The Medical-Surgical Nurse and Clinical Judgment

Medical-surgical nursing is the largest specialty in the profession and the floor where most new graduates begin. You will carry four, five, sometimes six adults at once, each with a different diagnosis, a different set of drips and drains, and a different way of falling apart. What separates a safe nurse from an unsafe one is not how many facts she has memorised — it is whether she notices the change in the patient at 0300 before the change becomes a code at 0500. That noticing has a name: clinical judgment. It can be taught, it can be practised, and since 2023 the licensure examination has been built around it. This chapter gives you the mental architecture for every chapter that follows: how the med-surg shift is structured, how nurses think, how to decide who to see first, how to recognise deterioration early, and how to delegate and escalate without dropping anything.

Section 1The Work: Who the Medical-Surgical Nurse Is

The specialty and its patients

Medical-surgical nursing is the care of adults with acute and chronic illness who are ill enough to need hospital-level monitoring but not ill enough for an intensive care bed. Historically it was called “the floor,” as though it were the place you worked before you found a real specialty. That framing is dead. Med-surg is now recognised as a distinct body of knowledge with its own certification, and its patients are sicker than the ICU patients of thirty years ago. Your assignment on any given day may include a seventy-eight-year-old admitted with community-acquired pneumonia who also has heart failure and type 2 diabetes, a post-operative day one bowel resection with a nasogastric tube and a patient-controlled analgesia pump, a forty-year-old in sickle cell crisis, and a patient waiting on a bed upstairs because his creatinine will not come down.

The defining feature of the work is simultaneity. Emergency nurses manage one crisis intensely and hand it off. Critical care nurses manage one or two patients with enormous depth. The med-surg nurse manages four to six people whose conditions are changing at different rates, in different directions, while the phone rings, the pharmacy calls, a family member wants an update and someone’s bed alarm is going off down the hall. Every skill in this book — assessment, pharmacology, pathophysiology — is only useful if it can be executed inside that reality.

Because you are with the patient continuously and the physician is not, you are the surveillance system. Research on hospital deaths repeatedly identifies failure to rescue — not failure to diagnose — as the mechanism of preventable mortality. The abnormality was documented; nobody acted on it. Most patients who arrest on a medical-surgical unit show deranged vital signs for six to eight hours beforehand. The clinical value of the med-surg nurse lies precisely in that window.

The nursing process is still the operating system

Everything the RN does is organised by the nursing process: assessment, diagnosis, planning, implementation, evaluation (ADPIE). It looks academic on paper and feels invisible at the bedside, but it is the legal and professional structure of practice. Assessment is the systematic collection of subjective and objective data. Nursing diagnosis is the RN’s independent clinical determination of the human response to that illness — not the medical diagnosis. Planning sets measurable, patient-centred, time-bound outcomes. Implementation carries out independent, dependent and collaborative interventions. Evaluation asks whether the outcome was met and, if not, restarts the loop.

Two points matter more than the acronym. First, the process is cyclical and continuous, not a form you fill out on admission. Second, the entire process belongs to the registered nurse and cannot be handed to anyone else. An LPN may collect data; the RN interprets it. A UAP may report that the patient looks tired; the RN decides what that means. When a test question asks what the nurse should delegate, the answer never includes assessment, teaching, evaluation, care planning or any unstable patient.

The shape of a shift

New nurses drown less from lack of knowledge than from lack of structure. A shift has a predictable architecture, and imposing it deliberately buys you the cognitive space to notice things. Receive handoff. Lay eyes on every patient within the first thirty to forty-five minutes — a fast safety check before a full assessment, because you cannot prioritise patients you have not seen. Then complete focused assessments, cluster your medication passes, chart in real time rather than at 1830, and re-evaluate anyone whose status changed or who received an as-needed medication.

Section 2How Nurses Think: The Clinical Judgment Model

From intuition to a model

Experienced nurses used to describe their best saves as a “gut feeling.” Patricia Benner’s work on novice-to-expert practice and Christine Tanner’s model of clinical judgment showed that the gut feeling is actually pattern recognition built from repeated exposure. Tanner described four movements: noticing (a perceptual grasp that something is off), interpreting (making sense of it), responding (acting or deliberately not acting) and reflecting (evaluating in the moment and afterwards). The value of naming these steps is that a student who has not yet accumulated ten thousand patients can borrow the structure while the pattern library is still being built.

The National Council of State Boards of Nursing operationalised this into the Clinical Judgment Measurement Model, whose third layer gives six cognitive steps that the Next Generation NCLEX measures directly. Learn these six as a bedside routine, not as trivia. They are simply the nursing process rewritten in the language of decision-making, with the analytic middle made explicit because that middle is where new graduates fail.

Recognise cues, then analyse them

Recognising cues means identifying which pieces of data are relevant, which are expected and which are irrelevant. A post-operative day one patient with a temperature of 38.0 °C (100.4 °F), incisional pain of 6 out of 10 and a hemoglobin of 10.9 g/dL has three abnormal-looking findings and possibly zero problems: low-grade fever in the first twenty-four to forty-eight hours is the inflammatory cytokine response to surgical tissue injury rather than infection (atelectasis is common after surgery and is prevented with incentive spirometry and early mobilisation, but it does not cause the fever), pain is expected, and mild post-operative anemia after blood loss is expected. The same patient on day four with a temperature of 38.6 °C, purulent drainage and a white blood cell count of 18,000/mm³ has cues that cluster into an actual problem. Relevance is always judged against the timeline, the diagnosis and the patient’s own baseline.

Analysing cues is the linking step: connecting the cluster to a pathophysiologic explanation. A patient with a heart rate of 118, a blood pressure that has drifted from 132/78 to 98/56, a respiratory rate of 24 and confusion is not four unrelated abnormalities. She has one story — inadequate perfusion — and your job is to ask which kind: hypovolemic from bleeding, distributive from sepsis, cardiogenic from pump failure. This is where the pathophysiology in every subsequent chapter earns its keep. If you understand that early sepsis vasodilates and that compensatory tachycardia precedes hypotension, you do not have to memorise a manifestation list.

Prioritise, act, evaluate

Prioritising hypotheses ranks the possible explanations by urgency and likelihood: what will kill this patient soonest, and what is most probable given the history. Pulmonary embolism and anxiety can both produce tachypnea in a post-operative patient; you rule out the lethal one first. Generating solutions identifies the interventions that address the prioritised hypothesis and, just as importantly, names the ones that are contraindicated. Taking action is the implementation, in the correct order, with attention to what you must do before the intervention (assess apical pulse before digoxin, check blood glucose before insulin, verify placement before a tube feed). Evaluating outcomes asks whether the patient responded and what the next move is if she did not.

Why the exam changed, and what that means for how you study

The Next Generation NCLEX arrived in April 2023 because entry-level nurses were passing a knowledge test and then making errors of judgment in their first year. The new item formats — case studies with six linked items, bow-tie items, trend items that show three sets of vital signs over time, matrix grids that ask you to classify each finding — exist to force you out of recognition memory and into reasoning. A partial-credit scoring model means a half-correct answer earns something, which rewards students who reason rather than guess.

Practically, this changes how you should read every remaining chapter of this book. Do not build flashcards that say “signs of hypokalemia.” Build the chain: potassium falls, the resting membrane potential becomes more negative, excitable tissue becomes harder to depolarise, therefore muscle weakness, decreased bowel motility, flattened T waves and U waves, and therefore a digoxin-toxicity risk because digoxin and potassium compete at the same pump. One mechanism replaces a list of nine symptoms and survives being asked in a format you have never seen.

Section 3Prioritization: What Do You Do First

The frameworks, in the order you apply them

Students lose more points on prioritization than on any other single skill, because prioritization questions look like knowledge questions and are not. All four options are usually correct nursing actions. The question is sequence. Apply the frameworks in a fixed order and the ambiguity mostly disappears.

Start with ABC: airway, breathing, circulation. An obstructed or threatened airway outranks everything, because a patient without an airway has minutes. Breathing problems outrank circulation problems, and circulation outranks everything below. The single deliberate exception is the pulseless, unresponsive patient, where basic life support uses C-A-B — compressions first, because the oxygen already in the blood is useless if nothing is circulating it. In trauma with visible exsanguinating hemorrhage, control of that bleeding also precedes airway management, because the patient is losing the fluid that carries the oxygen.

Once ABC is satisfied, move to Maslow: physiological needs (oxygen, fluid, nutrition, elimination, sleep, pain relief) before safety needs (fall prevention, infection control, correct identification) before love and belonging, esteem and self-actualization. Then apply the discriminators: acute over chronic, unstable over stable, actual over potential, and unexpected over expected. Finally, when two patients are equally unstable, use survival potential — the logic of triage — and treat the one whom intervention is most likely to save.

Choosing among four patients

The classic examination stem gives you a fresh assignment and asks whom you assess first. Read every option for the cue that signals an airway, breathing or perfusion threat, or a change from baseline. Change is the key word. “A patient with chronic obstructive pulmonary disease with an oxygen saturation of 89 percent” may be that patient’s normal, because chronic carbon dioxide retainers are often targeted to 88–92 percent. “A patient with COPD whose saturation has fallen from 91 to 84 percent and who is now using accessory muscles” is an emergency. The number alone is rarely the answer; the trajectory is.

Be equally alert to distractors dressed as urgency. Severe pain is distressing and must be treated, but pain is not an ABC problem unless it signals one — crushing substernal chest pain, sudden severe abdominal pain with rigidity, or calf pain with unilateral swelling all point to circulation. A patient who is anxious about discharge, a family member demanding to speak with you, and an overdue dressing change are real work but they are not first.

Time management and the interruption problem

Nurses on medical-surgical units are interrupted roughly every six to twelve minutes, and interruption during medication preparation measurably increases error rates. Defend the tasks that must be uninterrupted: medication preparation, high-alert double checks, blood product verification and any calculation. Use whatever your unit provides — a no-interruption zone, a sash, a designated space — and do not compute doses in a hallway.

Cluster care so the patient is disturbed less and you walk less: bring the medications, the assessment, the linens and the teaching into one entry. Batch documentation immediately after each room rather than at the end of the shift, when recall degrades and the chart becomes fiction. And protect the first hour: if you allow yourself to be pulled into a non-urgent task before you have seen everyone, you are working blind for the rest of the shift.

Section 4Assessment, Trends and Recognising Deterioration

The baseline belongs to you

Your admission and beginning-of-shift assessment creates the reference point against which every later finding is judged. If you do not know that this patient’s baseline mentation is alert and oriented to person, place, time and situation, you cannot recognise that being oriented only to person at 1400 is an emergency. If you did not palpate and mark the pedal pulses on admission, you cannot tell whether the absent pulse after the arteriogram is new. Document the baseline in specific, comparable terms: not “neuro intact,” but “alert, oriented ×4, moves all four extremities to command, grips equal, pupils 3 mm equal and reactive.”

A focused assessment targets the systems relevant to the diagnosis and the complaint and is repeated far more often than the head-to-toe. Heart failure: weight, lung sounds, jugular venous distension, edema, oxygen saturation, urine output. Post-abdominal surgery: bowel sounds, abdominal distension, incision, drain output, pain, ability to void. Neurologic admission: level of consciousness, pupils, motor symmetry, speech. Learn the four or five things that matter for each condition and check them every time.

Vital-sign trends and early warning

Single vital signs are weak evidence; trends are strong evidence. Respiratory rate is the most sensitive and the most frequently falsified vital sign in hospital charts. Count it for a full thirty to sixty seconds. A respiratory rate rising from 16 to 22 to 28 across three sets is one of the earliest signals of sepsis, pulmonary embolism, metabolic acidosis and impending respiratory failure — and it is often documented as “18” three times in a row.

Many hospitals use an aggregated early warning score, such as NEWS2, that assigns points for respiratory rate, oxygen saturation, supplemental oxygen use, temperature, systolic blood pressure, heart rate and level of consciousness. The clinical function is not the number but the requirement to escalate when the number rises. If your unit does not use one, use the standard rapid-response triggers in the table below, plus the criterion that exists in every published set and is the one nurses under-use: the nurse is worried.

Laboratory values you must know cold

You will not calculate these; you will recognise them in a stem and decide whether to hold a drug, call someone or act. Memorise the ranges below and, more importantly, memorise the action attached to the critical value. A potassium of 6.8 mEq/L is not a number to chart — it is a reason to obtain an electrocardiogram, hold every potassium source (potassium-containing fluids, oral supplements, potassium-sparing diuretics such as spironolactone, and ACE inhibitors), and call the provider now. Expect the treatment to run in a fixed order: intravenous calcium gluconate first to stabilise the myocardium, then insulin with dextrose or a nebulised beta agonist to drive potassium into the cell, then a binder or dialysis to actually remove it — only that last step lowers total body potassium.

Red flags and the SBAR call

When you escalate, the quality of your communication determines the speed of the response. SBAR gives you a script: Situation — who you are, who the patient is, what is happening right now. Background — diagnosis, day of admission or post-operative day, relevant history, current therapy. Assessment — your vital signs, your findings and what you think is going on. Recommendation — what you want, specifically. New nurses omit the R because it feels presumptuous. Do not omit it. “I would like you to come and see her now” or “I am requesting a stat chest x-ray and an arterial blood gas” is the sentence that produces action.

A complete call sounds like this: “This is Marisol Reyes, RN, on 4 West. I am calling about Mr. Lin in 412. Situation: his respiratory rate has risen from 18 to 30 over three hours and his oxygen saturation is 88 percent on 4 litres by nasal cannula. Background: he is post-operative day two from a right hemicolectomy, has a history of atrial fibrillation, and his enoxaparin was held yesterday for a procedure. Assessment: he is tachycardic at 122, blood pressure 96/58, lungs clear, right calf is swollen and tender, and he is anxious. I am concerned about a pulmonary embolism. Recommendation: I am requesting that you come now and that we obtain a stat CT pulmonary angiogram and blood gas. I have increased his oxygen and raised the head of the bed.”

The older adult does not follow the textbook

More than half of your medical-surgical patients will be over sixty-five, and physiologic reserve declines invisibly until it is stressed. Baseline temperature is lower, so a “normal” 37.2 °C may represent a fever; infection in an older adult often presents with no fever, no leukocytosis and no cough — only delirium, falls, anorexia or urinary incontinence. Up to a third of older adults having a myocardial infarction have no chest pain at all, presenting instead with dyspnea, fatigue, syncope, epigastric discomfort or confusion; this is likewise common in women and in people with long-standing diabetes and autonomic neuropathy.

Delirium is the single most important thing to recognise. It is acute, fluctuating and caused by something physiologic; dementia is chronic and progressive. The most common form is hypoactive delirium — the quiet, withdrawn patient — and it is the most frequently missed and carries the worst prognosis. Screen with a validated tool such as the Confusion Assessment Method, then hunt the cause: hypoxia, infection, pain, dehydration, electrolyte derangement, urinary retention, constipation, sleep deprivation and medications, particularly anticholinergics, benzodiazepines and diphenhydramine, all of which the Beers criteria flag as potentially inappropriate in older adults. Reorient, mobilise, restore hearing aids and glasses, normalise the day-night cycle, and treat the cause. Restraints and sedatives make delirium worse.

Section 5Safety, Delegation and the Handoff

Delegation: the five rights and the hard boundaries

You cannot carry six patients alone, and you are legally accountable for the outcome of everything you delegate. The five rights of delegation are the right task, the right circumstance, the right person, the right direction and communication, and the right supervision and evaluation. In practice this means the task must be within the delegatee’s scope and competence, the patient must be stable and the outcome predictable, the instruction must be specific with a reporting parameter attached, and you must follow up.

The hard boundary never moves: the RN cannot delegate the nursing process. Assessment, nursing diagnosis, evaluation of care, initial patient teaching, care planning, and the care of any unstable or unpredictable patient stay with the registered nurse. If an option in a question involves an LPN or a UAP assessing, teaching or evaluating anything, it is wrong. Also wrong: delegating any task on a patient whose condition is changing, no matter how routine the task looks.

Medication safety and high-alert drugs

Medication administration is the highest-volume risk activity of the med-surg shift. Use the rights of medication administration every time: right patient (two identifiers, never the room number), right drug, right dose, right route, right time, right documentation, right reason and right response. The last two are the ones students skip and the ones the examination loves — giving a beta blocker without knowing the heart rate, or documenting a dose of hydralazine without rechecking the blood pressure, is a defect even if the correct pill reached the correct mouth.

The Institute for Safe Medication Practices maintains a high-alert list: insulins, opioids, anticoagulants including heparin and warfarin, concentrated electrolytes such as potassium chloride and hypertonic saline, neuromuscular blockers, chemotherapeutic agents and sedatives. These require an independent double check and are involved in a disproportionate share of fatal errors. Two absolutes worth tattooing on your forearm: concentrated potassium chloride is never given by IV push, and neuromuscular blocking agents are never given to a patient who is not being ventilated. Know your key assessments before administration — apical pulse for one full minute before digoxin and hold if under 60, blood pressure before antihypertensives, blood glucose before insulin, respiratory rate and sedation level before opioids, and an aPTT or anti-Xa before heparin dose changes.

Handoff, documentation and getting the patient home

Most sentinel events trace back to a communication failure, and handoff is where communication most often fails. Use a structured format — SBAR or I-PASS — conduct it at the bedside when possible so the patient can correct you, allow questions, and include what is pending and what to watch for. “Everything is fine” is not a handoff. Read back and verify all telephone orders and critical laboratory values, and never accept an abbreviation from the do-not-use list.

Documentation is contemporaneous, factual, objective and complete. Chart what you assessed, what you did, and how the patient responded — the response is the part most often missing. Chart late entries as late entries. Never chart in advance, never chart for someone else, and never delete: correct with a single line, your initials and the date. Report errors and near-misses through the incident reporting system; the occurrence report is a quality document and is not referenced in the medical record.

Discharge teaching starts on admission, not at 1500 on the day of discharge. Prioritise ruthlessly: the medication changes, the red-flag symptoms that mean return to the emergency department, the follow-up appointment, activity and diet restrictions, and any device or wound care. Use plain language at a fifth- to sixth-grade level, teach one concept at a time, involve the caregiver, and close the loop with teach-back — “tell me how you will take this at home” — because a nod is not comprehension. Confirm the patient can afford and obtain the medications and can physically perform what you are asking, and use a professional interpreter, never a family member, when a language barrier exists.

Words worth knowing

Fluid, Electrolyte and Acid-Base Balance

Almost every patient on a medical-surgical floor is there because water, salt or acid has moved somewhere it should not be. The vomiting patient, the heart-failure patient, the patient three days post-op who has not eaten, the patient on furosemide and lisinopril, the patient with a nasogastric tube to suction — each of them is a fluid and electrolyte problem wearing a different diagnosis. This chapter teaches you to read the body’s water and its chemistry the way an experienced nurse does: mechanism first, so the manifestations are predictable rather than memorised; then the assessment findings, the labs with real reference ranges, the treatment and the complications. You will learn a ninety-second method for arterial blood gases that works every time, the electrolyte thresholds that mean stop and call, and the administration rules — particularly for potassium — that separate a safe nurse from a headline. Nothing here is abstract. All of it turns up on the NCLEX and in your first month on the floor.

Section 1Fluid Compartments, Fluid Movement and Volume Imbalance

Where the water lives and what makes it move

Water is roughly 60 percent of a healthy adult male and about 50 to 55 percent of a healthy adult female, because adipose tissue holds far less water than muscle. Two thirds of that water sits inside cells as intracellular fluid. The remaining third is extracellular fluid, and it is divided again: about three quarters of it bathes the cells as interstitial fluid, and only about one quarter of it is plasma inside blood vessels. Hold on to that last number. The intravascular compartment — the one that carries the blood pressure, the one that perfuses the brain and the kidneys — is a small fraction of total body water. Losing a few litres from it is a catastrophe; losing the same volume slowly from the intracellular space produces thirst and a dry mouth.

Water crosses membranes by osmosis, moving from the side with fewer dissolved particles toward the side with more. The concentration of those particles is osmolality, normally 275 to 295 mOsm/kg in serum, and it is governed almost entirely by sodium, glucose and urea. You can estimate it as twice the serum sodium plus the glucose divided by 18 plus the BUN divided by 2.8. Because sodium dominates that equation, sodium is effectively the body’s water thermostat. Where sodium goes, water follows. This single sentence will get you through most of the sodium content in this chapter.

Inside the capillary bed, two other forces argue with each other. Hydrostatic pressure is the push of blood against the vessel wall, driving fluid out into the interstitium. Oncotic pressure, generated mostly by albumin (normal 3.5 to 5.0 g/dL), is the pull that keeps fluid in. Raise hydrostatic pressure — heart failure, venous obstruction, over-aggressive infusion — and fluid leaks out and becomes edema. Drop the albumin — cirrhosis, nephrotic syndrome, malnutrition, burns — and fluid leaks out for the opposite reason. Both look like swelling at the bedside, but the fix is different, and knowing which force is broken tells you whether the patient needs a diuretic or protein and a different plan entirely.

Regulation is hormonal and quick. Osmoreceptors in the hypothalamus sense a rising osmolality and release antidiuretic hormone, which tells the kidney to reabsorb water and concentrate the urine. Baroreceptors sensing a falling volume activate the renin-angiotensin-aldosterone system; aldosterone reabsorbs sodium (and therefore water) and excretes potassium. Stretched atria release natriuretic peptides that do the reverse. Every one of these systems is blunted in the older adult, which is why an eighty-eight-year-old with two days of diarrhoea arrives in acute kidney injury while a twenty-eight-year-old with the same illness simply feels awful.

Fluid volume deficit

Fluid volume deficit, or hypovolemia, is the isotonic loss of water and electrolytes together: haemorrhage, vomiting, diarrhoea, nasogastric suction, wound and burn exudate, excessive diuresis, fever with insensible loss, and simple failure to drink. This is not the same as dehydration in the strict sense, which is loss of water alone and raises the serum sodium. In practice the two overlap, and the nursing assessment is the same at the start.

The findings follow the physiology. With less volume in the vessels, the heart compensates first: tachycardia is the earliest reliable sign, often before the blood pressure moves at all. Then comes orthostatic hypotension — a drop of 20 mmHg systolic or 10 mmHg diastolic, or a rise in pulse of 20 beats, when the patient sits or stands. Neck veins flatten. Capillary refill lengthens beyond three seconds. Mucous membranes go dry and the tongue develops longitudinal furrows. Skin turgor tents, though in an older adult you must test it over the sternum or forehead rather than the back of the hand, where lost elastin makes it meaningless. Urine output falls below 0.5 mL/kg/hr (about 30 mL/hr in an average adult) and the urine becomes dark and concentrated, with a specific gravity above 1.030 (normal 1.005 to 1.030). Weight falls. Late findings are hypotension, weak thready pulse, cool mottled extremities and altered mental status — by which point you are in hypovolemic shock.

Laboratory work confirms haemoconcentration. Haematocrit rises above the normal 42 to 52 percent in men and 37 to 47 percent in women. BUN rises out of proportion to creatinine, so a BUN-to-creatinine ratio above 20 to 1 (normal 10 to 20 to 1, with BUN 10 to 20 mg/dL and creatinine 0.6 to 1.2 mg/dL) points to a prerenal, volume-responsive cause. Serum osmolality and sodium rise if the loss was mostly water. Urine sodium falls below 20 mEq/L as the kidney clings to salt.

Management is replacement, and the first-line fluid for an isotonic loss is an isotonic crystalloid: 0.9% sodium chloride or lactated Ringer’s. Nursing care is deceptively simple and relentlessly important — strict intake and output, daily weight on the same scale at the same time in the same clothing, vital signs with orthostatics, safety precautions because these patients faint, oral fluids when they can take them, and reassessment of lung sounds every time you increase a rate, because the same patient you are filling can be flooded.

Fluid volume excess and third spacing

Fluid volume excess is isotonic retention of water and sodium, and its causes cluster around three organs: the failing heart, the failing kidney and the failing liver. Add iatrogenic causes — over-resuscitation, excessive normal saline, corticosteroids, hypertonic solutions given too fast — and you have the majority of cases you will see. The signs are the mirror image of deficit: weight gain, bounding pulse, elevated blood pressure, distended neck veins at 45 degrees, an S3 gallop, dependent pitting edema (sacral in the bedbound, pedal in the ambulatory), periorbital puffiness, and the finding that matters most, crackles in the lung bases with dyspnoea and a falling oxygen saturation. Laboratory values show haemodilution: a low haematocrit, a low BUN, a dilute urine with a specific gravity below 1.010.

Third spacing is the awkward middle case, and students routinely miss it. Fluid shifts out of the vascular space into a compartment where it does no useful work — the peritoneum in ascites, the interstitium in burns and sepsis, the bowel wall in obstruction, the retroperitoneum in acute pancreatitis. The patient therefore looks fluid-overloaded (swollen, heavy, weight up) while being functionally hypovolemic (tachycardic, hypotensive, oliguric). Treat the intravascular deficit even though the patient appears wet. In the days that follow, the fluid reabsorbs, and the same patient can flip into overload without a single millilitre being added — which is why they need diuretics later, not sooner.

Management of true excess is sodium and fluid restriction, loop diuretics such as furosemide, positioning with the head of the bed elevated, oxygen, and vigilant monitoring of potassium because loop diuretics waste it. Nursing priorities are respiratory: assess breath sounds and saturation before anything else, then daily weights, then intake and output, then skin care over edematous tissue, which breaks down quickly and heals slowly.

Reading volume status at the bedside

Assemble the picture from several sources rather than trusting any one. Weight trend is first. Intake and output over 24 and 72 hours is second, and you should look at the balance, not the individual numbers. Vital signs including orthostatics are third. Then the focused physical: neck veins, lung bases, dependent edema graded 1 to 4 plus, mucous membranes, capillary refill, skin turgor at a reliable site. Then the labs: sodium, BUN, creatinine, haematocrit, albumin, urine specific gravity. In the critical care setting central venous pressure and dynamic measures such as pulse pressure variation refine the estimate, but on a medical-surgical floor the scale and the stethoscope will carry you.

One caution about mental status. Confusion is not a soft finding in fluid imbalance — it is often the first hard one, especially in the older adult and especially with sodium disorders. A patient who was oriented at 0800 and is picking at the sheets at 1600 has a physiologic cause until proven otherwise, and dehydration, hyponatremia and hypercalcemia are all on that list. Do not chart it as sundowning and move on.

Section 2Sodium and Potassium

Sodium: a water problem in disguise

Serum sodium is normally 135 to 145 mEq/L. Ninety percent of the time an abnormal sodium is not a sodium problem at all — it is a water problem. Hyponatremia usually means too much water relative to salt; hypernatremia usually means too little water relative to salt. If you fix that idea in place now, the management logic follows without memorisation: dilute sodium is treated by removing water, concentrated sodium is treated by adding water.

Because sodium sets the osmolality of the extracellular fluid, sodium disorders are brain disorders. When serum sodium falls, extracellular fluid becomes hypotonic relative to brain cells, water moves into neurons and the brain swells inside a rigid skull. When sodium rises, water is pulled out of neurons and the brain shrinks, tearing bridging veins in severe cases. Every major manifestation of a sodium disorder — headache, confusion, lethargy, seizure, coma — is a consequence of the size of the brain cell.

Hyponatremia

Hyponatremia is sodium below 135 mEq/L. The common causes on a medical-surgical floor are the syndrome of inappropriate antidiuretic hormone (SIADH, seen with small-cell lung cancer, head injury, pneumonia, and drugs such as SSRIs and carbamazepine), heart failure and cirrhosis (where total body water is high but effective circulating volume is low), excessive hypotonic intravenous fluid, adrenal insufficiency, and gastrointestinal losses replaced with plain water. Thiazide diuretics deserve special mention. They are not a cause of SIADH; they act at the distal tubule and impair the kidney’s ability to dilute urine while causing mild volume depletion, and by that separate mechanism they produce hyponatremia far more often than loop diuretics do.

Symptoms track both the level and the speed of the fall. Above 130 mEq/L most patients are asymptomatic. Between 125 and 130 you see headache, nausea, malaise and muscle cramps. Below 125 you see confusion, lethargy and diminished deep tendon reflexes. Below 120, or with any rapid drop, expect seizures, respiratory arrest and coma. Chronic hyponatremia is far better tolerated than acute, because the brain exports osmoles over days to protect itself — and that adaptation is exactly why correcting it too fast is dangerous.

Management depends on volume status and on symptoms. In hypervolemic hyponatremia (heart failure, cirrhosis — edematous, weight up) and in euvolemic hyponatremia (SIADH, where the patient looks neither dry nor overloaded) the treatment is fluid restriction, commonly 800 to 1000 mL per day, with a loop diuretic in the hypervolemic patient or a vasopressin antagonist such as tolvaptan. In hypovolemic hyponatremia the treatment is isotonic 0.9% sodium chloride. For severe symptomatic hyponatremia — seizing, obtunded — the treatment is small-volume 3% hypertonic saline, given through a pump, ideally through a central line, with the patient on continuous monitoring and serum sodium drawn every two to four hours.

The rule that keeps your patient out of a wheelchair: do not raise the serum sodium faster than about 8 to 10 mEq/L in any 24-hour period (many institutions cap it at 8, and lower still in high-risk patients such as those with alcohol use disorder, malnutrition or hypokalemia). Correcting faster causes osmotic demyelination syndrome — formerly central pontine myelinolysis — a delayed, largely irreversible injury producing dysarthria, dysphagia, quadriparesis and locked-in syndrome. Seizure precautions, neurologic checks and hourly documentation of the infusion rate are nursing responsibilities, not the pharmacy’s.

Hypernatremia

Hypernatremia is sodium above 145 mEq/L, and it almost always means a water deficit in a patient who cannot obtain water: the tube-fed patient without free-water flushes, the intubated patient, the patient with dementia, the patient with diabetes insipidus passing litres of dilute urine with a specific gravity below 1.005, the patient on osmotic diuresis from hyperglycaemia, and the patient who received hypertonic saline or excessive sodium bicarbonate.

Manifestations are thirst (if the patient can perceive and express it), dry sticky mucous membranes, a swollen dry tongue, restlessness progressing to agitation, twitching, hyperreflexia, seizures and coma. Note that hypernatremic patients are often agitated rather than lethargic, which fools people into calling for a sedative when they need water. Serum osmolality is high, above 295 mOsm/kg.

Treatment is water, given orally or enterally when possible and as a hypotonic intravenous solution such as 0.45% sodium chloride or D5W when not. The same caution applies in reverse: lower the sodium no faster than about 0.5 mEq/L per hour, or 10 to 12 mEq/L in 24 hours, because a brain that has adapted to a hypertonic environment will swell if you rehydrate it abruptly. Cerebral edema and seizures during correction of hypernatremia are the mirror image of osmotic demyelination. Nursing care includes oral hygiene every two hours, free-water flushes with tube feeds, and offering fluids on a schedule to patients who no longer feel thirst.

Potassium: the rhythm electrolyte

Serum potassium is normally 3.5 to 5.0 mEq/L, and that narrow window contains only about two percent of the body’s potassium — the rest is intracellular. A small movement across the membrane therefore produces a large change in the serum number and a large change in the resting membrane potential of cardiac muscle. Potassium is the electrolyte that kills quickly, in both directions, and it is the one you will be asked about most.

Hypokalemia (below 3.5 mEq/L) comes from loop and thiazide diuretics, vomiting, nasogastric suction, diarrhoea, laxative abuse, corticosteroids, hyperaldosteronism, poor intake, insulin therapy and alkalosis (which drives potassium into cells). The findings are of a hyperpolarised, sluggish neuromuscular system — a low extracellular potassium makes the resting membrane potential more negative, so the cell sits further from threshold and is harder to excite: fatigue, generalised weakness that starts in the legs, leg cramps, diminished deep tendon reflexes, decreased bowel sounds and paralytic ileus, shallow respirations from weak respiratory muscles, orthostatic hypotension, and on the monitor a flattened or inverted T wave, ST depression and a prominent U wave. Two clinical dangers deserve emphasis: severe hypokalemia can produce respiratory muscle failure, and hypokalemia dramatically potentiates digoxin toxicity even at therapeutic digoxin levels (0.5 to 2.0 ng/mL). Treatment is oral potassium when the patient can swallow and the deficit is mild, and diluted intravenous potassium when it is not. Always check the magnesium: hypokalemia that will not correct is hypomagnesemia until proven otherwise.

Hyperkalemia (above 5.0 mEq/L) comes from kidney injury and chronic kidney disease above all, then from potassium-sparing diuretics such as spironolactone, ACE inhibitors and angiotensin receptor blockers, tissue destruction (crush injury, burns, rhabdomyolysis, tumour lysis, massive haemolysis), acidosis, and iatrogenic over-replacement. A haemolysed specimen is a common false positive — if the value does not fit the patient, redraw before you treat, but do not delay treatment in a patient who looks sick or has ECG changes. Findings are muscle weakness progressing to flaccid paralysis, paraesthesias, hyperactive bowel sounds with diarrhoea and abdominal cramping, and the sequence on the monitor that you must know cold: tall peaked T waves, then a prolonged PR interval with flattened or absent P waves, then a widened QRS, then a sine wave, then ventricular fibrillation or asystole.

Treatment of hyperkalemia is layered, and the order tells you the priority. First, stabilise the myocardium with intravenous calcium gluconate (commonly 10 mL of a 10% solution over 2 to 3 minutes with continuous cardiac monitoring). This does not lower the potassium at all — it raises the threshold potential and buys you thirty to sixty minutes. Second, shift potassium into cells with regular insulin 10 units IV accompanied by 25 g of dextrose (onset 15 to 30 minutes, lasting 4 to 6 hours — check blood glucose hourly), high-dose nebulised albuterol, and sodium bicarbonate if the patient is acidotic. Third, remove potassium from the body with a loop diuretic if the kidneys work, with a gastrointestinal binder such as sodium polystyrene sulfonate, patiromer or sodium zirconium cyclosilicate, or definitively with haemodialysis. Stop all potassium sources — the IV fluid, the salt substitute, the supplement, the lactated Ringer’s.

Section 3Calcium, Magnesium and Phosphorus

Calcium and neuromuscular excitability

Total serum calcium is normally 8.5 to 10.5 mg/dL, and ionised (free, physiologically active) calcium is 4.5 to 5.6 mg/dL. Roughly half of circulating calcium is bound to albumin, so a hypoalbuminaemic patient will show a low total calcium while the ionised fraction is perfectly normal. Correct it before you panic: add 0.8 mg/dL to the total calcium for every 1 g/dL that albumin sits below 4.0 g/dL. In critically ill patients, order the ionised calcium and skip the arithmetic. Calcium is regulated by parathyroid hormone (which raises it by pulling from bone, reabsorbing it in the kidney and activating vitamin D), by calcitonin (which lowers it), and by vitamin D (which absorbs it from the gut).

Calcium stabilises the neuronal membrane. Less calcium therefore means a twitchier membrane and more calcium means a sleepier one, which is the entire clinical picture in one sentence. Hypocalcemia (below 8.5 mg/dL) causes circumoral and digital numbness and tingling, muscle cramps, hyperactive reflexes, tetany, laryngospasm and stridor, bronchospasm, seizures and a prolonged QT interval that can degenerate into torsades de pointes. Two classic bedside signs: Chvostek sign is a facial twitch when you tap over the facial nerve just anterior to the ear, and Trousseau sign is carpopedal spasm when a blood pressure cuff is inflated 20 mmHg above systolic for three minutes. Trousseau is the more specific of the two.

Causes of hypocalcemia are surgical (thyroidectomy or parathyroidectomy with inadvertent parathyroid injury — watch the first 24 to 48 hours), chronic kidney disease, vitamin D deficiency, acute pancreatitis, massive transfusion with citrated blood, and alkalosis, which increases albumin binding and drops the ionised fraction even when the total is unchanged. That is why a hyperventilating patient gets tingly fingers. Treatment is oral calcium with vitamin D for chronic cases and intravenous calcium gluconate given slowly with continuous cardiac monitoring for acute symptomatic cases. After thyroid surgery keep calcium gluconate and a tracheostomy tray at the bedside and assess the voice and the airway every time you enter the room.

Hypercalcemia (above 10.5 mg/dL) is most often caused by malignancy — bone metastases and paraneoplastic parathyroid hormone-related peptide — or by primary hyperparathyroidism; add thiazides, prolonged immobility, and excessive supplements. Remember it as stones, bones, groans, moans and thrones: renal calculi, bone pain and pathologic fracture, abdominal pain and constipation, lethargy and psychiatric changes, and polyuria from a nephrogenic diabetes insipidus effect. The ECG shows a shortened QT interval. Treatment begins with aggressive isotonic 0.9% sodium chloride to restore volume and promote urinary excretion, then calcitonin for a rapid but short-lived drop, then a bisphosphonate such as zoledronic acid, which works well but takes 48 to 72 hours. Stop thiazides, stop calcium and vitamin D supplements, mobilise the patient, and use dialysis for refractory or renal-failure cases.

Magnesium: the electrolyte nobody checks until it is too late

Serum magnesium is normally 1.5 to 2.5 mEq/L (about 1.8 to 3.0 mg/dL depending on your laboratory’s units — always read the units on the report). Magnesium is a cofactor for hundreds of enzymes and a regulator of both potassium and calcium handling. Its manifestations parallel calcium almost exactly: low magnesium makes membranes irritable, high magnesium makes them sluggish.

Hypomagnesemia (below 1.5 mEq/L) is common in alcohol use disorder, malnutrition and refeeding, prolonged diarrhoea or nasogastric suction, diuretic therapy, proton pump inhibitors and some chemotherapy agents. Findings are tremor, hyperactive reflexes, positive Chvostek and Trousseau signs, muscle cramps, confusion, and dysrhythmias — notably a prolonged QT and torsades de pointes. The critical nursing insight is that hypomagnesemia causes refractory hypokalemia and refractory hypocalcemia. If you have replaced potassium three times and it will not budge, the magnesium is low. Replace magnesium first and the potassium follows.

Hypermagnesemia (above 2.5 mEq/L) is nearly always iatrogenic or renal: magnesium-containing antacids and laxatives in a patient with chronic kidney disease, or magnesium sulfate infusion in obstetric care. The progression is orderly and therefore easy to monitor. First the deep tendon reflexes disappear — check the patellar reflex before and during any magnesium infusion. Then come flushing, warmth, hypotension, bradycardia, lethargy, and finally respiratory depression and cardiac arrest. Any patient on a magnesium infusion needs hourly reflexes, a respiratory rate of at least 12, a urine output of at least 30 mL/hr, and calcium gluconate at the bedside as the antidote. Stop the infusion and call if reflexes are lost.

Phosphorus and the calcium seesaw

Serum phosphorus is normally 2.5 to 4.5 mg/dL, and it moves inversely with calcium: when one rises the other falls. Phosphorus is essential for ATP, for 2,3-DPG in red cells and for the phospholipid membrane, so its deficiency shows up as weakness in every energy-hungry tissue.

Hypophosphatemia (below 2.5 mg/dL) appears in refeeding syndrome, alcohol use disorder, diabetic ketoacidosis treatment, respiratory alkalosis, and with prolonged use of phosphate-binding antacids. Manifestations are muscle weakness including diaphragmatic weakness that can prevent ventilator weaning, bone pain, confusion, and in severe cases haemolysis and cardiomyopathy. Refeeding syndrome is the version you will meet on a medical-surgical floor: a chronically malnourished patient is fed, insulin surges, and phosphorus, potassium and magnesium all plunge into cells within 24 to 72 hours. Advance nutrition slowly and check electrolytes daily.

Hyperphosphatemia (above 4.5 mg/dL) is essentially a marker of chronic kidney disease. Its own symptoms are minimal; the trouble comes from the reciprocal hypocalcemia it produces (tetany) and from calcium-phosphate deposition in soft tissue, vessels and joints. Treatment is dietary phosphorus restriction — dairy, cola, processed meats, nuts — and phosphate binders given with meals, not between them. Calcium acetate, sevelamer and lanthanum all work by binding dietary phosphorus in the gut, so a binder taken an hour after eating has nothing to bind. That timing point is a favourite examination item and a genuine reason for treatment failure.

Section 4Acid-Base Balance and Arterial Blood Gas Interpretation

The buffer, the lung and the kidney

Arterial pH is held between 7.35 and 7.45, a range so narrow that a pH of 7.20 or 7.60 is a medical emergency. Three systems defend it. Chemical buffers — bicarbonate, phosphate, protein and haemoglobin — act in seconds but have limited capacity. The lungs act in minutes by changing the rate and depth of ventilation, blowing off carbon dioxide (an acid) or retaining it. The kidneys act over hours to days by excreting hydrogen ions and reclaiming or generating bicarbonate; they are slow but nearly limitless.

The four numbers you need from an arterial blood gas are pH 7.35 to 7.45, PaCO2 35 to 45 mmHg (the respiratory value, an acid), HCO3 22 to 26 mEq/L (the metabolic value, a base) and PaO2 80 to 100 mmHg with an SaO2 of 95 to 100 percent (oxygenation, which is a separate question from acid-base). Base excess, normally negative 2 to positive 2, is a supporting metabolic number. Draw the specimen from an artery, apply firm pressure for at least five minutes afterward (twenty minutes if the patient is anticoagulated), and get it to the laboratory without air bubbles for analysis within about fifteen minutes. Ice the specimen only if that window cannot be met, because delay and air both falsify the result, and routinely icing a plastic syringe falsely raises the PaO2.

A method you can do in ninety seconds

Use ROME: Respiratory Opposite, Metabolic Equal. In a respiratory disorder, the pH and the PaCO2 move in opposite directions. In a metabolic disorder, the pH and the HCO3 move in the same direction. That is the whole rule.

Run it as three steps. Step one: look at the pH. Below 7.35 is acidosis, above 7.45 is alkalosis, and inside the range is either normal or fully compensated. Step two: look at the PaCO2 and the HCO3, and decide which one is abnormal in the direction that would explain the pH. If the PaCO2 explains it, the disorder is respiratory; if the HCO3 explains it, the disorder is metabolic. Step three: look at the other value to judge compensation — if it has not moved, the disorder is uncompensated; if it has moved in the compensating direction but the pH is still abnormal, it is partially compensated; if the pH has returned to normal while both values remain abnormal, it is fully compensated.

The tic-tac-toe method is the same logic drawn on paper, and it is faster once you have practised it. Draw a grid with three columns labelled ACID, NORMAL and BASE. Down the left side write pH, then CO2, then HCO3. Place each value in the column its own number belongs to: for pH, acid is below 7.35 and base is above 7.45; for CO2, acid is above 45 and base is below 35 (because carbon dioxide is an acid, high is acidic); for HCO3, acid is below 22 and base is above 26 (because bicarbonate is a base, low is acidic). Now look at what lines up. Whichever value shares a column with the pH is the primary disorder. If the third value is in the opposite column, it is compensating. If the third value is in the normal column, there is no compensation yet.

Work an example. A 34-year-old with diabetic ketoacidosis: pH 7.21, PaCO2 26 mmHg, HCO3 10 mEq/L. Step one, pH 7.21 is acidosis. Step two, the PaCO2 of 26 is low, which would be alkalotic, so it cannot be the cause; the HCO3 of 10 is low, which is acidic, and it matches — so this is a metabolic acidosis. Step three, the PaCO2 has dropped well below normal in the opposite direction, which is the lung trying to blow off acid, but the pH is still 7.21, so this is partially compensated metabolic acidosis. The deep rapid breathing you observe at the bedside has a name: Kussmaul respirations. Do not sedate it and do not give this patient an opioid — that respiratory drive is keeping him alive.

Work a second. A 71-year-old with COPD found drowsy: pH 7.30, PaCO2 62 mmHg, HCO3 30 mEq/L. pH is acidotic. The PaCO2 of 62 is high, and high carbon dioxide is acid, so it matches: respiratory acidosis. The HCO3 of 30 is elevated in the compensating alkaline direction, but the pH is still low, so it is partially compensated respiratory acidosis. Now a third, the same patient two days later: pH 7.37, PaCO2 60 mmHg, HCO3 34 mEq/L. The pH is normal but both other values are abnormal, so this is fully compensated respiratory acidosis — and because the pH is on the acidic half of normal (below 7.40), the respiratory value is the primary problem. That last trick — using which half of the normal range the pH sits in — identifies the primary disorder in every fully compensated gas.

The four disorders as you will meet them

Respiratory acidosis is a ventilation failure: retained carbon dioxide from COPD exacerbation, opioid or sedative overdose, neuromuscular disease, chest wall trauma, atelectasis, obesity hypoventilation or an obstructed airway. The patient is dyspnoeic, drowsy, headachy, flushed and eventually somnolent, with a rising PaCO2 and a falling pH. Priority is airway and ventilation: position upright, improve gas exchange, reverse the opioid with naloxone if that is the cause, and support ventilation non-invasively or invasively. Bicarbonate is not the answer — the lung is.

Respiratory alkalosis is over-ventilation: anxiety and panic, pain, fever, early sepsis, pulmonary embolism, high altitude, salicylate toxicity, or a ventilator set too aggressively. The patient reports light-headedness, circumoral and digital tingling, and carpopedal spasm from the fall in ionised calcium. Never assume anxiety. A patient hyperventilating for the first time after hip surgery is having a pulmonary embolism until you rule it out. Treat the cause, coach slow breathing, and reduce the ventilator rate or tidal volume where relevant.

Metabolic acidosis is either acid gained or bicarbonate lost. Acid gained shows a high anion gap: diabetic ketoacidosis, lactic acidosis from shock or sepsis, kidney failure, and toxic ingestions such as methanol, ethylene glycol and salicylates. Bicarbonate lost shows a normal gap: severe diarrhoea, high-output ileostomy, pancreatic fistula, and renal tubular acidosis. Calculate the anion gap as sodium minus the sum of chloride and bicarbonate; normal is 8 to 12 mEq/L (using chloride 98 to 106 mEq/L). Treat the cause — insulin and fluids for ketoacidosis, perfusion for lactic acidosis, dialysis for uraemia — and reserve bicarbonate for severe acidaemia, usually a pH below 7.10, because it generates carbon dioxide and can worsen intracellular acidosis. Watch potassium closely: acidosis pushes potassium out of cells, so the serum potassium looks high even when total body potassium is depleted, and it will fall sharply as you correct the acidosis.

Metabolic alkalosis is either acid lost or base gained: protracted vomiting, prolonged nasogastric suction, loop and thiazide diuretics, hyperaldosteronism, excessive antacid or bicarbonate administration, and massive citrate load from transfusion. The patient shows tingling, tremor, hypertonic reflexes, tetany and dysrhythmias, and there is almost always a coexisting hypokalemia and hypochloremia. Treatment is 0.9% sodium chloride to replace chloride, potassium chloride to replace potassium, and correction of the cause — antiemetics, an appropriate irrigant for the nasogastric tube (isotonic saline, never plain water), and a review of diuretic dosing.

Section 5Intravenous Therapy, Safe Replacement and Nursing Priorities

Choosing the fluid

Intravenous solutions are classified by their tonicity relative to plasma, and that single property determines where the water ends up. Isotonic solutions stay in the extracellular space and expand the intravascular volume without shifting water into or out of cells: 0.9% sodium chloride (308 mOsm/L) and lactated Ringer’s (273 mOsm/L). These two are the fluids of resuscitation, of hypovolemia, of vomiting and diarrhoea, and of the hypotensive post-operative patient. D5W (252 mOsm/L) is the trap here. It is isotonic only inside the bag; the dextrose is metabolised within minutes and what remains is free water that distributes across total body water, so only about a twelfth of the infused volume stays in the vessels. D5W therefore behaves as a hypotonic fluid, does not expand the intravascular space, and must never be given for volume resuscitation or for hypotension — it will fail to restore perfusion and will drop the serum sodium while it fails. Note two further cautions: lactated Ringer’s contains 4 mEq/L of potassium, so avoid it in hyperkalemia and in significant renal failure, and its lactate is converted to bicarbonate by the liver, so it is a poor choice in severe hepatic failure. Only 0.9% sodium chloride may be hung with blood products.

Hypotonic solutions — 0.45% sodium chloride (154 mOsm/L), 0.33% sodium chloride, and D5W once the dextrose is metabolised — have fewer particles than plasma, so water moves out of the vessels and into cells. They treat cellular dehydration and hypernatremia, and they are used after the initial resuscitation phase of diabetic ketoacidosis. They are dangerous in anyone with cerebral edema, head injury or stroke, because they swell the brain, and they can worsen hypotension because they do not stay in the vascular space.

Hypertonic solutions — 3% sodium chloride, 5% sodium chloride, D5 in 0.9% NaCl, D5 in lactated Ringer’s, D10W and parenteral nutrition — pull water out of cells into the vascular space. They are used for severe symptomatic hyponatremia and for cerebral edema, and increasingly concentrated solutions require a central line because of vein damage. Their risks are fluid overload, pulmonary edema and cell shrinkage, so infuse them on a pump, assess lung sounds frequently, and follow serum sodium on the schedule ordered. Colloids raise oncotic pressure and pull fluid in from the interstitium; albumin is used in hypoalbuminaemia, large-volume paracentesis and some burn protocols, and the nurse watches for volume overload and, rarely, allergic reaction. Hydroxyethyl starch appears in older textbooks but is no longer recommended for volume resuscitation, because trials in critically ill and septic patients showed more acute kidney injury, more bleeding and higher mortality.

Giving potassium safely

Potassium chloride is a high-alert medication and the classic source of fatal nursing error. Learn these rules as absolutes.

Never give potassium by IV push, IM or subcutaneously. Undiluted potassium delivered as a bolus stops the heart in asystole. It is not a matter of a slow push or a small dose; there is no safe way to push it. Potassium is always diluted and always infused. Use commercially premixed bags whenever they exist rather than compounding at the bedside, and if a bag ever must be mixed, invert and agitate it thoroughly, because potassium is dense and will pool at the bottom and be delivered as an accidental bolus. Never add potassium to a bag that is already hanging and infusing.

Always use an electronic infusion pump, never gravity. Standard concentration limits are up to 10 mEq per 100 mL for a peripheral line and up to 20 mEq per 100 mL through a central line, per institutional policy. Standard rate limits are no more than 10 mEq per hour peripherally in a patient without continuous cardiac monitoring, and up to 20 mEq per hour only with central access, continuous ECG monitoring and usually an intensive care setting. Know your facility’s policy and do not exceed it because a provider verbally asks you to.

Assess renal function and urine output before you hang it. The kidney is the only meaningful route of potassium excretion, so confirm the patient is producing at least 30 mL/hr or 0.5 mL/kg/hr and check the most recent creatinine. Recheck the serum potassium after the ordered replacement is complete rather than assuming it worked. Place the patient on a cardiac monitor for any rapid or high-dose replacement, and check the magnesium level, because potassium will not correct in a magnesium-depleted patient.

Expect burning and act on it. Potassium irritates veins; pain at the site is common and is not itself an emergency, but it demands a response: assess for infiltration first, then slow the rate, increase the dilution, apply a warm compress, and discuss central access for continued therapy. If the site is cool, swollen, blanched or leaking, stop the infusion, disconnect the tubing while leaving the catheter in place to attempt aspiration, notify the provider, elevate the limb and follow your infiltration protocol. Oral potassium is equally irritating in a different way — give it with a full glass of water or with food, never on an empty stomach, and never crush an extended-release tablet.

Complications of infusion therapy

Infiltration is the leak of a non-vesicant solution into surrounding tissue: swelling, coolness, pallor, discomfort and a sluggish or absent flow. Extravasation is the same event with a vesicant such as a vasopressor, concentrated potassium or many chemotherapy agents, and it causes tissue necrosis. For both, stop the infusion immediately, leave the catheter in place until you have attempted aspiration and considered an antidote, notify the provider, elevate the extremity, and document the site, the volume and the appearance. Phlebitis is inflammation of the vein — redness, warmth, tenderness and a palpable cord along the vein. Discontinue the line, apply warm compresses, and restart in the opposite extremity.

Circulatory overload is the complication that will find you on a busy shift. Signs are dyspnoea, new crackles, a cough that may be productive of frothy sputum, distended neck veins, tachycardia, a rising blood pressure and a falling oxygen saturation. Act in this order: slow the infusion to a keep-vein-open rate rather than stopping it entirely and losing the access, raise the head of the bed, apply oxygen, take a full set of vital signs, and notify the provider — anticipating an order for a loop diuretic. Air embolism presents with sudden dyspnoea, chest pain, hypotension and often a churning murmur; clamp the catheter, place the patient on the left side in Trendelenburg to trap air in the right ventricular apex, give high-flow oxygen and call rapid response. Catheter-related bloodstream infection is prevented by hand hygiene, scrubbing the hub for at least fifteen seconds, aseptic dressing changes and prompt removal of lines nobody needs.

Priorities, delegation, the older adult and teaching

When two problems compete, use the standard hierarchy and use it out loud. Airway, breathing, circulation comes first, so a patient with new crackles and a saturation of 88 percent outranks a patient with a potassium of 3.1. Within circulation, a lethal rhythm risk outranks a stable abnormal value, so a potassium of 6.8 with peaked T waves outranks a sodium of 129 in a comfortable patient. Acute outranks chronic, so a sodium that fell from 138 to 126 overnight outranks a sodium that has been 128 for a year. Unstable outranks stable, and actual outranks potential. When a question asks what you do first and both options are reasonable, ask which patient dies sooner if you get it wrong.

Delegate deliberately. The UAP may obtain and record daily weights, measure and record intake and output, provide oral care, assist with ambulation and toileting, offer scheduled oral fluids, take routine vital signs on a stable patient and report findings to you. The UAP may not assess, interpret, teach or evaluate. The LPN or LVN may, within state scope and facility policy, administer many oral and intramuscular medications, monitor a stable patient receiving an established infusion, perform sterile dressing changes, reinforce teaching you have already provided, and collect focused data. The RN retains the initial and ongoing assessment, the plan of care, all intravenous push medications, the initiation and titration of high-alert infusions including potassium and hypertonic saline, blood product initiation, patient teaching, evaluation of response, and every unstable patient. Delegating a task never delegates the accountability.

The older adult deserves a separate paragraph because the presentation genuinely differs. Total body water falls toward 50 percent or less; thirst sensation blunts, so a dehydrated eighty-year-old may not ask for a drink; the kidney loses concentrating ability and the glomerular filtration rate declines, so both dehydration and overload arrive faster; skin turgor is unreliable and must be checked over the sternum or forehead; and polypharmacy — diuretics, ACE inhibitors, NSAIDs, laxatives, proton pump inhibitors — multiplies risk. Most importantly, the first sign is frequently acute confusion rather than any classic symptom. New delirium in an older patient should prompt a basic metabolic panel, not a sedative. Older adults also tolerate rapid infusion poorly, so the same litre of saline that helps a young adult can put a frail patient into pulmonary edema in an hour.

Teaching closes the loop. Patients on fluid restriction need the daily allowance divided across the day, ice chips counted as half their volume, and hard candy or lemon swabs for thirst. Patients on diuretics need to weigh themselves daily at the same time and call for a gain of 2 to 3 pounds in a day or 5 pounds in a week. Patients on ACE inhibitors, angiotensin receptor blockers or potassium-sparing diuretics need to know that salt substitutes are potassium chloride and are not safe for them. Patients on potassium supplements need to take them with food and water and to report muscle weakness, palpitations or persistent gastrointestinal upset. Patients on phosphate binders need them with meals. Every patient going home on a diuretic should be told the signs of dehydration and the signs of overload, in plain words, before they leave.

Words worth knowing

Perioperative Nursing

Surgery is a controlled injury. Everything the perioperative nurse does — the med rec at the preop phone call, the sip of water withheld, the warming blanket, the count of sponges, the jaw thrust in the recovery bay, the tenth incentive spirometer breath on postoperative day one — exists because tissue trauma sets off a predictable neuroendocrine and inflammatory cascade that stresses every organ system at once. The patient who dies after an uncomplicated cholecystectomy almost never dies of the cholecystectomy. They die of aspiration, of a pulmonary embolus, of an unrecognised bleed, of an opioid given on top of untreated obstructive sleep apnoea, of a delirium that was called “sundowning” and left alone. This chapter follows one patient through three phases — preoperative, intraoperative, postanaesthesia and unit recovery — and at each stop asks the only question that matters on the floor and on the examination: of everything in front of me, what do I do first?

Section 1Preoperative Assessment and Risk Stratification

The surgical stress response: why the patient looks the way they look

The moment tissue is cut, afferent nociceptive traffic and circulating cytokines — interleukin-1, interleukin-6 and tumour necrosis factor alpha — reach the hypothalamus. The sympathetic nervous system fires and the hypothalamic–pituitary–adrenal axis switches on. Catecholamines, cortisol, glucagon, growth hormone, aldosterone and antidiuretic hormone all rise. This is an evolutionarily sensible response to a sabre-tooth injury: conserve volume, mobilise fuel, clot the wound, fight the bacteria that got in. It is also the explanation for nearly every postoperative vital sign and laboratory value your student brain is about to be quizzed on.

Cortisol and glucagon drive gluconeogenesis and produce peripheral insulin resistance, so the patient who has never had diabetes runs a glucose of 180 to 220 mg/dL on the evening of surgery. Aldosterone and antidiuretic hormone conserve sodium and water, so urine output falls and urine concentrates for roughly 24 to 48 hours even in a well-hydrated patient — expect an oliguric-looking first shift, and be suspicious rather than reassured when it persists past 48 hours. Third-spacing shifts fluid into the traumatised interstitium, so the patient gains two to four kilograms of weight while being intravascularly dry. Around postoperative day two or three that fluid mobilises back into the vasculature, which is why the frail cardiac patient who was doing fine suddenly becomes short of breath and crackly on day three. Catecholamines raise heart rate and vascular tone; the inflammatory response raises fibrinogen and platelet reactivity, which is one leg of Virchow’s triad and one reason surgery is a prothrombotic event.

Two practical consequences follow. First, a modest tachycardia and a low-grade temperature in the first 24 hours are usually the stress response and not sepsis — but they are never to be dismissed without a look at the wound, the lungs and the volume status. Second, anything that blunts recovery of the stress response — malnutrition, uncontrolled diabetes, smoking, glucocorticoid therapy, immunosuppression — predicts a poor wound and a longer stay. That is exactly what your preoperative assessment is hunting for.

History, physical and the systems that actually decide risk

Preoperative assessment is organised by risk, not by habit. Start with the American Society of Anesthesiologists physical status classification, because it is the shorthand the whole team uses. Class I is a healthy patient; class II has mild systemic disease that is well controlled, such as treated hypertension or a body mass index of 31; class III has severe systemic disease that limits activity but is not incapacitating, such as poorly controlled diabetes with early nephropathy, a prior myocardial infarction, or moderate chronic obstructive pulmonary disease; class IV has severe systemic disease that is a constant threat to life, such as an ejection fraction under 30 per cent, a myocardial infarction within the past three months, or end-stage renal disease that is not on a regular dialysis schedule — note that a patient dialysing on schedule is usually class III, not IV; class V is a moribund patient not expected to survive without the operation, such as a ruptured abdominal aortic aneurysm; class VI is a declared brain-dead organ donor. An E suffix is added for emergency cases, and emergency status roughly doubles risk at every class.

Cardiac reserve is measured in metabolic equivalents. A patient who can climb two flights of stairs or walk four blocks without stopping has a functional capacity of at least four METs and generally tolerates non-cardiac surgery. A patient who cannot — or who cannot tell you, because arthritis or a walker limits them — deserves more scrutiny. Ask directly about chest pain, exertional dyspnoea, orthopnoea, syncope, palpitations, prior stents and the date they were placed, and prior cardiac surgery. Elective non-cardiac surgery is generally deferred at least 30 days after a bare-metal stent and ideally six months after a drug-eluting stent, because interrupting dual antiplatelet therapy earlier risks stent thrombosis, which is frequently fatal.

Pulmonary risk is dominated by three things: smoking, obstructive sleep apnoea and reactive airway disease. Screen every surgical patient with STOP-BANG — Snoring, Tiredness, Observed apnoea, Pressure (treated hypertension), BMI over 35, Age over 50, Neck circumference over 40 cm and male Gender. Three or more affirmative items is intermediate-to-high risk and changes postoperative practice: continuous pulse oximetry, cautious opioid dosing, the patient’s own CPAP machine at the bedside, and elevation of the head of the bed. Counsel smoking cessation at least four weeks before surgery; stopping less than four weeks out still helps carboxyhaemoglobin and ciliary function but does not reliably reduce pulmonary complications, and telling a patient it is “too late to bother” is both untrue and unkind.

Then work the remaining systems fast and deliberately: renal (dialysis schedule, baseline creatinine, nephrotoxins), hepatic (drug metabolism, coagulopathy, albumin), endocrine (diabetes control, thyroid, chronic steroids requiring stress dosing), neurologic (prior stroke, seizures, baseline cognition — document it, because you cannot diagnose delirium without a baseline), musculoskeletal (arthritis limits positioning and mobility), and haematologic (bleeding history, anaemia, sickle cell trait or disease). Ask about alcohol and substance use honestly and without judgement; the patient who drinks a fifth a day will withdraw on postoperative day two or three, and CIWA-guided management planned in advance is far safer than a code called at 0300. Ask about prior anaesthesia problems and about a family history of malignant hyperthermia or of “a relative who died on the table.” Ask about latex, iodine, adhesive and food allergies — banana, kiwi, avocado and chestnut cross-react with latex.

Preoperative diagnostics and what the numbers mean

Routine shotgun testing has been abandoned; tests are ordered because the history, the physical or the operation demands them. What follows are the ones you will see, with the reference ranges you should carry in your head.

Medication reconciliation: the highest-value nursing task in the whole chapter

Ask about prescription drugs, over-the-counter drugs, herbals, supplements, vitamins, cannabis and anything borrowed from a spouse. Patients routinely omit inhalers, eye drops, insulin, and “that shot I take on Sundays.” Ask the last dose and time of every anticoagulant by name. Then apply the hold-or-continue logic below, which is decided by the surgeon and anaesthetist but is checked, taught and enforced by you.

Section 2Preparing the Patient: Consent, Fasting, Teaching and the Day of Surgery

Informed consent and the nurse’s actual legal role

Students lose points on this every single year, so learn it precisely. The surgeon (or the provider performing the procedure) is legally responsible for obtaining informed consent. That means explaining the diagnosis, the nature and purpose of the proposed procedure, the risks and benefits, reasonable alternatives including doing nothing, and the likely consequences of refusal. The nurse witnesses the signature. In witnessing, you attest to three things: the signature is the patient’s, the patient signed voluntarily and without coercion, and the patient appears competent to sign at that moment. You also serve as the patient’s advocate by confirming their understanding — and this is where the examination question lives.

If the patient says “I’m not really sure what they’re taking out” or “my daughter said I should just sign it,” you stop. Do not explain the operation yourself — that is outside the nurse’s scope for informed consent and it does not cure the defect. Withhold the preoperative sedative, notify the surgeon, and document. A consent signed after midazolam has been given is not valid consent, because the patient was not competent at the moment of signing. In a true life-or-limb emergency where the patient cannot consent and no surrogate is reachable, implied consent applies and the surgery proceeds; document the circumstances thoroughly. Minors require a parent or legal guardian except in the specific circumstances your state recognises — emancipated minors, and often care related to pregnancy, sexually transmitted infection or substance use. Consent must be obtained in the patient’s preferred language using a qualified medical interpreter; a family member is not an acceptable interpreter for consent.

Fasting, aspiration and ERAS

The reason for fasting is a single, specific, lethal event: regurgitation of gastric contents into the airway during induction, when protective reflexes are abolished. The old “NPO after midnight” ritual dehydrated patients for 12 to 16 hours without improving gastric volume, and modern guidance is different and better. For elective procedures in patients without gastroparesis or bowel obstruction: clear liquids up to 2 hours before induction; breast milk up to 4 hours; infant formula and non-human milk up to 6 hours; a light meal up to 6 hours; and a fried, fatty or meat-containing meal up to 8 hours. Clear liquids means water, black coffee or tea without milk, pulp-free juice, clear carbohydrate drinks — anything you can read newsprint through. Milk in coffee makes it not a clear liquid, because milk curdles into a solid in gastric acid.

Certain patients are treated as full stomachs regardless of the clock: trauma, bowel obstruction, active vomiting, advanced pregnancy, symptomatic gastro-oesophageal reflux, gastroparesis and patients on GLP-1 receptor agonists. These patients receive a rapid sequence induction with cricoid pressure at the anaesthetist’s discretion, and may receive a non-particulate antacid such as sodium citrate, a histamine-2 blocker or metoclopramide.

Enhanced Recovery After Surgery protocols bundle the evidence into a pathway: no prolonged fasting and often a carbohydrate-rich clear drink two hours preoperatively, no routine bowel preparation for many procedures, multimodal opioid-sparing analgesia, goal-directed rather than liberal fluids, active warming, aggressive postoperative nausea prophylaxis, removal of catheters and drains early, feeding within 24 hours, and ambulation the day of surgery. ERAS shortens length of stay and reduces complications, and your ability to get a patient out of bed six hours after a colectomy is not a comfort measure — it is the intervention.

Preoperative teaching that prevents postoperative complications

Teach before surgery, because after surgery the patient is sedated, in pain and will not retain it. Cover, and have the patient demonstrate: incentive spirometry — sit upright, seal the lips, inhale slowly and deeply, hold three to five seconds, ten breaths every hour while awake; splinting the incision with a pillow or folded blanket before coughing and before moving; turn, cough and deep breathe every one to two hours; ankle pumps and calf exercises ten times per hour; how to get out of bed by rolling to the side and pushing up rather than sitting straight up; and how to rate pain on the scale that will be used, with the honest message that the goal is function, not zero. If a patient-controlled analgesia pump is planned, teach it now and teach the family the single most important rule about it.

Also set expectations: what the incision and drains will look like, that there will be a urinary catheter or a nasogastric tube if planned, that the first ambulation will be hard and will happen anyway, how long the hospital stay is expected to be, and who will be with them at discharge. Anxiety is not a soft finding — catecholamine surge raises myocardial oxygen demand and increases postoperative pain scores. Address it directly, allow questions, involve the family and use the facility’s spiritual care resources when the patient wants them.

The day-of-surgery checklist and preoperative medications

The preoperative checklist exists so that nothing depends on memory. Confirm: two patient identifiers and an intact identification band; allergy band and documented allergies; NPO status and time of last intake; signed and dated consent on the chart with the correct procedure and side; history and physical and required laboratory, ECG and imaging results present; site marked by the surgeon with the patient participating while awake; vital signs and a documented baseline neurological status; blood products available if ordered; that the patient has voided or a catheter is in place; that dentures, partial plates, contact lenses, glasses, hearing aids, prostheses, jewellery, body piercings, nail polish and make-up are removed and documented (hearing aids and glasses are frequently left in place until the operating room so the patient can participate in the time out — follow policy); valuables secured or given to family with documentation; antiembolism stockings or sequential compression devices applied; and preoperative medications given and charted.

Preoperative medications typically include an anxiolytic such as midazolam, an antibiotic timed so infusion is complete within 60 minutes before incision (cefazolin 2 g, or 3 g for patients weighing 120 kg or more; vancomycin and fluoroquinolones are started within 120 minutes because they infuse slowly), an antiemetic, and sometimes a proton pump inhibitor or an anticholinergic to dry secretions. After sedation is given, the side rails go up, the bed goes low and the patient does not get out of bed unassisted. If beta blockers, inhalers or antiseizure medications are on the continue list, give them with a sip of water — and document that too.

Section 3Intraoperative Care: Anaesthesia, the Sterile Field and Patient Safety

Anaesthesia by type, and what each one does to the patient

General anaesthesia produces unconsciousness, amnesia, analgesia and often muscle relaxation, and it abolishes airway protection. It is delivered by intravenous induction agents (propofol, etomidate, ketamine), maintained with inhaled volatile agents (sevoflurane, desflurane, isoflurane) with or without nitrous oxide, and supported by neuromuscular blocking agents. Propofol drops blood pressure; etomidate is haemodynamically kind but suppresses adrenal cortisol; ketamine preserves blood pressure and respiration but can produce emergence hallucinations. Nursing implications after general anaesthesia are airway, airway, airway, plus hypothermia, nausea and residual sedation.

Neuromuscular blocking agents deserve their own paragraph, because they kill people. Succinylcholine is depolarising, works in under a minute and wears off in five to ten, which makes it ideal for rapid sequence induction — but it releases potassium and is contraindicated in burns beyond about 24 to 48 hours, crush injury, denervating conditions such as spinal cord injury and muscular dystrophy, and pre-existing hyperkalaemia, where it can cause cardiac arrest. It is also a trigger for malignant hyperthermia. Rocuronium and vecuronium are non-depolarising and are reversed by neostigmine plus glycopyrrolate, or by sugammadex. Residual paralysis is a real PACU problem: the patient looks awake but cannot lift the head for five seconds, has a weak grip, uses accessory muscles and desaturates. Support ventilation, keep the head of the bed up and call anaesthesia. One teaching point patients are rarely given: sugammadex can reduce the effectiveness of hormonal contraception for about seven days, so a backup method is needed.

Regional anaesthesia blocks a region while the patient remains conscious or lightly sedated. Spinal anaesthesia injects local anaesthetic into the subarachnoid space, produces dense rapid block, and reliably causes sympathetic blockade — expect hypotension and bradycardia, and expect it fast. Treat with fluids, positioning and vasopressors such as ephedrine or phenylephrine. If the block rises too high (a “high spinal”), the patient reports numb fingers, difficulty breathing or difficulty speaking, and this is an airway emergency. Post-dural puncture headache is positional — severe when upright, relieved when supine — and is managed with fluids, caffeine, analgesia and, if persistent, an epidural blood patch. Epidural catheters give continuous analgesia but carry the risk of epidural haematoma, particularly in anticoagulated patients: new or worsening back pain with new lower-extremity weakness, numbness or bowel or bladder dysfunction is a surgical emergency requiring immediate imaging and decompression, ideally within hours. Assess motor and sensory function at least every four hours — more often if policy or the infusion rate demands — on every patient with an epidural, and continue those checks for 24 hours after the catheter is removed, because removal is itself a bleeding event. Coordinate anticoagulant timing with pharmacy and anaesthesia.

Monitored anaesthesia care and moderate procedural sedation preserve spontaneous ventilation and the ability to respond to verbal or light tactile stimulation. The registered nurse monitoring moderate sedation must have no other responsibilities, must monitor level of consciousness, oxygen saturation, capnography where used, heart rate and blood pressure continuously, and must have reversal agents — naloxone for opioids, flumazenil for benzodiazepines — and emergency airway equipment immediately available. Local anaesthesia is infiltration only, but is not risk-free: local anaesthetic systemic toxicity begins with perioral numbness, tinnitus, metallic taste, dizziness and agitation, and progresses to seizure and cardiovascular collapse. Stop the injection, call for help, manage the airway, and give 20 per cent intravenous lipid emulsion per protocol.

The surgical team, the Universal Protocol and the counts

The circulating nurse is a registered nurse and is not scrubbed; they manage the room, verify consent and the count, position the patient, prepare the skin, document, connect equipment, monitor the sterile field for breaks, and speak for the patient. The scrub person — a registered nurse or a certified surgical technologist — sets up and maintains the sterile field and passes instruments. The registered nurse first assistant retracts, provides haemostasis and closes under the surgeon’s direction.

The Joint Commission Universal Protocol itself has three elements: a pre-procedure verification process, marking of the procedure site by the person performing it, and a time out immediately before the start. In practice most operating rooms deliver it inside the WHO Surgical Safety Checklist, which has three pauses. Sign in occurs before induction and confirms identity, procedure, site, consent, allergies, airway risk and blood availability. The time out occurs immediately before incision: all activity stops, everyone in the room participates, and the team confirms correct patient, correct procedure, correct site and side, correct position, availability of implants and imaging, and antibiotic administration. Any team member — including you as a student — can and must stop the process if something does not match. Sign out occurs before the patient leaves the room and confirms the procedure performed, the counts, specimen labelling and equipment problems.

Surgical counts of sponges, sharps and instruments are performed by the scrub person and the circulating nurse together, audibly and visibly: before the procedure begins, before closure of a cavity, at the start of skin closure, and at the end. If a count is incorrect, the surgeon is notified, the count is repeated, the wound and the floor are searched, and a radiograph is obtained before the patient leaves the room. Retained surgical items are never-events, and the count is a nursing responsibility, not a formality.

Positioning, temperature, skin and fire

An anaesthetised patient has no protective reflexes and no ability to report that an arm hurts. Positioning injuries are therefore nursing-preventable injuries. Common ones: brachial plexus stretch when the arm is abducted beyond 90 degrees on an arm board; ulnar nerve compression at the elbow; peroneal nerve compression at the fibular head in lithotomy, producing foot drop; and pressure injury over the sacrum, heels and occiput during long cases. Pad bony prominences, keep the body in neutral alignment, use a safety strap above the knees, raise and lower lithotomy legs simultaneously and slowly, and re-evaluate. Trendelenburg increases intracranial and intraocular pressure and pushes abdominal contents against the diaphragm; the prone position risks eye and breast and genital pressure injury.

Maintain normothermia: core temperature at or above 36 degrees Celsius. Hypothermia is not a comfort issue. It impairs platelet function and the coagulation cascade, causes vasoconstriction that lowers wound oxygen tension and roughly triples surgical site infection risk, slows drug metabolism so the patient wakes late, and causes shivering that can increase oxygen consumption several-fold in a patient with limited cardiac reserve. Use forced-air warming, warmed intravenous fluids and warmed irrigation.

Prepare skin with a chlorhexidine–alcohol solution unless contraindicated, working from the incision outward. Remove hair only if necessary and only with clippers — razors create microabrasions that colonise. And respect the operating-room fire triad: an oxidiser (oxygen or nitrous oxide), an ignition source (electrosurgery, laser) and fuel (alcohol prep, drapes, hair). Alcohol-based preps must be allowed to dry completely and must not pool under the patient or in the umbilicus before drapes go on.

Malignant hyperthermia: the emergency you must know cold

Malignant hyperthermia is an inherited (commonly RYR1 mutation) disorder of skeletal muscle calcium handling. Exposure to a volatile anaesthetic or to succinylcholine causes uncontrolled calcium release from the sarcoplasmic reticulum, producing sustained muscle contraction, an explosive rise in metabolism, and a hypermetabolic crisis with a mortality that is low with treatment and very high without it.

The earliest signs are metabolic, not thermal: an unexplained rise in end-tidal carbon dioxide that does not respond to increased ventilation, unexplained tachycardia and tachypnoea, and masseter or generalised muscle rigidity. Hyperthermia — which can rise 1 to 2 degrees Celsius every five minutes — is a late sign, and a question that offers “temperature of 40 degrees” as the earliest indicator is testing whether you know that. Later come mixed acidosis, hyperkalaemia, dysrhythmias, rhabdomyolysis with cola-coloured myoglobinuric urine, disseminated intravascular coagulation and cardiac arrest.

Management: stop the triggering agents immediately and hyperventilate with 100 per cent oxygen at high flow; call for the MH cart and for help; give dantrolene sodium 2.5 mg/kg intravenous push, repeated as needed to a usual maximum around 10 mg/kg (the newer concentrated formulation reconstitutes far faster than the older one, which required 60 mL of sterile water per vial and many hands); cool the patient with cold intravenous saline, surface ice packs to the groin, axillae and neck, and cold lavage if needed, stopping active cooling around 38 degrees to avoid overshoot; treat hyperkalaemia with intravenous insulin and dextrose, calcium and bicarbonate as ordered; treat dysrhythmias with amiodarone or lidocaine but avoid calcium channel blockers, which can cause hyperkalaemia and cardiovascular collapse with dantrolene; maintain urine output at 1 to 2 mL/kg per hour to protect the kidneys from myoglobin; and monitor in an intensive care setting for at least 24 hours because recrudescence occurs. Refer the patient and their blood relatives for testing and counselling.

Section 4Postanaesthesia Care: The First Two Hours

Airway first, always

The most common complication in the postanaesthesia care unit is airway obstruction, and the most common cause is the tongue falling back against the posterior pharynx in a patient whose muscle tone has not returned. The findings are snoring or crowing respirations, paradoxical see-saw chest and abdominal movement, use of accessory muscles, and a falling oxygen saturation — and by the time the saturation falls, obstruction has already been present for a while. The first action is a physical airway manoeuvre: stimulate the patient, reposition the head, and perform a chin lift or jaw thrust. Then suction, then supplemental oxygen, then an oral or nasal airway, then call anaesthesia. Notice the order — a question that offers “increase the oxygen” and “perform a jaw thrust” is asking whether you know that oxygen delivered above an obstruction goes nowhere.

Other airway threats: laryngospasm, presenting with stridor or a completely silent airway with vigorous effort, treated with positive pressure, jaw thrust and, if needed, a small dose of succinylcholine; laryngeal oedema after difficult intubation or a long prone case; bronchospasm in the asthmatic; residual neuromuscular blockade, tested at the bedside by asking the patient to lift the head off the pillow for five seconds or squeeze your hand; and opioid-induced respiratory depression, in which the respiratory rate falls and the tidal volume shrinks. Remember the sequence: sedation precedes respiratory depression. A patient who is difficult to rouse but still breathing 12 times a minute is already in trouble. Use a sedation scale, stop the opioid, stimulate, oxygenate, and give naloxone in small diluted increments titrated to respiration — a full ampoule pushed fast produces agonising pain, hypertension, vomiting and, occasionally, flash pulmonary oedema.

Position the recovering patient on their side or with the head turned to the side unless contraindicated, so that if they vomit it drains out rather than in. Keep suction assembled and working at the head of every bed.

Circulation, bleeding, and the vital signs that lie

Once the airway is secure, work circulation. Hypotension in the PACU is most often hypovolaemia — from fasting, insensible losses, third-spacing and blood loss — but also comes from residual anaesthetic vasodilation, sympathetic blockade from a spinal, cardiac dysfunction, and rarely adrenal insufficiency or anaphylaxis. Hypertension is usually pain, a full bladder, hypoxia, hypercarbia or the patient’s own withheld antihypertensives.

The critical concept for haemorrhage is that the young, healthy patient compensates, and their vital signs lie to you until they do not. The sequence is: anxiety and restlessness first (a hypoxic brain is an agitated brain), then tachycardia, then a narrowing pulse pressure as the diastolic rises with vasoconstriction, then cool clammy pale skin and delayed capillary refill, then falling urine output, and only last a falling systolic blood pressure. A blood pressure that has finally dropped means the patient has already lost roughly 30 per cent or more of their blood volume. Restlessness in a postoperative patient is a respiratory and haemodynamic finding until you have proven otherwise — it is not a request for lorazepam.

Assess bleeding directly. Look at the dressing, then slide your hand underneath the patient, because blood runs downhill and a dry-looking abdominal dressing can sit above a soaked bed. Mark and time the border of any drainage so the next nurse can measure progression. Measure drain output. Check that a haemovac or Jackson-Pratt drain is actually compressed and holding suction; an uncompressed drain measures nothing and drains nothing. Reinforce the initial dressing rather than changing it — the first dressing change after surgery is generally performed by the surgeon — and notify. Expect urine output of at least 0.5 mL/kg per hour, roughly 30 mL per hour in an average adult; less than that for two consecutive hours is reportable.

Pain, nausea, shivering and emergence delirium

Manage pain multimodally so that opioids are the smallest part of the plan. Scheduled acetaminophen (maximum 4 g per day, and 3 g or less in older adults, low body weight or hepatic disease) plus an NSAID such as ketorolac (15 to 30 mg intravenously every six hours, limited to five days total, reduced dose in patients 65 and over, under 50 kg, or with renal impairment; avoided in some bowel anastomoses and in active bleeding) plus a regional block covers a remarkable amount of postoperative pain. Reserve opioids for breakthrough, and monitor sedation and respiratory rate every time you give one. Avoid meperidine for routine analgesia: its metabolite normeperidine accumulates and causes tremor, myoclonus and seizures, especially in older adults and renal impairment. Low-dose meperidine remains a standard treatment for postanaesthesia shivering, which is a different indication entirely.

Postoperative nausea and vomiting is not a nuisance; retching pops staples, raises intracranial and intraocular pressure and causes aspiration. Risk is scored by the Apfel criteria — female sex, non-smoker, history of PONV or motion sickness, and expected postoperative opioids — and prophylaxis is layered accordingly: ondansetron 4 mg intravenously, dexamethasone 4 to 8 mg at induction, scopolamine transdermally (an anticholinergic to be avoided in older adults and in glaucoma), and droperidol or aprepitant in selected cases. Promethazine is a vesicant and can cause severe tissue injury with extravasation or inadvertent arterial injection; many facilities restrict it. Keep the patient still, cool the room, avoid strong odours, and advance oral intake slowly.

Emergence delirium — thrashing, disorientation, agitation — is common and usually self-limited, but the nurse’s first move is not restraint or sedation. Rule out hypoxia, hypercarbia, hypoglycaemia, hypotension, a distended bladder and pain, in that spirit. Then orient, reduce stimulation, protect the airway and lines, and stay with the patient. Restraints are a last resort with an order and a documented failure of alternatives.

Handoff, Aldrete scoring and discharge from PACU

Handoff from anaesthesia to the PACU nurse is a structured, uninterrupted report: procedure performed, anaesthetic type and agents, reversal agents given, airway difficulty, estimated blood loss and fluids and blood products given, urine output, medications given including antibiotics and analgesia and the times, allergies, comorbidities, complications, drains and lines, and the plan. The PACU nurse then reports out to the receiving unit in the same structured way. Use SBAR and expect the receiving nurse to ask questions.

Readiness for discharge from Phase I recovery is documented with the modified Aldrete score: activity, respiration, circulation, consciousness and oxygen saturation, each scored 0, 1 or 2, for a maximum of 10. Most facilities require a score of 9 or greater, with stable vital signs at or near baseline, a patent airway with adequate ventilation on room air or the patient’s baseline oxygen, controlled pain and nausea, no active bleeding, adequate urine output, and normothermia. Patients who received spinal anaesthesia additionally need documented return of sensation and motor function, and outpatients typically need to be able to ambulate, tolerate fluids and, in many settings, void, with a responsible adult to drive them home.

Section 5Postoperative Unit Care: Complications, Recovery and Discharge

Pulmonary: atelectasis, pneumonia and the postoperative fever timeline

Atelectasis is alveolar collapse, and after surgery it is nearly universal. General anaesthesia reduces functional residual capacity, the diaphragm sits higher in a supine patient, opioids reduce tidal volume and suppress sighing, and pain makes a patient with an upper abdominal or thoracic incision refuse to take a deep breath. Collapsed alveoli are perfused but not ventilated, so the patient shunts and desaturates. Findings are diminished or absent breath sounds in the bases and fine crackles that typically clear, or markedly diminish, with coughing, deep breathing or a change of position, because the collapsed alveoli re-open — crackles that do not clear point away from simple atelectasis and toward pulmonary oedema, pneumonia or interstitial disease, which is exactly what the day-three patient re-absorbing third-spaced fluid has — together with tachypnoea, low-grade temperature and a falling oxygen saturation. Prevention and treatment are the same thing: incentive spirometry ten breaths hourly while awake, deep breathing and splinted coughing, adequate analgesia so the patient can breathe deeply, sitting upright, and early and frequent ambulation. Untreated atelectasis becomes postoperative pneumonia around day three to five, with productive cough, purulent sputum, fever over 38.3 degrees Celsius, leucocytosis and an infiltrate on chest radiograph.

The classic fever timeline — the five Ws — is worth carrying, with one honest caveat: modern evidence suggests early fever is usually the inflammatory stress response rather than atelectasis itself. The timeline still reliably tells you where to look.

Vascular: venous thromboembolism, pulmonary embolism and late bleeding

Surgery satisfies all three legs of Virchow’s triad: venous stasis from immobility and positioning, endothelial injury from the operation itself and from calf compression on the table, and hypercoagulability from the acute-phase response. Risk multiplies with orthopaedic surgery of the hip and knee, pelvic and abdominal cancer surgery, obesity, prior venous thromboembolism, oestrogen therapy and prolonged operative time. Prophylaxis is mechanical and pharmacological: sequential compression devices applied before induction and worn whenever in bed, graduated compression stockings, ambulation on the day of surgery when possible, and enoxaparin 40 mg subcutaneously daily (30 mg every 12 hours in many joint-replacement protocols) or unfractionated heparin 5,000 units subcutaneously every 8 to 12 hours. Never massage a calf that hurts.

Pulmonary embolism presents suddenly: dyspnoea out of nowhere, pleuritic chest pain, tachypnoea, tachycardia, hypoxia, sometimes haemoptysis, and very often an overwhelming sense of impending doom that the patient will describe before the monitor shows anything. Your first actions are nursing actions: raise the head of the bed to high Fowler position, apply high-flow oxygen, stay with the patient, obtain vital signs and oxygen saturation, call the rapid response team and notify the provider. Anticipate a CT pulmonary angiogram, anticoagulation with heparin, and in massive embolism thrombolysis or embolectomy. A related entity after long-bone or pelvic fracture is fat embolism syndrome, typically 24 to 72 hours after injury, with hypoxaemia, confusion out of proportion and a petechial rash across the chest, axillae and conjunctivae.

Late bleeding on the unit shows up as tachycardia, falling haemoglobin, a distended tense abdomen after abdominal surgery, an expanding neck swelling after thyroid or carotid surgery (an airway emergency — keep a tracheostomy tray at the bedside after thyroidectomy), or brisk drain output. Trend the haemoglobin and haematocrit, but remember that in acute haemorrhage the haemoglobin lags because the patient loses whole blood; a normal haemoglobin 30 minutes into a bleed is not reassurance.

Gastrointestinal, genitourinary and the wound

Paralytic ileus is the temporary arrest of coordinated peristalsis after bowel handling, anaesthesia, opioids, immobility and electrolyte derangement — particularly hypokalaemia. Normal return of motility is staged: small intestine within hours, stomach in 24 to 48 hours, and colon in 3 to 5 days, which is why the passage of flatus is the milestone everyone waits for. Ileus is diagnosed when that does not happen: absent or hypoactive bowel sounds, abdominal distension and tympany, nausea and vomiting, no flatus or stool. Management is supportive — NPO or clear liquids, nasogastric decompression to low intermittent suction if vomiting or marked distension, correction of potassium and magnesium, minimising opioids in favour of multimodal analgesia, and ambulation, which genuinely works. Distinguish ileus from mechanical small-bowel obstruction, which produces high-pitched hyperactive bowel sounds proximal to the blockage early on, colicky pain and, if strangulation develops, fever, tachycardia and peritoneal signs. Advance diet only after bowel function returns and never against the surgeon’s order.

Postoperative urinary retention follows anaesthesia, anticholinergics, opioids, pelvic surgery and simply being unable to void lying flat with a stranger in the room. The patient should void within six to eight hours of surgery or catheter removal. Suprapubic fullness, restlessness, small frequent voids and lower abdominal discomfort are the findings; the assessment is a bladder scan, not a straight catheter, because the scan is non-invasive and tells you the answer. Try privacy, running water, warm perineal water, upright positioning and ambulation first; intermittent catheterisation follows facility thresholds, commonly a scanned residual over 300 to 500 mL. Remove indwelling catheters as early as possible — every catheter day is a urinary tract infection risk.

Wounds heal by primary intention when edges are approximated, by secondary intention when a defect granulates in, or by tertiary intention when a contaminated wound is deliberately left open and closed later. Drainage progresses in a predictable order: sanguineous (bright red, first hours) to serosanguineous (pink, watery) to serous (clear straw) — and any drainage that goes backward in that sequence or becomes thick, opaque, malodorous and purulent means infection. Surgical site infection typically declares itself around day 3 to 7 with fever, increasing rather than decreasing incisional pain, erythema extending beyond the wound margin, warmth, induration and purulent drainage.

Dehiscence is separation of the wound layers, classically postoperative day 4 to 14 and most often 5 to 10, when the wound has lost the strength of sutures and has not yet gained collagen strength. It is often heralded by a sudden gush of serosanguineous drainage or by the patient saying “something gave way.” Evisceration is protrusion of viscera through the separation and is a surgical emergency. Your actions, in order: stay with the patient and call for help; place them in low Fowler position with the knees bent to reduce abdominal tension; cover the protruding tissue with sterile gauze moistened with sterile normal saline and keep it moist; do not attempt to replace the organs; keep the patient NPO; take vital signs and monitor for shock; notify the surgeon and prepare for the operating room. Risk factors are obesity, malnutrition, diabetes, steroids, infection, coughing, vomiting and straining — which is exactly why splinting, antiemetics and stool softeners are part of wound care.

The older adult, delirium, delegation and discharge

The older surgical patient is not a young patient with grey hair. Cardiac reserve is reduced and the stiff ventricle depends on preload, so both over-resuscitation and dehydration are poorly tolerated. Glomerular filtration falls with age even when the creatinine looks normal, because there is less muscle to make creatinine — so a creatinine of 1.1 mg/dL in an 82-year-old may represent substantially reduced clearance and mandates renal dosing. Chest wall compliance and cough strength fall, raising atelectasis and aspiration risk. Thermoregulation is blunted, so hypothermia comes faster and lasts longer. Skin is thinner and pressure injuries develop in hours, not days. Polypharmacy and the Beers criteria matter: benzodiazepines, anticholinergics such as diphenhydramine and scopolamine, and meperidine are all deliriogenic and are avoided.

Presentation is atypical, and this is where students are caught. Myocardial infarction may present as dyspnoea, fatigue, syncope or confusion with no chest pain at all. Infection may present with a normal temperature and a new confusion, because the febrile response is blunted — a temperature of 37.6 degrees Celsius in a frail 85-year-old may represent a significant fever. And delirium is frequently the first sign of anything going wrong: hypoxia, hypoglycaemia, urinary retention, uncontrolled pain, infection, a new medication. Screen with the Confusion Assessment Method and look for the acute onset with fluctuating course, inattention, and either disorganised thinking or altered level of consciousness. Remember that hypoactive delirium — the quiet, withdrawn, sleepy patient — is more common than the agitated form, carries a worse prognosis, and is the one that gets missed because a quiet patient does not generate a call light. Prevention is not pharmacological: orient frequently, restore glasses and hearing aids, get the patient up and into daylight, protect sleep, treat pain adequately, hydrate, remove tethers such as catheters and telemetry leads that are no longer needed, and involve family.

Delegation on a busy postoperative floor is a competency, not an afterthought. Unlicensed assistive personnel may take and report vital signs on stable patients, assist with ambulation and positioning that is already established, apply sequential compression devices, record intake and output, provide hygiene and oral care, remind and coach a patient who has already been taught incentive spirometry, and report findings to you. They may not assess, teach, evaluate, or care for an unstable patient. Licensed practical or vocational nurses may gather data and monitor stable patients, reinforce teaching you have already provided, perform routine dressing changes and sterile procedures per policy, insert catheters, administer most oral and subcutaneous and intramuscular medications, and monitor infusions per state scope. The registered nurse retains the initial and ongoing assessment, the plan of care, all teaching and evaluation, blood product administration, intravenous push medications and titrated drips in most settings, care of the unstable patient, and the witnessing of consent. When you are handed a five-option delegation question, ask which option requires nursing judgement — that one stays with you.

An SBAR escalation for the fourth of these sounds like this. Situation: “This is Marcus Vela, RN, on 5 East. I’m calling about Mrs Okonkwo in 512, postoperative day four from a right hemicolectomy. She has sudden shortness of breath and chest pain.” Background: “She is 71, has hypertension and obesity, and has been on enoxaparin prophylaxis but has ambulated only twice since surgery.” Assessment: “Heart rate 124 and regular, respirations 32, blood pressure 98 over 62, oxygen saturation 86 per cent on room air and 92 per cent on 6 litres, lungs clear, right calf is warm and 3 cm larger than the left. I think she has a pulmonary embolus.” Recommendation: “I have her in high Fowler on oxygen and I’ve called rapid response. I need you to come now, and I’d like orders for a CT pulmonary angiogram and therapeutic anticoagulation.” Notice that the nurse acted first and called second, and that the recommendation is specific.

Finally, discharge teaching is not the last ten minutes; it starts at the preoperative visit and is reinforced every shift. Cover, using teach-back: incision care and when it may get wet; how to recognise infection — increasing pain, redness spreading, purulent drainage, fever at or above 38 degrees Celsius (100.4 degrees Fahrenheit); activity restrictions including the specific lifting limit, driving restriction while on opioids, and when to resume work and sexual activity; the analgesic plan, including scheduled acetaminophen, safe opioid storage and disposal, and the naloxone kit if one is prescribed; a bowel regimen, because opioids plus reduced mobility plus reduced intake equals constipation and straining that threatens the wound; the anticoagulant plan with dose, duration and bleeding precautions; diet and protein for healing; the signs of venous thromboembolism; the follow-up appointment date; and the specific phone number to call, with a clear statement of what warrants a call and what warrants emergency services. Confirm they have the medications they can afford, a ride, a caregiver and a way to get up the stairs at home. A perfect operation undone by a discharge the patient did not understand is still a failure.

Words worth knowing

PAIN, COMFORT AND PALLIATIVE CARE

Pain is the reason most of your patients came to the hospital and the symptom they will remember longest. It is also the one clinical problem where the nurse holds nearly all the levers: you assess it, you medicate it, you reposition, you reassure, you decide whether the physician needs to know now or at rounds. Done well, analgesia lets a post-operative patient cough, walk and go home without a pneumonia or a clot. Done poorly, it produces splinting, atelectasis, delirium, immobility, tachycardia, poor wound healing and a patient who no longer trusts you. This chapter builds pain from the nerve ending up — how a signal becomes a sensation, how to measure it in a patient who cannot speak, how to combine drugs so that each does less harm, how to recognise the sedation that precedes respiratory arrest, and how to shift the goal from cure to comfort when cure is no longer possible.

Section 1How Pain Is Made, and What Untreated Pain Costs

Four steps, four places to intervene

Pain is not a single event; it is a relay with four handoffs, and almost every drug you will give interrupts one of them. Transduction happens at the peripheral nerve ending, where tissue damage releases prostaglandins, bradykinin, histamine, substance P and hydrogen ions. These chemicals open sodium channels on the nociceptor and convert a mechanical, thermal or chemical insult into an electrical impulse. NSAIDs act here by blocking cyclooxygenase and therefore prostaglandin synthesis; local anaesthetics act here by blocking the sodium channel outright.

Transmission carries that impulse along A-delta fibres (myelinated, fast, sharp, well localised — the pain that makes you pull your hand back) and C fibres (unmyelinated, slow, dull, aching, poorly localised — the pain that keeps a patient awake at 0300) to the dorsal horn of the spinal cord. There the signal crosses to the opposite side and ascends the spinothalamic tract. Opioids act partly here, on presynaptic mu receptors in the dorsal horn, reducing the release of substance P. This is exactly why epidural and intrathecal opioids work at tiny doses: they are delivered to the receptor rather than to the whole body.

Perception occurs when the thalamus distributes the signal to the somatosensory cortex, which locates and quantifies it, and simultaneously to the limbic system, which supplies the fear, the anticipation and the memory. This is not a soft point — it is why the same incision hurts more in an anxious, exhausted, isolated patient, and why a warm blanket, an explanation and a family member at the bedside are genuine analgesic interventions rather than niceties. Modulation is the descending brake: the periaqueductal grey and brainstem send serotonin, norepinephrine and endogenous opioids (endorphins, enkephalins, dynorphins) back down to dampen the dorsal horn. Serotonin–norepinephrine reuptake inhibitors such as duloxetine and tricyclics such as nortriptyline work by strengthening this brake, which is why they relieve neuropathic pain independently of any effect on mood — tricyclics at nightly doses well below their antidepressant range, duloxetine at its usual antidepressant dose. Teach that the analgesic benefit builds over one to two weeks, so the drug must not be judged a failure after two doses.

Nociceptive, neuropathic and nociplastic pain

Nociceptive pain comes from actual tissue damage with an intact nervous system. Somatic nociceptive pain arises from skin, muscle, bone and joint; patients localise it precisely and describe it as aching, throbbing or sharp — a surgical incision, a fractured hip, a pressure injury. Visceral nociceptive pain arises from organ capsules and hollow viscera; it is poorly localised, described as cramping, squeezing or deep pressure, frequently referred to a distant dermatome, and characteristically accompanied by autonomic signs such as nausea, diaphoresis and pallor. Cholecystitis referring to the right scapula and myocardial ischaemia referring to the left jaw are the classic examples. Nociceptive pain responds well to acetaminophen, NSAIDs and opioids.

Neuropathic pain arises from damage to the nervous system itself — diabetic peripheral neuropathy, postherpetic neuralgia, chemotherapy-induced neuropathy, phantom limb pain, sciatica, spinal cord injury. Patients use a distinctive vocabulary: burning, shooting, electric, stabbing, pins-and-needles, numb-but-painful. Two findings are almost diagnostic: allodynia, pain from a stimulus that should not hurt (a bedsheet on the feet), and hyperalgesia, exaggerated pain from a stimulus that should hurt only a little. Neuropathic pain responds poorly to opioids and well to gabapentinoids, SNRIs, tricyclics and topical lidocaine. When a patient with burning foot pain reports that four escalating doses of oxycodone did nothing, that is not drug-seeking behaviour — that is the wrong drug class.

Nociplastic pain is the newest category: real pain generated by altered central processing without identifiable tissue damage or nerve lesion. Fibromyalgia, irritable bowel syndrome and many chronic low back pain syndromes sit here. These patients are frequently disbelieved, and they arrive on your unit having been disbelieved for years. Management leans on exercise, sleep restoration, cognitive behavioural approaches, duloxetine, milnacipran and pregabalin; opioids are generally unhelpful and may worsen the condition through opioid-induced hyperalgesia, a paradoxical state in which escalating opioid doses increase pain sensitivity.

Acute, persistent, and the price of leaving pain alone

Acute pain has an identifiable cause, a predictable trajectory and a sympathetic response: tachycardia, hypertension, tachypnoea, diaphoresis, dilated pupils, restlessness. It is protective and it should resolve as tissue heals, generally within days to three months. Persistent (chronic) pain lasts beyond three months or beyond expected healing. Crucially, the sympathetic signs are absent — the autonomic system adapts. A patient with chronic pancreatitis reporting 9 out of 10 pain while lying still with a heart rate of 72 and normal blood pressure is not lying. Normal vital signs never rule out pain, and this single point costs students more examination items than almost any other.

Untreated pain is not merely uncomfortable, and you should be able to recite the physiologic bill. Splinting and shallow breathing after abdominal or thoracic surgery produce atelectasis, retained secretions and pneumonia. Immobility produces venous stasis and deep vein thrombosis, deconditioning, pressure injury and constipation. Catecholamine surge increases myocardial oxygen demand and can precipitate ischaemia in a patient with coronary disease. Cortisol and catecholamines cause hyperglycaemia, immune suppression and impaired wound healing. Sleep deprivation and pain are the two most modifiable contributors to delirium in hospitalised older adults. And unrelieved acute pain is itself the strongest predictor of the transition to persistent post-surgical pain, through the phenomenon of central sensitisation — the dorsal horn learns to amplify. Treating pain early and adequately is therefore not comfort care layered on top of medical care; it is medical care.

Section 2Assessment: Believing It, Measuring It, Documenting It

Self-report is the standard, and the standard is not negotiable

The patient’s report of pain is the single most reliable indicator of its existence and intensity. Not the vital signs, not the grimace, not your impression of how much a laparoscopic cholecystectomy “should” hurt. Research on nurse–patient pain agreement is consistent and unflattering: nurses systematically underestimate pain, and underestimate it most in older adults, in patients of a different race or language than their own, and in patients with a history of substance use. Your first professional obligation in this chapter is to accept the number you are given and then decide what to do about it.

Structure the history rather than asking “how bad is it?” and moving on. OLDCARTS works well on a med-surg floor: Onset, Location, Duration, Characteristics, Aggravating factors, Relieving factors, Treatment tried, Severity. PQRSTU is the equivalent: Provocation and Palliation, Quality, Region and Radiation, Severity, Timing, and Understanding — what does the patient believe is causing it, and what is an acceptable level? That last element is the one students skip and the one that changes care. Ask for a functional goal, not just a number: “What number lets you take a deep breath, cough and walk to the bathroom?” A patient whose goal is 3 out of 10 to ambulate gives you a target you can titrate to and document against. Chasing a numeric zero with opioids alone is how patients are oversedated.

Intensity is conventionally banded as mild 1–3, moderate 4–6 and severe 7–10 on a 0–10 numeric rating scale, and those bands drive order-set selection. Note that pain was formally retired as “the fifth vital sign” because tying opioid dosing to a number alone contributed to overprescribing. The number remains essential; it simply is not a stand-alone order for an opioid. Assess intensity, function, sedation and respiratory status together.

Choosing the right tool

The correct scale is the one the patient can actually use, and once chosen, it must be used consistently — switching tools between shifts destroys trend data. The Numeric Rating Scale (NRS) 0–10 is the default for alert adults. The Verbal Descriptor Scale (none, mild, moderate, severe, worst possible) suits older adults and those with mild cognitive impairment, who often manage words better than numbers. The Faces Pain Scale – Revised and the Wong-Baker FACES scale serve children over three, patients with limited literacy and non-English speakers; teach that the faces represent how much it hurts, not how happy or sad the patient feels.

For patients who cannot self-report, behavioural tools are valid and required. FLACC (Face, Legs, Activity, Cry, Consolability) scores five behaviours 0–2 for a total of 0–10, and is used in children two months to seven years and in non-verbal patients of any age. The Critical-Care Pain Observation Tool (CPOT) scores facial expression, body movement, muscle tension and either ventilator compliance or vocalisation, total 0–8; a score above 2 indicates significant pain. The Behavioral Pain Scale (BPS) ranges 3–12 with a threshold above 5. PAINAD (Pain Assessment in Advanced Dementia) scores breathing, negative vocalisation, facial expression, body language and consolability, total 0–10, mapping onto the familiar bands. Remember the hierarchy of pain assessment: attempt self-report first; then look for pathology known to be painful; then observe behaviours; then ask the family or caregiver who knows this person’s baseline; then, if the situation is one that would hurt anyone, offer an analgesic trial and evaluate the behavioural response.

Older adults, cognitive impairment and cultural variation

Older adults are the most undertreated group in the hospital, for reasons that stack. They under-report because they believe pain is an expected part of ageing, because they fear addiction or the loss of independence, and because they do not want to bother a busy nurse. They may use words other than pain — “discomfort,” “aching,” “it’s sore,” “my arthritis is acting up” — so ask about all of them. Sensory losses interfere with scales: enlarge the print, ensure hearing aids and glasses are in place, reduce background noise, and allow longer response time.

In dementia, pain frequently presents as a behaviour change rather than a complaint: new agitation, resistance to care, striking out during a bath, pacing, calling out, withdrawal, refusal to eat, or an acute delirium. Untreated pain is one of the most common reversible causes of delirium in hospitalised older adults, and the reflex to reach for an antipsychotic before ruling out pain, urinary retention, constipation and infection is a documented harm. When a resident with advanced dementia becomes newly combative during transfers, a scheduled low-dose acetaminophen trial is a legitimate and evidence-supported diagnostic step. Culture also shapes expression — some patients are raised to bear pain stoically, others to express it vocally — and neither pattern tells you anything about intensity. Use professional interpreters, never family members, for pain assessment in a patient with limited English proficiency.

Reassessment, red flags and escalation

Reassessment timing is a testable, chartable standard: after intravenous opioid, reassess in 15 to 30 minutes; after oral analgesic, in 60 minutes; after a non-pharmacologic intervention, in 30 to 60 minutes. Document the intensity, the sedation level, the respiratory rate and the effect on function. “Medicated for pain” without a reassessment entry is both a care failure and a legal one.

Some pain is a message rather than a symptom, and these are the calls that must not wait for morning rounds. Pain that is out of proportion to the injury, escalating despite opioids, and worsened by passive stretch of the muscle group — particularly in a casted or splinted extremity, after a tibial fracture, or after a crush injury — is acute compartment syndrome until proven otherwise. Do not elevate the limb above heart level (that reduces perfusion pressure), do not apply ice, loosen or bivalve the cast per protocol, and call the surgeon immediately; pulselessness and paralysis are late signs and their absence is reassuring about nothing. New back pain with lower-extremity weakness, numbness or bowel or bladder dysfunction in a patient with an epidural catheter suggests spinal or epidural haematoma — a surgical emergency requiring immediate notification of anaesthesia and urgent MRI. Sudden severe chest pain, a rigid abdomen, a cold pulseless leg, a sudden severe headache described as the worst of the patient’s life, or calf pain with unilateral swelling all demand assessment before analgesia. And never medicate escalating post-operative pain with a rising heart rate and falling blood pressure without evaluating for haemorrhage.

Section 3Pharmacologic Management: Multimodal Analgesia

The non-opioid foundation: acetaminophen and NSAIDs

Every analgesic plan starts with scheduled non-opioids, because they reduce opioid requirement by 30 to 50 percent and therefore reduce every opioid side effect proportionally. Acetaminophen acts centrally, has no anti-inflammatory or antiplatelet effect, and does not injure the gastric mucosa or the kidney. Its ceiling is hepatic: the maximum for a healthy adult is 4 g in 24 hours, and you should reduce this to 2 to 3 g in older adults, in chronic alcohol use, in malnutrition and in known liver disease. The hazard on a med-surg floor is duplication — the patient receives 650 mg scheduled, then a combination product such as oxycodone/acetaminophen or hydrocodone/acetaminophen, then a cold preparation from home. Add every source before you give the next dose. Baseline transaminases matter: ALT 7–56 U/L and AST 10–40 U/L are typical reference ranges, and a rising ALT with an INR climbing above 1.2 in a patient on multi-day acetaminophen is a hold-and-call situation. The antidote for overdose is N-acetylcysteine, most effective within 8 to 10 hours of ingestion.

The non-selective NSAIDs (ibuprofen, naproxen, ketorolac) inhibit both cyclooxygenase isoenzymes and are outstanding for inflammatory, bone and post-operative pain — often superior to opioids after dental and orthopaedic procedures. Their toxicities are predictable from the mechanism. COX-1 inhibition removes gastric prostaglandin protection, producing dyspepsia, ulceration and gastrointestinal bleeding; give with food, add a proton pump inhibitor in high-risk patients, and monitor haemoglobin (12–16 g/dL in women, 13–17 g/dL in men) and stool for melaena. COX-1 inhibition also blocks platelet aggregation — reversibly for the non-selective NSAIDs, irreversibly for aspirin — so these agents add to surgical and gastrointestinal bleeding risk. Prostaglandin inhibition reduces renal afferent arteriolar dilation, so NSAIDs cause acute kidney injury in the volume-depleted, the elderly, and anyone on an ACE inhibitor and diuretic — the “triple whammy.” Check creatinine (0.6–1.2 mg/dL) and avoid NSAIDs when creatinine clearance is below 30 mL/min. They raise cardiovascular risk and are avoided in active peptic ulcer disease and heart failure. In pregnancy, avoid NSAIDs from 20 weeks’ gestation onward because of fetal renal dysfunction and oligohydramnios, and treat them as absolutely contraindicated from about 30 weeks because of premature closure of the ductus arteriosus. Celecoxib is different: it is COX-2 selective, so it largely spares COX-1 — it does not meaningfully inhibit platelet aggregation, which means it does not add to surgical bleeding and is not held for a platelet effect, and it causes substantially less ulceration and gastrointestinal bleeding than the non-selective agents. It keeps the renal and cardiovascular risks of the class in full, and because it is a sulfonamide it is contraindicated in patients with sulfonamide allergy. Ketorolac deserves particular caution: 15 to 30 mg IV every 6 hours, dose-reduced to 15 mg in patients over 65, under 50 kg, or with renal impairment, and limited to five days total across all routes.

Opioids: mechanism, route, equianalgesia and PCA

Opioids bind mu receptors in the dorsal horn, brainstem and limbic system, reducing both transmission and the affective distress of pain. There is no ceiling dose for pure mu agonists — the limit is side effects, chiefly sedation and respiratory depression. Route determines onset and therefore your reassessment window: intravenous onset 5 to 10 minutes with peak at 15 to 30; oral onset 30 to 45 minutes with peak at 60; subcutaneous intermediate. Intramuscular administration is essentially obsolete for pain — erratic absorption, painful injection, and no advantage.

Know a small number of agents deeply. Morphine is the reference standard; its active metabolite morphine-6-glucuronide accumulates in renal impairment and produces prolonged sedation, myoclonus and respiratory depression, so avoid morphine when creatinine clearance is below 30 mL/min. It causes histamine release, hence pruritus and occasional hypotension. Hydromorphone is roughly five to seven times more potent than morphine intravenously, has fewer active metabolites and is preferred in renal impairment — and is also the drug most often involved in fatal ten-fold dosing errors, so read the concentration twice. Fentanyl is highly lipophilic, onset within 1 to 2 minutes intravenously, short duration, haemodynamically stable, and safe in renal failure. The transdermal fentanyl patch is for stable chronic pain only, never for opioid-naive patients and never for acute or post-operative pain; it takes 12 to 24 hours to reach effect and up to 72 hours for steady state, external heat (fever, heating pad, hot shower) accelerates absorption dangerously, and the old patch must be removed and the site documented. Oxycodone and hydrocodone are oral workhorses, frequently combined with acetaminophen. Codeine and tramadol are prodrugs requiring CYP2D6 activation: ultra-rapid metabolisers convert too much and can arrest, poor metabolisers get no relief, and both are contraindicated in children under 12, after tonsillectomy or adenoidectomy, and in breastfeeding. Tramadol additionally lowers the seizure threshold and contributes to serotonin syndrome with SSRIs, SNRIs and triptans. Meperidine should essentially not be used: its metabolite normeperidine accumulates, is not reversed by naloxone, and causes tremor, myoclonus and seizures — it is on the Beers list and contraindicated with MAO inhibitors. Mixed agonist–antagonists such as nalbuphine and butorphanol have a ceiling effect and will precipitate withdrawal in an opioid-dependent patient.

Equianalgesic tables vary between references and are estimates, not equivalences. When rotating a patient from one opioid to another, calculate the equivalent dose and then reduce it by 25 to 50 percent to account for incomplete cross-tolerance, then titrate up. Round doses down, never up, and always verify high-alert opioid doses with a second nurse per policy.

Patient-controlled analgesia gives the patient a small on-demand bolus with a programmed lockout interval (commonly 6 to 10 minutes) and a one- or four-hour limit. It produces better analgesia with lower total dose and higher satisfaction, and its safety rests on one principle: pressing the button requires enough consciousness to press it, so the sedated patient stops dosing. That principle collapses if anyone else presses it. PCA by proxy — a spouse, a well-meaning daughter, or a nurse pressing the button for a sleeping patient — is a recognised cause of fatal respiratory depression, and teaching the family that only the patient presses the button is a required nursing intervention. Continuous basal infusions markedly increase risk in opioid-naive patients and are generally avoided. Nursing responsibilities include verifying pump settings and concentration with a second RN, documenting attempts versus delivered doses (a high attempt-to-delivery ratio means the regimen is inadequate, not that the patient is drug-seeking), monitoring sedation and respiratory rate with continuous pulse oximetry or capnography per policy, and ensuring naloxone is available.

Adjuvants: the drugs that are not analgesics

Adjuvants were developed for other purposes and are indispensable for neuropathic and mixed pain. Gabapentin and pregabalin bind the alpha-2-delta subunit of voltage-gated calcium channels, reducing excitatory neurotransmitter release. They are titrated slowly, cause dizziness, somnolence, ataxia and peripheral oedema, require dose reduction when creatinine clearance falls below 60 mL/min, and must never be stopped abruptly. Their most important nursing implication is additive central nervous system and respiratory depression when combined with opioids, particularly in older adults — a real and under-recognised cause of falls and hypoventilation. Duloxetine, an SNRI, is first-line for diabetic peripheral neuropathy and fibromyalgia; monitor blood pressure and for serotonin syndrome. Tricyclics such as nortriptyline and amitriptyline work at low nightly doses, but their anticholinergic burden — dry mouth, urinary retention, constipation, orthostatic hypotension, confusion — and their cardiac conduction effects place amitriptyline on the Beers list; nortriptyline is the better-tolerated choice in older adults.

Other adjuvants earn their place in specific situations. Corticosteroids (dexamethasone) shrink peritumoural and neural oedema and are excellent for bone pain, malignant spinal cord compression and raised intracranial pressure; monitor glucose. Bisphosphonates and radiotherapy treat metastatic bone pain. Low-dose ketamine infusions blunt NMDA-mediated central sensitisation and are increasingly used for opioid-tolerant patients and refractory pain; watch for dissociation, vivid dreams, hypertension and hypersalivation. Lidocaine 5% patches for postherpetic neuralgia are applied 12 hours on and 12 hours off, up to three patches, to intact skin only. Topical capsaicin depletes substance P but burns on initial application — warn the patient and instruct them not to touch the eyes. Muscle relaxants such as cyclobenzaprine and methocarbamol help acute spasm but sedate; baclofen is used for spasticity and is never stopped abruptly.

Regional and interventional analgesia

Regional techniques deliver the drug to the nerve rather than the whole patient. Peripheral nerve blocks — interscalene for shoulder, femoral or adductor canal for knee, transversus abdominis plane for abdominal surgery — provide hours to days of analgesia with minimal systemic effect. Your teaching points: the limb is numb and weak, so it is at risk for injury and falls; protect it from heat, cold and pressure; do not bear weight until the block has resolved and the physiotherapist clears it; and expect “rebound” pain when it wears off, so take the oral analgesic before sensation fully returns.

Epidural analgesia, typically a local anaesthetic plus a low-dose opioid, is standard after thoracic, abdominal and major orthopaedic surgery and in labour. Monitor for hypotension from sympathetic blockade (have fluids and vasopressors available), for excessive motor block (a patient who cannot lift the leg needs the infusion rate reduced and the provider notified), for urinary retention (bladder scan; neuraxial morphine is a frequent culprit), for pruritus and for respiratory depression, which with hydrophilic neuraxial morphine can occur as late as 12 to 24 hours after the dose. Inspect the insertion site for leakage, erythema and drainage. The catastrophic complication is spinal epidural haematoma: anticoagulation must be timed against catheter placement and removal — with prophylactic enoxaparin, remove the catheter no sooner than 12 hours after the last dose and give the next dose no sooner than 4 hours after removal — and new or progressive lower-extremity weakness, numbness or incontinence requires immediate escalation.

Section 4Opioid Safety, Stewardship and the Patients Who Get It Worst

Sedation comes before respiratory depression — every time

This is the single most important safety concept in the chapter. Opioid-induced respiratory depression is almost never sudden; it is preceded by progressive sedation over minutes to hours. A nurse who assesses only respiratory rate, or who charts “sleeping comfortably” on a patient who cannot be roused to complete a sentence, will miss it. Use a validated sedation scale at every opioid administration and every reassessment. The Pasero Opioid-induced Sedation Scale (POSS) is the standard.

Adjunct monitoring matters. A respiratory rate below 8 to 10 per minute, shallow or irregular respirations, snoring or airway obstruction in a previously quiet patient, or a falling oxygen saturation are all late relative to sedation. Note that supplemental oxygen masks desaturation — a patient on 4 L nasal cannula can hypoventilate to an end-tidal carbon dioxide of 60 mmHg (normal 35–45) while maintaining a saturation of 96 percent. Capnography, where available, detects hypoventilation earlier than pulse oximetry. Highest-risk patients are those who are opioid-naive, over 65, obese, have obstructive sleep apnoea (screen with STOP-BANG), have renal or hepatic impairment, or are receiving concurrent sedatives — benzodiazepines, gabapentinoids, muscle relaxants, antihistamines, sleep aids. Opioid plus benzodiazepine is the most lethal combination on the medical floor.

Naloxone is a pure competitive mu antagonist with onset in 1 to 2 minutes intravenously. In a hospitalised patient receiving therapeutic opioids, giving a full 0.4 mg ampoule is a mistake: it precipitates acute withdrawal, severe uncontrolled pain, hypertension, tachycardia, vomiting, agitation and occasionally pulmonary oedema. Dilute instead — 0.4 mg (1 mL) in 9 mL of normal saline to yield 0.04 mg/mL — and give 0.5 to 1 mL (0.02 to 0.04 mg) intravenously every 1 to 2 minutes, titrating to an adequate respiratory rate and arousability, not to full alertness. In a witnessed apnoeic arrest, give the full dose. Because naloxone’s duration (roughly 30 to 90 minutes) is shorter than that of most opioids, and far shorter than that of extended-release preparations or a fentanyl patch, re-sedation is expected: the patient must be monitored continuously, may require repeat doses or an infusion, and an applied fentanyl patch must be removed. Community naloxone — 4 mg intranasal or auto-injector — should be prescribed and taught to patients at risk and to their families, and that teaching is a nursing responsibility.

The side effects you manage every shift

Tolerance develops to most opioid effects within days — sedation, nausea, respiratory depression, euphoria — but never to constipation. Opioid-induced constipation therefore requires prophylaxis from the first dose, not treatment after five days: a stimulant laxative such as senna 8.6 mg, one to two tablets at bedtime, with or without a stool softener, plus fluid, fibre and mobility as tolerated. Bulk-forming agents such as psyllium alone can worsen impaction in a slow gut and should not be relied upon. When the regimen fails, peripherally acting mu-opioid receptor antagonists — methylnaltrexone subcutaneously, naloxegol or naldemedine orally — reverse gut receptors without reversing analgesia. Track the last bowel movement on every opioid patient; ileus, impaction and perforation start as an undocumented third day.

Nausea and vomiting usually abate in a few days; treat with ondansetron 4 mg or metoclopramide, and consider rotating opioids if persistent. Pruritus is a central mu effect rather than a true allergy, particularly with morphine; low-dose nalbuphine or a naloxone infusion works better than diphenhydramine, which mostly adds sedation. Urinary retention is common after neuraxial opioids and in older men — bladder scan before assuming oliguria. Myoclonus and confusion suggest metabolite accumulation and call for opioid rotation or dose reduction. Distinguish a true allergy (urticaria, angio-oedema, bronchospasm, hypotension) from a predictable side effect (nausea, itching, constipation); labelling a patient “allergic to morphine” because it made them itch narrows every future option they have.

Tolerance, dependence, addiction — and the patients we treat worst

These terms are not synonyms and confusing them harms patients. Tolerance is a physiologic need for more drug to achieve the same effect. Physical dependence is the expected occurrence of withdrawal when the drug is stopped abruptly — it develops in anyone on opioids for more than a week or two and is not addiction. Opioid use disorder is a chronic brain disease defined by compulsive use, craving and continued use despite harm. What used to be called “pseudoaddiction” describes drug-seeking behaviour driven by undertreated pain that resolves when analgesia becomes adequate — clock-watching, requesting a specific drug that has worked before, or appearing anxious before a scheduled dose are all consistent with inadequate dosing rather than misuse.

Two populations pay the price of this confusion. Patients with sickle cell disease in vaso-occlusive crisis wait longer for analgesia in the emergency department than patients with any comparably painful condition, receive smaller doses, and are more often labelled drug-seeking. The standard of care is individualised dosing based on the patient’s own written pain plan or prior effective dose, with the first parenteral opioid given within 30 to 60 minutes of arrival and reassessment every 15 to 30 minutes until controlled; add scheduled non-opioids, maintain hydration and normothermia, provide oxygen only for hypoxaemia, and never use meperidine. Patients with known opioid use disorder on buprenorphine or methadone maintenance need their baseline maintenance dose continued and additional analgesia for acute pain — the maintenance dose treats the disorder, not the fracture. Involve the acute pain service and use regional techniques and non-opioid adjuvants generously. Withholding analgesia from a patient in acute pain does not treat their substance use disorder; it simply causes suffering.

Non-pharmacologic comfort, delegation and discharge teaching

Non-drug measures are not filler; several have real effect sizes and all of them are free of respiratory depression. Cold reduces oedema, spasm and conduction velocity in the first 24 to 48 hours after injury (20 minutes on, with a barrier, and never over an insensate or ischaemic area). Heat relaxes muscle and improves flow in chronic musculoskeletal pain (contraindicated over acute inflammation, bleeding or numbness). Repositioning, splinting an incision with a pillow before coughing, a properly supported limb, an emptied bladder and a quiet dark room at night are the interventions patients report as most helpful. Distraction, guided imagery, music, controlled breathing, progressive muscle relaxation, massage and mindfulness all reduce reported intensity and anxiety. Transcutaneous electrical nerve stimulation, acupuncture, physiotherapy and cognitive behavioural therapy have supporting evidence in persistent pain.

Discharge teaching for an opioid prescription has become a patient-safety intervention in its own right. Cover the following, and document it: take the non-opioid on schedule and the opioid only for breakthrough; never combine with alcohol, benzodiazepines, sleep aids or cannabis; do not drive or operate machinery; start the bowel regimen the same day; count the acetaminophen in every combination product against the 4 g (or lower) daily maximum; store the medication locked and out of reach of children and visitors; dispose of leftovers at a take-back site or per the FDA flush list rather than leaving them in the cabinet; and keep naloxone at home with a family member who knows how to use it. Teach the expected trajectory too — that post-operative opioid need should fall substantially within three to five days — so that patients are not alarmed when they taper, and so they call if pain instead escalates.

Section 5Palliative Care, Symptom Management and Comfort When Cure Is Not the Goal

Palliative care is not hospice, and neither is giving up

Students conflate these constantly and it changes what they tell families. Palliative care is specialised care focused on relief of symptoms, distress and suffering for anyone with a serious illness, at any stage, of any prognosis, delivered alongside curative or life-prolonging treatment. A 34-year-old on induction chemotherapy for leukaemia with a curative intent, a patient with severe COPD, a patient with heart failure awaiting transplant, a patient with advanced dementia — all are appropriate palliative referrals. Trials in advanced lung cancer showed early palliative care improved quality of life, reduced depression, reduced aggressive end-of-life treatment, and in at least one landmark study was associated with longer survival. Hospice is a subset of palliative care with specific eligibility: a prognosis of six months or less if the disease follows its usual course, certified by two physicians, with the patient electing comfort-focused care and generally forgoing disease-directed treatment for the terminal diagnosis. Under the Medicare hospice benefit, hospice provides the interdisciplinary team, medications related to the terminal diagnosis, equipment and bereavement support for up to a year after the death. Hospice care is delivered wherever the patient lives — most often at home.

Advance care planning documents are the other frequent confusion. An advance directive is a legal document created by a competent adult; a living will states what treatments the person would want under specified conditions; a durable power of attorney for health care (health care proxy) names a surrogate decision-maker, and is generally more useful because it covers situations the living will never anticipated. A POLST or MOLST is different in kind: it is a portable medical order set signed by a clinician, actionable by emergency personnel, appropriate for patients with advanced illness. A DNR or AND (allow natural death) order addresses cardiopulmonary resuscitation only — and the teaching point students must be able to deliver to a distressed family is that a DNR order does not mean do not treat. Antibiotics, oxygen, transfusion, analgesia, dialysis, hydration and admission to the ICU all remain on the table unless separately declined. Under the Patient Self-Determination Act, every admitted patient must be asked about advance directives, and the nurse is usually the person who asks.

Managing the symptoms that actually cause suffering

Pain at end of life is treated with the same pharmacology as elsewhere, with two shifts in emphasis: analgesia is given on a scheduled basis with breakthrough doses (typically 10 to 20 percent of the 24-hour total) rather than as needed, and dose ceilings driven by long-term toxicity become irrelevant. When swallowing fails, opioids may be given by concentrated sublingual solution, rectally, subcutaneously or transdermally — intravenous access is rarely required at home.

Dyspnoea is the symptom patients and families fear most, and its first-line treatment surprises students: low-dose opioids. Morphine 2.5 to 5 mg orally, or 1 to 2 mg intravenously, reduces the sensation of breathlessness by reducing respiratory drive and the central perception of air hunger. Supplemental oxygen helps only if the patient is actually hypoxaemic; in a normoxic patient, a handheld fan directed at the face is as effective as oxygen, working through trigeminal nerve stimulation. Add a benzodiazepine such as lorazepam when anxiety compounds the breathlessness, reposition upright, cool the room, reduce clutter and stay in the room — a nurse who leaves during air hunger amplifies it. Treat reversible contributors when consistent with goals: bronchospasm, effusion, anaemia, heart failure.

Nausea is managed by mechanism rather than by habit. Chemoreceptor trigger zone or drug-induced nausea (including opioids) responds to dopamine antagonists — haloperidol or prochlorperazine; delayed gastric emptying responds to metoclopramide; chemotherapy and radiation nausea responds to ondansetron; vestibular nausea responds to scopolamine or meclizine; raised intracranial pressure responds to dexamethasone. Constipation must be prevented relentlessly, because in a bed-bound patient on opioids it becomes obstruction. Excessive oropharyngeal secretions — the “death rattle” — distress the family far more than the patient, who is usually unconscious. Reposition to the side, elevate the head, stop or reduce artificial hydration, suction only the mouth (deep suctioning is traumatic and ineffective), and explain to the family what the sound is and is not. Antimuscarinics such as glycopyrrolate or a scopolamine patch reduce further secretion but do not clear what is already there, so give them early or not at all.

Terminal delirium and restlessness — picking at bedclothes, agitation, reversal of day and night, hallucination — occur in the majority of dying patients. Screen for reversible causes first: pain, urinary retention, faecal impaction, hypoxia, hypercalcaemia, hypoglycaemia, infection, and medications (anticholinergics, benzodiazepines, steroids). Then treat with low-dose haloperidol, reorient gently, keep lighting and the environment consistent, and keep a familiar person present. Physical restraints worsen delirium and are avoided. Anorexia, cachexia and dehydration in the final weeks are the body shutting down, not starvation; artificial nutrition and hydration at this stage do not improve survival or comfort and increase oedema, secretions and aspiration risk. Offer comfort feeding — whatever the patient wants, whenever they want it — and meticulous mouth care with a moist swab and lip balm, which relieves the sensation of thirst far better than an intravenous bag.

The last days, the ethics, and the family you are also caring for

Recognising the final days lets you prepare the family, and preparing the family is the intervention they remember. Expect progressive weakness and bed-bound status, withdrawal from surroundings, minimal intake, decreased urine output that becomes dark and scant, cool and mottled extremities beginning at the knees and feet, blood pressure that falls and a pulse that becomes thready, Cheyne-Stokes respirations with lengthening apnoeic pauses, terminal secretions, and reduced level of consciousness. Tell the family what is coming before it happens, in plain language, and tell them that hearing is believed to persist — encourage them to speak, to say what needs saying, and to give permission. Many families need to be told it is acceptable to leave the room, to eat, to sleep, and that patients sometimes die in the few minutes a vigil steps out.

Two ethical points recur on examinations and at the bedside. The principle of double effect holds that an intervention with a good intended effect (relief of pain or air hunger) is ethically permissible even if it carries a foreseen but unintended risk (hastened death), provided the intent is comfort, the dose is titrated to symptom relief, and the good effect is not achieved through the bad one. In practice, appropriately titrated opioids at end of life have not been shown to shorten survival; the fear of “giving the dose that kills them” causes far more suffering than the drug ever has. Palliative sedation — lowering consciousness to relieve refractory symptoms — is distinct in intent and method from euthanasia and physician-assisted death, and requires documented refractory symptoms, informed consent and interdisciplinary review. Nurses have a right to conscientious objection in jurisdictions permitting medical aid in dying, but never a right to abandon a patient; you must transfer care safely.

After the death: confirm and document per policy, allow the family as much time as they need, offer to help with bathing and dressing if they wish to participate, honour cultural and religious practices around handling the body, provide information on funeral arrangements and bereavement resources, and remember organ or tissue donation referral where applicable. Then take care of yourself. Repeated exposure to death without processing produces compassion fatigue and moral distress; debriefing, peer support, employee assistance and a genuine break at the end of a shift are professional obligations, not weakness. You cannot pour comfort from an empty cup for a whole career.

Words worth knowing

Infection, Sepsis and the Immunocompromised Patient

Infection is the one problem that will follow you into every room on a med-surg floor. It arrives as a post-operative wound that suddenly smells wrong, as a urinary catheter that should have come out two days ago, as an oncology patient whose only complaint is that she feels “a little off,” and as the eighty-four-year-old who is not febrile at all but is confused for the first time in his life. Sepsis is the deadliest thing that happens on general medical-surgical units, and it is deadly largely because it is recognised late. This chapter builds the reasoning from the inside out: why a pathogen produces the vital signs you see, how the laboratory confirms or refutes your suspicion, what must happen in the first hour, which antimicrobials demand which monitoring, and how all of it changes when the patient’s immune system has been removed by disease, by chemotherapy or by a bottle of prednisone.

Section 1Infection, Host Defence and the Chain of Transmission

Why infection looks the way it does

An organism becomes a clinical problem only when it crosses a barrier and multiplies faster than the host can clear it. What happens next is not the microbe attacking you; it is your own immune system responding. Bacterial cell walls, flagella and DNA carry repeating molecular signatures called pathogen-associated molecular patterns. Tissue macrophages and dendritic cells recognise these signatures through toll-like receptors and release the first wave of cytokines: tumour necrosis factor alpha, interleukin-1 and interleukin-6. Every classic sign of infection traces back to that wave.

Interleukin-1 and interleukin-6 travel to the hypothalamus and drive prostaglandin E2 synthesis, which raises the thermoregulatory set point. The body is not simply hot; it now believes 39 degrees Celsius is correct, which is why the patient shivers, complains of cold and pulls up blankets while the thermometer climbs. Rigors are the muscular work of reaching the new set point. When the set point falls — spontaneously or after antipyretics — the patient diaphoreses. This is also why covering a rigoring patient with warm blankets is humane rather than counterproductive: you are not fighting the fever, you are letting the set point do its work while you treat the cause.

The same cytokines make endothelium leaky and vasodilated. Locally that produces the four cardinal signs Celsus described: redness and heat from vasodilation, swelling from plasma leaking into the interstitium, pain from bradykinin and prostaglandins on nociceptors. Neutrophils marginate, roll along the activated endothelium, squeeze between cells and phagocytose; the residue of that battle is pus. Systemically the identical process produces warm flushed skin, a bounding pulse, a widened pulse pressure and a falling blood pressure — the paradox of a patient who looks pink and feels warm while perfusing poorly. Understanding that one mechanism spares you from memorising two separate lists of manifestations.

The chain of infection and where nursing breaks it

Six links must connect for transmission to occur: an infectious agent, a reservoir where it lives, a portal of exit, a mode of transmission, a portal of entry and a susceptible host. Nursing practice is essentially a set of deliberate attacks on specific links. Sterilising instruments attacks the agent. Changing the bed of a patient with draining wounds attacks the reservoir. Covering a cough attacks the portal of exit. Hand hygiene attacks the mode of transmission and is the highest-yield intervention available to you. Removing an indwelling urinary catheter or a peripheral IV attacks the portal of entry. Immunisation, glycaemic control and nutrition attack host susceptibility.

The World Health Organization’s five moments for hand hygiene are the operational form of this reasoning: before touching a patient, before a clean or aseptic procedure, after body fluid exposure risk, after touching a patient, and after touching the patient’s surroundings. That last moment is the one most often skipped and the one that seeds outbreaks, because bed rails, pumps and keyboards are reservoirs. Alcohol-based rub is preferred for routine decontamination because it is faster, more effective against most vegetative bacteria and gentler on skin than soap. Soap and water are required when hands are visibly soiled and when the organism forms spores — Clostridioides difficile and Bacillus anthracis — because alcohol does not kill spores; the friction and rinsing physically remove them.

Healthcare-associated infection and the bundles

Roughly one hospitalised patient in thirty-one carries a healthcare-associated infection on any given day, and four categories dominate med-surg practice: central line-associated bloodstream infection, catheter-associated urinary tract infection, ventilator-associated pneumonia and surgical site infection. These are treated as preventable events, which means the interventions are bundled, audited and, in most institutions, nurse-driven. Bundles work only when every element is performed every time; partial compliance produces most of the burden and none of the benefit.

For central lines: full-barrier precautions at insertion, chlorhexidine skin antisepsis, avoidance of the femoral site, scrub the hub for at least fifteen seconds with alcohol or chlorhexidine before every access, sterile dressing changes every seven days for transparent dressings or every two days for gauze, and daily review of whether the line is still needed. For urinary catheters: insert only for accepted indications, maintain a closed system, keep the bag below the level of the bladder and off the floor, secure the tubing to prevent traction, and remove the catheter as early as possible — the single strongest predictor of catheter-associated infection is duration. For ventilated patients: head of bed elevated 30 to 45 degrees, daily sedation interruption and spontaneous breathing trials, oral care with chlorhexidine per protocol, and subglottic suctioning. For surgical patients: appropriate prophylactic antibiotic within sixty minutes before incision (120 minutes for vancomycin and fluoroquinolones), normothermia, glucose control and clippers rather than razors for hair removal.

Standard and transmission-based precautions

Standard precautions apply to every patient regardless of diagnosis and assume that all blood, body fluids, secretions, excretions except sweat, non-intact skin and mucous membranes may be infectious. Transmission-based precautions layer on top of — never instead of — standard precautions. Selecting them correctly is a reliable NCLEX item and a reliable source of real harm when it is done wrong, because a patient with pulmonary tuberculosis placed on droplet precautions exposes an entire unit.

Section 2Recognising Infection: Assessment, Laboratory and Cultures

The bedside assessment: trends beat single numbers

Infection is usually announced by a trend rather than by a threshold. A heart rate that has drifted from 78 to 96 to 112 over three sets of vital signs is more informative than one reading of 112, and a respiratory rate that has crept from 16 to 24 is the earliest and most neglected vital sign in deterioration. Tachypnoea appears early because rising lactate is buffered by bicarbonate, producing carbon dioxide that the patient must blow off; the respiratory system compensates before the blood pressure fails. This is why counting respirations for a full minute, rather than copying the monitor, catches sepsis hours ahead of hypotension.

Fever is defined as a single oral temperature of 38.3 degrees Celsius (101 degrees Fahrenheit) or higher, or a temperature of 38.0 degrees Celsius (100.4 degrees Fahrenheit) sustained for at least one hour. Hypothermia below 36.0 degrees Celsius (96.8 degrees Fahrenheit) in a patient who looks unwell is more ominous than fever, not less, because it signals a host response that has failed. Assess mental status every shift and compare it to the family’s description of baseline; new confusion, lethargy or agitation is organ dysfunction of the brain. Then localise: lungs (cough, sputum change, crackles, falling saturation), urine (dysuria, frequency, flank or suprapubic pain, cloudy or malodorous urine), skin and wounds (erythema extending beyond the incision, purulent drainage, dehiscence, tenderness out of proportion), lines (insertion-site erythema, tenderness, purulence), abdomen (distension, absent bowel sounds, rebound) and the mouth and perineum, which are the two areas students most often skip.

Many units run an automated screening score — MEWS, NEWS2 or a sepsis alert — that fires on combinations of temperature, heart rate, respiratory rate, blood pressure, oxygen saturation and level of consciousness. Treat a positive screen as a mandate to lay eyes on the patient within minutes, not as a task to acknowledge in the chart. Treat a negative screen as no reassurance at all when your assessment says otherwise; scores miss the atypical presentations that kill.

Reading the laboratory picture

The white blood cell count with differential is the starting point but it is frequently misread. Leukocytosis supports infection; leukopenia in an acutely ill patient supports overwhelming infection or marrow failure and is a worse prognostic sign. What matters most is the differential. Neutrophils are produced and released in stages; under demand the marrow discharges immature band forms. When bands exceed about 10 percent of the differential — bandemia, the “left shift” — the marrow is being driven hard, and a left shift can be present when the total count is still normal. A patient with a white count of 9,000 and 18 percent bands is more infected than a patient with a count of 14,000 and no bands.

Lactate deserves its own sentence of caution. It is treated as a marker of anaerobic metabolism, but it also rises from catecholamine-driven glycolysis, from impaired hepatic clearance and from albuterol, metformin and seizures. That does not make it useless — a lactate above 2 mmol/L in a patient with suspected infection independently predicts mortality — but it means you interpret it beside the patient, and you repeat it. A lactate that falls after fluid is reassuring; a lactate that climbs from 2.6 to 4.8 despite resuscitation is a call to the provider whether or not the blood pressure has moved.

Cultures, collected correctly

Cultures are the difference between guessing and knowing, and the nurse controls their quality. Draw two sets of blood cultures from two separate venipuncture sites, each set consisting of an aerobic and an anaerobic bottle, with 8 to 10 mL of blood per bottle in adults. Volume is the strongest determinant of yield; under-filled bottles are the commonest reason a true bacteraemia is missed. Disinfect the skin with chlorhexidine-alcohol and let it dry fully, scrub the bottle tops with alcohol, and do not palpate the site after prep unless you re-glove. If a central line is present, one set may be drawn through the line and one peripherally so the laboratory can compare time to positivity and decide whether the line itself is the source.

Cultures go before antibiotics — but they never delay antibiotics in a patient with septic shock. The working standard is that culture collection should not push the first dose beyond about 45 minutes. If you cannot obtain access, you say so out loud and the antibiotic goes in. Collect urine from the sampling port of a catheter after cleaning it, never from the drainage bag, and change a catheter that has been in more than two weeks before culturing. Expectorated sputum should be deep-cough material, not saliva; a specimen with abundant squamous epithelial cells will be rejected. Wound cultures are taken from viable tissue after cleansing with normal saline, not by swabbing surface slough or pus, which grows colonisers.

Then interpret with judgement. A single blood culture bottle growing coagulase-negative staphylococcus at 48 hours in a well patient is usually skin contamination; the same organism in both sets from a patient with a tunnelled catheter is real. Bacteria in the urine of an asymptomatic older adult is asymptomatic bacteriuria and should not be treated — treating it drives resistance and C. difficile without improving anything. Colonisation is presence; infection is presence plus host response.

The older adult presents differently — expect it

Baseline temperature falls with age, so an older adult’s “normal” may be 36.4 degrees Celsius and a temperature of 37.8 degrees Celsius (100 degrees Fahrenheit) may represent a substantial fever. Up to half of frail older adults with serious infection never mount a temperature above 38 degrees Celsius at all. Use the geriatric definitions: a persistent oral temperature above 37.2 degrees Celsius (99 degrees Fahrenheit), a rectal temperature above 37.5 degrees Celsius, or a rise of 1.1 degrees Celsius (2 degrees Fahrenheit) over the patient’s own baseline is significant.

What appears instead is functional: new confusion or delirium, a fall, incontinence in a previously continent patient, anorexia, weakness, or simply “she is not herself.” Delirium is an infection until proven otherwise in a hospitalised older adult. Beta blockers blunt the tachycardia you expect, so a heart rate of 88 may already be relative tachycardia. Chronic hypertension shifts the autoregulatory curve, so a systolic pressure of 110 in a patient who usually runs 165 is functional hypotension even though it clears every threshold on the screening tool. The lesson is not that older adults are confusing; it is that you must know their baseline before the shift begins.

Section 3Sepsis and Septic Shock: the First Hour

From infection to organ failure

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Every word carries weight. It is not simply a severe infection; it is a response that has stopped being proportionate and has begun injuring the host. The cytokine storm that was helpful at the wound edge becomes systemic. The endothelial glycocalyx — the sugar-protein layer that keeps vessels sealed — is stripped away, and plasma pours into the interstitium. The patient becomes intravascularly dry and interstitially waterlogged at the same time, which is why she gains six kilograms of oedema while remaining hypotensive.

Simultaneously, inducible nitric oxide synthase floods the vasculature with nitric oxide, producing vasodilation that no longer responds normally to endogenous catecholamines. Systemic vascular resistance falls, cardiac output initially rises, and the classic warm shock appears: warm extremities, brisk capillary refill, bounding pulses and a low diastolic pressure. Meanwhile the coagulation cascade activates, tissue factor is expressed, and microthrombi plug capillary beds while anticoagulant pathways are consumed — disseminated intravascular coagulation, in which the patient clots and bleeds at once. Blood is present in the organ but cannot be distributed to the cells that need it, and mitochondria injured by inflammatory mediators cannot use the oxygen that does arrive. That combination of maldistribution and cytopathic hypoxia is what raises lactate and what kills kidneys, liver, lungs and brain.

The clinical picture follows the organs as they fail: brain (confusion, agitation, obtundation), lung (tachypnoea, hypoxaemia, the bilateral infiltrates of acute respiratory distress syndrome), kidney (urine output under 0.5 mL/kg/hr, rising creatinine), liver (rising bilirubin), marrow (falling platelets), gut (ileus) and skin (mottling of the knees, delayed capillary refill in late or cold shock). Septic shock is the subset in which vasopressors are required to maintain a mean arterial pressure of at least 65 mmHg and lactate remains above 2 mmol/L after adequate fluid resuscitation; hospital mortality in that group exceeds 40 percent.

Screening: SIRS, qSOFA and SOFA

Three frameworks coexist and students are tested on all of them. Systemic inflammatory response syndrome criteria — temperature above 38 or below 36 degrees Celsius, heart rate above 90, respiratory rate above 20 or PaCO2 under 32 mmHg, white count above 12,000 or under 4,000 or more than 10 percent bands — are sensitive and non-specific; two of four in a patient with suspected infection is a screen, not a diagnosis. Quick SOFA uses three bedside items: respiratory rate 22 or higher, altered mentation, and systolic blood pressure 100 mmHg or lower. Two of three identifies patients at higher risk of dying, but qSOFA is deliberately insensitive and current Surviving Sepsis guidance recommends against using it as the sole screening tool; NEWS or MEWS perform better for screening. The full Sequential Organ Failure Assessment score grades six systems — respiration, coagulation, liver, cardiovascular, central nervous system and renal — and an acute rise of 2 points or more defines organ dysfunction and therefore sepsis.

Practically, on the floor, you are screening constantly and informally: is there a plausible source, and is any organ behaving badly? Suspected infection plus new confusion, plus a respiratory rate of 26, plus a systolic of 96 is sepsis until proven otherwise, and the correct response is to escalate before the laboratory confirms you.

The Hour-1 bundle and the order of operations

The Surviving Sepsis Campaign consolidated resuscitation into a bundle begun immediately upon recognition. For septic shock or high-probability sepsis, antibiotics go in within one hour; where sepsis is possible but not certain and shock is absent, a rapid focused work-up within three hours is acceptable.

Order matters, and NCLEX will make you choose. Airway and breathing come first: if the patient is hypoxaemic, oxygen goes on before anything else, and you do not leave the room to fetch it. Circulation is next, which in practice means establishing two large-bore intravenous lines — without access, nothing else in the bundle can happen. Cultures precede antibiotics only because they take ninety seconds; if access is difficult, antibiotics win. Fluids and antibiotics then run concurrently. Insert a urinary catheter only if hourly output measurement is genuinely needed, remembering you are trading information for a portal of entry. Recheck the blood pressure, mental status and lactate rather than assuming the bundle worked.

Fluid responsiveness is judged dynamically, not by a single central venous pressure. A passive leg raise that raises stroke volume, or pulse-pressure variation on an arterial line, predicts benefit from more fluid; a patient with new crackles, rising oxygen requirement and jugular venous distension has moved past that point and needs vasopressors rather than another litre. Norepinephrine is the first-line agent because it raises systemic vascular resistance with modest chronotropy; vasopressin is commonly added at a fixed 0.03 units/min to spare norepinephrine dose; epinephrine is added for inadequate response. Intravenous hydrocortisone, typically 200 mg per day, is considered for shock that continues to require vasopressors. Transfuse red cells at a haemoglobin threshold of 7 g/dL unless there is active bleeding or ischaemia, keep glucose at or below 180 mg/dL with an insulin infusion, and pursue source control — abscess drainage, infected line removal, debridement — as soon as it is feasible, because antibiotics cannot sterilise undrained pus.

Escalating: red flags and SBAR

Escalate in SBAR so nothing gets lost. Situation: “This is Marcus, RN, on 4 West. Room 412, Mrs. Alvarez, 68, post-op day 3 from a sigmoid colectomy. I am concerned she is septic.” Background: “She has diabetes and hypertension, home lisinopril and metformin, no known drug allergies. She has been afebrile until this evening.” Assessment: “Temperature 38.7, heart rate 118 sinus tachycardia, respirations 26, blood pressure 92/48 with a MAP of 63, saturation 91 percent on room air, and she is confused, which is new. Her abdomen is distended and tender and the incision has purulent drainage. Urine output is 15 mL over the last two hours. Lactate is 3.9.” Recommendation: “I would like sepsis orders now: two sets of blood cultures and a wound culture, broad-spectrum antibiotics, a 30 mL/kg lactated Ringer bolus, a repeat lactate in two hours, and I think she needs surgical evaluation and probably a higher level of care. I have started oxygen at 2 litres and placed a second large-bore IV. Can you come see her?”

Section 4Antimicrobial Therapy, Toxicity and Stewardship

Empiric therapy, then de-escalation

The first antibiotic a septic patient receives is a guess, but an educated one. Empiric selection is driven by the suspected source, the likely organisms for that source, whether the infection was acquired in the community or in a healthcare setting, the patient’s prior cultures and resistance history, local antibiogram data and drug allergies. Broad coverage is chosen deliberately because the cost of missing the organism in a shocked patient is death, while the cost of two extra days of a broad agent is manageable.

The corresponding obligation is de-escalation. At 48 to 72 hours the cultures and susceptibilities return, and therapy should narrow to the narrowest effective drug, switch from intravenous to oral when the patient is stable and the gut works, and stop at a defined duration. Prolonged broad therapy is not caution; it selects resistant organisms, invites C. difficile and fungal superinfection, prolongs line days and adds toxicity. Nurses drive this by ensuring cultures are actually collected, by flagging the day-three antibiotic review, and by advocating for the oral switch and the line removal that follows it.

Classes by mechanism

The four monitoring problems that come up on every floor

Vancomycin. Dosing for serious MRSA infection now targets an area-under-the-curve to minimum inhibitory concentration ratio of 400 to 600, calculated by pharmacy; where trough monitoring is still used, the goal is 15 to 20 mcg/mL for serious infection and the trough is drawn within 30 minutes before the fourth dose. Monitor creatinine at least every two to three days, and more often when the patient also receives piperacillin-tazobactam, an aminoglycoside, a contrast load or a diuretic. Vancomycin infusion reaction — flushing, erythema of the face, neck and upper torso, pruritus, sometimes hypotension — is a rate-related direct release of histamine from mast cells, not an IgE allergy. The correct response is to stop the infusion, give an antihistamine as ordered, and restart at a slower rate, infusing each gram over at least 60 minutes. Documenting it as an allergy wrongly denies the patient the best MRSA drug for the rest of their life.

Aminoglycosides. With traditional dosing, gentamicin and tobramycin peaks run 5 to 10 mcg/mL and troughs must be under 2 mcg/mL; the trough is what predicts toxicity. Many institutions use extended-interval dosing with a single random level. Ototoxicity is often permanent and often first reported by the patient as tinnitus, fullness or a feeling of unsteadiness when turning the head — ask specifically, every day, and report it immediately.

Allergy versus intolerance. Nausea from erythromycin is an intolerance. Hives, wheeze, angioedema or hypotension after a beta-lactam is an allergy. Take the history precisely: what drug, what happened, how long after the dose, what treatment was needed. Most patients labelled penicillin-allergic are not, and the label pushes them toward vancomycin and fluoroquinolones with worse outcomes. If anaphylaxis occurs, stop the infusion, maintain the airway, call for help, and give epinephrine 0.3 to 0.5 mg of the 1 mg/mL concentration intramuscularly into the lateral thigh, repeating every 5 to 15 minutes as needed — epinephrine is the treatment; antihistamines and steroids are adjuncts that do nothing for airway oedema in the first minutes.

Clostridioides difficile. Antibiotic exposure, especially fluoroquinolones, clindamycin, cephalosporins and carbapenems, allows toxin-producing C. difficile to overgrow the colon. Suspect it with three or more unformed stools in 24 hours; do not test formed stool, and do not repeat testing after a positive result. Place the patient on contact precautions in a private room with dedicated equipment, perform hand hygiene with soap and water, and clean with a sporicidal bleach agent. First-line treatment is oral vancomycin 125 mg four times daily for 10 days or oral fidaxomicin 200 mg twice daily for 10 days; metronidazole is now reserved for when neither is available. Intravenous vancomycin does not treat colitis because it does not reach the colonic lumen — a classic examination distractor. Antimotility agents such as loperamide are avoided because retaining toxin risks toxic megacolon; report abdominal distension, absent bowel sounds and a rising white count urgently.

Stewardship, resistance and what the patient must hear

Multidrug-resistant organisms — MRSA, vancomycin-resistant enterococcus, extended-spectrum beta-lactamase producers, carbapenem-resistant Enterobacterales and Candida auris — are the direct product of antimicrobial pressure combined with imperfect hand hygiene. Stewardship programmes exist to shorten courses, narrow spectra and stop unnecessary therapy, and they depend on bedside data that nurses generate: accurate temperature trends, documented stool frequency, honest allergy histories and timely cultures.

Teaching is short and non-negotiable. Complete the full prescribed course even after feeling better, unless the prescriber stops it. Never save or share leftover antibiotics. Take doses at even intervals to keep concentrations above the inhibitory level. Report rash, watery diarrhoea, new tendon or heel pain, hearing change and severe nausea. Understand which drug needs food and which needs an empty stomach, which requires sun protection, and which forbids alcohol. The old blanket warning that every antibiotic defeats an oral contraceptive is not supported; only rifampin and rifabutin meaningfully reduce hormonal contraceptive efficacy, so backup contraception is taught with those agents rather than routinely. And a viral upper respiratory infection does not need an antibiotic — a sentence you will say hundreds of times.

Section 5The Immunocompromised Patient

Who is immunocompromised, and which defence is missing

“Immunocompromised” is not one condition; it is at least four different holes, and the hole determines the organism. A neutropenic patient has lost the phagocytic arm and is vulnerable to gram-negative bacilli including Pseudomonas, gram-positive skin organisms and, after prolonged neutropenia, Aspergillus and Candida. A patient with impaired cell-mediated immunity — advanced HIV, solid organ transplant on tacrolimus, high-dose corticosteroids, TNF-alpha inhibitors — is vulnerable to intracellular organisms: tuberculosis, Pneumocystis jirovecii, cytomegalovirus, Listeria, fungi and reactivating herpes viruses. A patient with impaired humoral immunity or absent spleen cannot opsonise encapsulated bacteria and is at risk of fulminant pneumococcal, meningococcal and Haemophilus influenzae type b sepsis. And a patient with broken barriers — burns, mucositis, central lines, drains, poorly controlled diabetes — is vulnerable to whatever is on their skin.

Corticosteroids deserve specific attention because they are everywhere on a med-surg floor. Prednisone at 20 mg per day or more, continued for two weeks or longer, is generally considered clinically significant immunosuppression. Steroids also blunt the febrile response and can mask peritonitis, so a patient on chronic prednisone with a perforated viscus may present with a soft, minimally tender abdomen and almost no fever — distrust the absence of rigidity in a steroid-treated patient rather than explaining rigidity away. Anti-TNF biologics such as infliximab and adalimumab require tuberculosis screening with an interferon-gamma release assay or tuberculin skin test before initiation because they reactivate latent disease. Uncontrolled diabetes impairs neutrophil chemotaxis and phagocytosis; glycaemic control is infection control.

The unifying clinical consequence is that immunocompromised patients cannot generate the signs you rely on. Without neutrophils there is no pus, so an abscess may show only tenderness; a chest radiograph may be clear in early neutropenic pneumonia because the infiltrate is made of neutrophils; peritoneal signs may be absent. Fever, or sometimes only hypothermia and hypotension, may be the entire presentation — and it must be treated as if it were the whole picture, because it is.

The absolute neutrophil count and neutropenic fever

The absolute neutrophil count is the number that matters. Calculate it as the total white blood cell count multiplied by the sum of the percentage of segmented neutrophils and the percentage of bands, divided by 100. A patient with a white count of 2,100 cells/mm³, 18 percent segs and 4 percent bands has an ANC of 2,100 × 0.22, or 462 cells/mm³ — severe neutropenia, even though the white count alone does not look alarming. Do the arithmetic yourself; do not assume the laboratory reported it.

Febrile neutropenia is defined as a single oral temperature of 38.3 degrees Celsius (101 degrees Fahrenheit) or a temperature of 38.0 degrees Celsius (100.4 degrees Fahrenheit) sustained over one hour, in a patient with an ANC under 500 or an ANC expected to fall below 500 within 48 hours. It is an oncologic emergency with the same urgency as chest pain. The nursing sequence is: recognise the fever, notify the provider immediately, draw blood cultures including one set from every lumen of any central line, and give the first dose of an antipseudomonal beta-lactam — cefepime, piperacillin-tazobactam or meropenem — within 60 minutes. Vancomycin is added for suspected line infection, skin or soft-tissue infection, haemodynamic instability or known MRSA colonisation. Do not wait for the white count to result, do not wait for the radiograph, and do not administer an antipyretic before the provider has seen the temperature, because acetaminophen can mask the next fever.

Protecting the patient: environment, prophylaxis and vaccines

Neutropenic precautions on a med-surg unit are practical rather than mystical: a private room, meticulous hand hygiene by everyone entering, no visitors with respiratory or gastrointestinal illness, no fresh flowers or potted plants and no standing water in vases or humidifiers, no construction dust exposure, scrupulous oral care with a soft brush and non-alcohol rinse, daily skin and perineal inspection, and daily bathing. Allogeneic stem cell transplant recipients require a true protective environment: a positive-pressure room with HEPA filtration and at least 12 air exchanges per hour, and a mask on the patient whenever they leave it. Strict low-microbial diets have largely been abandoned as unhelpful, but food safety remains: thoroughly cooked food, no unpasteurised dairy, no raw eggs, no undercooked meat or raw seafood, and thorough washing of any fresh produce.

Pharmacologic support matters too. Granulocyte colony-stimulating factors, filgrastim and pegfilgrastim, shorten the duration of neutropenia; warn the patient about bone pain, which is expected, treatable with acetaminophen or a non-steroidal agent, and a sign the marrow is responding. Prophylaxis follows the missing defence: trimethoprim-sulfamethoxazole for Pneumocystis when the CD4 count falls under 200 cells/mm³ or during prolonged high-dose steroids; azithromycin for Mycobacterium avium complex when the CD4 count falls under 50; acyclovir for herpes reactivation; an antifungal for prolonged profound neutropenia. Asplenic patients need pneumococcal, meningococcal and Haemophilus influenzae type b vaccination and must carry documentation, because overwhelming post-splenectomy infection can kill within hours.

Vaccination teaching has one hard rule: inactivated vaccines — inactivated influenza, pneumococcal, tetanus-diphtheria-pertussis, recombinant zoster, hepatitis B — are safe and encouraged, while live attenuated vaccines are contraindicated in significant immunosuppression. That list includes measles-mumps-rubella, varicella, live attenuated zoster, intranasal influenza, oral typhoid and yellow fever. Household contacts should be vaccinated, which protects the patient by cocooning; the one caution is that a household contact who receives live oral polio or develops a varicella vaccine rash needs temporary separation.

Priorities, delegation and discharge

When you have four patients and one is immunocompromised, the prioritisation logic is unchanged but the thresholds move. Airway, breathing and circulation still come first. Unstable outranks stable. Acute outranks chronic. Actual outranks potential risk. What changes is what counts as unstable: a temperature of 38.3 degrees Celsius in a neutropenic patient outranks chest tightness that has already been evaluated and treated, because the neutropenic fever is an untreated emergency with a one-hour clock. When two patients seem equal, ask which problem will kill faster if you guess wrong.

Discharge teaching for the immunocompromised patient is a short list repeated until it is automatic. Take your temperature any time you feel unwell and call immediately for 38.0 degrees Celsius (100.4 degrees Fahrenheit) or higher — do not take acetaminophen and wait to see what happens. Know your nadir, the seven-to-fourteen-day window after chemotherapy when counts are lowest. Wash hands, avoid crowds and sick contacts during the nadir, wear a mask when advised. Do not garden, change cat litter, clean bird cages or handle reptiles. Use an electric razor and a soft toothbrush; avoid flossing if the platelet count is low. Call for chills or rigors, cough, shortness of breath, burning on urination, new mouth sores, redness or drainage at a line site, diarrhoea, or a rash. Keep the phone number for the on-call oncology service on the refrigerator, and bring the medication list to every visit. Confirm understanding by teach-back rather than by asking whether they have questions.

Words worth knowing

Respiratory Disorders: Airway and Obstructive Disease

Obstructive lung disease is the quiet backbone of every med-surg floor. The patient in 412 with a COPD exacerbation, the twenty-two-year-old in 408 whose asthma flared after a viral illness, the man in 415 with a new tracheostomy and a mucus plug he cannot clear — all three are failing at the same physiologic step, which is moving air out. In obstructive disease the problem is not getting air in; it is emptying the chest before the next breath arrives. Air stacks, the chest hyperinflates, the diaphragm flattens, the work of breathing climbs, and eventually carbon dioxide rises. Everything you will do — positioning, bronchodilators, pursed-lip breathing, oxygen titration, airway clearance, teaching — is aimed at that single mechanical problem. This chapter builds the mechanism first, then the assessment, the diagnostics with real numbers, the drug classes by what they actually do, and the priority logic the NCLEX and your charge nurse will both demand of you.

Section 1Gas Exchange, Focused Assessment and the Tests That Matter

Ventilation, perfusion and why obstruction hurts on the way out

Two things must happen for a patient to oxygenate: air must reach the alveoli (ventilation) and blood must reach those same alveoli (perfusion). When the two are matched, gas exchange is efficient. When they are mismatched — ventilated alveoli with no blood flow, as in pulmonary embolism, or perfused alveoli with no air, as in a mucus-plugged lobe — oxygenation falls. Obstructive disease is fundamentally a ventilation problem, and the specific place it fails is exhalation.

Inhalation is active. The diaphragm contracts, the thorax enlarges, intrathoracic pressure drops and air is pulled in; the negative pressure around the airways actually helps hold them open. Exhalation in a healthy person is passive, driven by the elastic recoil of lung tissue. In obstructive disease that recoil is lost (emphysema destroys the elastin scaffolding) or the lumen is narrowed by smooth-muscle spasm, mucosal oedema and thick secretions (asthma, chronic bronchitis). Now the patient must push air out, and pushing raises the pressure around the small airways, which collapses them before the alveoli have emptied. Air stacks behind the closed airway. This is air trapping, and it is the single mechanism that explains nearly every finding in this chapter.

Follow the consequences. Trapped air means the lungs sit at a larger resting volume, so the chest becomes hyperinflated and the anteroposterior diameter approaches the lateral diameter — the barrel chest. Hyperinflation flattens the diaphragm; a flat diaphragm is a mechanically inefficient muscle, so the patient recruits sternocleidomastoid, scalene and intercostal muscles and leans forward onto their elbows to fix the shoulder girdle and give those accessory muscles something to pull against. That is the tripod position, and it is not a comfort preference — it is a compensation. Trapped air also means each new breath begins against a positive alveolar pressure the patient must overcome before any air moves, which is the intrinsic PEEP that makes these patients so exhausting to breathe for. Finally, because carbon dioxide is cleared by ventilation, failure to empty the chest eventually raises PaCO₂.

The focused respiratory assessment

Start before you touch the patient. From the doorway, count the respiratory rate for a full minute (normal 12–20 breaths per minute in an adult) and watch the ratio of inspiration to expiration. Normal is roughly 1 to 2. In obstruction it stretches to 1 to 3 or 1 to 4, and a prolonged expiratory phase is one of the most reliable and most under-documented findings on a med-surg floor. Note the position, the ability to speak in full sentences, the use of accessory muscles, nasal flaring, and whether the skin at the suprasternal notch or between the ribs pulls in with each breath. A patient who can speak only three or four words between breaths is in significant distress regardless of what the pulse oximeter reads.

Auscultate systematically, comparing side to side, apex to base, anterior and posterior, over bare skin. Wheezes are continuous musical sounds produced by air moving through narrowed airways, classically expiratory in obstruction; inspiratory and expiratory wheezing means more severe narrowing. Rhonchi are low-pitched, snoring or gurgling sounds from secretions in larger airways and characteristically change or clear with coughing. Crackles are discontinuous popping sounds from the opening of collapsed alveoli or from fluid, and they point you toward pneumonia, heart failure or atelectasis rather than pure obstruction. Stridor is a high-pitched inspiratory crow heard without a stethoscope and means upper airway obstruction until proven otherwise — it is an emergency.

The finding students most often mis-read is the silent chest. Wheezing requires airflow. A patient who was wheezing loudly an hour ago and is now quiet, with a rising respiratory rate, rising heart rate, a drowsy affect and a falling ability to speak, has not improved — they have stopped moving enough air to make noise. That is impending respiratory arrest, and the correct action is to call for help, apply oxygen, prepare for continuous nebulised bronchodilator and anticipate intubation, not to chart “lungs clear.”

Round out the exam with percussion (hyperresonance over hyperinflated lung), a look at the fingernails for clubbing, and the sputum. Clubbing is worth memorising because it is not a feature of uncomplicated COPD or asthma. When you see it, think bronchiectasis, cystic fibrosis, lung cancer or interstitial disease. Document sputum by colour, consistency, volume and whether it changed — a change from clear-white to thick yellow-green with increased volume is one of the three cardinal signs of a COPD exacerbation.

Arterial blood gases, oximetry and capnography

Learn the reference values cold, because you will be asked to interpret gases at three in the morning: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, PaO₂ 80–100 mmHg and SaO₂ 95–100 percent on room air. Read a gas in three steps. First, is the pH acidotic, alkalotic or normal? Second, which value moves in the direction that would explain the pH — a high PaCO₂ explains an acidosis (respiratory), a low HCO₃⁻ also explains an acidosis (metabolic). Third, has the other system compensated? If the pH has returned into range while both PaCO₂ and HCO₃⁻ are abnormal, compensation is complete.

Apply that to obstruction. A patient in an early, frightening asthma attack hyperventilates: pH 7.48, PaCO₂ 28, HCO₃⁻ 23 — an acute respiratory alkalosis, which is the expected gas. If that same patient is rechecked an hour later and the gas reads pH 7.36, PaCO₂ 41, the temptation is to relax. Do not. A tachypneic, struggling asthmatic should be blowing off carbon dioxide. A normalising PaCO₂ in that setting means the patient is tiring and can no longer sustain the minute ventilation. It is the gas that precedes intubation.

Contrast that with the patient who has lived with COPD for fifteen years: pH 7.36, PaCO₂ 58, HCO₃⁻ 32, PaO₂ 62 on 2 L nasal cannula. That is a compensated respiratory acidosis and it may be this patient’s baseline. The kidney has retained bicarbonate over months to buffer chronic hypercapnia. You do not treat that number; you treat the change from it. If the same patient presents with pH 7.24 and PaCO₂ 78, that is acute-on-chronic respiratory acidosis and it earns a rapid response call, non-invasive ventilation and an intensivist.

Two bedside adjuncts deserve mention. Continuous waveform capnography reports end-tidal CO₂, normally 35–45 mmHg, and in obstruction the waveform loses its square shape and takes on a “shark-fin” upslope that visibly improves as bronchodilators work — it is the earliest objective sign of response. Arterial line draws and radial punctures require you to hold pressure for five minutes, or twenty minutes if the patient is anticoagulated. Then expel any air bubbles, cap the syringe, mix it and have it run at room temperature within thirty minutes. A modern plastic syringe is not routinely iced: chilling plastic accelerates oxygen diffusion through the barrel wall and falsely raises the PaO₂, and prolonged cooling leaks potassium out of the cells. Ice only a glass syringe, or a plastic syringe whose analysis will be delayed well beyond thirty minutes, and note on the requisition that the specimen was chilled.

Spirometry, peak flow and imaging

Spirometry is the diagnostic gold standard for obstructive disease. Two numbers matter. FVC is the total volume forcibly exhaled after a maximal inhalation. FEV₁ is the volume exhaled in the first second. In obstruction the FEV₁ falls further and faster than the FVC, so the ratio drops. A post-bronchodilator FEV₁/FVC ratio below 0.70 confirms persistent, incompletely reversible airflow limitation and is the diagnostic threshold for COPD. In restrictive disease the ratio is normal or high while both volumes shrink — a useful contrast to keep straight.

Reversibility separates asthma from COPD. Repeat spirometry ten to fifteen minutes after a short-acting bronchodilator; an increase in FEV₁ of at least 12 percent and at least 200 mL is a significant bronchodilator response and supports asthma. When baseline spirometry is normal but the history is suggestive, a methacholine challenge is used; a fall in FEV₁ of 20 percent or more is positive for airway hyperresponsiveness. Fractional exhaled nitric oxide (FeNO) of 25 ppb or higher in an adult suggests eosinophilic airway inflammation likely to respond to inhaled corticosteroids.

Peak expiratory flow is the home version — less precise, but the number the patient will actually use. Teach the patient to establish a personal best over two weeks of good control and then to act on zones: green is 80–100 percent of personal best (continue current plan), yellow is 50–79 percent (use the reliever, follow the written action plan, contact the provider if not back to green), red is below 50 percent (take the reliever and seek emergency care now). Nursing pointers: stand up, seal the lips tightly, blow one hard fast blast, do three attempts and record the highest, and measure at the same time each day before bronchodilators.

Imaging is supportive rather than diagnostic in obstruction. A chest radiograph in advanced COPD shows hyperinflation, flattened hemidiaphragms, a narrow vertical heart and increased retrosternal air space; its real job is to rule out pneumonia, pneumothorax, effusion or a mass. High-resolution CT is the test of choice for bronchiectasis, where it shows dilated, thickened airways with “tram-track” and “signet-ring” signs. Supporting labs include a CBC (white cells 5,000–10,000/mm³; haematocrit above 55 percent suggests chronic hypoxemia), a blood eosinophil count (300 cells/µL or more predicts steroid responsiveness), alpha-1 antitrypsin level in emphysema under age 45 or without smoking history, and BNP, where a value below 100 pg/mL makes heart failure an unlikely cause of the dyspnoea.

Section 2Asthma: Reversible Obstruction and the Rescue Plan

Pathophysiology: three narrowings, not one

Asthma is a chronic inflammatory disorder of the airways with variable, largely reversible obstruction. An inhaled trigger — allergen, cold air, exercise, viral infection, smoke, aspirin or an NSAID, a beta-blocker, gastro-oesophageal reflux, emotional stress — activates mast cells and eosinophils in a sensitised airway. Mediators including histamine, leukotrienes and prostaglandins are released, and three things happen at once: bronchial smooth muscle contracts (bronchospasm), the mucosa becomes oedematous, and goblet cells pour out thick tenacious mucus. Each narrowing is additive. This is why a bronchodilator alone opens the airway only partially and why the inflammation must be treated as well.

There are two phases. The early phase begins within minutes and is dominated by bronchospasm; it responds beautifully to a short-acting beta₂-agonist. The late phase arrives four to twelve hours later, is dominated by eosinophilic inflammation and mucosal swelling, and does not respond well to bronchodilators at all. That biphasic pattern is the reason a patient who feels better in the emergency department can deteriorate at home overnight, and the reason systemic corticosteroids are given even when the patient improves acutely.

Over years, repeated inflammation produces airway remodelling — subepithelial fibrosis, smooth-muscle hypertrophy and mucous gland hyperplasia — which converts some of the reversible obstruction into fixed obstruction. Preventing remodelling is the entire argument for adherence to controller therapy in a patient who feels perfectly well between attacks, and it is the single most important thing you will teach.

Assessment, severity and diagnostics

The classic triad is wheezing, cough (often nocturnal or early morning) and chest tightness with dyspnoea. Ask about the pattern: what triggers it, how often the reliever inhaler is used, whether symptoms wake the patient at night, whether school or work is missed, and — the highest-yield question — whether the patient has ever been intubated or admitted to intensive care for asthma. A history of intubation identifies a patient at high risk of a fatal attack and changes your threshold for escalation permanently.

Grade severity at the bedside using speech, posture, accessory muscles, mental status and peak flow rather than a single number. In a mild-to-moderate exacerbation the patient speaks in phrases, wheezes on expiration, has a peak flow of 50–79 percent of personal best and an oxygen saturation above 92 percent. In a severe exacerbation the patient speaks in single words, sits upright or tripods, uses accessory muscles, wheezes throughout inspiration and expiration, has a peak flow below 50 percent and a saturation below 90 percent. In life-threatening asthma the chest is silent, the patient is drowsy or confused, the effort is feeble, and cyanosis, bradycardia or hypotension appear.

Diagnostics: spirometry with a bronchodilator response of at least 12 percent and 200 mL, peak flow variability, FeNO, blood eosinophils, and allergy testing when triggers are unclear. During an acute attack, obtain an ABG only if the patient is severe or deteriorating — and interpret it against the effort, as above. Serum potassium (normal 3.5–5.0 mEq/L) matters more than students expect, because repeated beta₂-agonist dosing drives potassium into cells and a patient on continuous albuterol can become genuinely hypokalaemic.

Pharmacology: relievers, controllers and the ones that are never rescue

Short-acting beta₂-agonists (SABA) — albuterol, levalbuterol — stimulate beta₂ receptors on bronchial smooth muscle, relaxing it within five minutes and lasting four to six hours. This is the rescue drug. Expect tachycardia, tremor, nervousness and hypokalaemia; teach the patient that these effects are common and not an allergy. Short-acting muscarinic antagonists (SAMA) — ipratropium — block acetylcholine-mediated bronchoconstriction, take about fifteen minutes to work, and are added to albuterol in moderate-to-severe exacerbations but are not a rescue drug on their own. Anticholinergic effects are dry mouth, urinary retention and blurred vision, and the drug is used cautiously in narrow-angle glaucoma and benign prostatic hyperplasia.

Inhaled corticosteroids (ICS) — fluticasone, budesonide, beclomethasone — are the cornerstone controller. They suppress airway inflammation over days to weeks and have no acute effect whatsoever, which is why a patient must be told explicitly, in plain language, that this inhaler will not help during an attack and must still be taken every day. Teach rinsing and spitting after each use to prevent oral candidiasis and hoarseness, and use of a valved holding chamber or spacer to reduce oropharyngeal deposition. Long-acting beta₂-agonists (LABA) — salmeterol, formoterol — provide twelve hours of bronchodilation and must never be used as monotherapy in asthma; they are always combined with an inhaled corticosteroid. Current guidance increasingly favours an ICS–formoterol combination used as both maintenance and reliever, because it treats the inflammation every time the patient reaches for relief.

Leukotriene receptor antagonists — montelukast, zafirlukast — block leukotriene-mediated bronchoconstriction and inflammation, are oral, and are useful in exercise-induced and aspirin-sensitive asthma. The two are not interchangeable at the bedside, and the difference is entirely a nursing-teaching difference. Montelukast is taken once daily in the evening, with or without food, and it is montelukast — not the class — that carries a boxed warning for serious neuropsychiatric events including agitation, depression, sleep disturbance and suicidal thinking; ask about mood at every encounter and tell families what to watch for. Zafirlukast is 20 mg twice daily and must be taken on an empty stomach, at least one hour before or two hours after a meal, because food reduces its absorption by roughly 40 percent. Zafirlukast also needs liver-enzyme monitoring, since hepatic injury has been reported — teach the patient to report anorexia, nausea, right upper quadrant pain, dark urine or jaundice — and it raises warfarin levels, so the INR is watched closely when the two are given together. Biologics — omalizumab (anti-IgE), mepolizumab and benralizumab (anti-IL-5), dupilumab (anti-IL-4/13) — are reserved for severe eosinophilic or allergic asthma; omalizumab carries a risk of anaphylaxis, so observe the patient after injection and ensure epinephrine is available. Methylxanthines — theophylline — are rarely used now because of a narrow therapeutic index; the therapeutic serum level is roughly 10–20 mcg/mL and many clinicians target 5–15 mcg/mL. Toxicity begins with nausea, vomiting, insomnia and tachycardia and progresses to dysrhythmias and seizures. Caffeine potentiates it; smoking accelerates its metabolism.

Status asthmaticus, priorities and teaching

Status asthmaticus is a severe exacerbation that does not respond to standard bronchodilator and corticosteroid therapy. Priorities in order: place the patient in high Fowler or tripod position, apply oxygen titrated to a saturation of 93–95 percent, give continuous or back-to-back nebulised albuterol with ipratropium, establish IV access, give systemic corticosteroids (methylprednisolone IV or prednisone orally — onset four to six hours, so give early), and stay with the patient. Add magnesium sulfate, typically 2 g IV over twenty minutes, for severe refractory bronchospasm; it relaxes smooth muscle, and you monitor for hypotension, flushing and loss of deep tendon reflexes. Subcutaneous or intramuscular epinephrine is used when anaphylaxis is part of the picture. Heliox and non-invasive ventilation are bridges; intubation is the endpoint if the patient tires.

Sedatives and opioids are avoided in an unstable asthmatic outside of controlled intubation because they blunt respiratory drive. Do not give a beta-blocker — even an ophthalmic one such as timolol — and check the home list for it. Hydrate the patient adequately to thin secretions, but remember that a struggling asthmatic often cannot drink; IV fluids may be needed.

Teaching is where nursing changes outcomes. Every asthmatic goes home with a written asthma action plan in zones tied to their own peak flow numbers and symptoms. Demonstrate inhaler technique and have the patient teach it back — studies consistently show most patients use inhalers incorrectly, and a mis-used inhaler is an untaken drug. Cover trigger avoidance concretely (dust-mite covers, no indoor smoking, pet management, humidity control, pre-medicating with a SABA fifteen minutes before exercise), annual influenza vaccination and current COVID-19 and pneumococcal vaccination as indicated, and the specific circumstances that mean go to the emergency department now: peak flow below 50 percent of personal best, no relief from the reliever, inability to speak a full sentence, or lips and nail beds turning blue.

Section 3COPD: Emphysema, Chronic Bronchitis and the Exacerbation

Two mechanisms under one name

Chronic obstructive pulmonary disease is persistent, largely irreversible airflow limitation caused by an abnormal inflammatory response to noxious particles — cigarette smoke above all, plus occupational dust, biomass cooking fuel and air pollution. It is conventionally described as two overlapping processes, and understanding both explains the whole clinical picture.

In emphysema, proteolytic enzymes released by inflammatory cells digest the alveolar walls. Alveoli merge into large floppy air sacs called bullae. Two things are lost: surface area for gas exchange, and the elastic recoil that drives passive exhalation and tethers the small airways open. The result is severe air trapping, hyperinflation, a barrel chest, marked dyspnoea, minimal cough, weight loss from the caloric cost of breathing, and pursed-lip breathing adopted spontaneously because it creates back-pressure that splints the airways open. Because ventilation and perfusion are lost together in the same destroyed unit, hypoxemia is relatively mild until late — this is the patient older texts called the “pink puffer.”

In chronic bronchitis, defined clinically as a productive cough for at least three months in each of two consecutive years, the insult is to the airway lining. Goblet cells and mucous glands hypertrophy, cilia are destroyed, and the airway fills with mucus it can no longer clear. Perfused alveoli sit behind plugged airways, so shunt physiology produces earlier and more severe hypoxemia and hypercapnia, with cyanosis, polycythaemia, right-sided heart strain and peripheral oedema — the “blue bloater.” Most real patients sit somewhere between these two portraits. A separate cause worth knowing is alpha-1 antitrypsin deficiency. Alpha-1 antitrypsin is not an enzyme; it is an anti-enzyme — a protease inhibitor made by the liver whose job is to neutralise the neutrophil elastase that inflammatory cells release into the airway. When it is hereditarily deficient that elastase is left unopposed and digests the alveolar walls. Suspect it in emphysema before age 45, in a never-smoker, or with a strong family history, and note that it produces lower-lobe rather than upper-lobe disease.

Assessment, staging and diagnostics

Expect a barrel chest with an anteroposterior-to-lateral ratio approaching 1 to 1, prolonged expiration, diminished breath sounds (the destroyed lung transmits sound poorly — quiet is bad here too), hyperresonance to percussion, distant heart sounds, use of accessory muscles, and often a thin, wasted body habitus with a large chest. The patient may sleep in a recliner. Ask about the pack-year history: packs per day multiplied by years smoked. Grade functional dyspnoea by what the patient can no longer do — one flight of stairs, walking to the mailbox, dressing.

Diagnosis requires post-bronchodilator spirometry showing an FEV₁/FVC ratio below 0.70. Severity is then graded by FEV₁ as a percentage of predicted: GOLD 1 (mild) FEV₁ 80 percent or more, GOLD 2 (moderate) 50–79 percent, GOLD 3 (severe) 30–49 percent, GOLD 4 (very severe) below 30 percent. Additional expected findings: an ABG showing compensated respiratory acidosis, a haematocrit above 55 percent from chronic hypoxemic stimulation of erythropoietin, a chest film with flattened diaphragms and increased retrosternal air space, and an ECG that may show right axis deviation or P pulmonale from right heart strain.

Management: what actually changes the trajectory

Only three interventions are proven to prolong survival in COPD: smoking cessation, long-term oxygen therapy in patients with resting hypoxemia, and lung volume reduction surgery or transplantation in carefully selected patients. Everything else improves symptoms and reduces exacerbations, which matters enormously for quality of life but does not change the slope of decline. Smoking cessation is the only intervention that slows the annual loss of FEV₁, and it works at any age and any stage — say so, every admission, without lecturing. Offer nicotine replacement, varenicline or bupropion and a referral.

Bronchodilators are the pharmacologic backbone. Long-acting muscarinic antagonists (LAMA) — tiotropium, umeclidinium, aclidinium — are first-line and reduce exacerbations; tiotropium is a once-daily maintenance drug and is never a rescue inhaler. If it comes as a capsule for a dry-powder device, teach the patient that the capsule is placed in the inhaler and is never swallowed. LABAs are added or combined. Inhaled corticosteroids are added in COPD only for frequent exacerbators, particularly those with a blood eosinophil count of 300 cells/µL or more, because in COPD they raise the risk of pneumonia. Roflumilast, a phosphodiesterase-4 inhibitor, reduces exacerbations in severe chronic-bronchitis-predominant disease with FEV₁ below 50 percent; monitor for weight loss, diarrhoea and psychiatric symptoms. Chronic low-dose azithromycin reduces exacerbations in selected patients but requires baseline ECG for QT and hearing monitoring.

Long-term oxygen therapy is indicated when resting PaO₂ is 55 mmHg or less, or SpO₂ is 88 percent or less; or when PaO₂ is 56–59 mmHg in the presence of cor pulmonale, right heart failure or a haematocrit above 55 percent. To improve survival it must be worn at least fifteen hours a day, and ideally continuously. This is a teaching problem more than a prescribing problem: patients take it off to shower, to eat, to go out, and the survival benefit evaporates. Set the target saturation at 88–92 percent in a chronically hypercapnic patient. Titrating far above that risks worsening hypercapnia through several mechanisms — release of hypoxic pulmonary vasoconstriction worsening ventilation–perfusion matching, the Haldane effect, and to a lesser degree reduced respiratory drive. That said, never withhold oxygen from a hypoxemic patient out of fear of CO₂ retention. Give what is needed, titrate down, and watch.

Non-pharmacologic care is where nurses do the most good. Teach pursed-lip breathing (inhale through the nose for a count of two, exhale slowly through pursed lips for a count of four to six) to prevent airway collapse and reduce air trapping, and diaphragmatic breathing with a hand on the abdomen. Refer to pulmonary rehabilitation, which reliably improves exercise capacity and dyspnoea. Address nutrition directly: these patients burn extra calories to breathe and become breathless while eating, so offer small frequent calorie-dense high-protein meals, rest before eating, use bronchodilators before meals, avoid gas-forming foods that splint the diaphragm, and monitor weight weekly. Ensure influenza vaccination annually plus pneumococcal, COVID-19, RSV and Tdap vaccination as indicated. Assess mood; anxiety and depression are extremely common and worsen dyspnoea.

Exacerbations and complications

A COPD exacerbation is diagnosed by the three cardinal signs: increased dyspnoea, increased sputum volume, and increased sputum purulence. Viral or bacterial infection is the most common trigger. Management is bronchodilators (nebulised albuterol with ipratropium), systemic corticosteroids for roughly five days, antibiotics when all three cardinal signs are present, or when two are present and one of them is increased sputum purulence, or when the patient needs invasive or non-invasive ventilatory support, controlled oxygen to a target of 88–92 percent, and non-invasive positive pressure ventilation (BiPAP) for acute hypercapnic respiratory acidosis. BiPAP in this setting reduces intubation rates and mortality; it is one of the highest-value interventions in respiratory medicine, and the nursing work is skin protection at the mask, monitoring for gastric distension and aspiration risk, and reassessing the gas in one to two hours.

Complications to anticipate: cor pulmonale, right ventricular failure secondary to chronic hypoxic pulmonary vasoconstriction, presenting with jugular venous distension, dependent oedema, hepatomegaly, ascites and a loud pulmonic second heart sound — treated by correcting the hypoxemia, with diuretics for congestion. Secondary polycythaemia raises viscosity and thrombotic risk. Spontaneous pneumothorax occurs when a bulla ruptures; suspect it with sudden unilateral pleuritic pain, absent breath sounds on that side and tracheal deviation away from the affected side in tension physiology. Respiratory failure, pneumonia, venous thromboembolism, osteoporosis from chronic steroids and inactivity, and skeletal muscle wasting round out the list.

Escalate immediately — and use SBAR — for a change in mental status, a respiratory rate above 30 or falling toward exhaustion, saturation that will not rise despite appropriate oxygen, accessory muscle use with paradoxical abdominal motion, a pH below 7.30, or new haemodynamic instability. Situation: “This is Maria, RN, on 4 West. Mr. Alvarez in 412 with a COPD exacerbation has become confused in the last thirty minutes.” Background: “He is day two, on 2 L nasal cannula, baseline gas last night pH 7.36, PaCO₂ 56.” Assessment: “Respiratory rate 32, saturation 86 percent on 2 L, using accessory muscles, oriented to person only, breath sounds markedly diminished.” Recommendation: “I have him upright and I have increased oxygen while I call. I need you at the bedside now, and I would like an ABG and an order for BiPAP.”

Section 4Bronchiectasis, Cystic Fibrosis and Sleep-Disordered Breathing

Bronchiectasis: the airway that cannot clear itself

Bronchiectasis is permanent, abnormal dilation and destruction of bronchial walls, usually the consequence of a vicious cycle: an initial insult (severe pneumonia, tuberculosis, aspiration, an inhaled foreign body, immunodeficiency, cystic fibrosis) impairs mucociliary clearance; retained secretions become colonised; chronic infection releases enzymes that destroy the elastic and muscular wall; the floppy dilated airway clears even less well; and the cycle accelerates.

The hallmark is a chronic productive cough with copious purulent sputum — often described in cupfuls, worst on rising, and layering into three levels when left standing. Expect crackles, wheezes, recurrent respiratory infections, fatigue, weight loss and digital clubbing. Haemoptysis is common because the dilated airway wall erodes into bronchial arteries; small streaks are frequent, but massive haemoptysis is a genuine emergency in which the patient is positioned with the bleeding lung down to protect the good lung, oxygen is applied and interventional bronchial artery embolisation is arranged.

Diagnosis is by high-resolution CT. Management is chronic and unglamorous: daily airway clearance (active cycle of breathing, oscillating positive expiratory pressure device such as a flutter or Acapella, high-frequency chest wall oscillation vest, postural drainage), hydration, bronchodilators, sputum cultures to guide antibiotics, treatment of exacerbations with a longer antibiotic course of ten to fourteen days, vaccination, and pulmonary rehabilitation. Nursing role: schedule airway clearance before meals to avoid vomiting, document sputum volume and character every shift as an objective outcome measure, and reinforce that clearance is done every day, not only when sick.

Cystic fibrosis: one gene, many organs

Cystic fibrosis is an autosomal recessive disorder of the CFTR chloride channel. Defective chloride transport at epithelial surfaces means water is not drawn into secretions, so mucus everywhere in the body becomes thick and sticky. In the lungs this produces obstruction, chronic infection (Staphylococcus aureus early, Pseudomonas aeruginosa later) and progressive bronchiectasis. In the pancreas, thick secretions plug the ducts and cause exocrine insufficiency with malabsorption, steatorrhoea and failure to thrive, and eventually CF-related diabetes. Sweat glands cannot reabsorb chloride, so the sweat is salty — the parent’s report that the baby tastes salty is a genuine clinical clue.

Diagnosis is by newborn screening followed by a sweat chloride test: a value of 60 mmol/L or greater is diagnostic, 30–59 mmol/L is intermediate and requires further testing, and below 30 mmol/L is normal. Genetic testing identifies the specific CFTR variant, which now determines therapy.

Management has been transformed by CFTR modulators such as elexacaftor–tezacaftor–ivacaftor, which partially correct the defective protein in patients with eligible variants; monitor liver enzymes and for cataracts. Respiratory care follows a specific and testable order: bronchodilator first to open the airway, then mucolytics — inhaled dornase alfa, which cleaves the DNA released by dead neutrophils, and hypertonic saline 7 percent, which draws water onto the airway surface — then airway clearance to move the loosened secretions, and finally inhaled antibiotics such as tobramycin so the drug is deposited in a cleared airway. Nutritional care is equally essential: pancreatic enzyme replacement with every meal and every snack, taken with the food and never crushed or chewed if enteric-coated; fat-soluble vitamins A, D, E and K; a high-calorie, high-protein diet; and added salt, especially in hot weather or with exercise, because salt losses are large. Teach strict infection prevention and segregation from other CF patients to prevent cross-infection.

Obstructive sleep apnea and upper airway obstruction

Obstructive sleep apnea is repetitive collapse of the pharyngeal airway during sleep despite continued respiratory effort. Each apnoea produces desaturation and a surge of sympathetic activity that arouses the patient briefly; the arousals fragment sleep and the desaturations plus sympathetic surges drive hypertension, atrial fibrillation, pulmonary hypertension, stroke risk, insulin resistance and daytime somnolence. Risk factors are obesity, a large neck circumference, male sex, older age, retrognathia, tonsillar hypertrophy, alcohol and sedatives.

Screen with STOP-BANG (Snoring, Tiredness, Observed apnoea, Pressure, BMI above 35, Age above 50, Neck circumference above 40 cm, Gender male); a score of three or more indicates elevated risk. Diagnosis is by polysomnography, reported as the apnea–hypopnea index: 5–15 events per hour is mild, 15–30 moderate, and above 30 severe. Treatment is CPAP, plus weight loss, positional therapy, avoidance of alcohol and sedating drugs, and in selected patients an oral appliance or surgery.

The med-surg relevance is perioperative and pharmacologic. A patient with untreated or unrecognised OSA who receives opioids, benzodiazepines or anaesthesia is at high risk of postoperative airway obstruction and respiratory arrest, particularly in the first 24 hours and particularly during the first uninterrupted sleep. Bring the patient’s own CPAP machine into the hospital and use it whenever they sleep, including naps; nurse them with the head of bed elevated and in a lateral rather than supine position; use continuous pulse oximetry and, when opioids are given, capnography; use multimodal non-opioid analgesia; and never assume a quiet, sleeping postoperative patient is a comfortable one.

Acute upper airway obstruction — from a foreign body, angioedema, anaphylaxis, epiglottitis, tumour, trauma or post-extubation laryngeal oedema — announces itself with stridor, drooling, an inability to speak, severe anxiety and rapidly progressive distress. This is the most time-critical scenario in the chapter. Do not leave the patient. Call for emergency help, keep the patient upright and calm, give high-flow oxygen, avoid anything that agitates them, and prepare for a difficult airway with intubation or surgical airway equipment at the bedside. For a conscious choking adult with a complete obstruction, perform abdominal thrusts; if the patient becomes unresponsive, begin CPR and look in the mouth for a visible object before each set of ventilations. In anaphylaxis, intramuscular epinephrine into the lateral thigh is the first drug and antihistamines and steroids are adjuncts, never substitutes.

Section 5Airway Management, Oxygen Delivery and Setting Priorities

Oxygen delivery devices and oxygen safety

Oxygen is a drug. It requires an order (or protocol), a dose, a route, a target and reassessment, and it carries real toxicity: prolonged high concentrations cause absorption atelectasis and, over days, oxidative alveolar injury. Choose the device by how much oxygen the patient needs and how precisely you need to control it, and remember that with any low-flow device the actual inspired concentration falls as the patient’s minute ventilation rises — a tachypneic patient entrains more room air and gets a lower effective dose.

Safety teaching for home oxygen is a board favourite and a genuine fire-prevention issue: no smoking by the patient or anyone in the home, no open flames or gas stoves near the tubing, keep cylinders upright and secured at least six to ten feet from heat sources, use cotton rather than wool or synthetic blankets to limit static, avoid petroleum-based products on the face (use water-soluble lubricant for dry nares), post “oxygen in use” signage, and keep a working fire extinguisher and smoke alarms. Never adjust the litre flow without an order or a protocol, and always re-check saturation and work of breathing after any change.

Tracheostomy care and suctioning

Keep at the bedside of every tracheostomy patient: the obturator for the current tube, a spare tube of the same size, a spare tube one size smaller, a suction setup, an Ambu bag, and sterile saline and gloves. If the tube becomes dislodged in a mature tract, hyperextend the neck, spread the stoma with a curved haemostat and reinsert the spare tube with the obturator in place, then immediately remove the obturator so the patient can breathe. If the tract is fresh — less than seven days — do not attempt blind reinsertion; call for emergency help, occlude the stoma and ventilate over the mouth and nose with a bag-valve-mask.

Routine care: assess the site every shift for redness, drainage, subcutaneous emphysema and skin breakdown; clean the inner cannula or replace a disposable one per policy; use pre-cut or manufactured tracheostomy dressings and never cut gauze, because loose fibres can be aspirated; secure ties with one to two fingers’ space beneath them; and always have a second person hold the tube while ties are changed. Maintain cuff pressure at 20–25 cmH₂O — higher pressures compress tracheal mucosal capillaries and cause ischaemia, stenosis and fistula, while lower pressures allow aspiration. A cuffed tube prevents aspiration and permits positive-pressure ventilation but blocks airflow through the larynx, so the patient cannot speak; a speaking valve is used only with the cuff fully deflated, and placing one on an inflated cuff is a fatal error.

Suction only when indicated — audible or visible secretions, coarse rhonchi, a rise in peak airway pressure, a fall in saturation, or an ineffective cough — not on a schedule. Technique: explain the procedure, hyperoxygenate with 100 percent oxygen for thirty to sixty seconds, use sterile technique for tracheal suctioning, choose a catheter no larger than half the internal diameter of the airway, set wall suction to 80–120 mmHg for an adult, insert without suction until resistance is met and then withdraw about 1 cm, apply intermittent suction for no more than 10–15 seconds while withdrawing in a rotating motion, allow the patient to recover and re-oxygenate between passes, and limit to two or three passes. Do not instil normal saline before suctioning — it does not thin secretions, it does dislodge bacteria from the tube into the lower airway, and it causes desaturation. Watch for hypoxemia, dysrhythmias from vagal stimulation, bronchospasm, bleeding and raised intracranial pressure. Stop and re-oxygenate for bradycardia, a drop in saturation, or new dysrhythmia.

Inhaler and nebuliser technique — the teaching that actually changes outcomes

For a metered-dose inhaler: shake for five seconds, attach a spacer whenever one is available, exhale fully away from the device, seal the lips around the mouthpiece, begin a slow deep inhalation while actuating one puff, continue inhaling over three to five seconds, hold the breath for ten seconds, exhale slowly, and wait about one minute between puffs of the same drug. When two different inhalers are due, give the bronchodilator first and wait five minutes before the corticosteroid, so the second drug reaches an opened airway. Rinse and spit after any inhaled corticosteroid.

For a dry-powder inhaler, the technique reverses in two important ways: do not shake, do not exhale into the device (humidity clumps the powder), and inhale quickly and forcefully rather than slowly, because the patient’s own effort disaggregates the powder. For a small-volume nebuliser, the patient sits upright and breathes normally with occasional deep breaths through the mouthpiece until the mist stops, typically eight to twelve minutes; tapping the reservoir recovers the last of the dose. Assess heart rate before and after a beta-agonist, and reassess lung sounds, respiratory rate, saturation and the patient’s subjective breathing afterward — that reassessment is the nursing evaluation step and it belongs in your note.

Priorities, delegation and the older adult

When two respiratory patients need you at once, sort with the same three filters every time. First, ABC: airway before breathing before circulation, and within breathing, the patient with the least effective air movement wins. Second, acute over chronic: a new finding beats a chronic one, so a COPD patient at their documented baseline of 89 percent waits while the post-operative patient who has dropped from 97 to 91 percent gets seen. Third, unstable over stable and actual over potential problems. Applying that: a patient with stridor outranks a patient with a silent chest, who outranks a patient wheezing loudly, who outranks a patient asking for a scheduled inhaler. A drowsy patient with a “good” saturation on a non-rebreather outranks nearly everyone, because that combination means CO₂ is climbing.

Older adults change the picture in ways that catch students out. Ageing reduces chest wall compliance and elastic recoil, weakens respiratory muscles, blunts the cough and ciliary clearance, and dulls the ventilatory response to both hypoxia and hypercapnia — so an older patient can be significantly hypoxemic and neither look nor feel distressed. The first sign of hypoxemia or pneumonia in an older adult is frequently new confusion, restlessness or a fall, sometimes with a normal temperature and no cough at all. Treat acute change in mental status in an older patient as hypoxia or infection until proven otherwise, and check a saturation before you reach for anything else. Anticholinergic inhalers may precipitate urinary retention in a man with prostatic enlargement or worsen narrow-angle glaucoma; beta-agonists cause more tremor and tachycardia; theophylline clearance falls, so toxicity appears at doses that were previously safe; and arthritic hands and reduced inspiratory flow may make a metered-dose inhaler or dry-powder device unusable, in which case a spacer or nebuliser is the right accommodation, not a compliance problem.

Words worth knowing

Respiratory Disorders: Infection, Trauma and Failure

Chapter 6 dealt with lungs that cannot move air. This chapter deals with lungs that cannot exchange it — alveoli flooded with pus, pleural spaces filled with blood or air, pulmonary arteries plugged by clot, and finally the whole system failing at once. These are the patients who deteriorate fastest on a med-surg floor, and they almost always warn you before they crash: the respiratory rate climbs, the confusion starts, the oxygen requirement creeps up two litres at a time. Everything that follows rests on one habit — look at the patient, count the respirations yourself, and treat a rising rate as the emergency it is. You will learn the mechanism first, because a student who understands why a shunt does not respond to oxygen never has to memorise the fact. Then assessment, then diagnostics with real numbers, then what you do first, and who on your team may safely do it with you.

Section 1Pneumonia and Lower Respiratory Infection

Why the alveolus fills, and why the patient looks the way she does

Pneumonia begins when an organism reaches the distal airway in a number the host cannot clear. Neutrophils and macrophages arrive, capillary permeability rises, and the alveolar sac fills with protein-rich exudate, cellular debris and bacteria. That single mechanical fact explains nearly every finding at the bedside. A fluid-filled alveolus still receives blood but no longer receives air, so blood leaves that unit as unoxygenated as it arrived — an intrapulmonary shunt. Shunted blood mixes with well-oxygenated blood in the left atrium and drags the arterial saturation down. Because the alveolus is full rather than merely underventilated, adding oxygen to the inspired gas helps less than students expect; this is why a patient with dense multilobar consolidation may sit at 88 percent on a non-rebreather.

Fluid also conducts sound better than air. That is the whole of the physical examination: crackles (air popping open fluid-lined alveoli), bronchial breath sounds heard over the periphery where they do not belong, increased tactile fremitus, dullness to percussion, and egophony — the spoken letter E heard through the stethoscope as A. Inflammation reaching the visceral and parietal pleura produces sharp pleuritic chest pain that worsens on deep inspiration, so the patient splints, breathes shallowly, does not cough, and retains more secretions. The cycle feeds itself, which is precisely why early mobility, analgesia and incentive spirometry are nursing interventions and not comfort measures.

Systemically, cytokines reset the hypothalamic set point (fever, rigors), raise the metabolic rate and increase insensible losses. Tachypnea blows off carbon dioxide, producing an early respiratory alkalosis; a normal or rising PaCO₂ in a tachypneic pneumonia patient is not reassurance, it is fatigue, and it is a call to the provider.

Classifying pneumonia — because the class decides the antibiotic

Community-acquired pneumonia (CAP) develops outside a healthcare facility or within 48 hours of admission. Streptococcus pneumoniae remains the commonest bacterial cause; atypicals (Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella) and respiratory viruses (influenza, SARS-CoV-2, RSV) account for a large share. Hospital-acquired pneumonia (HAP) appears 48 hours or more after admission, and ventilator-associated pneumonia (VAP) 48 hours or more after intubation. Both skew toward Pseudomonas aeruginosa, Staphylococcus aureus including MRSA, and resistant gram-negative rods, so empiric therapy is broader and de-escalation depends on cultures. Aspiration pneumonia follows entry of oropharyngeal or gastric contents and typically involves the dependent segments — the right lower lobe in an upright patient, the posterior segments in a supine one, because the right mainstem bronchus is wider and more vertical.

The older label “healthcare-associated pneumonia” has been retired; current guidance is to treat by local risk factors for resistance rather than by residence. What still matters clinically is the question you ask on admission: has this patient been hospitalised, had IV antibiotics in the last 90 days, or is she immunosuppressed? Those answers drive coverage more than the address on the face sheet.

Assessment, diagnostics and severity scoring

Expect fever (often 38.3 °C or higher), productive cough with rust-coloured or purulent sputum, dyspnea, pleuritic pain, tachycardia and tachypnea. Count the respiratory rate for a full minute — a rate of 30 or more is one of the strongest predictors of deterioration and is the vital sign most often fabricated on a busy floor. Assess mental status every shift; in the older adult, new confusion may be the only presenting sign, arriving before fever, before cough and before any change in saturation.

Chest radiography confirms the diagnosis; a negative film early in dehydration does not exclude it. Laboratory findings support the picture: WBC above the normal 5,000–10,000/mm³ with a left shift (or a frankly low count, which is more ominous), procalcitonin above roughly 0.25 ng/mL suggesting bacterial rather than viral cause, and lactate above 2 mmol/L (normal 0.5–2.0) flagging tissue hypoperfusion and possible sepsis. A pulse oximetry reading below 92 percent on room air, or an ABG showing PaO₂ under 60 mmHg (normal 80–100), signals hypoxemic failure. Send blood cultures, sputum Gram stain and culture, and in the right setting urinary antigens for pneumococcus and Legionella, plus viral PCR panels.

Management, prevention and the aspiration patient

Empiric therapy follows severity and comorbidity. A previously healthy outpatient may receive high-dose amoxicillin, doxycycline or a macrolide. An outpatient with comorbidities, or any inpatient, receives a beta-lactam such as ceftriaxone or ampicillin–sulbactam plus a macrolide, or a respiratory fluoroquinolone (levofloxacin 750 mg, moxifloxacin 400 mg) as monotherapy. Add MRSA coverage (vancomycin, trough-guided, or linezolid) and antipseudomonal coverage (piperacillin–tazobactam, cefepime, meropenem) when risk factors or cultures justify it. Treat for a minimum of five days and until the patient has been afebrile 48–72 hours and clinically stable. Influenza gets oseltamivir 75 mg twice daily for five days, most effective within 48 hours of symptom onset. Hospitalised COVID-19 requiring supplemental oxygen receives dexamethasone 6 mg daily for up to ten days.

Nursing management is unglamorous and decisive. Position upright or in semi-Fowler’s; place the “good lung down” in unilateral disease so gravity delivers perfusion to the lung that can still oxygenate. Encourage 2–3 L of fluid daily unless heart failure or renal disease restricts it, because thick secretions do not clear. Teach incentive spirometry — ten breaths per hour while awake, held three seconds — splinting the chest with a pillow to cough. Give analgesia so the patient can cough. Mobilise early; a patient in a chair for meals develops fewer complications than one on strict bed rest. Monitor vancomycin levels — current guidance for serious MRSA infection is AUC-guided dosing (AUC/MIC 400–600) rather than trough alone, though many facilities still report a trough target of 15–20 mcg/mL for pneumonia — along with renal function.

Prevention is a nursing responsibility you can document. Verify pneumococcal vaccination per current ACIP recommendations (PCV20, or PCV15 followed by PPSV23, for all adults at or above the recommended age and for younger adults with chronic heart, lung, liver or kidney disease, diabetes, immunocompromise, cochlear implants or CSF leak), annual influenza vaccine, and RSV vaccination for eligible older adults. For aspiration risk, screen swallowing before the first oral intake after any stroke or prolonged intubation, keep the head of bed at 30–45 degrees, sit the patient fully upright for meals and 30 minutes afterward, use thickened liquids and chin-tuck if the speech-language pathologist prescribes them, and provide meticulous oral care — colonised plaque is the inoculum.

Section 2Tuberculosis and the Infected Pleural Space

Transmission, latency and reactivation

Mycobacterium tuberculosis travels in droplet nuclei one to five micrometres across, which remain suspended in room air for hours and are inhaled directly to the alveolus. Alveolar macrophages engulf the bacillus but cannot kill it; the organism survives inside the phagosome, and the immune system walls it off in a granuloma. In roughly ninety percent of immunocompetent hosts the story stops there — the person has latent tuberculosis infection: not sick, not infectious, not symptomatic, but harbouring viable organisms with a five to ten percent lifetime risk of reactivation. Anything that weakens cell-mediated immunity raises that risk sharply: HIV, TNF-alpha inhibitors, chronic corticosteroids at 15 mg of prednisone daily or more, transplant immunosuppression, end-stage renal disease, diabetes, malnutrition, and advancing age.

Active pulmonary tuberculosis reactivates most often in the apical and posterior segments of the upper lobes, where oxygen tension is highest. Caseous necrosis liquefies and drains into a bronchus, producing a cavity and making the patient contagious. The classic presentation is deliberately slow: cough of more than three weeks, low-grade afternoon fever, drenching night sweats, unintentional weight loss, anorexia, fatigue and eventually hemoptysis. Because the onset is gradual and the symptoms are nonspecific, patients frequently present after weeks of exposing family, roommates and staff.

Testing, and what airborne precautions actually require

Screening tests detect infection, not disease. The tuberculin skin test (TST) is read at 48–72 hours by palpating induration, never erythema, measured transversely in millimetres. Cut-points are risk-stratified: 5 mm is positive in HIV infection, recent close contacts, patients with fibrotic changes on chest film consistent with prior TB, and the pharmacologically immunosuppressed; 10 mm in recent immigrants from high-prevalence countries, injection drug users, residents and employees of congregate settings, mycobacteriology laboratory staff, and people with diabetes, silicosis, chronic kidney disease or gastrectomy; 15 mm in people with no risk factors. Interferon-gamma release assays (IGRAs) require one blood draw, need no return visit and are not confounded by prior BCG vaccination — the preferred test in anyone BCG-vaccinated or unlikely to return.

A positive screen obligates a chest radiograph and, if abnormal or if symptoms exist, sputum for acid-fast bacilli smear and culture — three specimens collected at least eight hours apart with at least one early-morning sample — plus a nucleic acid amplification test on the first specimen for rapid confirmation. Culture remains the gold standard and the only source of drug-susceptibility data, but takes one to three weeks in liquid media and up to six to eight weeks on solid media. Treatment starts on clinical suspicion; nobody waits for culture.

Suspected or confirmed active pulmonary TB requires airborne precautions: a negative-pressure airborne infection isolation room with six to twelve air exchanges per hour and air exhausted outside or HEPA-filtered, the door kept closed, and a fit-tested N95 respirator or higher for every person entering. The patient wears a surgical mask — not an N95 — whenever leaving the room, and transport is limited to what is essential. Precautions are discontinued only when the patient is clinically improving, has completed at least two weeks of effective therapy, and has three consecutive negative AFB smears collected at least eight hours apart with one early-morning specimen. Tuberculosis is a reportable disease; the public health department manages contact tracing.

RIPE therapy, adherence and the monitoring that matters

Standard therapy for drug-susceptible pulmonary tuberculosis is an intensive phase of four drugs for two months followed by a continuation phase of isoniazid and rifampin for four months — six months total. Multiple drugs are used because spontaneous resistant mutants exist within any large bacillary population; monotherapy selects them. Latent infection is treated differently — commonly three months of weekly isoniazid plus rifapentine, four months of daily rifampin, or nine months of isoniazid. Directly observed therapy, in which a healthcare worker watches each dose swallowed, is the single most effective intervention against acquired resistance and is standard for active disease.

Teach that the sputum usually converts and symptoms resolve within weeks — and that this is exactly when patients stop taking the drugs, which is how multidrug-resistant TB is created. Reinforce that the full course is non-negotiable, that all household contacts need screening, and that a woman of childbearing age on rifampin needs alternative contraception.

Pleural effusion, empyema and thoracentesis

The pleural space normally holds five to fifteen millilitres of lubricating fluid. Infection, malignancy, heart failure, hypoalbuminemia and pulmonary embolism can all expand it. A transudate is thin and results from altered hydrostatic or oncotic pressure (heart failure, cirrhosis); an exudate is protein- and LDH-rich and results from inflammation or malignancy — the distinction is made with Light’s criteria on the fluid. When infected fluid becomes frankly purulent it is an empyema, which usually requires tube thoracostomy drainage, sometimes intrapleural fibrinolytics, and occasionally surgical decortication.

Findings mirror the physics: decreased or absent breath sounds over the effusion, dullness to percussion, decreased fremitus, tracheal shift away from a large effusion, dyspnea and pleuritic pain. Upright chest radiograph shows blunting of the costophrenic angle once about 200 mL has accumulated; ultrasound is more sensitive and is used to mark the site. For thoracentesis, position the patient sitting upright leaning forward over the bedside table, arms supported; verify consent and coagulation studies; instruct the patient to remain still and not to cough or talk during needle insertion. Limit removal to roughly 1,000–1,500 mL in a single sitting — draining more risks re-expansion pulmonary edema. Afterward monitor for sudden dyspnea, chest pain, cough or hypoxemia, which suggest pneumothorax, and obtain the post-procedure chest film.

Section 3Pulmonary Embolism and Pulmonary Vascular Disorders

Ventilation without perfusion — the dead-space lung

Most pulmonary emboli begin as deep vein thrombi in the proximal leg or pelvis, break free, travel through the right heart and lodge in a pulmonary artery. Distal to the occlusion the alveoli are ventilated but not perfused — dead space. Gas exchange fails, and the physiology cascades. Loss of pulmonary capillary blood flow reduces surfactant production over hours, causing regional atelectasis and worsening shunt. Serotonin and thromboxane released from platelets on the clot constrict adjacent vessels. Pulmonary vascular resistance rises abruptly; if enough of the vascular bed is obstructed, the thin-walled right ventricle cannot generate the pressure to overcome it, dilates, and fails. A failing right ventricle cannot fill the left, cardiac output falls, and the patient becomes hypotensive. That is massive (high-risk) PE, and it kills within hours.

Risk follows Virchow’s triad: venous stasis (immobility, long travel, heart failure, obesity), endothelial injury (surgery — especially orthopedic hip and knee, trauma, central venous catheters) and hypercoagulability (malignancy, pregnancy and the postpartum period, estrogen-containing contraceptives, factor V Leiden, smoking, sepsis, inflammatory bowel disease). Any patient on your floor with two of the three deserves prophylaxis and a low threshold of suspicion.

Recognition, scoring and diagnostics

The presentation is abrupt: sudden dyspnea, pleuritic chest pain, apprehension or a sense of impending doom, tachypnea, tachycardia, low-grade fever, and hypoxemia. Hemoptysis, a pleural friction rub and a focal wedge infiltrate suggest pulmonary infarction. A large embolus adds jugular venous distension, a loud second heart sound, syncope and hypotension. The most consistent finding across all presentations is unexplained tachypnea — a respiratory rate that does not match the chest film.

The characteristic arterial blood gas is hypoxemia with respiratory alkalosis: PaO₂ below 80 mmHg, PaCO₂ below 35 mmHg and pH above 7.45, because the patient hyperventilates around the dead space. D-dimer below roughly 500 ng/mL FEU has excellent negative predictive value in a low-probability patient and effectively rules PE out; above that it is nonspecific, rising with surgery, trauma, pregnancy, malignancy and infection, and age-adjusted thresholds (age × 10 in patients over 50) reduce false positives. The Wells score stratifies pretest probability using clinical signs of DVT, PE as the most likely diagnosis, heart rate above 100, immobilisation or surgery within four weeks, prior DVT/PE, hemoptysis and malignancy. CT pulmonary angiography is the diagnostic test of choice; a ventilation–perfusion (V/Q) scan substitutes when contrast is contraindicated by renal impairment, allergy or pregnancy. Echocardiography assesses right ventricular strain, and an elevated troponin or BNP in confirmed PE marks a higher-risk patient. The classic but insensitive ECG finding is S1Q3T3; sinus tachycardia is far more common.

Anticoagulation, thrombolysis and nursing priorities

Anticoagulation does not dissolve the existing clot; it stops propagation while endogenous fibrinolysis does the work. Start it on strong clinical suspicion, before imaging, when bleeding risk is acceptable. Options include unfractionated heparin infusion titrated to an aPTT of roughly 1.5–2.5 times the laboratory’s control value (the reported therapeutic range is lab-specific, commonly about 60–80 seconds) or anti-Xa 0.3–0.7 units/mL; low-molecular-weight heparin such as enoxaparin 1 mg/kg subcutaneously every 12 hours; or a direct oral anticoagulant — apixaban 10 mg twice daily for seven days then 5 mg twice daily, or rivaroxaban 15 mg twice daily for 21 days then 20 mg daily with food. Warfarin, if used, overlaps with a parenteral agent for at least five days and until the INR is 2.0–3.0 on two consecutive days. Antidotes to know: protamine sulfate for heparin, vitamin K (phytonadione) for warfarin, idarucizumab for dabigatran, andexanet alfa for apixaban and rivaroxaban.

Monitor the platelet count. Heparin-induced thrombocytopenia presents as a fall of more than 50 percent from baseline or a count below 150,000/mm³ (normal 150,000–400,000), typically five to ten days after exposure, and paradoxically causes thrombosis. Stop all heparin including flushes and coated catheters, and expect a direct thrombin inhibitor such as argatroban. For massive PE with sustained hypotension, systemic thrombolysis with alteplase 100 mg over two hours, catheter-directed lysis or embolectomy may be used; absolute contraindications include active internal bleeding, any prior hemorrhagic stroke, ischemic stroke within three months, known intracranial neoplasm or recent intracranial surgery. An inferior vena cava filter is reserved for patients who cannot be anticoagulated or who embolise despite therapy.

Nursing priorities are ordered by airway, breathing, circulation. Stay with the patient. Raise the head of the bed and apply high-flow oxygen to keep saturation above 92 percent. Establish IV access, obtain vital signs and continuous oximetry, place the patient on cardiac monitoring, and notify the provider immediately. Anticipate ABG, D-dimer, troponin, BNP, ECG and CT angiography. Do not massage the legs, and do not have the patient perform Valsalva. Once anticoagulated, institute bleeding precautions: soft toothbrush, electric razor, no rectal temperatures or suppositories, pressure to venipuncture sites for five minutes, and assessment for occult bleeding — melena, hematuria, bruising, and any new headache or change in level of consciousness. Prevention on every med-surg patient is the real intervention: early ambulation, sequential compression devices, adequate hydration, and prophylactic enoxaparin 40 mg daily or heparin 5,000 units subcutaneously every eight to twelve hours as ordered.

Fat embolism, air embolism and pulmonary hypertension

Fat embolism syndrome follows long-bone or pelvic fracture, usually 24 to 72 hours after injury, and is distinguished by a triad of hypoxemia, neurologic change (confusion, restlessness, decreased level of consciousness) and a petechial rash over the chest, axillae, neck and conjunctivae. Prevention is prompt immobilisation and early surgical fixation; management is supportive oxygenation and ventilation. Venous air embolism is an iatrogenic emergency associated with central line insertion, removal or disconnection: sudden dyspnea, chest pain, hypotension and sometimes a mill-wheel murmur. Immediately clamp the catheter, place the patient in left lateral Trendelenburg to trap air in the right atrial apex, administer 100 percent oxygen and call for help.

Pulmonary arterial hypertension is a mean pulmonary artery pressure above 20 mmHg at rest, confirmed by right heart catheterisation. It presents insidiously with exertional dyspnea, fatigue, chest pain and syncope, and progresses to right-sided heart failure — cor pulmonale — with jugular venous distension, hepatomegaly, ascites and dependent edema. Therapies act on three pathways: endothelin receptor antagonists (bosentan — monitor liver enzymes, teratogenic), phosphodiesterase-5 inhibitors (sildenafil, tadalafil — never with nitrates), and prostacyclin analogues (epoprostenol, treprostinil). Continuous intravenous epoprostenol has a half-life of minutes; an interrupted infusion is a life-threatening event, so the line is never used for anything else and a backup pump and cassette stay at the bedside.

Section 4Chest Trauma, Pneumothorax and Chest Drainage

Rib fractures, flail chest and pulmonary contusion

Breathing depends on a negative intrapleural pressure of roughly −4 to −8 cm H₂O generated by an intact, rigid chest wall. Break the wall and the mechanics fail. Simple rib fractures are the commonest blunt chest injury and are dangerous not because of the bone but because of the splinting: pain limits tidal volume, the patient will not cough, atelectasis becomes pneumonia. The management is therefore aggressive analgesia — scheduled multimodal agents, patient-controlled analgesia, or an intercostal or epidural block — combined with incentive spirometry, splinting with a pillow, and early mobility. Never apply a circumferential binder or tight strapping; it guarantees hypoventilation. Fractures of ribs one through three imply enormous force and raise concern for great-vessel injury; ribs nine through twelve raise concern for liver, spleen and kidney.

Flail chest is the fracture of two or more adjacent ribs in two or more places, creating a free-floating segment that moves paradoxically — inward on inspiration and outward on expiration. Ventilation becomes inefficient, but the true killer is the underlying pulmonary contusion: bruised lung that leaks blood and fluid into alveoli, worsening over 24 to 72 hours and often progressing to ARDS. Findings include increasing dyspnea, hypoxemia, hemoptysis and a chest film that looks worse each day. Management is analgesia, humidified oxygen, pulmonary hygiene, judicious fluid administration — over-resuscitation floods a contused lung — and mechanical ventilation with PEEP when oxygenation fails. Surgical rib fixation is used in selected patients.

Pneumothorax, tension pneumothorax and hemothorax

A pneumothorax is air in the pleural space. It may be spontaneous (classically a tall, thin, young male smoker with a ruptured apical bleb), traumatic, or iatrogenic after central line placement, thoracentesis or barotrauma from positive-pressure ventilation. Assess for sudden pleuritic pain, dyspnea, diminished or absent breath sounds on the affected side, hyperresonance to percussion, decreased fremitus and asymmetric chest expansion. A small, stable pneumothorax may be observed with oxygen; a large or symptomatic one needs a chest tube.

An open pneumothorax — a sucking chest wound — allows air to move through the chest wall with each breath. Cover it with a sterile occlusive dressing taped on three sides, which lets air escape on expiration but not enter on inspiration. If the patient worsens after the dressing is applied, lift a corner to release trapped air. A tension pneumothorax is a one-way valve: air enters the pleural space and cannot leave, pressure rises, the lung collapses completely and the mediastinum shifts, kinking the great veins and abolishing venous return. This is obstructive shock and it is a clinical diagnosis — you do not wait for a chest film.

A hemothorax is blood in the pleural space and produces dullness to percussion rather than hyperresonance, plus the signs of hypovolemia. Management is a large-bore chest tube placed low (fourth or fifth intercostal space, midaxillary line) with volume resuscitation. Report to the surgeon immediately if initial drainage exceeds 1,500 mL or if output exceeds roughly 200 mL per hour for two to four consecutive hours — that patient needs a thoracotomy, not another unit of blood. Also remember cardiac tamponade in penetrating chest trauma: Beck’s triad of hypotension, jugular venous distension and muffled heart tones, with pulsus paradoxus, treated by pericardiocentesis.

Closed chest drainage — what to expect and what to fix

A chest tube restores negative intrapleural pressure by draining air, blood or fluid and preventing its return. Air is removed by a tube placed high and anteriorly (second intercostal space, midclavicular line); fluid by a tube placed low and laterally. The modern disposable unit has three functional chambers: a collection chamber that measures drainage, a water-seal chamber that acts as a one-way valve, and a suction control chamber regulated either by a column of water (usually 20 cm, producing gentle continuous bubbling) or by a dry dial with a float indicator. Keep the entire unit upright and below the level of the patient’s chest at all times, keep tubing free of dependent loops, and never strip or milk the tubing — the negative pressure it generates damages tissue.

Keep a sterile occlusive dressing and a bottle of sterile water at the bedside. Do not clamp a chest tube routinely — clamping a tube that is still leaking air converts a pneumothorax into a tension pneumothorax. Brief clamping is acceptable only to change the drainage unit, to locate a leak, or immediately before a planned removal with an order. Assess breath sounds, respiratory effort, insertion-site dressing, subcutaneous emphysema (a crackling, rice-crispy feel under the skin) and drainage character every shift and with any change. Encourage deep breathing, incentive spirometry, coughing and repositioning; the tube does not excuse the patient from pulmonary hygiene, it makes it more important. For removal, premedicate for pain, then have the patient take a deep breath and hold it at the end of inspiration or bear down (Valsalva) while the tube is withdrawn, and apply an airtight petrolatum gauze dressing immediately. Obtain the post-removal chest film and watch for recurrent dyspnea.

Section 5Acute Respiratory Failure, ARDS and Mechanical Ventilation

Two kinds of failure, and the gas that tells them apart

Acute respiratory failure means the lungs can no longer meet metabolic demand. There are exactly two ways to fail, and the arterial blood gas separates them. Type I — hypoxemic (oxygenation) failure is a PaO₂ below 60 mmHg on room air with a normal or low PaCO₂. The problem is at the alveolar-capillary interface: shunt, V/Q mismatch or diffusion limitation from pneumonia, ARDS, pulmonary edema, PE or atelectasis. Type II — hypercapnic (ventilatory) failure is a PaCO₂ above 50 mmHg with a pH below 7.35. The lungs may be capable but the bellows are not: opioid or sedative overdose, COPD exacerbation, neuromuscular disease such as Guillain–Barré or myasthenic crisis, spinal cord injury, morbid obesity or sheer respiratory muscle fatigue. Many patients have both.

Normal values you must know cold: pH 7.35–7.45; PaCO₂ 35–45 mmHg; HCO₃⁻ 22–26 mEq/L; PaO₂ 80–100 mmHg; SaO₂ 95–100 percent. Read the gas in order — pH first (acidotic or alkalotic), then PaCO₂ (respiratory), then bicarbonate (metabolic), then decide whether compensation is absent, partial or full, and finally look at oxygenation separately. Remember that in a patient with chronic CO₂ retention the baseline PaCO₂ may be 55 mmHg with a compensating bicarbonate of 32 and a pH of 7.36; what makes that patient sick is a change from their baseline, shown by a falling pH.

Clinically, watch the sequence rather than a single number. Early hypoxemia produces restlessness, anxiety, tachypnea, tachycardia and hypertension — restlessness is the earliest sign of hypoxia and is too often charted as agitation and medicated. Late hypoxemia brings bradycardia, hypotension, cyanosis and loss of consciousness. Hypercapnia produces headache, flushed warm skin, drowsiness, bounding pulse and eventually CO₂ narcosis. Accessory muscle use, tripod positioning, nasal flaring, paradoxical abdominal motion and the inability to speak a full sentence are the physical signs that a patient is losing the work-of-breathing contest. A quiet chest in a previously wheezing patient means air is no longer moving — that is worse, not better.

Acute respiratory distress syndrome

ARDS is diffuse injury to the alveolar-capillary membrane. An insult — sepsis (the most common cause), aspiration, pneumonia, trauma, pancreatitis, massive transfusion, near-drowning, inhalation injury — triggers a systemic inflammatory response. Neutrophils release proteases and reactive oxygen species, the membrane becomes permeable, and protein-rich fluid floods the alveoli even though the left atrial pressure is normal. This is non-cardiogenic pulmonary edema. Surfactant is inactivated, alveoli collapse, lungs stiffen (compliance falls), and the result is massive shunt and refractory hypoxemia — hypoxemia that does not correct as FiO₂ is increased, which is the single most characteristic clinical feature. If the patient survives the exudative phase, a proliferative and then a fibrotic phase may follow over one to three weeks.

The Berlin criteria require all four: onset within one week of a known insult; bilateral opacities on chest imaging not fully explained by effusion, collapse or nodules; respiratory failure not fully explained by cardiac failure or fluid overload; and a PaO₂/FiO₂ ratio of 300 or less with PEEP of at least 5 cm H₂O. Severity grades as mild (P/F 201–300), moderate (101–200) and severe (100 or less). Compute it: a PaO₂ of 70 on an FiO₂ of 0.70 gives a ratio of 100 — severe ARDS.

Management is supportive and evidence-driven. Treat the underlying cause, above all sepsis. Ventilate with a lung-protective strategy: tidal volume 6 mL/kg of predicted body weight, plateau pressure kept at or below 30 cm H₂O, higher PEEP to recruit collapsed alveoli, and tolerance of permissive hypercapnia (an elevated PaCO₂ with pH allowed down to about 7.25) because a smaller breath in a stiff lung is safer than a normal gas. Use conservative fluid management once the patient is out of shock. Prone positioning for 12 to 16 hours a day improves survival in moderate-to-severe ARDS by recruiting dorsal lung; it demands a trained team, protection of the eyes, face, ears and bony prominences, secured airway and lines, and pressure-injury vigilance. Neuromuscular blockade may be used early in severe disease — and a paralysed patient must receive continuous sedation and analgesia, with paralysis depth monitored by train-of-four. Corticosteroids have a role in selected patients.

Oxygen, non-invasive support and intubation

Escalate deliberately. A nasal cannula at 1–6 L/min delivers roughly 24–44 percent oxygen; a simple mask at 6–10 L/min, 40–60 percent; a partial rebreather at 6–11 L/min, 60–75 percent; a non-rebreather at 10–15 L/min, 80–95 percent (the reservoir bag must stay inflated and must never fully collapse on inspiration); a Venturi mask delivers a precise 24–50 percent and is the device of choice when a specific concentration matters, as in the chronic CO₂ retainer. High-flow nasal cannula delivers heated humidified gas at up to 60 L/min with a controlled FiO₂ and modest PEEP effect, and is often the step before intubation.

Non-invasive positive-pressure ventilation (BiPAP or CPAP) can avert intubation in COPD exacerbation with hypercapnic acidosis, cardiogenic pulmonary edema and obstructive sleep apnea. It requires a cooperative, alert patient who can protect the airway. Contraindications are the exam favourites: decreased level of consciousness, inability to protect the airway or clear secretions, vomiting, hemodynamic instability, facial trauma or surgery, and untreated pneumothorax. Watch for gastric distension, aspiration and skin breakdown over the nasal bridge.

Prepare for intubation when the patient cannot maintain oxygenation or ventilation despite maximal support, cannot protect the airway, or is visibly exhausting. Confirm tube placement with continuous waveform capnography — the standard — then auscultate over the epigastrium first and then bilaterally over the lung fields, and confirm the tip 2–6 cm above the carina on chest radiograph. Record and monitor the centimetre marking at the lip or teeth every shift, and maintain cuff pressure at 20–30 cm H₂O — higher risks tracheal mucosal ischemia, lower permits microaspiration.

Caring for the ventilated patient — prevention, weaning and the team

Ventilator complications follow the pressure: barotrauma and pneumothorax, ventilator-induced lung injury, decreased venous return and hypotension from PEEP, gastrointestinal stress ulceration, delirium, immobility and VAP. The prevention bundle is nursing work. Keep the head of the bed at 30–45 degrees unless contraindicated; perform structured oral care with suctioning; use an endotracheal tube with subglottic secretion drainage where available; provide stress-ulcer and venous thromboembolism prophylaxis; interrupt sedation daily and pair it with a spontaneous breathing trial; mobilise early; and manage delirium (the ABCDEF bundle). Suction only when indicated — audible or visible secretions, a high-pressure alarm, a sawtooth flow waveform, or desaturation — not on a schedule. Pre-oxygenate with 100 percent for 30 to 60 seconds, limit each pass to 10–15 seconds, and do not instil normal saline; it does not thin secretions and it does displace bacteria into the lower airway.

Weaning readiness is assessed, not guessed: the underlying cause is resolving, the patient is hemodynamically stable off or on minimal vasopressors, adequately oxygenating on an FiO₂ of 0.40 or less with PEEP of 5–8 cm H₂O, afebrile, able to initiate breaths, and metabolically and electrolytically sound. Objective measures include a rapid shallow breathing index (respiratory rate divided by tidal volume in litres) below 105, a negative inspiratory force more negative than −20 to −25 cm H₂O, and vital capacity above 10–15 mL/kg. During a spontaneous breathing trial, terminate for a respiratory rate above 35, saturation below 90 percent, heart rate change greater than 20 percent, new dysrhythmia, agitation, diaphoresis or paradoxical breathing. After extubation, watch for stridor, hoarseness and progressive respiratory distress; keep the patient NPO until a swallow screen is passed, and have reintubation equipment available.

Communication is a nursing intervention here, not a courtesy. An intubated patient is awake more often than families realise; provide a communication board, yes/no questions, writing materials, and explain every procedure before you touch. Reorient frequently, preserve the day-night cycle, and involve family. Delirium in the ventilated patient predicts longer stay and worse cognitive outcomes.

Words worth knowing

Cardiac Disorders: Coronary Artery Disease and Heart Failure

Two problems account for an enormous share of the patients you will care for on a medical floor, and they are the same disease at two different stages. Coronary artery disease starves myocardium of oxygen; when a coronary artery closes, muscle dies. Dead muscle does not contract, so the pump weakens, pressure backs up behind it, fluid moves into the lungs and the legs, and the patient returns months later with heart failure. Understanding that continuity means you never have to memorise two unrelated lists. In this chapter you build the mechanism first — supply versus demand, plaque rupture, remodelling, neurohormonal compensation — and then layer on the assessment findings, the diagnostics with real numbers, the drug classes by what they actually do, and the priority reasoning that decides what you handle first when four patients need you at once. Chest pain and shortness of breath are the two complaints that will define your shift. Learn to think through both.

Section 1Coronary Perfusion, Plaque and the Anginas

Supply, demand and the arithmetic of ischaemia

The myocardium is the most oxygen-greedy tissue in the body and it has almost no reserve. Most tissues extract roughly a quarter of the oxygen delivered to them and can extract more when demand rises. Cardiac muscle already extracts about seventy-five percent at rest. That single fact drives the whole chapter: when the heart needs more oxygen, the only way to get it is to increase coronary blood flow. If the artery cannot dilate — because a plaque holds the lumen fixed — demand outruns supply and the tissue becomes ischaemic.

Supply depends on three things. First, the diameter of the coronary artery, which is where plaque does its damage. Second, the oxygen-carrying capacity of the blood, which is why a haemoglobin of 7 g/dL (normal roughly 12 to 16 g/dL in women and 14 to 18 g/dL in men) can precipitate angina in a patient whose arteries have not changed at all. Third, diastolic time. The coronaries fill during diastole, when the aortic valve has closed and the myocardium is relaxed. Tachycardia shortens diastole disproportionately, so a heart rate of 150 both raises demand and cuts supply at the same moment. This is the single most useful piece of physiology in cardiac nursing, and it explains why rate control is therapeutic, why beta-blockers reduce angina, and why the patient in atrial fibrillation with a rapid ventricular response develops chest pain.

Demand rises with heart rate, contractility, and wall tension (preload and afterload). Anything that increases those — exertion, cold, a heavy meal, emotional stress, fever, hyperthyroidism, hypertension, cocaine — can tip a fixed lesion into symptoms. Note that a plaque generally has to obstruct about seventy percent of the lumen before it limits flow during exertion, and about ninety percent before it limits flow at rest. That is why patients feel entirely well for decades while the disease builds.

Anatomy matters for prediction. The left anterior descending artery feeds the anterior wall, the anterior two-thirds of the septum and much of the left ventricle — occlusion here is the “widow-maker” and the infarct most likely to cause heart failure and cardiogenic shock. The left circumflex feeds the lateral wall. The right coronary artery feeds the inferior wall, the right ventricle and, in most people, the SA and AV nodes — which is why inferior infarcts come with bradycardia and heart block. Since the coronaries perfuse from the epicardial surface inward, the innermost layer, the subendocardium, is the watershed and dies first. Partial-thickness subendocardial damage produces ST depression; full-thickness transmural damage produces ST elevation.

Building a plaque and the risk factors that actually change outcomes

Atherosclerosis begins with endothelial injury from shear stress at branch points, hypertension, tobacco toxins, hyperglycaemia or oxidised LDL. The damaged endothelium becomes sticky and permeable. LDL particles slip into the intima and oxidise. Monocytes follow, transform into macrophages, gorge on the oxidised lipid and become foam cells, which pile up as a fatty streak. Smooth muscle migrates in and lays down a fibrous cap over a soft, inflammatory, lipid-rich core. The plaque is now a two-part structure, and how it behaves depends on which part predominates.

A stable plaque has a thick fibrous cap and a small lipid core. It narrows the lumen slowly and produces predictable exertional angina. A vulnerable plaque has a thin cap over a large, inflamed lipid core — and here is the point students miss: vulnerable plaques are often not the tightest lesions. Roughly two-thirds of infarctions arise from plaques that were obstructing less than fifty percent of the lumen. When the thin cap erodes or tears, the thrombogenic core is exposed to flowing blood. Platelets adhere, activate and aggregate, the coagulation cascade fires, and a thrombus forms in minutes. Partial occlusion produces unstable angina or NSTEMI; complete, sustained occlusion produces STEMI. That is the whole mechanism of acute coronary syndrome in one paragraph, and every drug you will give — aspirin, P2Y12 inhibitors, heparin, fibrinolytics — targets one step in it.

Non-modifiable risk factors are age (men 45 and older, women 55 and older or post-menopausal), male sex until menopause equalises the risk, family history of premature coronary disease (a first-degree male relative under 55 or female relative under 65), and ethnicity. The modifiable ones are where nursing lives: tobacco use, hypertension, diabetes (a coronary risk equivalent), dyslipidaemia, obesity with central adiposity, physical inactivity, an atherogenic diet, excess alcohol, chronic kidney disease and untreated obstructive sleep apnoea. Metabolic syndrome — three or more of waist circumference above 40 inches in men or 35 inches in women, triglycerides 150 mg/dL or higher, HDL below 40 mg/dL in men or 50 mg/dL in women, blood pressure 130/85 mmHg or higher, and fasting glucose 100 mg/dL or higher — bundles several of them.

Know the lipid targets, because you will teach them. A standard fasting panel reports total cholesterol (desirable below 200 mg/dL), LDL (optimal below 100 mg/dL, and below 70 mg/dL for patients with established disease or diabetes), HDL (protective at 60 mg/dL or higher, a risk factor below 40) and triglycerides (normal below 150 mg/dL). Modern practice puts less weight on chasing a single LDL number and more on statin intensity matched to risk, but the numbers still anchor patient teaching. Smoking cessation is the single highest-yield intervention you can deliver: risk of a coronary event begins falling within a year of quitting.

Stable angina — and the two anginas that are not stable

Stable angina is the symptom of a fixed lesion under load. It is predictable: the same amount of exertion produces the same substernal pressure, tightness or squeezing, lasting three to five minutes, relieved by rest or by sublingual nitroglycerin. Patients often describe it with a fist over the sternum rather than a fingertip. It may radiate to the left arm, both arms, the jaw, the neck, the epigastrium or between the shoulder blades. There is no myocardial necrosis, so troponin stays normal and the resting ECG is frequently normal — ST depression appears only during the episode or during stress testing.

Unstable angina is the same pain that has broken its pattern: new onset, occurring at rest, lasting longer, occurring with less exertion than before, or no longer fully relieved by rest or nitroglycerin. Mechanistically this is plaque rupture with a partially occluding thrombus. It is an acute coronary syndrome, it is admitted, and it carries a real short-term risk of progressing to infarction. Troponin is negative — and that negative troponin is precisely what distinguishes unstable angina from NSTEMI, not the severity of the pain.

Vasospastic (Prinzmetal or variant) angina is a different animal. It results from coronary spasm rather than fixed obstruction, occurs at rest and characteristically between midnight and early morning, may occur in relatively young patients without classic risk factors, and produces transient ST elevation that resolves when the spasm breaks. Calcium channel blockers and nitrates are the treatment; non-selective beta-blockers can worsen it by leaving alpha-mediated vasoconstriction unopposed. Cocaine and methamphetamine cause the same picture in a much more dangerous form, and in cocaine-associated chest pain benzodiazepines and nitrates come before beta-blockers.

Chronic stable angina is managed with the goal of shifting the supply-demand balance. Nitrates dilate veins to cut preload and dilate coronaries. Beta-blockers lower heart rate, contractility and blood pressure, and lengthen diastolic filling time. Calcium channel blockers relax vascular smooth muscle and, in the case of the non-dihydropyridines diltiazem and verapamil, also slow the rate. Ranolazine is added for refractory angina without meaningful effect on heart rate or blood pressure. Aspirin and a high-intensity statin address plaque stability rather than symptoms. Cardiac rehabilitation, weight management, glycaemic control and blood pressure control complete the plan.

Section 2Acute Coronary Syndrome: Reading the Presentation

One ruptured plaque, three diagnoses

Acute coronary syndrome is an umbrella covering unstable angina, non-ST-elevation myocardial infarction and ST-elevation myocardial infarction. All three begin with the same event — plaque disruption and thrombosis — and differ only by how completely and for how long the artery is occluded. Think of it as a spectrum of one disease, because the initial nursing response is identical no matter which of the three it turns out to be.

The classic presentation is crushing substernal chest pressure, often described as an elephant on the chest, lasting more than twenty minutes, unrelieved by rest or nitroglycerin, accompanied by diaphoresis, nausea, dyspnoea, weakness and a sense of impending doom. Radiation to the left arm, jaw, neck, back or epigastrium is common. Skin is often cool, ashen and clammy because sympathetic outflow shunts blood centrally. Blood pressure may be elevated from catecholamines or low if the pump is failing.

Now unlearn the assumption that this is universal. Up to a third of infarcts present without chest pain. Women more often report fatigue that preceded the event by days or weeks, dyspnoea, indigestion, nausea, anxiety, and pain between the shoulder blades or in the jaw. Patients with diabetes may have autonomic neuropathy that blunts the pain signal entirely — the silent MI. Older adults commonly present with dyspnoea, sudden confusion or delirium, syncope, a fall, weakness or new-onset heart failure rather than with pain, and delirium in an older adult should always raise the possibility of an acute cardiac or infectious event. Do not require chest pain before you obtain an ECG.

One further distinction shapes treatment. Type 1 MI is the plaque-rupture event described above and it is what reperfusion therapy is designed for. Type 2 MI is myocardial injury from supply-demand mismatch without plaque rupture — severe anaemia, sepsis, sustained tachydysrhythmia, hypotension, hypertensive crisis, respiratory failure. Troponin rises in both. A patient in septic shock with a troponin of 250 ng/L usually needs the sepsis treated, not the catheterisation lab. Knowing that the number has more than one explanation keeps you from anchoring.

The 12-lead ECG: territory, timing and the leads you forget

A 12-lead ECG must be obtained and interpreted within ten minutes of a patient reporting ischaemic symptoms — in the emergency department, on your floor, anywhere. That ten-minute standard is a national quality measure, and on the NCLEX “obtain a 12-lead ECG” is nearly always among the first actions in a chest-pain stem, alongside aspirin and continuous cardiac monitoring.

Read the tracing in three layers. Ischaemia shows as ST depression or symmetric T-wave inversion and is reversible. Injury shows as ST elevation and represents tissue that is dying but salvageable — this is the finding that starts the clock. Infarction shows as a pathologic Q wave, which develops over hours to days and is permanent, the electrical scar. Diagnostic ST elevation is measured at the J point in two anatomically contiguous leads: at least 1 mm (0.1 mV) in all leads except V2 and V3, where the threshold is 2 mm in men aged 40 and older, 2.5 mm in men under 40, and 1.5 mm in women. A new left bundle branch block with an ischaemic presentation is managed as a STEMI equivalent.

Localisation lets you predict the complications before they happen, which is what separates a nurse who documents from a nurse who anticipates. Two lead groups deserve special attention. First, posterior infarction produces no ST elevation on a standard 12-lead; it shows as tall R waves and ST depression in V1 and V2 — a mirror image — and requires posterior leads V7 to V9 to confirm. Second, and more important at the bedside, whenever you see an inferior STEMI in II, III and aVF, obtain a right-sided ECG with V4R, because up to half of these involve the right ventricle.

Troponin, the other markers, and the rest of the workup

Cardiac troponin I and T are structural proteins of the contractile apparatus and they are the diagnostic standard because they are essentially specific to cardiac muscle. Timing is what students get wrong, so learn it precisely. With conventional assays troponin begins to rise about three to six hours after the onset of injury, peaks at twelve to twenty-four hours, and remains detectable for seven to fourteen days. That long tail makes troponin excellent for diagnosing an event the patient sat on at home for two days, and poor for detecting a re-infarction a few days later. High-sensitivity troponin assays detect a rise within one to three hours and are used in serial 0-hour and 1-hour, or 0-hour and 2-hour, rule-out protocols. Cut-points are assay-specific and often sex-specific — the 99th-percentile upper reference limit for high-sensitivity troponin T is commonly around 14 ng/L, with separate thresholds for men and women. Always use your own laboratory’s reference range, and interpret the delta — the change between draws — not a single value.

Two consequences follow. First, a normal troponin drawn one hour into chest pain does not rule out infarction; serial sampling is mandatory, and a patient who is discharged on a single negative troponin has been failed. Second, you never wait for a troponin result to activate reperfusion in a STEMI. The ECG, not the laboratory, triggers the catheterisation lab. CK-MB retains a narrow role: it rises in four to six hours, peaks at eighteen to twenty-four hours and normalises within forty-eight to seventy-two hours, so a second rise after it has normalised is useful evidence of re-infarction. Myoglobin rises earliest but is so non-specific that it has largely been abandoned.

The rest of the workup rounds out the picture. Order a CBC (haemoglobin, because anaemia worsens ischaemia), a basic metabolic panel with potassium 3.5 to 5.0 mEq/L and magnesium 1.5 to 2.5 mg/dL because both derangements provoke ventricular dysrhythmias, creatinine 0.6 to 1.2 mg/dL before contrast exposure, coagulation studies before anticoagulation, a lipid panel within twenty-four hours, a glucose and A1C, and a BNP if failure is suspected. Echocardiography quantifies the ejection fraction (normal 55 to 70 percent) and shows regional wall-motion abnormalities that correspond to the infarcted territory, plus complications such as acute mitral regurgitation or a pericardial effusion.

For patients who are not in an acute syndrome, non-invasive testing sorts out chest pain. Exercise stress testing is preferred when the patient can walk; pharmacologic stress with adenosine, regadenoson or dipyridamole is substituted when they cannot. Nursing preparation matters and is frequently tested: nothing by mouth for four to six hours, no caffeine for twelve to twenty-four hours (caffeine blocks adenosine and invalidates the test), hold beta-blockers if instructed, wear walking shoes, and hold theophylline. Adenosine-class agents are contraindicated in bronchospastic disease because they can provoke severe bronchoconstriction — dobutamine stress is used instead. Coronary CT angiography and coronary calcium scoring are increasingly used for risk stratification, and cardiac catheterisation with angiography remains the definitive anatomic test.

Section 3Managing ACS: The First Ten Minutes and the Next Ten Days

The immediate bundle, and what is wrong with MONA

When a patient reports chest pain, your actions overlap rather than queue. Stay with the patient and call for help. Place them in semi-Fowler position, obtain a full set of vital signs including bilateral blood pressures, apply continuous cardiac monitoring with defibrillator available, obtain the 12-lead ECG within ten minutes, establish two large-bore intravenous lines, draw troponin and the baseline labs, and give aspirin 162 to 325 mg chewed (non-enteric-coated, chewed so it is absorbed in minutes) unless there is a true allergy or active bleeding. Then treat pain and arrange reperfusion.

You were probably taught MONA — morphine, oxygen, nitroglycerin, aspirin. It is a useful memory hook and a poor treatment order, and current practice has revised nearly every letter. Learn the critiques, because they are now tested directly.

Aspirin comes first, not last. It is the intervention with the clearest mortality benefit and it takes seconds to give. Oxygen is not routine. Supplemental oxygen in a normoxic patient causes coronary vasoconstriction and confers no benefit; large trials showed no reduction in mortality or infarct size. Give oxygen only if the SpO₂ is below 90 percent (some protocols use 94 percent) or the patient is dyspnoeic or in respiratory distress, and titrate to that target rather than running high flow reflexively.

Nitroglycerin is given as 0.4 mg sublingually, repeated every five minutes for up to three doses, with blood pressure checked before each dose; hold it and reassess for a systolic pressure below 90 mmHg or a drop of more than 30 mmHg from baseline, for heart rate below 50 or above 100, and for suspected right ventricular infarction. The absolute contraindication you must never miss is recent phosphodiesterase-5 inhibitor use: sildenafil or vardenafil within 24 hours, tadalafil within 48 hours. The combination causes refractory, potentially fatal hypotension. Ask every patient of any age and any sex, privately and without embarrassment, and remember that these drugs are also prescribed for pulmonary hypertension. Teach outpatients to take one tablet at the first sign of pain, sit or lie down first because of the hypotension and headache, and call emergency services if the pain is unimproved five minutes after the first dose rather than finishing all three at home. Tablets are stored in the original dark glass bottle away from heat and light and replaced every six months once opened.

Morphine has moved from routine to selective. It relieves pain, reduces sympathetic drive and venodilates, which lowers preload — helpful in pulmonary oedema, harmful in right ventricular infarction. It also slows gastric emptying and measurably delays absorption of oral P2Y12 inhibitors, and observational data raised concern about outcomes in NSTEMI. Reserve it for pain that persists despite nitrates and anti-ischaemic therapy, give 2 to 4 mg intravenously, and monitor blood pressure, respiratory rate and level of consciousness. Never treat ongoing ischaemic pain with analgesia alone: pain that continues means muscle that is still dying, and the answer is reperfusion.

Reperfusion: PCI, fibrinolysis and the clock

Time is muscle. Necrosis begins within twenty to thirty minutes of complete occlusion and is largely complete by six hours, so every minute of delay is myocardium that will not come back. Primary percutaneous coronary intervention is the preferred strategy: a catheter is advanced from the radial or femoral artery, the thrombosed segment is crossed, a balloon expands the lesion and a stent holds it open. The benchmark is first medical contact to device within 90 minutes at a PCI-capable facility, or within 120 minutes when the patient must be transferred.

If PCI cannot be delivered within 120 minutes, fibrinolytic therapy is given, with a door-to-needle time of 30 minutes and greatest benefit within the first twelve hours of symptom onset. Alteplase, reteplase and tenecteplase convert plasminogen to plasmin and dissolve the clot. Screening is a nursing responsibility. Absolute contraindications include any prior intracranial haemorrhage, known cerebral vascular malformation or intracranial malignancy, ischaemic stroke within three months, active bleeding or a bleeding diathesis, suspected aortic dissection, and significant closed head or facial trauma within three months. Relative contraindications include uncontrolled hypertension above 180/110 mmHg, recent major surgery or internal bleeding, pregnancy, current anticoagulant use and prolonged CPR. After administration, monitor neurologic status closely, avoid unnecessary punctures and invasive lines, hold pressure longer at any site, watch for signs of reperfusion (relief of pain, resolution of ST elevation, and reperfusion dysrhythmias such as accelerated idioventricular rhythm, which is usually transient and benign), and observe for bleeding — a sudden change in level of consciousness or a new headache is intracranial haemorrhage until proven otherwise.

Post-catheterisation nursing is high-yield and reliably tested. Assess the access site and the distal pulses, colour, temperature, capillary refill and sensation of the affected extremity on the standard schedule — typically every fifteen minutes for the first hour, then tapering. With femoral access keep the leg straight, maintain bed rest with the head of the bed no higher than about 30 degrees, and do not let the patient flex the hip. With radial access a compression band is used, the wrist is kept straight, and the patient may sit up much sooner. Watch for haematoma, and for the complication students forget: retroperitoneal bleeding, which presents as flank or back pain, hypotension, tachycardia and a falling haematocrit with an unremarkable-looking groin. Contrast is nephrotoxic, so hydrate, monitor urine output and creatinine, and follow institutional policy on holding metformin for 48 hours after contrast in patients with renal impairment because of lactic acidosis risk. Report chest pain after PCI immediately — it may signal acute stent thrombosis.

Complications, priorities and communicating the deterioration

Complications cluster by time, and knowing the timeline lets you anticipate. In the first hours, dysrhythmias dominate and ventricular fibrillation is the leading cause of pre-hospital death — which is why continuous monitoring, patent intravenous access and an available defibrillator are non-negotiable. Inferior infarcts bring bradycardia and AV block. Within the first day to week, pump failure appears: acute heart failure, pulmonary oedema, and cardiogenic shock when more than roughly forty percent of the left ventricle is lost, presenting as hypotension, cool mottled skin, oliguria, altered mentation and a rising lactate.

Mechanical complications typically appear between day two and day seven, as necrotic tissue softens before scar forms. Papillary muscle rupture produces sudden acute mitral regurgitation — a new loud holosystolic murmur at the apex with abrupt flash pulmonary oedema. It follows an inferior infarct most often, because the posteromedial papillary muscle has only one blood supply, from the posterior descending branch of the right coronary artery. Ventricular septal rupture produces a new harsh murmur with a thrill and rapid decompensation. Free wall rupture produces sudden pulseless electrical activity from tamponade and is usually fatal. Any new murmur in a post-MI patient is an emergency, not a charting detail. Later still come ventricular aneurysm, mural thrombus with embolic stroke, and Dressler syndrome — an autoimmune pericarditis one to eight weeks out with pleuritic pain that improves sitting forward, fever, a friction rub and diffuse ST elevation, treated with anti-inflammatories rather than reperfusion.

Priority reasoning is what the NCLEX rewards. Apply ABC first: airway and breathing problems and lethal rhythms outrank everything. Then unstable over stable, acute over chronic, actual over potential. Given four post-MI patients, you see the one with new dyspnoea and crackles before the one whose pain is relieved and vital signs are stable, and you see the patient with a run of ventricular tachycardia before either. Red flags that mean call now: chest pain unrelieved after three sublingual nitroglycerin doses; new or worsening ST elevation; systolic pressure below 90 mmHg with signs of poor perfusion; heart rate below 50 or a new high-grade block; sustained ventricular tachycardia or any new ventricular ectopy with instability; a new murmur; sudden severe dyspnoea with pink frothy sputum; altered mentation; and signs of bleeding after fibrinolysis or PCI.

Escalate using SBAR, and rehearse it until it is automatic. Situation: “Dr. Reyes, this is Jordan Park, RN, on 4 West. Mr. Alvarez in 412, day one after an inferior STEMI, has new chest pain rated 8 out of 10 that has not responded to three sublingual nitroglycerin.” Background: “He had a right coronary stent yesterday and is on aspirin, ticagrelor and a heparin infusion.” Assessment: “Blood pressure is 88 over 54, heart rate 48 and sinus bradycardic, SpO₂ 93 percent on room air, skin cool and diaphoretic. The repeat 12-lead shows new ST elevation in II, III and aVF and I have obtained a right-sided lead.” Recommendation: “I have held the nitroglycerin, started a 250 mL fluid bolus and I need you to see him now. Should I activate the catheterisation lab?”

Recovery teaching begins before discharge. Refer every patient to cardiac rehabilitation. Teach that activity is resumed gradually, that sexual activity may generally be resumed when the patient can climb two flights of stairs or walk a block without symptoms, that nitroglycerin must never be combined with erectile dysfunction drugs, and that isometric straining, heavy lifting and extremes of temperature increase cardiac work. Address smoking cessation at every contact, review a heart-healthy dietary pattern, and make sure the patient can state which symptoms mean call 911 rather than wait for the clinic to open.

Section 4Heart Failure: When the Pump Cannot Keep Up

Forward failure, backward failure, and compensation that turns on the patient

Heart failure is a clinical syndrome in which the ventricle cannot fill or eject sufficiently to meet metabolic demand at normal filling pressures. Two consequences follow from that one sentence and they generate every sign and symptom. Forward failure — inadequate cardiac output — produces fatigue, exercise intolerance, weakness, cool extremities, oliguria and, in the older adult, confusion. Backward failure — congestion behind the failing chamber — produces the fluid findings. If you can name which ventricle is failing, you can predict the assessment.

The common causes are coronary artery disease and prior infarction (dead muscle does not contract), long-standing hypertension (the ventricle hypertrophies against afterload and eventually stiffens and dilates), valvular disease, cardiomyopathies, dysrhythmias, myocarditis, and high-output states such as thyrotoxicosis or severe anaemia. Precipitants of decompensation in a previously stable patient are worth memorising because they are largely preventable and dominate the readmission data: dietary sodium indiscretion, medication non-adherence, new atrial fibrillation, infection, anaemia, uncontrolled hypertension, NSAIDs (which cause sodium and water retention), thiazolidinediones, excess intravenous fluid, and myocardial ischaemia.

The cruelty of heart failure is that the compensations are helpful for weeks and destructive for years. When cardiac output falls, the sympathetic nervous system fires: heart rate and contractility rise and vessels constrict, which maintains blood pressure but raises both afterload and myocardial oxygen demand and shortens diastolic filling. Reduced renal perfusion activates the renin-angiotensin-aldosterone system: angiotensin II vasoconstricts and aldosterone retains sodium and water, which restores preload but worsens congestion. Antidiuretic hormone retains free water and produces dilutional hyponatraemia (sodium normally 135 to 145 mEq/L). Over months these signals drive ventricular remodelling — hypertrophy, chamber dilation, fibrosis and a shift to a spherical, inefficient shape.

Once you see that, modern therapy stops looking like a random list. Every disease-modifying drug in heart failure blocks one of those compensations: ACE inhibitors, ARBs and ARNIs block RAAS; beta-blockers block sympathetic drive; mineralocorticoid receptor antagonists block aldosterone; SGLT2 inhibitors act through metabolic and renal pathways that reduce congestion and remodelling. Diuretics, by contrast, relieve symptoms without changing the trajectory of the disease. That distinction — symptom relief versus mortality benefit — explains why the patient who “feels fine” still must take four medications.

HFrEF, HFpEF and the left-right split

Classify by ejection fraction, the percentage of end-diastolic volume ejected each beat; normal is 55 to 70 percent. HFrEF (reduced, 40 percent or less) is a systolic problem: the ventricle is dilated and weak and cannot eject. It follows infarction and dilated cardiomyopathy, and it is the phenotype with proven drug therapy. HFpEF (preserved, 50 percent or higher) is a diastolic problem: the ventricle is stiff and non-compliant and cannot fill, so filling pressures rise and back up even though the squeeze looks normal on echo. HFpEF is typical of older women with long-standing hypertension, diabetes, obesity and atrial fibrillation, and it accounts for roughly half of all heart failure. A patient can be drowning in pulmonary congestion with an ejection fraction of 60 percent, and telling a family “the pump is fine” on that basis is a common and damaging error. Ejection fraction between 41 and 49 percent is termed mildly reduced.

Left-sided failure backs up into the pulmonary circulation. Expect dyspnoea on exertion, orthopnoea (quantified by how many pillows the patient sleeps on), paroxysmal nocturnal dyspnoea (waking at two in the morning gasping and needing to sit up or open a window, caused by reabsorption of interstitial fluid when recumbent), bibasilar crackles that do not clear with coughing, a dry hacking nocturnal cough, frothy or pink-tinged sputum in pulmonary oedema, fatigue, nocturia, an S3 gallop, tachycardia and a laterally displaced point of maximal impulse. The S3 is worth chasing with the bell at the apex in the left lateral position: in an adult it is one of the earliest and most specific signs of volume overload.

Right-sided failure backs up into the systemic venous circulation. Expect jugular venous distension, hepatojugular reflux, dependent pitting oedema (ankles in an ambulatory patient, sacrum in a bedbound one — always check the sacrum), weight gain, hepatomegaly and right upper quadrant fullness or tenderness, splenomegaly, ascites, anorexia, nausea and early satiety from gut congestion. The most common cause of right-sided failure is left-sided failure; when it arises from pulmonary disease alone it is called cor pulmonale. Most hospitalised patients have findings on both sides.

Diagnostics: BNP, imaging and the numbers you must know

B-type natriuretic peptide is released by ventricular myocytes in response to stretch, so it rises with volume overload. Learn the interpretation, not just the number. A BNP below 100 pg/mL makes heart failure an unlikely explanation for acute dyspnoea; 100 to 400 pg/mL is a grey zone requiring clinical correlation; above 400 pg/mL strongly supports it, and values above 1,000 are common in decompensation. For NT-proBNP, a level below 300 pg/mL effectively rules out acute heart failure, and the confirming thresholds are age-adjusted — roughly above 450 pg/mL under age 50, above 900 between 50 and 75, and above 1,800 over 75. BNP is most useful for answering the question that actually arises at 3 a.m.: is this dyspnoeic patient in failure or having a COPD exacerbation?

Three caveats separate a nurse who reports a number from one who interprets it. Renal impairment and atrial fibrillation raise BNP independently of failure. Obesity lowers it, so a value of 250 pg/mL in a patient with a BMI of 45 may represent significant congestion. And sacubitril/valsartan raises BNP because the neprilysin inhibitor blocks BNP degradation — in a patient on that drug, follow NT-proBNP instead, which is unaffected. Trend the value against the patient’s own baseline rather than against the reference range.

The rest of the workup: chest radiography shows cardiomegaly, cephalisation of pulmonary vessels, Kerley B lines, interstitial and then alveolar oedema, and pleural effusions. Echocardiography is the central test — it gives ejection fraction, chamber sizes, wall motion, diastolic function and valve assessment. ECG identifies infarction, hypertrophy, atrial fibrillation and bundle branch block (a QRS of 150 ms or more with left bundle branch block, in a symptomatic patient whose ejection fraction remains 35 percent or below on optimal therapy, is what qualifies a patient for resynchronisation therapy). Laboratory monitoring is relentless in these patients: potassium, sodium, magnesium, BUN 10 to 20 mg/dL and creatinine 0.6 to 1.2 mg/dL (a rising ratio suggests poor renal perfusion), liver enzymes with hepatic congestion, thyroid studies, CBC for anaemia and iron studies, and a digoxin level where relevant. Right heart catheterisation is reserved for uncertain cases, where the numbers to recognise are CVP 2 to 6 mmHg, pulmonary artery wedge pressure 6 to 12 mmHg and cardiac output 4 to 8 L/min.

Two classification systems coexist and both appear on examinations. The New York Heart Association functional classes describe symptoms and can move up and down: class I, no limitation; class II, slight limitation with ordinary activity; class III, marked limitation with less-than-ordinary activity; class IV, symptoms at rest. The ACC/AHA stages describe structural progression and only move forward: stage A, at risk with no structural disease; stage B, structural disease without symptoms; stage C, structural disease with current or prior symptoms; stage D, refractory disease requiring advanced interventions. Staging drives therapy; NYHA class drives the conversation about how the patient is actually living.

Section 5Treating Heart Failure and Teaching the Patient to Live With It

Guideline-directed medical therapy: four pillars and the drugs around them

For HFrEF, four drug classes each independently reduce mortality, and the current standard is to start all four early at low doses and titrate upward rather than maximising one before adding the next. Students should be able to name them cold. First, a renin-angiotensin blocker: an ARNI (sacubitril/valsartan) is preferred, with an ACE inhibitor or ARB as the alternative. Second, an evidence-based beta-blocker — only carvedilol, metoprolol succinate (the extended-release salt) and bisoprolol have been shown to work, so metoprolol tartrate is not a substitute. Third, a mineralocorticoid receptor antagonist: spironolactone or eplerenone. Fourth, an SGLT2 inhibitor: dapagliflozin or empagliflozin, which benefit patients with and without diabetes. Beyond the four, hydralazine plus isosorbide dinitrate is added for self-identified Black patients on optimal therapy and for those who cannot take RAAS blockade, ivabradine is added when the sinus rate remains at 70 or above, and digoxin reduces hospitalisation without reducing mortality. Loop diuretics are used at the lowest effective dose for congestion; they make patients feel better but do not extend life. For HFpEF, the evidence base is thinner: control blood pressure, control rate and rhythm in atrial fibrillation, diurese for congestion, treat obesity and sleep apnoea, and use an SGLT2 inhibitor, with an MRA considered.

Three safety points recur on examinations and in practice. Switching from an ACE inhibitor to sacubitril/valsartan requires a 36-hour washout to avoid angioedema, and the two are never given together. Beta-blockers are started when the patient is euvolaemic and stable, not during an acute decompensation, and are titrated slowly because they transiently worsen symptoms before they help. And potassium is the recurring hazard of the whole regimen: loop diuretics drive it down while ACE inhibitors, ARBs, ARNIs, MRAs and potassium supplements drive it up. Never assume the direction — look at the actual value. And when potassium must be replaced, it is given orally or as a dilute intravenous infusion on a pump, never as an intravenous push and never as a concentrated bolus — undiluted intravenous potassium stops the heart.

Acute decompensation, pulmonary oedema and cardiogenic shock

Acute decompensated heart failure is the most common reason these patients are admitted, and flash pulmonary oedema is its most frightening form: extreme dyspnoea, severe anxiety and air hunger, tachypnoea, tachycardia, diffuse crackles, wheezing, cyanosis and pink frothy sputum from plasma forced into the alveoli. The patient will not lie down, and you should not make them. Interventions, in order: sit the patient upright with the legs dependent (this pools blood peripherally and immediately reduces preload — it is the fastest intervention you own and requires no order), apply oxygen and titrate to saturation, obtain vital signs and an ECG, establish intravenous access, and prepare for an intravenous loop diuretic, nitroglycerin infusion for afterload and preload reduction if the blood pressure tolerates it, and non-invasive positive pressure ventilation (CPAP or BiPAP), which pushes fluid out of the alveoli and often prevents intubation. Morphine, once routine here, is now used sparingly. Insert a urinary catheter if precise output measurement is required, and monitor potassium closely as diuresis proceeds.

Cardiogenic shock is failure of the pump severe enough to compromise tissue perfusion: systolic pressure below 90 mmHg or a sustained fall of more than 30 mmHg, urine output below 0.5 mL/kg/hour, cool mottled extremities, weak thready pulses, altered mentation and a rising serum lactate (normal roughly 0.5 to 2.2 mmol/L). Mortality is high and the patient belongs in intensive care. Management combines inotropic support (dobutamine or milrinone), vasopressor support (norepinephrine is generally first-line), careful volume assessment, treatment of the underlying cause — usually urgent revascularisation when the cause is infarction — and mechanical support such as an intra-aortic balloon pump or a percutaneous ventricular assist device. Your role on the floor is early recognition and fast escalation, because the window is short.

For advanced, refractory disease, options include an implantable cardioverter-defibrillator for primary prevention of sudden death when the ejection fraction remains 35 percent or below after at least three months of optimal therapy, cardiac resynchronisation therapy for a wide QRS with left bundle branch block, a left ventricular assist device as a bridge to transplant or as destination therapy, and cardiac transplantation. Palliative care is not a failure of treatment and belongs in the conversation earlier than most teams introduce it — symptom burden in advanced heart failure rivals that of many cancers, and goals-of-care discussions should include device deactivation planning.

Daily weights, sodium, delegation and the discharge conversation

Heart failure has one of the highest thirty-day readmission rates in medicine, and most of those readmissions are preventable with teaching that the patient actually retains. Lead with the scale. Teach the patient to weigh every morning, after voiding, before eating, in similar clothing, on the same scale, and to write it down. The action threshold you must teach in these exact terms: call the provider for a gain of 2 to 3 pounds in 24 hours, or 5 pounds in a week. That gain is fluid, not fat, and it precedes symptoms by days. Many patients will also have a diuretic action plan permitting an extra dose within defined limits — confirm the patient can state theirs.

Diet is the second pillar. Sodium is limited to roughly 2 to 3 grams per day, and teaching that works is concrete: read labels for sodium per serving, avoid canned soups, deli meats, frozen dinners, pickled and smoked foods, cheese and restaurant meals, cook with herbs and citrus instead of salt, and do not switch to a salt substitute without asking, because most contain potassium chloride and are dangerous with an ACE inhibitor, ARB or MRA. Fluid is restricted to about 1.5 to 2 litres per day in advanced disease or hyponatraemia; teach the patient to measure it, spread it across the day, count ice chips and gelatine, and manage thirst with hard candy, chewing gum, frequent mouth care and cold water rinses. Add daily activity as tolerated, alcohol moderation or abstinence, smoking cessation, annual influenza and appropriate pneumococcal and COVID-19 vaccination (infection is a leading trigger of decompensation), and a plan for medication adherence including a pill organiser and a realistic conversation about cost.

Delegation is tested constantly and misunderstood constantly. The UAP may obtain and record daily weights, measure and record intake and output, take vital signs on stable patients, assist with hygiene and repositioning, ambulate a stable patient and report findings back to you. The LPN or LVN may administer most oral and many routine medications within their state scope, reinforce teaching that the RN has already provided, monitor an established stable patient, and perform many procedures. The RN retains initial and ongoing assessment, initial patient teaching, evaluation of the response to therapy, care of the unstable patient, and titration of intravenous vasoactive infusions including nitroglycerin, dobutamine and heparin. The rule that will carry you through most items: you may delegate a task, never the assessment, the teaching, the evaluation or the unstable patient — and you remain accountable for the outcome of anything you delegate.

Older adults deserve a final paragraph because their presentation and their pharmacology both differ. Heart failure in the older adult may present as confusion, delirium, falls, anorexia, weakness or functional decline long before the classic dyspnoea, and a sudden change in mental status warrants a cardiac and infectious workup rather than a sedative. Reduced lean body mass and declining renal clearance raise digoxin levels at unchanged doses, so toxicity presents insidiously as nausea, anorexia and confusion. Diuretics plus vasodilators produce orthostatic hypotension and falls — teach patients to rise in stages and check orthostatic vital signs. Polypharmacy is the rule, and NSAIDs taken over the counter for arthritis are a frequent and hidden cause of decompensation. Ask about them by name. Red flags in heart failure that mean call now: weight gain of 2 to 3 pounds in a day or 5 in a week; new or worsening orthopnoea or paroxysmal nocturnal dyspnoea; resting dyspnoea, pink frothy sputum or a falling oxygen saturation; chest pain; syncope, palpitations or a new irregular rhythm; systolic pressure below 90 with poor perfusion; urine output below 0.5 mL/kg/hour; and any new confusion.

Words worth knowing

Cardiac Disorders: Dysrhythmias, Valves and Vascular Disease

Chapter 8 gave you the pump and its fuel supply. This chapter gives you the wiring, the doors and the plumbing. A dysrhythmia is an electrical problem that becomes a mechanical problem the instant it steals filling time or the atrial kick; a valve lesion is a mechanical problem that becomes an electrical problem the instant a stretched atrium fibrillates; and vascular disease is what happens when the conduit itself narrows, clots, dilates or tears. On a busy medical–surgical floor these three live together in the same patient: the eighty-two-year-old with aortic stenosis, new atrial fibrillation, a heparin drip and a cool, pulseless foot. Your job is not to memorise every strip in the book. It is to recognise the handful of rhythms that kill, to know whether the patient in front of you is stable or unstable, and to know which intervention comes first. Everything else in this chapter hangs off that skeleton.

Section 1Reading the Rhythm: Conduction, the Six-Step Strip and the Sinus Rhythms

The conduction system and what each waveform means

Cardiac muscle is unusual because it generates its own signal. Specialised pacemaker cells depolarise spontaneously, and the fastest one in the heart sets the pace. Normally that is the sinoatrial (SA) node in the high right atrium, firing at 60 to 100 times a minute. The impulse spreads across both atria, producing the P wave and the atrial contraction that tops off ventricular filling — the atrial kick, worth roughly 20 to 30 per cent of cardiac output in a healthy adult and considerably more in a stiff, hypertrophied or ischaemic ventricle. The signal then reaches the atrioventricular (AV) node, which deliberately delays it by about a tenth of a second so the atria can finish emptying before the ventricles squeeze. That delay is the flat part of the PR interval.

From the AV node the impulse races down the bundle of His, splits into right and left bundle branches and fans out through the Purkinje fibres, depolarising both ventricles almost simultaneously. That is the QRS complex, and it is narrow — 0.06 to 0.10 seconds — precisely because the specialised conduction tissue is fast. A wide QRS tells you the impulse took the slow route, muscle cell to muscle cell, which means it either started in the ventricle or met a blocked bundle branch on the way down. The ST segment is the quiet interval after the whole ventricle has depolarised and before repolarisation begins, and it should sit on the isoelectric line; the T wave is ventricular repolarisation, the electrical reset. Atrial repolarisation happens too, but it is buried inside the QRS and you never see it.

The system has redundancy. If the SA node fails, the AV junction takes over at 40 to 60 beats a minute, producing a narrow QRS with an absent, inverted or retrograde P wave — a junctional escape rhythm. If the junction fails too, the ventricle itself will fire at 20 to 40 beats a minute with a wide, bizarre QRS — an idioventricular rhythm. Escape rhythms are the heart’s last-resort generators. They are slow, they are unreliable, and they are never something to suppress with an antiarrhythmic; if you abolish the escape you are left with asystole.

Finally, remember that electricity is not perfusion. A monitor can show a textbook rhythm while the patient has no pulse at all — that is pulseless electrical activity. The first response to any alarming rhythm is always the same: look at your patient, touch your patient, check a central pulse and a blood pressure. Treat the person, not the screen.

A systematic six-step strip analysis

Students who guess at strips get them wrong; students who follow the same six steps every single time get them right. Step one: rate. Count the QRS complexes in a six-second strip and multiply by ten, or for a regular rhythm divide 300 by the number of large boxes between two R waves. Step two: rhythm. March out the R-to-R intervals with calipers or the edge of a piece of paper. Are they regular, regularly irregular (a repeating pattern, as in Wenckebach) or irregularly irregular (no pattern at all, the signature of atrial fibrillation)? Step three: P waves. Is there one, is it upright, and does it look like every other P wave on the strip?

Step four: P-to-QRS relationship. Is there exactly one P for every QRS? More P waves than QRS complexes means beats are being dropped — a block. Step five: PR interval. Measure it and, just as importantly, ask whether it is constant. A PR that lengthens progressively before a dropped beat is Mobitz I; a PR that stays fixed and then drops a beat without warning is Mobitz II; a PR that varies randomly with no relationship at all is third-degree block. Step six: QRS duration. Narrow or wide? Narrow tells you the impulse came from above the ventricles, and that is reassuring even when the rate is fast. Wide and fast, in an adult with cardiac disease, is ventricular tachycardia until proven otherwise.

Two habits will save you. First, always run and mount a strip when the rhythm changes, label it with the date, time and the patient’s symptoms, and compare it to the previous one; a rhythm change with no symptoms is a different problem from a rhythm change with chest pain and a systolic of 78. Second, when telemetry alarms, verify at the bedside before you act. Loose electrodes, a patient brushing their teeth, and a shivering patient all produce artefact that looks alarming. Artefact has one giveaway: you can usually march the underlying QRS complexes straight through the noise.

Sinus rhythms, sinus arrest and the bradycardia response

Sinus bradycardia is a normal-looking strip at a rate below 60. In a conditioned athlete or a sleeping adult it is normal. It becomes a problem when it produces symptoms: dizziness, syncope, fatigue, hypotension, confusion, chest pain or heart failure. Common causes are vagal stimulation (suctioning, vomiting, straining at stool, carotid pressure), inferior wall myocardial infarction, hypothyroidism, raised intracranial pressure, hypothermia and drugs — beta blockers, non-dihydropyridine calcium channel blockers, digoxin, amiodarone and cholinesterase inhibitors. Always look at the medication administration record before you conclude the node is diseased.

For symptomatic bradycardia the sequence is: assess airway, breathing and circulation, give oxygen if the patient is hypoxaemic, obtain intravenous access, apply the monitor and get a twelve-lead. Atropine 1 mg intravenous push is the first drug, repeated every three to five minutes to a maximum total of 3 mg. If atropine fails, move to transcutaneous pacing or a chronotropic infusion — dopamine 5 to 20 micrograms per kilogram per minute or epinephrine 2 to 10 micrograms per minute. Two cautions matter: atropine is unlikely to work and should not delay pacing when the block is below the AV node (Mobitz II or third-degree block with a wide QRS), and transcutaneous pacing hurts, so the conscious patient needs analgesia and sedation while you confirm both electrical capture on the monitor and mechanical capture by palpating a pulse.

Sinus tachycardia is almost never the primary problem. It is a symptom. Fever, pain, anxiety, hypovolaemia, hypoxaemia, anaemia, sepsis, hyperthyroidism, alcohol withdrawal, caffeine, nicotine and stimulants all drive it, and so do beta agonists such as albuterol. Treat the cause, not the number. Slowing a compensatory tachycardia in a hypovolaemic patient removes the only thing keeping their cardiac output up. Sick sinus syndrome, common in older adults, is a diseased node that alternates between inappropriate bradycardia and bursts of atrial tachycardia — the tachy–brady syndrome — and it is a leading reason for permanent pacemaker implantation after age 70.

Electrolytes, drugs and the vulnerable QT interval

A remarkable number of dysrhythmias on a medical–surgical floor are metabolic, not cardiac, and they are the ones you can actually fix. Potassium 3.5 to 5.0 mEq/L is the number to watch. Hypokalaemia flattens the T wave, produces a U wave, provokes premature ventricular contractions and sets the stage for torsades de pointes; it is common in patients on loop diuretics, which is to say most patients with heart failure. Hyperkalaemia peaks the T waves, then widens the QRS, then flattens the P wave and finally produces a sine wave and arrest. Magnesium 1.3 to 2.1 mEq/L travels with potassium: you cannot correct a stubborn hypokalaemia until the magnesium is replaced. Two replacement rules are absolute. Potassium is never given by intravenous push or bolus — it is always diluted and infused on a pump, conventionally no faster than 10 mEq per hour on a general floor and only faster in a monitored setting through a central line, because a bolus stops the heart. And never add potassium to a hanging bag; use the premixed one. Ionised calcium 4.5 to 5.6 mg/dL shortens or lengthens the QT interval when it is high or low respectively.

The QT interval deserves its own paragraph because prolonging it is the most common way a well-meaning drug order kills a patient. Corrected QT above 500 milliseconds is the threshold at which most institutions require notification. The offenders you will actually hang are amiodarone, sotalol, procainamide, ibutilide, haloperidol, ondansetron, methadone, fluoroquinolones such as levofloxacin, macrolides such as azithromycin, and many antipsychotics and antidepressants. Two or three of these together, in a patient who is also hypokalaemic and hypomagnesaemic, is a recipe for polymorphic ventricular tachycardia. Before giving a QT-prolonging drug, look at the most recent QTc and the most recent potassium and magnesium. That is a nursing intervention, not a pharmacy one.

Finally, digoxin. Therapeutic serum level is 0.5 to 2.0 ng/mL, and in heart failure most clinicians now target 0.5 to 0.9 ng/mL. Hold the dose and notify the provider if the apical pulse is below 60 in an adult. Early toxicity is deceptively vague — anorexia, nausea, vomiting, fatigue, confusion — and the classic yellow-green or halo visual disturbance comes late. Any new dysrhythmia in a patient on digoxin should be treated as toxicity until the level and the potassium return, because hypokalaemia dramatically potentiates digoxin binding. The antidote is digoxin immune Fab.

Section 2Atrial Fibrillation, Flutter and the Supraventricular Tachycardias

Why atrial fibrillation matters: the lost kick and the quiet appendage

In atrial fibrillation the atria stop contracting and instead quiver at 350 to 600 impulses a minute. The AV node acts as a gatekeeper, letting through an unpredictable subset of those impulses, which is why the ventricular response is irregularly irregular — the single most reliable bedside finding. On the strip there are no organised P waves, only a wavy or flat fibrillatory baseline, and the QRS complexes are narrow unless there is a coexisting bundle branch block.

Two consequences follow, and every intervention in atrial fibrillation aims at one of them. First, the atrial kick is lost. In a young healthy heart that costs perhaps 20 per cent of cardiac output; in an older patient with a stiff, hypertrophied ventricle or aortic stenosis it can cost 30 to 40 per cent, and the drop is felt immediately as fatigue, dyspnoea, hypotension or frank pulmonary oedema. A rapid ventricular response makes it worse by shortening diastole, which is both the filling time for the ventricle and the perfusion time for the coronary arteries. This is why new-onset atrial fibrillation with a rate of 150 can precipitate angina in a patient whose coronary disease was previously silent.

Second, blood stagnates. The left atrial appendage is a blind pouch that, without coordinated contraction, becomes a thrombus factory. A clot that forms there and embolises travels to the brain, and this is why atrial fibrillation raises stroke risk roughly fivefold and why cardioembolic strokes tend to be large and disabling. Understanding this one anatomical fact makes the entire anticoagulation discussion make sense. It also explains the pulse deficit you may find: because many ventricular beats are too weak to open the aortic valve, the apical rate counted at the chest can exceed the radial rate counted at the wrist. Always take an apical pulse for a full minute in atrial fibrillation, and never rely on the automated blood pressure cuff’s heart rate.

Atrial fibrillation is provoked by hypertension, heart failure, valvular disease (especially mitral stenosis), coronary disease, hyperthyroidism, obstructive sleep apnoea, obesity, alcohol, sepsis, pulmonary embolism, electrolyte derangement and cardiac or thoracic surgery. Postoperative atrial fibrillation after cardiac surgery is so common — roughly a third of patients — that it is anticipated rather than surprising. Screening a new case means a twelve-lead ECG, an echocardiogram, thyroid studies, electrolytes including magnesium, a complete blood count and renal function.

Rate, rhythm and the cardioversion clock

For the unstable patient — hypotensive, ischaemic, confused, in pulmonary oedema because of the rhythm — the answer is immediate synchronised cardioversion, typically 120 to 200 joules biphasic, with sedation if time allows. For everyone else, the first goal is rate control, usually a target resting ventricular rate under about 110 in an asymptomatic patient or under 80 if symptoms persist. The workhorse agents are intravenous beta blockers (metoprolol 5 mg slow push, may repeat) and the non-dihydropyridine calcium channel blocker diltiazem (0.25 mg/kg over two minutes, then an infusion). Both drop blood pressure and slow conduction, so take an apical pulse and a blood pressure immediately before and after every dose; the usual hold parameters are a heart rate below 60 or a systolic pressure below 100, and if the order does not specify them, get them clarified before the first dose. Avoid diltiazem in a patient with reduced ejection fraction because of its negative inotropy. Digoxin is a second-line choice reserved for patients with heart failure or hypotension; it controls the rate at rest but poorly with activity. Amiodarone both slows the rate and may chemically convert the rhythm, which is exactly why it cannot be given casually.

That brings us to the rule students most often miss. If atrial fibrillation has lasted more than 48 hours, or the duration is unknown, the patient must not be converted — electrically or chemically — until either three weeks of therapeutic anticoagulation has been completed or a transoesophageal echocardiogram has excluded a left atrial thrombus. Converting a fibrillating atrium restores coordinated contraction and can fire an existing clot straight into the cerebral circulation. After any conversion, anticoagulation continues for at least four weeks, because the atrium is mechanically stunned and remains thrombogenic even though the rhythm on the monitor looks normal.

Atrial flutter is the organised cousin: a single re-entrant circuit, usually around the tricuspid annulus, producing a sawtooth flutter-wave baseline at an atrial rate of 250 to 350. When conduction is a fixed 2:1 you get a very regular ventricular rate near 150, which is the classic trap — a regular narrow tachycardia at exactly 150 should make you look hard for hidden flutter waves. Flutter carries the same embolic risk as fibrillation and the same anticoagulation rules, converts at lower energy (50 to 100 joules), and is often curable by catheter ablation of the cavotricuspid isthmus. Left atrial appendage occlusion devices offer an alternative for patients who cannot tolerate long-term anticoagulation.

Anticoagulation: scoring the risk and giving the drug safely

Stroke prevention is decided by the CHA2DS2-VASc score, not by whether the rhythm is paroxysmal, persistent or permanent. In general, a score of 2 or more in men and 3 or more in women warrants long-term oral anticoagulation. Bleeding risk is estimated separately (HAS-BLED and similar tools), but a high bleeding score is a prompt to correct modifiable risks — uncontrolled hypertension, alcohol, concurrent non-steroidal anti-inflammatory drugs — not an automatic reason to withhold anticoagulation. Aspirin alone is not adequate stroke prophylaxis in atrial fibrillation.

The direct oral anticoagulants — apixaban, rivaroxaban, edoxaban (factor Xa inhibitors) and dabigatran (a direct thrombin inhibitor) — are now first-line for non-valvular atrial fibrillation. They require no routine coagulation monitoring and have few food interactions, but they must be dose-adjusted for renal function and age, they have short half-lives so a single missed dose genuinely matters, and they are contraindicated in patients with mechanical heart valves or moderate-to-severe mitral stenosis, who still require warfarin. Warfarin is monitored by the international normalised ratio, target 2.0 to 3.0 in atrial fibrillation. Its antidote is vitamin K (with prothrombin complex concentrate for serious bleeding); idarucizumab reverses dabigatran and andexanet alfa reverses apixaban and rivaroxaban.

Teaching is where the nursing happens. Patients on warfarin need a consistent intake of vitamin K–rich foods rather than avoidance of them, no new over-the-counter medicine or herbal product without checking (ginkgo, ginseng, garlic, vitamin E and St John’s wort all interact), an electric razor and a soft toothbrush, and a medical alert identification. Every anticoagulated patient must be taught the bleeding report list: black or tarry stools, blood in urine or vomit, coughing blood, a nosebleed that will not stop after ten minutes of pressure, unusual bruising, and — the one they forget — a fall or any blow to the head, which requires evaluation even when they feel fine because of the risk of a delayed intracranial bleed.

Paroxysmal supraventricular tachycardia, vagal manoeuvres and adenosine

Paroxysmal supraventricular tachycardia is a re-entrant circuit, usually within or near the AV node, producing an abrupt-onset, abrupt-offset, perfectly regular narrow-complex tachycardia at 150 to 250 beats a minute. P waves are typically buried in the preceding T wave. Patients describe a sudden pounding in the chest or neck, lightheadedness, dyspnoea and anxiety; young, otherwise healthy people tolerate it for hours, while an older patient with coronary disease may become ischaemic within minutes.

For the stable patient, start with vagal manoeuvres: ask the patient to bear down as if having a bowel movement (Valsalva) for 10 to 15 seconds, or apply a cold stimulus to the face. Carotid sinus massage is a provider manoeuvre and is avoided in older adults and anyone with carotid bruits because of stroke risk. Have the monitor running and a strip recording; the transient AV block a vagal manoeuvre produces is diagnostic even when it does not convert the rhythm, because it unmasks flutter waves or fibrillation.

If vagal manoeuvres fail, the drug is adenosine 6 mg by rapid intravenous push over one to two seconds, immediately followed by a 20 mL normal saline flush with the arm elevated, using the port closest to the patient and preferably an antecubital or larger vein. If there is no conversion in one to two minutes, give 12 mg the same way. Adenosine has a half-life under 10 seconds, so a slow push simply does not work. Warn the patient in advance: they will feel flushing, chest pressure and a sense of impending doom, and the monitor will show a few seconds of asystole or bradycardia before sinus rhythm resumes. Adenosine is used cautiously or avoided in asthma because it can provoke bronchospasm, and its effect is blunted by caffeine and theophylline. If the patient is unstable at any point, skip all of this and go to synchronised cardioversion at 50 to 100 joules. Definitive long-term therapy for recurrent supraventricular tachycardia is catheter ablation, which is curative in the great majority of patients.

Section 3Ventricular Dysrhythmias, Heart Block and Electrical Therapy

From premature ventricular contractions to ventricular tachycardia

A premature ventricular contraction is an early, wide, bizarre QRS with no preceding P wave, usually followed by a full compensatory pause. Because it fires before the ventricle has filled, it produces little or no stroke volume, which is why a patient with frequent premature ventricular contractions may have a pulse deficit and feel a “skipped beat” or a thud. Occasional premature ventricular contractions are common and benign in a structurally normal heart. They become concerning when they are frequent (more than about six a minute), multifocal (differently shaped, meaning multiple irritable sites), coupled (pairs), run in threes or more, or fall on the T wave of the preceding beat — the R-on-T phenomenon, which can trigger ventricular fibrillation because it lands in the vulnerable period of repolarisation.

The nursing response to new or increasing premature ventricular contractions is not a drug. It is a search for the cause: check oxygenation, check the potassium and magnesium, check for ischaemia with a twelve-lead, review the drug list for QT prolongers and stimulants, check for caffeine and nicotine, and look at any central line or pulmonary artery catheter, because a catheter tip irritating the right ventricle is a classic and immediately reversible cause. Assess whether the patient is symptomatic and whether they are perfusing.

Three or more consecutive ventricular beats is ventricular tachycardia — a run if it is brief and self-limiting, sustained if it lasts more than 30 seconds or causes haemodynamic collapse. Monomorphic ventricular tachycardia is regular and wide at 100 to 250 beats a minute with all complexes the same shape, and it usually arises from scar tissue after a myocardial infarction. A wide-complex tachycardia in an adult with known heart disease should be treated as ventricular tachycardia until proven otherwise; the mistake of calling it supraventricular tachycardia with aberrancy and giving a calcium channel blocker can be fatal. Assess for a pulse immediately, because the treatment path forks entirely on that finding. Stable ventricular tachycardia with a pulse is treated with intravenous amiodarone 150 mg over 10 minutes (alternatives include procainamide and sotalol); unstable monomorphic ventricular tachycardia with a pulse gets synchronised cardioversion; pulseless ventricular tachycardia is a cardiac arrest.

Torsades de pointes is polymorphic ventricular tachycardia in the setting of a prolonged QT interval, and it looks like the QRS complexes are twisting around the baseline. It is its own diagnosis because it has its own treatment: magnesium sulfate 1 to 2 g intravenously, plus removal of every QT-prolonging drug and correction of potassium and magnesium. It frequently self-terminates and just as frequently degenerates into ventricular fibrillation, so the patient stays on the monitor with the defibrillator at the bedside. Know in advance what to do if it does not self-terminate: because the QRS complexes are constantly changing shape, there is no consistent R wave for the machine to synchronise to, and pressing sync on unstable torsades commonly ends with the defibrillator refusing to discharge while the patient deteriorates. Unstable or pulseless polymorphic ventricular tachycardia is therefore treated as ventricular fibrillation — an immediate high-energy unsynchronised shock — while the magnesium, the drug review and the electrolyte correction continue.

The code: defibrillation, synchronised cardioversion and what not to shock

Ventricular fibrillation is chaotic, disorganised depolarisation with no coordinated contraction and therefore no cardiac output. The patient is pulseless, apnoeic and unresponsive within seconds. Along with pulseless ventricular tachycardia it is one of the two shockable rhythms, and survival falls by roughly 7 to 10 per cent for every minute that defibrillation is delayed. The response is to confirm unresponsiveness and pulselessness, call for help and the defibrillator, and begin high-quality compressions at 100 to 120 per minute, 2 to 2.4 inches deep, allowing full recoil and minimising interruptions, at a 30:2 ratio until an advanced airway is placed.

Defibrillation is unsynchronised: it delivers energy the instant the button is pressed, because in ventricular fibrillation there is no R wave to synchronise to. Use 120 to 200 joules biphasic per the manufacturer, or 360 joules monophasic. Resume compressions immediately after the shock without pausing to check a rhythm. Give epinephrine 1 mg intravenously or intraosseously every three to five minutes and, after the second or third shock, amiodarone 300 mg followed by 150 mg, or lidocaine 1 to 1.5 mg/kg. Throughout, work the reversible causes — hypovolaemia, hypoxia, hydrogen ion (acidosis), hypo- and hyperkalaemia, hypothermia, tension pneumothorax, tamponade, toxins, and thrombosis of the coronary or pulmonary circulation.

Synchronised cardioversion is different and the difference is examinable. The machine times the shock to the R wave so that it does not land on the T wave and induce ventricular fibrillation. It is used for unstable rhythms that still have a pulse: atrial fibrillation at 120 to 200 joules, atrial flutter and supraventricular tachycardia at 50 to 100 joules, and monomorphic ventricular tachycardia with a pulse at 100 joules. Every one of those rhythms is organised enough to give the machine an R wave; polymorphic ventricular tachycardia is not, so an unstable or pulseless polymorphic rhythm is defibrillated rather than cardioverted. Sedate the conscious patient. Press and hold the discharge buttons, because the machine waits for the next R wave. If the rhythm degenerates to ventricular fibrillation, turn the sync function off and defibrillate. Safety is the nurse’s job for both procedures: ensure everyone is clear including yourself, remove supplemental oxygen from the immediate area, verify no one is touching the bed, and never place a pad directly over an implanted device.

The two non-shockable rhythms are asystole and pulseless electrical activity. Shocking them does nothing and delays what does work: compressions, epinephrine and an aggressive hunt for the reversible cause. Asystole should be confirmed in a second lead and the leads and gain checked, because a disconnected electrode produces a flat line on a living patient.

The atrioventricular blocks and when atropine is the wrong drug

The two things students confuse are Mobitz I versus Mobitz II, and when atropine helps. Mobitz I lengthens the PR before it drops a beat; Mobitz II drops without warning. The mechanism explains everything else. Mobitz I is a fatiguing AV node, and the AV node is richly innervated by the vagus nerve, so blocking the vagus with atropine speeds it up. Mobitz II and complete block with a wide QRS sit in the His–Purkinje system, which has little vagal innervation, so atropine does nothing useful there — and by speeding the atrial rate it can actually worsen the ratio of conducted beats. For Mobitz II and third-degree block, the answer is pacing, and atropine must never delay it. Third-degree block is recognised by marching out the P waves at one regular rate and the QRS complexes at a different, slower regular rate, with no fixed relationship between them.

Pacemakers, implantable defibrillators and the nursing that surrounds them

A permanent pacemaker delivers an impulse when the heart’s own rate falls below a programmed threshold; the spike appears on the strip immediately before the captured complex. Three malfunctions are testable. Failure to capture is a pacer spike with no complex after it — the impulse fired but the myocardium did not respond, often because of lead displacement, a low output setting, or electrolyte or ischaemic change. Failure to sense is a spike that appears where it should not, marching into the patient’s own beats and risking an R-on-T event. Failure to pace is no spike at all when one is due, from battery depletion, a lead fracture or oversensing. All three are reported promptly.

An implantable cardioverter–defibrillator adds the ability to detect and terminate ventricular tachycardia or fibrillation with antitachycardia pacing or an internal shock. Teach the patient to sit or lie down when they feel a warning symptom, to keep a log of every shock, and the reporting rule: one shock with recovery means call the clinic; more than one shock in 24 hours, or a shock accompanied by chest pain, syncope or dyspnoea, means call 911. Household members should learn cardiopulmonary resuscitation; a bystander touching the patient during a discharge may feel a harmless tingle. Driving restrictions vary by state and by whether the device was placed for primary or secondary prevention, and this conversation must not be skipped.

Post-implantation care for either device: monitor the incision for bleeding, haematoma, redness or drainage; restrict the arm on the operative side from lifting above shoulder height and from lifting more than about 10 pounds for four to six weeks so the leads can fibrose into place; use a sling only as ordered and encourage gentle range of motion so the shoulder does not freeze; and watch for pneumothorax, which presents as new dyspnoea and diminished breath sounds after subclavian access. Long term, the patient carries the device identification card, avoids arc welding, large running motors and high-voltage fields, keeps a mobile phone at least six inches from the generator and uses the opposite ear, walks briskly through and never lingers in airport security arches, and asks whether their device is MRI-conditional before any scan.

Section 4Valvular Heart Disease and Infective Endocarditis

Stenosis versus regurgitation: the mechanical logic

There are only two things a valve can do wrong. A stenotic valve will not open properly, so the chamber behind it must generate higher pressure to push blood through a smaller orifice; that chamber hypertrophies and pressure backs up behind it. A regurgitant (insufficient) valve will not close properly, so blood leaks backward with every beat; the receiving chamber has to handle its normal volume plus the regurgitant volume, so it dilates. Stenosis causes pressure overload and hypertrophy; regurgitation causes volume overload and dilation. Learn that sentence and you can reason out the findings of any valve lesion rather than memorising four separate lists.

Work out where the blood backs up and you have the symptoms. A mitral valve problem backs up into the left atrium and then into the pulmonary circulation, so the patient is dyspnoeic, orthopnoeic, has crackles and may cough pink or blood-tinged sputum. An aortic valve problem eventually backs up through the left ventricle into the left atrium and lungs as well, but its earlier symptoms are those of inadequate forward flow: exertional syncope, angina and fatigue. Tricuspid and pulmonic lesions back up into the systemic venous system, producing jugular venous distension, hepatomegaly, ascites and dependent oedema. A dilated left atrium, regardless of cause, stretches the atrial tissue and produces atrial fibrillation — which is how valve disease and Section 2 collide in the same patient.

Causes have shifted over time. Rheumatic heart disease, once the dominant cause worldwide and still important in immigrant and under-resourced populations, is now a smaller share in the United States, where degenerative calcific disease of the aortic valve in older adults, myxomatous degeneration of the mitral valve, congenital bicuspid aortic valve, infective endocarditis and dilation secondary to heart failure predominate. Transthoracic echocardiography is the diagnostic test of choice for all of them; it gives valve area, pressure gradient, ejection fraction and chamber size. Transoesophageal echocardiography is reserved for when better resolution is needed — vegetations, prosthetic valve dysfunction, left atrial thrombus. A B-type natriuretic peptide level (normal generally under 100 pg/mL) helps gauge how much the ventricle is straining.

The four lesions you must be able to describe

Aortic stenosis earns extra attention because of what it forbids. The hypertrophied, non-compliant left ventricle depends on adequate preload and on the atrial kick to fill. Remove preload with a nitrate or a large dose of a loop diuretic and stroke volume falls off a cliff; the patient becomes hypotensive and may syncopise. Put the same patient into rapid atrial fibrillation and the loss of the atrial kick plus shortened filling time does the same thing. This is why the classic teaching is to be cautious with nitroglycerin in severe aortic stenosis, and why new atrial fibrillation in these patients is treated urgently. Whenever a nitrate is on the order set, screen for a phosphodiesterase-5 inhibitor as well — sildenafil or vardenafil within 24 hours, or tadalafil within 48 hours, makes any nitrate an absolute contraindication because the combination causes profound, refractory hypotension. Once symptoms appear, untreated severe aortic stenosis carries an average survival measured in a few years, which is why symptom onset is the trigger for valve replacement.

Nursing assessment for any valve patient is a fatigue and activity history — what could you do six months ago that you cannot do now? — plus auscultation at all four valve areas with both the diaphragm and the bell, palpation for a thrill, assessment for jugular venous distension, hepatomegaly, dependent oedema and crackles, daily weights, and an accurate apical–radial pulse. Management before surgery is largely medical: diuretics and sodium restriction for congestion, rate control and anticoagulation for atrial fibrillation, treatment of hypertension, and prompt treatment of anaemia, fever and infection, because anything that raises cardiac demand decompensates a fixed valve.

Repair, replacement and life with a prosthetic valve

Options range from valve repair — preferred for the mitral valve where feasible because it preserves the native apparatus and avoids anticoagulation — through percutaneous balloon valvuloplasty for selected mitral stenosis, to full replacement. Transcatheter aortic valve replacement delivers a bioprosthetic valve through the femoral artery without sternotomy, and postoperative nursing focuses on the vascular access site (bleeding, haematoma, retroperitoneal bleed presenting as flank or back pain and unexplained hypotension), distal pulses, renal function after contrast, stroke assessment, and new conduction disturbance — the new valve sits next to the conduction system, so a new left bundle branch block or complete heart block requiring a permanent pacemaker is a recognised complication.

Surgical replacement uses either a mechanical valve or a bioprosthetic (tissue) valve, and the trade-off is durability against anticoagulation. Mechanical valves last decades but require lifelong warfarin — international normalised ratio 2.0 to 3.0 for most mechanical aortic valves and 2.5 to 3.5 for mechanical mitral valves — and direct oral anticoagulants are contraindicated. Tissue valves generally last 10 to 20 years and need only a shorter course of anticoagulation followed by aspirin, but they degenerate and may require reoperation. Younger patients therefore usually receive mechanical valves and older patients tissue valves, though patient preference about bleeding risk and pregnancy plans weighs heavily.

After open valve surgery, nursing priorities are the ones common to cardiac surgery: haemodynamic monitoring, chest tube patency and output, pain control adequate to permit deep breathing, incentive spirometry with a splinting pillow, sternal precautions, early mobilisation, glycaemic control and rhythm surveillance for postoperative atrial fibrillation. Watch specifically for cardiac tamponade — a sudden drop or cessation of chest tube drainage followed by hypotension, jugular venous distension, muffled heart tones, narrowing pulse pressure and pulsus paradoxus. That is a rapid-response call, not a wait-and-see. Discharge teaching for a mechanical valve includes the expected soft clicking sound, bleeding precautions, strict international normalised ratio follow-up, antibiotic prophylaxis before dental work, and reporting fever, new dyspnoea, a changed valve sound or an embolic symptom immediately.

Infective endocarditis and rheumatic heart disease

Infective endocarditis is infection of the endocardium, usually of a valve, in which platelets and fibrin build a vegetation around colonising organisms. Two things follow: the vegetation destroys the valve, producing acute regurgitation and heart failure, and pieces break off and embolise. Left-sided vegetations embolise to the brain, spleen, kidneys and extremities; right-sided vegetations, common in people who inject drugs, embolise to the lungs and present as septic pulmonary emboli. Risk factors are prosthetic valves, prior endocarditis, congenital heart disease, injection drug use, indwelling vascular catheters, haemodialysis and immunosuppression. Staphylococcus aureus causes most acute, aggressive disease; viridans group streptococci cause the subacute form that follows dental procedures.

The presentation is fever plus a new or changed murmur, with fatigue, night sweats, weight loss, arthralgias and anorexia. The peripheral findings are classic and worth knowing by name: Osler nodes (painful, tender nodules on finger and toe pads — Osler is Ouch), Janeway lesions (painless flat haemorrhagic macules on palms and soles), splinter haemorrhages under the nails, Roth spots on the retina, petechiae on the conjunctivae and oral mucosa, and clubbing in long-standing disease. Diagnosis rests on the modified Duke criteria, combining blood cultures with echocardiographic evidence of vegetation. Obtain at least three sets of blood cultures from separate venipuncture sites before the first dose of antibiotic; giving antibiotics first can sterilise the cultures and leave the team treating blind for six weeks.

Treatment is four to six weeks of intravenous antibiotics targeted to the organism, frequently completed at home or in a skilled facility through a peripherally inserted central catheter. Nursing care is line care with meticulous sterile technique, monitoring temperature trends, tracking renal function and drug levels for vancomycin and aminoglycosides, daily assessment for new murmur or heart failure, and a focused neurological check every shift because embolic stroke is the feared complication. Surgery is indicated for heart failure from valve destruction, uncontrolled infection, prosthetic valve involvement or recurrent emboli. Prophylaxis is now restricted to the highest-risk patients — prosthetic valves or prosthetic material, prior endocarditis, certain congenital heart disease and cardiac transplant recipients with valvulopathy — who take amoxicillin 2 g orally 30 to 60 minutes before dental procedures involving gingival or periapical manipulation; cephalexin, azithromycin or doxycycline are used for penicillin allergy. Teach meticulous oral hygiene and regular dental care, because everyday gum disease produces more cumulative bacteraemia than any single procedure.

Acute rheumatic fever remains the reason that untreated streptococcal pharyngitis is not a trivial illness. Two to three weeks after group A streptococcal throat infection, antibodies cross-react with cardiac, joint, skin and neural tissue, producing carditis, migratory polyarthritis, chorea, erythema marginatum and subcutaneous nodules. The mitral valve is most often scarred, and the stenosis may not declare itself for twenty years. The nursing message is simple and preventive: culture the sore throat, and finish the entire antibiotic course.

Section 5Vascular Disease: Arteries, Veins, the Aorta and the Crisis

Peripheral arterial disease and acute limb ischaemia

Peripheral arterial disease is atherosclerosis of the limb arteries, most often the lower extremities. The pathophysiology is identical to coronary disease, so the risk factors are identical — smoking above all, then diabetes, hypertension, dyslipidaemia, age and chronic kidney disease — and the presence of peripheral arterial disease means that patient almost certainly has coronary and cerebrovascular disease too. The cardinal symptom is intermittent claudication: reproducible cramping, aching or fatigue in the calf, thigh or buttock brought on by a predictable amount of walking and relieved within a few minutes of rest. As disease progresses, pain appears at rest, characteristically in the forefoot and toes at night, and is relieved by hanging the leg over the side of the bed, because gravity assists a circulation that can no longer overcome supine pressures.

Assessment findings follow the mechanism. The limb is cool and pale, with thin, shiny, hairless skin, thickened nails, muscle atrophy, diminished or absent pedal pulses, prolonged capillary refill, pallor on elevation and dependent rubor. Ulcers, when they come, sit on the toes, the lateral malleolus or pressure points; they are round with sharply demarcated “punched-out” edges, pale or necrotic at the base, exquisitely painful and minimally exudative. The diagnostic bedside test is the ankle–brachial index, the ratio of ankle to brachial systolic pressure by Doppler.

Management begins with risk-factor treatment, because the leg is the visible part of a systemic disease: complete tobacco cessation (the single highest-value intervention), a high-intensity statin, an antiplatelet agent such as aspirin 81 mg or clopidogrel 75 mg, blood pressure and glycaemic control. A supervised walking programme — walk to near-maximal claudication pain, rest, repeat, for 30 to 45 minutes three or more times a week — genuinely increases walking distance by promoting collateral vessels, and it is the intervention patients most need coaching to continue through the discomfort. Cilostazol, a phosphodiesterase III inhibitor, improves walking distance but is contraindicated in heart failure of any severity and takes weeks to work. Revascularisation, by angioplasty with stenting or by bypass grafting, is reserved for lifestyle-limiting claudication or critical limb ischaemia.

Positioning and foot care are where nursing decides outcomes. In arterial disease, keep the legs below heart level or neutral — never elevated — because elevation removes the gravitational assist. Keep the patient warm with socks and blankets, but never apply direct heat such as a heating pad or hot soak, because neuropathic skin will burn before the patient feels it. Avoid crossing the legs and avoid constricting clothing. Inspect the feet daily including between the toes with a mirror, wash with lukewarm water and mild soap, dry thoroughly, moisturise the skin but not between the toes, cut nails straight across or have a podiatrist do it, and never walk barefoot. Any new break in the skin is reported the same day. Acute arterial occlusion announces itself with the six P’s — pain, pallor, pulselessness, paraesthesia, poikilothermia (coolness) and paralysis — and it is a limb-threatening emergency with roughly six hours before irreversible tissue loss. Do not elevate, do not apply heat or cold, do not massage the limb: keep it dependent and protected, keep the patient nothing by mouth in anticipation of surgery, and call immediately for anticoagulation and revascularisation.

Venous thromboembolism and anticoagulation safety

Virchow’s triad explains every deep vein thrombosis you will ever see: venous stasis, endothelial injury and hypercoagulability. The hospitalised medical–surgical patient has all three — immobility, surgical or catheter-related vessel trauma, and the acute-phase hypercoagulable state of illness, malignancy, oestrogen therapy, pregnancy or inherited thrombophilia. Findings in the affected limb are unilateral oedema (measure and compare calf circumferences at a marked point), warmth, erythema, tenderness along the deep venous course and a dull ache. Homans sign is unreliable and is no longer recommended. Venous duplex ultrasonography is the diagnostic test; a D-dimer below about 500 ng/mL FEU is useful to exclude thrombosis in a low-probability patient but is non-specific and rises with surgery, infection, pregnancy, malignancy and age.

The feared complication is pulmonary embolism: sudden dyspnoea, pleuritic chest pain, tachypnoea, tachycardia, hypoxaemia, apprehension and, in massive embolism, hypotension and syncope. Any patient with a known or suspected deep vein thrombosis who becomes acutely short of breath is a rapid-response call. Prevention is a nursing responsibility on every shift: early and frequent ambulation, ankle pumps and leg exercises for the patient who cannot walk, adequate hydration, sequential compression devices worn as ordered, and pharmacologic prophylaxis such as enoxaparin 40 mg subcutaneously daily or heparin 5000 units subcutaneously two or three times a day unless contraindicated.

Treatment is anticoagulation, which does not dissolve the existing clot but stops its extension while the body lyses it. Options are a direct oral anticoagulant, low-molecular-weight heparin such as enoxaparin 1 mg/kg subcutaneously every 12 hours, or an unfractionated heparin infusion bridging to warfarin. Unfractionated heparin is monitored by activated partial thromboplastin time at 1.5 to 2.5 times control (commonly about 46 to 70 seconds) or by an anti-factor Xa level of 0.3 to 0.7 units/mL; its antidote is protamine sulfate. Low-molecular-weight heparin needs no routine monitoring except in renal impairment, obesity or pregnancy, where an anti-Xa level is used. Teach enoxaparin injection into the abdominal fat two inches from the umbilicus, alternating sides, without expelling the air bubble and without rubbing the site. Warfarin overlaps with heparin for at least five days and until the international normalised ratio has been therapeutic for 24 hours, because warfarin is transiently procoagulant at initiation.

Heparin-induced thrombocytopenia is the complication that must not be missed. An immune reaction to heparin–platelet factor 4 complexes causes the platelet count to fall by more than 50 per cent, typically five to ten days after exposure, and paradoxically causes thrombosis, not bleeding. Check a baseline platelet count and monitor it on every heparin patient. If it is suspected: stop all heparin, including flushes and heparin-bonded catheters, notify the provider, and anticipate a non-heparin anticoagulant such as argatroban, bivalirudin or fondaparinux. Do not transfuse platelets, and do not start warfarin until the platelet count has recovered. An inferior vena cava filter is reserved for patients in whom anticoagulation is contraindicated or has failed.

Chronic venous insufficiency and telling the two ulcers apart

Chronic venous insufficiency results from incompetent valves in the deep or perforating veins, often after a previous deep vein thrombosis, so blood refluxes and venous pressure stays high. Capillaries leak fluid, protein and red cells into the tissue; haemoglobin breakdown leaves the characteristic brown haemosiderin staining, and the skin becomes indurated, itchy and eczematous. The limb is warm, oedematous and heavy, worse at the end of the day and better after a night in bed. The ulcer that follows sits over the medial malleolus, is shallow with irregular sloping borders, has a beefy red granulating base, drains a good deal of fluid and is uncomfortable rather than agonising.

Management of venous disease is compression, elevation and skin care. Graduated compression stockings of 20–30 or 30–40 mmHg are the mainstay, applied first thing in the morning before the leg has become oedematous, removed at night, and replaced every three to six months when they lose elasticity. Layered compression wraps such as an Unna boot are used for active ulcers. The critical safety check is that compression must not be applied to a limb with significant arterial insufficiency — confirm the ankle–brachial index first, because squeezing a leg that cannot get arterial blood in will cause necrosis. Teach elevation above heart level for 20 minutes several times daily, avoidance of prolonged standing or sitting with legs dependent, ankle pumping every hour, weight management, and daily moisturising of intact skin. Venous ulcers are slow; healing is measured in weeks to months, and adherence to compression is the single strongest predictor of whether they close and stay closed.

Aneurysm, dissection and hypertensive crisis

An abdominal aortic aneurysm is a permanent dilation to more than one and a half times normal diameter, driven by atherosclerosis, hypertension, smoking, male sex, age and connective tissue disorders such as Marfan syndrome. It is usually silent and found incidentally; when there are findings they are a pulsatile mass at or above the umbilicus, a bruit and vague abdominal or low back pain. Do not palpate deeply on a suspected or known aneurysm. Surveillance imaging is by ultrasound or computed tomography, and elective repair — open or endovascular — is generally offered at about 5.5 cm, or sooner for rapid expansion of more than 0.5 cm in six months, symptoms, or in some women at a smaller diameter. Medical management in the meantime is blood pressure control, statin therapy and absolute smoking cessation. Rupture presents as sudden severe, tearing abdominal, flank or back pain with hypotension, tachycardia and a pulsatile mass, and it is an immediate surgical emergency: large-bore access, type and crossmatch, nothing by mouth, and the operating room. After endovascular repair, monitor peripheral pulses and limb perfusion hourly at first, renal function (contrast plus possible graft coverage of renal arteries), the groin access sites, and any new back or abdominal pain, which may signal an endoleak.

Aortic dissection is a tear in the intima that allows blood to split the layers of the aortic wall. The pain is abrupt, maximal at onset, and described as tearing or ripping, classically radiating to the back between the scapulae. Look for a systolic blood pressure difference of more than 20 mmHg between arms, a pulse deficit, a new diastolic murmur of aortic regurgitation, and neurological deficit if the arch vessels are involved. Type A dissection involves the ascending aorta and is a surgical emergency; type B is descending and usually managed medically. The medical goal is to reduce the shearing force fast: heart rate below 60 and systolic pressure to roughly 100 to 120 mmHg within about 20 minutes. Give the intravenous beta blocker first — esmolol or labetalol — and only then add a vasodilator such as nicardipine or nitroprusside, because a vasodilator given alone produces reflex tachycardia that increases the force per beat and can extend the dissection. Pain control with opioids is not optional; catecholamine release from pain raises pressure.

Hypertensive emergency is a systolic pressure above 180 or a diastolic above 120 with evidence of acute target organ damage — encephalopathy, stroke, papilloedema, acute heart failure or pulmonary oedema, myocardial ischaemia, acute kidney injury, dissection or eclampsia. Without organ damage, the same numbers are hypertensive urgency, treated with oral agents and follow-up over 24 to 48 hours. In an emergency the patient is admitted to an intensive setting for continuous intra-arterial or frequent non-invasive pressure monitoring and a titratable intravenous infusion — nicardipine, clevidipine, labetalol, esmolol or nitroprusside (protect from light, and watch for cyanide and thiocyanate toxicity with prolonged high-dose use). Lower the mean arterial pressure by no more than about 25 per cent in the first hour, then toward 160/100 to 110 over the next two to six hours, and to normal over 24 to 48 hours; dropping it faster can infarct a brain, kidney or coronary bed that has autoregulated to the higher pressure. The exceptions are aortic dissection, which demands rapid lowering, and acute ischaemic stroke, where pressure is permitted to run high unless thrombolysis is planned.

Words worth knowing

Hematologic and Oncologic Disorders

Blood is the only organ that travels. When it fails, it fails everywhere at once — the brain gets confused, the heart races, the wound will not close, the fever that should have come never arrives. This chapter walks the three jobs blood does and what happens when each one breaks: carrying oxygen (the anemias), stopping and starting clot (thrombocytopenia, disseminated intravascular coagulation, anticoagulation), and defending the body (neutropenia and the marrow malignancies). Then it takes you into transfusion therapy, where the nurse is the last safety check between a labelled bag and a fatal mismatch, and into oncology, where the emergencies are quiet at the start and lethal by the end of the shift. Throughout, the same discipline applies: understand the mechanism, read the actual number, and know which finding makes you pick up the phone before you finish charting.

Section 1Anemia: When the Blood Stops Carrying Oxygen

The mechanism, and why every anemia looks the same at first

Anemia is not a diagnosis. It is a finding — a reduction in circulating hemoglobin, hematocrit or red cell mass — and it always has a cause underneath it. Normal hemoglobin runs about 14 to 18 g/dL in men and 12 to 16 g/dL in women, with hematocrit roughly three times the hemoglobin (42 to 52 percent in men, 37 to 47 percent in women). When hemoglobin falls, oxygen delivery falls with it, and the body compensates in a predictable order: the heart speeds up and stroke volume rises, blood is shunted from skin and gut to brain and myocardium, and the respiratory rate climbs. That compensation is exactly why the early manifestations are so uniform — fatigue, pallor, tachycardia, exertional dyspnea, dizziness, cold intolerance — regardless of whether the patient is bleeding from a duodenal ulcer or missing intrinsic factor.

The manifestations also track how fast the anemia developed, not just how low the number is. A patient who bleeds two units in an hour is tachycardic, hypotensive and diaphoretic at a hemoglobin of 9 g/dL. A patient who has been oozing slowly from a colonic lesion for six months may walk into clinic at a hemoglobin of 6 g/dL with nothing but fatigue, because plasma volume expanded and cardiac output adapted. Do not let a stable-looking patient with a terrible number lull you, and do not dismiss a symptomatic patient because the hemoglobin is only mildly low.

Every anemia belongs to one of three buckets, and sorting the patient into a bucket is the single most useful thing a nurse can do at the bedside. Blood loss — obvious trauma or occult gastrointestinal bleeding. Increased destruction — hemolysis, whether inherited (sickle cell, G6PD deficiency, thalassemia) or acquired (autoimmune, mechanical valve, transfusion reaction). Decreased production — missing raw material (iron, B12, folate), missing signal (erythropoietin in chronic kidney disease), or a marrow that has stopped working (aplastic anemia, marrow infiltration by leukemia or metastasis).

Reading the numbers: MCV and reticulocytes do the sorting

Two indices narrow the field faster than anything else. Mean corpuscular volume (MCV, normal 80 to 100 fL) tells you cell size. Microcytic anemia (MCV under 80 fL) is iron deficiency until proven otherwise, with thalassemia and anemia of chronic disease as the other contenders. Macrocytic anemia (MCV over 100 fL) points to B12 or folate deficiency, alcohol use, liver disease or myelodysplasia. Normocytic anemia (MCV 80 to 100 fL) is acute blood loss, hemolysis, chronic kidney disease or marrow failure.

The reticulocyte count (normal 0.5 to 2 percent) tells you whether the marrow is trying. A high reticulocyte count means the marrow is responding appropriately — the problem is loss or destruction downstream. A low or normal reticulocyte count in the face of significant anemia means the marrow itself is the problem, either because it lacks material or because it is sick. Rising reticulocytes three to five days after starting iron or B12 is the earliest proof that therapy is working, and it is worth teaching patients that the fatigue lifts before the hemoglobin normalises.

Iron studies complete the microcytic workup. Ferritin below 30 ng/mL is diagnostic of iron deficiency (normal roughly 12 to 300 ng/mL in men, 12 to 150 ng/mL in women), serum iron falls (normal 60 to 170 mcg/dL), total iron-binding capacity rises (normal 240 to 450 mcg/dL) and transferrin saturation drops below 20 percent. Because ferritin is an acute-phase reactant, it can be falsely normal during infection or inflammation — a genuinely iron-deficient inflamed patient may show a ferritin of 80 ng/mL. For megaloblastic anemia, check serum B12 (normal 200 to 900 pg/mL) and folate (normal 3 to 20 ng/mL); methylmalonic acid rises in B12 deficiency but not in folate deficiency, which is how the laboratory tells them apart.

Sickle cell disease: the crisis you will actually manage

In sickle cell disease a single amino acid substitution produces hemoglobin S, which polymerises when it gives up oxygen. The red cell distorts into a rigid crescent, adheres to vascular endothelium and obstructs the microcirculation, producing the two consequences that define the disease: chronic hemolytic anemia and recurrent ischemic pain. Dehydration, hypoxia, infection, acidosis, cold exposure, high altitude and physical or emotional stress all precipitate sickling. Baseline hemoglobin usually sits between 6 and 9 g/dL, and the patient is genuinely accustomed to it — do not transfuse toward a normal number.

Vaso-occlusive crisis is severe, deep, unrelenting pain in bones, chest, abdomen or joints. Manage it as the emergency it is: scheduled or patient-controlled opioid analgesia rather than as-needed dosing that leaves the patient chasing pain, intravenous or oral hydration, warmth to the affected areas (never cold, which promotes sickling), and supplemental oxygen only when the pulse oximetry reading is below the patient’s baseline. Avoid meperidine — its metabolite normeperidine accumulates and lowers the seizure threshold. Patients with sickle cell disease are frequently and wrongly labelled drug-seeking; the literature on undertreatment in this population is unambiguous, and believing the patient’s report of pain is a clinical skill, not a courtesy.

Three complications kill. Acute chest syndrome — new pulmonary infiltrate with fever, chest pain, hypoxia and cough — is the leading cause of death and needs oxygen, antibiotics, incentive spirometry and often exchange transfusion. Splenic sequestration traps blood in the spleen, dropping hemoglobin precipitously with a rapidly enlarging left upper quadrant mass and hypovolemic shock. Aplastic crisis, usually triggered by parvovirus B19, shuts down erythropoiesis and is recognised by a collapsing reticulocyte count. Long-term therapy is hydroxyurea, which raises fetal hemoglobin and reduces crisis frequency; it causes myelosuppression, so the CBC is monitored, and it is teratogenic.

Priorities and the older adult

The first question in any anemia is airway, breathing, circulation. A patient with hemoglobin of 6 g/dL who is tachycardic at 130, hypotensive and confused needs oxygen, large-bore intravenous access, type and crossmatch and a provider at the bedside — not an iron teaching sheet. Once perfusion is secured, the priority shifts to finding and stopping the source, then to replacement and education. Restrictive transfusion thresholds are the standard: transfuse for hemoglobin below 7 g/dL in most hospitalised adults, below 8 g/dL in patients with cardiovascular disease or undergoing orthopedic surgery, and always in symptomatic patients regardless of number.

Anemia is never a normal consequence of aging, and in older adults it rarely announces itself as fatigue. It presents as a fall, as new-onset confusion or delirium, as worsening angina or heart failure, or as a decline in function that the family calls “slowing down.” The most common cause in this population is occult gastrointestinal blood loss, frequently from NSAID use, and every new iron-deficiency anemia in an adult over 50 requires endoscopic evaluation to rule out colorectal cancer. Older adults also have less marrow reserve, so they decompensate faster and recover more slowly. Delegation here is straightforward: the UAP may obtain vital signs, assist with ambulation and report dizziness; the LPN may administer oral iron and reinforce teaching; the RN performs the initial and ongoing assessment, interprets the CBC and initiates the transfusion.

Section 2Bleeding, Clotting and Anticoagulation

Platelets first, then the cascade

Hemostasis happens in two stages. Primary hemostasis is platelets adhering to injured endothelium and aggregating into a plug — fast, and responsible for controlling small-vessel bleeding in skin and mucous membranes. When it fails, the patient shows petechiae, purpura, easy bruising, gum bleeding, epistaxis and heavy menses. Secondary hemostasis is the coagulation cascade, which converts fibrinogen to a fibrin mesh that stabilises the plug. When it fails, the patient shows deep bleeding — hemarthrosis, muscle hematoma, delayed rebleeding after a procedure. That distinction alone tells you where to look before a single result comes back.

Normal platelet count is 150,000 to 400,000/mm³. Spontaneous bleeding is uncommon above 50,000, becomes a real risk below 20,000, and below 10,000 the danger is intracranial hemorrhage. Bleeding precautions begin around 50,000 and become strict below 20,000: electric razor only, soft toothbrush or oral sponges, no flossing if gums bleed, no rectal temperatures, suppositories or enemas, no intramuscular injections, avoid aspirin and NSAIDs, hold pressure at least five minutes after any venipuncture, humidify air and avoid forceful nose blowing, and use a stool softener so the patient does not strain.

The cascade is monitored by two tests. Prothrombin time (PT, normal 11 to 12.5 seconds) and its standardised expression the INR (normal 0.8 to 1.1) reflect the extrinsic and common pathways — the warfarin and liver-failure test. Activated partial thromboplastin time (aPTT, normal 30 to 40 seconds) reflects the intrinsic and common pathways — the unfractionated heparin and hemophilia test. Fibrinogen (normal 200 to 400 mg/dL) is the substrate; D-dimer (normal under 0.5 mcg/mL FEU) is the breakdown product and rises whenever clot is being lysed anywhere in the body.

The four thrombocytopenias you must tell apart

Immune thrombocytopenia (ITP) is autoantibody-mediated platelet destruction in the spleen. The patient is otherwise well but covered in petechiae with a platelet count that may be under 20,000; PT and aPTT are normal. Treatment is corticosteroids, intravenous immunoglobulin when the count must rise quickly, rituximab, thrombopoietin-receptor agonists such as eltrombopag or romiplostim, and splenectomy for refractory disease. Platelet transfusion is reserved for life-threatening bleeding because transfused platelets are destroyed as fast as native ones.

Heparin-induced thrombocytopenia (HIT) is the trap. Antibodies against the heparin–platelet factor 4 complex activate platelets, so despite a falling count the patient clots rather than bleeds. Suspect it when the platelet count falls more than 50 percent from baseline five to ten days after heparin exposure, or sooner with recent prior exposure. The nursing action is immediate and absolute: stop all heparin — infusions, subcutaneous prophylaxis, flushes, heparin-bonded catheters, dialysis circuits — and notify the provider. Anticoagulation continues with a non-heparin agent such as argatroban, bivalirudin or fondaparinux. Do not transfuse platelets, and do not start warfarin until the platelet count recovers above 150,000, because warfarin alone in acute HIT can cause venous limb gangrene.

Thrombotic thrombocytopenic purpura (TTP) results from deficient ADAMTS13 activity, leaving ultra-large von Willebrand multimers that shear red cells and consume platelets. The classic pentad is fever, thrombocytopenia, microangiopathic hemolytic anemia with schistocytes on smear, renal impairment and fluctuating neurologic changes. Treatment is urgent therapeutic plasma exchange; platelet transfusion is contraindicated because it fuels further microthrombi. Disseminated intravascular coagulation (DIC) is the fourth: widespread activation of coagulation, usually triggered by sepsis, obstetric catastrophe, major trauma, burns or malignancy, that consumes platelets and clotting factors until the patient bleeds from every puncture site while simultaneously infarcting organs.

Inherited bleeding disorders

Hemophilia A is deficiency of factor VIII, hemophilia B of factor IX; both are X-linked recessive, so males are affected and females are usually carriers. The aPTT is prolonged with a normal PT and normal platelet count. The characteristic bleed is hemarthrosis — a warm, swollen, exquisitely painful joint, most often knee, elbow or ankle — and repeated bleeds destroy cartilage and produce chronic arthropathy. Acute management is factor concentrate replacement first, then rest, ice, compression and elevation; the joint is immobilised briefly and then mobilised with physical therapy, because prolonged immobility causes contracture. Desmopressin releases stored factor VIII and von Willebrand factor and is useful in mild hemophilia A only. Aspirin and NSAIDs are contraindicated; acetaminophen is the analgesic of choice for minor pain.

Von Willebrand disease is the most common inherited bleeding disorder and behaves like a platelet problem — mucocutaneous bleeding, epistaxis, menorrhagia, prolonged bleeding after dental work — because von Willebrand factor is what lets platelets adhere. Management is desmopressin for mild disease, von Willebrand factor–containing concentrate for severe disease or surgery, and antifibrinolytics such as tranexamic acid for mucosal bleeding. Teach both groups to carry medical identification, avoid contact sports, use soft toothbrushes and electric razors, and notify every dentist and surgeon before any procedure.

Anticoagulants: the right test, the right antidote

Unfractionated heparin potentiates antithrombin and is monitored by aPTT (therapeutic range about 1.5 to 2.5 times control, roughly 60 to 100 seconds depending on the laboratory) or by anti-factor Xa level. It works within minutes, has a short half-life, and is reversed with protamine sulfate. Low-molecular-weight heparin such as enoxaparin gives a predictable response and needs no routine monitoring except anti-Xa levels in renal impairment, obesity or pregnancy. Give it deep subcutaneously in the abdomen at least two inches from the umbilicus, do not expel the air bubble in the prefilled syringe, do not aspirate, and do not massage the site. Both heparins can cause HIT, so a platelet count baseline and periodic recheck are standard.

Warfarin blocks vitamin K–dependent synthesis of factors II, VII, IX and X and takes three to five days for full effect, which is why it overlaps with a parenteral agent at initiation. It is monitored by INR: therapeutic range is 2 to 3 for atrial fibrillation and venous thromboembolism, and 2.5 to 3.5 for a mechanical mitral valve. The antidote is vitamin K (phytonadione), with prothrombin complex concentrate or fresh frozen plasma for serious bleeding. Teach dietary consistency rather than avoidance — the patient does not have to give up spinach, but the amount should not swing week to week — and review the enormous list of interacting drugs, antibiotics and herbals, including ginkgo, ginger, garlic and St. John’s wort. Direct oral anticoagulants (apixaban, rivaroxaban and edoxaban inhibit factor Xa; dabigatran inhibits thrombin directly) need no routine monitoring, are dose-adjusted for renal function, and are reversed with andexanet alfa for the Xa inhibitors and idarucizumab for dabigatran.

Section 3Transfusion Therapy and Reactions

Components and what each one actually does

Whole blood is rarely used outside massive hemorrhage protocols; modern practice is component therapy. One unit of packed red blood cells, roughly 250 to 350 mL, raises hemoglobin by about 1 g/dL and hematocrit by about 3 percent in an average adult who is not actively bleeding — a fact worth remembering when the post-transfusion CBC comes back and you need to judge whether it makes sense. Platelets are given for counts below 10,000, for counts below 20,000 with fever or sepsis, for counts below 50,000 before an invasive procedure, and for active bleeding; one apheresis unit typically raises the count by 30,000 to 50,000.

Fresh frozen plasma contains all the clotting factors and is used for multiple factor deficiencies, urgent warfarin reversal when prothrombin complex concentrate is unavailable, and dilutional coagulopathy in massive transfusion. Cryoprecipitate is the fibrinogen product — give it when fibrinogen falls below 100 mg/dL, and for factor VIII, factor XIII and von Willebrand factor replacement when specific concentrates are not available. Leukocyte-reduced products lower the rate of febrile nonhemolytic reactions and cytomegalovirus transmission. Irradiated products prevent transfusion-associated graft-versus-host disease in severely immunocompromised recipients, including stem cell transplant patients. Washed red cells remove plasma proteins and are used for recipients with IgA deficiency or recurrent severe allergic reactions.

The procedure, step by step

Verify a signed informed consent and a current type and crossmatch. Establish patent intravenous access — an 18- or 20-gauge catheter is preferred for red cells; smaller bores risk hemolysis and slow flow, though platelets and plasma tolerate a 22-gauge. Take a full set of baseline vital signs including temperature; if the patient is already febrile, report it before the product is released, because a fever after the transfusion starts is then impossible to interpret. Prime the blood administration set with 0.9 percent sodium chloride only. Never hang blood with dextrose solutions, which lyse red cells, or lactated Ringer’s, whose calcium can clot the line; no medication is ever added to a blood product or infused through the same lumen.

Two licensed personnel verify at the bedside, against the patient’s identification band and the unit tag, the patient name and second identifier, the ABO and Rh type, the unit number and expiration, and the crossmatch compatibility. Start the infusion within 30 minutes of release from the blood bank. Run it slowly for the first 15 minutes — about 2 mL per minute — and stay with the patient, because the most catastrophic reactions declare themselves in the first 15 minutes and as little as 10 to 15 mL of incompatible blood can be fatal. Recheck vital signs at 15 minutes, then per policy, and again at completion. A unit must finish within four hours because of bacterial growth risk at room temperature; if the patient cannot tolerate that rate, ask the blood bank to split the unit.

Delegation is tightly drawn here. Only the RN may initiate a transfusion, perform the verification, complete the first 15-minute assessment and evaluate a suspected reaction. The UAP may obtain vital signs once the transfusion is under way and stable, and must be told explicitly what to report immediately: any temperature rise of one degree Celsius or more, chills, rash, itching, back pain, shortness of breath or a feeling of impending doom. LPN scope for transfusion varies by state and facility — know your board of nursing rule rather than assuming.

Massive transfusion and special considerations

Massive transfusion — replacement of the patient’s entire blood volume within 24 hours, or 10 or more units of red cells — brings its own physiology. Citrate anticoagulant in the stored product binds calcium, so watch for hypocalcemia with perioral tingling, tetany, positive Chvostek and Trousseau signs and QT prolongation; ionized calcium (normal 4.5 to 5.6 mg/dL) is monitored. Potassium leaks from stored cells, so hyperkalemia is a risk, particularly in renal impairment. Cold product causes hypothermia, which itself worsens coagulopathy — use an approved blood warmer, never a microwave or hot water. And replacing red cells without plasma and platelets produces dilutional coagulopathy, which is why trauma protocols give red cells, plasma and platelets in balanced ratios.

Some patients decline transfusion on religious grounds, most commonly Jehovah’s Witnesses. The competent adult’s refusal must be honoured, documented and communicated to the whole team; the nursing role is to support the decision without coercion and to advocate for alternatives — erythropoiesis-stimulating agents, intravenous iron, cell salvage, tranexamic acid, minimising phlebotomy volumes. Older adults are at particular risk of TACO because of reduced ventricular compliance; transfuse them slowly, over three to four hours per unit when the clinical situation permits, and assess lung sounds before, during and after.

Section 4Leukemia, Lymphoma, Myeloma and the Neutropenic Patient

Leukemia: one mechanism, three consequences

Leukemia is malignant proliferation of white cell precursors in the bone marrow. The malignant clone does not work — a blast cannot phagocytose — and it crowds out normal hematopoiesis. That single mechanism explains the entire presentation. Loss of red cell production gives fatigue, pallor and dyspnea. Loss of platelet production gives petechiae, ecchymoses, epistaxis and gum bleeding. Loss of functional neutrophils gives recurrent infection and fever. Add bone pain from marrow expansion, lymphadenopathy, hepatosplenomegaly, weight loss and night sweats, and you have the classic picture. The white cell count may be strikingly high, normal or low; what matters is the differential and the blast percentage, confirmed by bone marrow aspiration and biopsy, usually from the posterior iliac crest.

Four types dominate. Acute lymphocytic leukemia (ALL) is the most common childhood cancer and carries a risk of central nervous system involvement, which is why intrathecal chemotherapy is standard. Acute myelogenous leukemia (AML) is the most common acute leukemia in adults; Auer rods on smear are characteristic, and disseminated intravascular coagulation is a recognised complication of the promyelocytic subtype. Chronic lymphocytic leukemia (CLL) occurs in older adults, is often found incidentally on a routine CBC with lymphocytosis, and may be observed rather than treated for years. Chronic myelogenous leukemia (CML) carries the Philadelphia chromosome and its BCR-ABL fusion protein, and is treated with tyrosine kinase inhibitors such as imatinib — a genuine success story of targeted therapy.

Treatment of acute leukemia proceeds in phases: induction to achieve remission, consolidation to eliminate residual disease, and maintenance. Induction deliberately destroys the marrow, so the nadir — the lowest blood counts — occurs roughly 7 to 14 days after therapy, and that is the window when the patient is most likely to become septic or bleed. Hematopoietic stem cell transplantation follows conditioning chemotherapy with or without total body irradiation; the transplant recipient is profoundly aplastic for weeks and is at risk for graft-versus-host disease, which attacks skin (maculopapular rash), gut (voluminous diarrhea) and liver (rising bilirubin).

Lymphoma and multiple myeloma

Lymphomas arise in lymphoid tissue rather than marrow. Hodgkin lymphoma is identified by Reed-Sternberg cells, has a bimodal age distribution in young adults and adults over 55, spreads predictably from one nodal group to the next, and is among the most curable of cancers. The typical presentation is a painless, firm, enlarged cervical or supraclavicular node, sometimes with the B symptoms — fever, drenching night sweats and unintentional loss of more than 10 percent of body weight — that carry prognostic weight. Non-Hodgkin lymphoma is far more common, occurs mostly in older adults, spreads unpredictably and is often widespread at diagnosis. Late effects of treatment matter for teaching: secondary malignancy, cardiomyopathy from anthracyclines, pulmonary fibrosis from bleomycin, hypothyroidism and infertility.

Multiple myeloma is malignant proliferation of plasma cells that secrete a monoclonal immunoglobulin and activate osteoclasts. The acronym CRAB captures it: hyperCalcemia, Renal insufficiency, Anemia and Bone lesions. Serum protein electrophoresis shows an M spike, urine may contain Bence Jones protein, and skeletal survey shows punched-out lytic lesions with diffuse osteoporosis. Nursing care runs on three rails. Hydration — at least 3 litres daily unless contraindicated — to protect the kidneys from light chains and calcium. Safety — the bones are structurally weak, so use gentle handling, avoid lifting under the arms, assess any new back pain for pathologic fracture, and never apply traction to an unassessed limb. Pain and calcium management — bone-modifying agents reduce skeletal events, and the two available agents belong to different drug classes. Zoledronic acid is a bisphosphonate; denosumab is not — it is a monoclonal antibody against RANK ligand. Denosumab is preferred when renal function is impaired, because it needs no renal dose adjustment, whereas zoledronic acid must be dose-reduced or withheld as creatinine clearance falls and can itself cause acute kidney injury. Monitor calcium on either agent and especially on denosumab, which commonly causes symptomatic hypocalcemia requiring calcium and vitamin D repletion. NSAIDs are avoided because of the renal risk.

Neutropenia, ANC and the fever that must not wait

The absolute neutrophil count, not the total white cell count, defines infection risk. Calculate it as total WBC multiplied by the sum of the percentage of segmented neutrophils and bands, divided by 100. A patient with a WBC of 2,000/mm³, 30 percent segs and 5 percent bands has an ANC of 700 — moderately neutropenic. An ANC below 1,500 is neutropenia, below 1,000 is moderate risk, and below 500 is severe neutropenia with high risk of life-threatening infection.

Here is the part students underestimate: without neutrophils, the patient cannot mount the signs of infection you were taught to look for. There is no purulent drainage, no infiltrate on chest film, no redness around the line site, because all of those are made of neutrophils. Fever may be the only manifestation — and in the older adult or the patient on corticosteroids, even fever may be blunted, so new confusion, unexplained tachycardia, hypotension or simply “not acting right” deserves the same response. A single oral temperature of 38.3°C (101°F), or 38.0°C (100.4°F) sustained for one hour, in a patient with an ANC below 500 is febrile neutropenia: an oncologic emergency.

The sequence is fixed and time-critical. Assess and take vital signs, notify the provider immediately, obtain blood cultures from a peripheral site and from every lumen of any central line plus urine and any other indicated culture, and administer broad-spectrum intravenous antibiotics within 60 minutes of the fever being identified. Do not wait for culture results. Do not give acetaminophen before cultures are drawn, because masking the fever delays recognition. Delegation during this event: the UAP may obtain vital signs and gather supplies; the RN draws cultures from central lines, administers the antibiotics and reassesses. Priority among several patients is straightforward — the neutropenic patient with a new fever outranks the stable patient with chronic pain or a scheduled dressing change, every time.

Section 5Cancer Treatment, Toxicity and Oncologic Emergencies

How the treatments work and what they cost the patient

Cytotoxic chemotherapy kills rapidly dividing cells. It cannot distinguish a tumour cell from any other fast-cycling cell, which is precisely why the toxicities are so predictable: bone marrow (myelosuppression), gastrointestinal mucosa from mouth to anus (mucositis, diarrhea, nausea), hair follicles (alopecia) and gonads (infertility). Certain agents carry signature organ toxicities that drive specific monitoring. Doxorubicin and the other anthracyclines are cardiotoxic in a cumulative, dose-dependent way, so ejection fraction is measured by echocardiogram or MUGA scan before and during therapy. Cisplatin is nephrotoxic and ototoxic — hydrate aggressively, monitor creatinine, and ask about tinnitus and hearing change. Vincristine causes peripheral neuropathy and is fatal if given intrathecally, so it is labelled for intravenous use only. Cyclophosphamide causes hemorrhagic cystitis, prevented with vigorous hydration, frequent voiding and mesna. Bleomycin causes pulmonary fibrosis; a new dry cough or exertional dyspnea is reported, not watched.

Chemotherapy-induced nausea and vomiting has three patterns — acute within 24 hours, delayed from day 2 to day 5, and anticipatory, a conditioned response triggered by the smell of the infusion suite. Management is scheduled and preventive, not rescue: a serotonin antagonist such as ondansetron, an NK-1 antagonist such as aprepitant, dexamethasone, and olanzapine for highly emetogenic regimens, with lorazepam for the anticipatory component. Mucositis is managed with a soft brush or sponge, saline or sodium bicarbonate rinses, no alcohol-containing mouthwash, no hot spicy or acidic food, and topical or systemic analgesia; oral cryotherapy during certain infusions reduces its severity.

Radiation damages DNA locally, so its toxicities are confined to the treatment field plus systemic fatigue. Teach skin care: wash gently with lukewarm water and mild soap, pat dry, use only the moisturiser the radiation oncology team approves, no powders or metal-containing products, never apply heat or ice to the field, wear loose cotton, protect from sun, and do not scrub off the treatment markings. With sealed-source brachytherapy the patient emits radiation: apply time, distance and shielding, assign the patient a private room, wear a dosimeter badge, limit each visitor to about 30 minutes per day at six feet, exclude pregnant staff and visitors and children under 18, and if an implant dislodges never touch it with your hands — use long-handled forceps to place it in the lead container kept in the room and call radiation safety.

Immunotherapy changes the toxicity profile entirely. Checkpoint inhibitors such as nivolumab and pembrolizumab release the brakes on T cells and produce immune-related adverse events — colitis with severe diarrhea, pneumonitis with cough and dyspnea, hepatitis, dermatitis, thyroiditis and adrenal insufficiency — managed with corticosteroids and, if severe, drug discontinuation. CAR-T cell therapy can trigger cytokine release syndrome with high fever, hypotension and hypoxia within days, treated with tocilizumab, and neurotoxicity that begins as a subtle handwriting or naming deficit. Monoclonal antibodies commonly cause infusion reactions during the first exposure; premedication and a slow initial rate are standard, and the nurse stays close.

The oncologic emergencies

These are the events that turn a scheduled admission into a code, and they are heavily tested because the first action separates a safe nurse from an unsafe one.

Teaching, survivorship and the older adult

Discharge teaching for the patient on active cancer therapy has a short non-negotiable core. Take your temperature and call for anything at or above 100.4°F (38°C) — do not take an antipyretic first and see how it goes. Call for bleeding that will not stop after ten minutes of pressure, black or bloody stools, new bruising or a severe headache. Call for inability to keep fluids down for 24 hours, for diarrhea more than four or five times above your normal, or for a new cough or shortness of breath. Wash your hands, keep away from anyone who is sick, avoid crowds during the nadir, and do not receive live vaccines or let household members receive live oral polio or the live-attenuated intranasal influenza vaccine. Handle body fluids as hazardous for 48 hours after chemotherapy — flush the toilet twice with the lid down, wash soiled linen separately, and have caregivers wear gloves.

Older adults tolerate cancer therapy differently. Renal function falls with age even when creatinine looks normal, so drugs cleared renally accumulate and doses are adjusted by estimated glomerular filtration rate rather than by creatinine alone. Marrow reserve is smaller, so the nadir is deeper and longer. Baseline cognitive impairment plus opioids plus antiemetics plus hypercalcemia produces delirium, which is frequently the first sign of infection, dehydration or metabolic derangement in this group — investigate it, do not sedate it. Polypharmacy and drug interactions, transportation barriers, financial toxicity and social isolation affect adherence as much as any pharmacologic factor, and a case management or social work referral is a clinical intervention, not an afterthought. Finally, palliative care is not hospice and is not a surrender; introduce it early, alongside curative treatment, because symptom control and goals-of-care conversations improve both quality of life and, in several studies, survival.

Words worth knowing

Gastrointestinal Disorders

The gastrointestinal tract is thirty feet of muscular tube whose only jobs are to move contents forward, absorb what the body needs and contain a staggering population of bacteria. Nearly every disorder in this chapter is a failure of one of those three jobs: motility fails and the bowel obstructs or ileus sets in; absorption fails and the patient wastes despite eating; containment fails and the gut bleeds, perforates or seeds the peritoneum. That framework matters on a busy floor because gastrointestinal complaints are common, mostly benign and occasionally lethal within the hour — the same abdominal pain that means constipation in one patient means a perforated ulcer in the next. Your work is triage disguised as assessment: recognise the bleed before the blood pressure falls, recognise the rigid abdomen before the sepsis, recognise the dusky stoma before the bowel dies. This chapter teaches the mechanisms, the numbers and the “what do you do first” logic that both the NCLEX and your patients require.

Section 1Assessment of the Abdomen and Gastrointestinal Bleeding

Reading the abdomen: sequence, pain patterns and what each finding means

Abdominal assessment is the one examination where the usual order is deliberately broken. You inspect, then auscultate, then percuss, then palpate. Percussion and palpation stimulate the bowel and alter what you would have heard, so listening must come first. Inspect for contour (flat, rounded, distended, scaphoid), symmetry, visible peristalsis, surgical scars, hernias, stoma and skin changes. Auscultate all four quadrants with the diaphragm; normal bowel sounds occur roughly five to thirty times per minute and are irregular. Before you chart “absent,” you must listen for a full five minutes in each quadrant. High-pitched, rushing, hyperactive sounds suggest early mechanical obstruction; a silent abdomen suggests ileus, late obstruction or peritonitis. Palpate lightly first (about one centimetre) in all quadrants, saving the painful quadrant for last, and stop if the abdomen is rigid.

Pain tells you more than any other single finding, and it comes in three flavours. Visceral pain arises from stretch or distention of a hollow organ; it is dull, crampy, poorly localised and often felt near the midline — the periumbilical ache of early appendicitis, the colic of obstruction. Parietal (somatic) pain arises when inflammation reaches the parietal peritoneum; it is sharp, constant, well localised and made worse by movement, coughing or a bumped stretcher — the right-lower-quadrant point tenderness of appendicitis several hours later. Referred pain is felt at a distance because of shared spinal segments: diaphragmatic irritation from a perforation or a post-laparoscopic gas is felt in the shoulder; biliary pain refers to the right scapula. A patient who moves from vague midline pain to focal pain that hurts when the bed is jostled has moved from irritated to inflamed, and that trajectory is the assessment.

Certain physical findings carry disproportionate weight. Rebound tenderness (pain worse on release than on pressure), involuntary guarding and a board-like rigid abdomen together mean peritoneal irritation until proven otherwise. Absent bowel sounds with distention and vomiting suggests obstruction or ileus. Palpable pulsatile mass in a hypotensive older adult suggests abdominal aortic aneurysm — do not palpate deeply again; notify. Also assess what the abdomen produces: last bowel movement, stool colour and consistency, emesis character, oral intake, weight change and abdominal girth measured at the same marked spot each time. Girth increasing by several centimetres in a shift with a tense abdomen is data, not a nuisance.

Upper versus lower gastrointestinal bleeding

Bleeding proximal to the ligament of Treitz is upper gastrointestinal bleeding; the usual culprits are peptic ulcer disease, erosive gastritis, esophageal or gastric varices and Mallory-Weiss tears from forceful retching. Blood exposed to gastric acid is denatured to a coffee-ground appearance, and haemoglobin degraded through the gut turns stool black, tarry and characteristically foul: melena. Hematemesis — bright red or coffee-ground vomitus — is upper by definition. Bleeding distal to the ligament of Treitz is lower; diverticular bleeding, angiodysplasia, haemorrhoids, ischaemic colitis, inflammatory bowel disease and colorectal cancer dominate, and the stool is bright red or maroon blood (hematochezia). One caution flips the rule: a brisk upper bleed can move so fast that it presents as hematochezia, and such a patient is usually the sickest one in the unit.

Laboratory findings follow the physiology. Haemoglobin (normal roughly 14–18 g/dL in men, 12–16 g/dL in women) and haematocrit (42–52 percent and 37–47 percent) may be normal in the first hours of a large bleed because whole blood is lost — the ratio does not change until plasma is replaced or fluid is given. Do not be reassured by an early haemoglobin. In upper bleeding, digested blood is absorbed as protein and the BUN rises out of proportion to creatinine, giving a BUN-to-creatinine ratio above 20:1 and often above 30:1 (normal BUN 10–20 mg/dL, creatinine 0.6–1.2 mg/dL). Draw a type and crossmatch, coagulation studies (INR normally 0.8–1.1), platelets (150,000–400,000/mm³) and a lactate; a lactate above 2 mmol/L suggests hypoperfusion and above 4 mmol/L is an emergency. Upper endoscopy within twenty-four hours is both diagnostic and therapeutic, allowing clipping, thermal coagulation or epinephrine injection.

Management is resuscitation before diagnosis. Two large-bore peripheral IVs (18 gauge or larger — a 22 gauge will not deliver blood at speed), isotonic crystalloid, supplemental oxygen, continuous monitoring and NPO status come first. Packed red cells are transfused using a restrictive threshold: haemoglobin below 7 g/dL for most patients, below 8 g/dL for those with coronary artery disease; one unit raises haemoglobin about 1 g/dL. A high-dose proton pump inhibitor (pantoprazole IV bolus followed by infusion) raises gastric pH so a clot can stabilise. If varices are suspected, octreotide reduces splanchnic flow and prophylactic antibiotics are given. Reversal is considered for anticoagulated patients and is drug-specific: vitamin K plus four-factor prothrombin complex concentrate for warfarin, followed by the INR; protamine sulfate for heparin, followed by the aPTT; idarucizumab for dabigatran; and andexanet alfa for apixaban or rivaroxaban — the direct oral anticoagulants are not reversed by vitamin K, and their effect is not tracked by the INR. Hold home NSAIDs, aspirin and anticoagulants pending provider decision — do not resume them on your own.

Priorities, red flags and who does what

When a patient vomits blood, the order of operations is airway first: position upright or lateral to protect against aspiration, suction available, oxygen on. Then circulation: assess level of consciousness, heart rate, blood pressure, capillary refill and urine output (a goal of at least 0.5 mL/kg/hr, or roughly 30 mL/hr in an average adult). Then access and blood products. Then notify. A common test trap asks whether to insert the nasogastric tube, send labs or start fluids first — the answer is nearly always the intervention that supports oxygenation and perfusion. Never insert or blindly reposition a nasogastric tube in a patient with known varices, recent esophageal surgery, facial trauma or a suspected basilar skull fracture without a specific order.

SBAR — escalating an acute bleed. Situation: “This is Maya Ortiz, RN, on 4 East. Mr. Delgado in 412, sixty-eight, admitted with anaemia, just had 400 mL of coffee-ground emesis.” Background: “He has osteoarthritis, takes daily ibuprofen and apixaban for atrial fibrillation. Admission haemoglobin was 9.1.” Assessment: “Heart rate 118, blood pressure 92/54 down from 138/78, he is pale and diaphoretic, alert but anxious. Two 18-gauge IVs are in, normal saline is running, type and cross is drawn.” Recommendation: “I think this is an active upper GI bleed. I need you to come see him now. Can I have orders for IV pantoprazole, transfusion parameters and a gastroenterology consult for urgent endoscopy?”

Older-adult variation. Older adults bleed silently. Reduced gastric mucosal defence, widespread NSAID and anticoagulant use, and blunted autonomic responses mean the presentation is often fatigue, dyspnoea on exertion, a fall or new delirium rather than pain or frank vomiting. Anaemia is frequently the first laboratory clue. Because thirst perception is blunted and renal concentrating ability is reduced, they decompensate with smaller volume losses. Treat new confusion in an older adult with any gastrointestinal complaint as a haemodynamic sign until you have proved otherwise.

Section 2Esophageal and Gastric Disorders

Gastroesophageal reflux disease and hiatal hernia

The lower esophageal sphincter is a zone of tonic contraction, not a true valve. When resting tone falls or transient relaxations become frequent, gastric contents move into an esophagus that has no protective mucus layer — and the acid burns. That single mechanism explains the whole syndrome: pyrosis (heartburn) thirty to sixty minutes after meals, worse lying flat or bending forward; regurgitation of sour fluid; water brash; dysphagia if the chronic inflammation has produced a stricture; chronic cough, hoarseness, sore throat and asthma exacerbations when refluxate reaches the larynx or airway. Anything that lowers sphincter tone or raises intra-abdominal pressure aggravates it: caffeine, chocolate, peppermint, alcohol, nicotine, fatty meals, calcium channel blockers, nitrates, anticholinergics, obesity, pregnancy and large late meals.

Diagnosis is often clinical, confirmed by response to therapy. Upper endoscopy is indicated for alarm features — dysphagia, odynophagia, weight loss, anaemia, bleeding, vomiting or age over sixty with new symptoms — and for surveillance of Barrett esophagus, in which chronic acid injury converts squamous epithelium to intestinal-type columnar epithelium. Barrett is a premalignant change carrying meaningful risk of esophageal adenocarcinoma, so those patients need scheduled endoscopic surveillance and lifelong acid suppression. Ambulatory pH monitoring and manometry are reserved for unclear cases or pre-surgical evaluation. Nursing after endoscopy is simple and non-negotiable: keep the patient NPO until the gag reflex returns, monitor for bleeding, crepitus and severe pain that could signal perforation.

Management begins with behaviour. Teach the patient to elevate the head of the bed six to eight inches on blocks (extra pillows bend the trunk and worsen reflux), to finish eating three hours before lying down, to eat smaller meals, to lose weight, to stop smoking and to avoid tight waistbands. Proton pump inhibitors such as pantoprazole and omeprazole irreversibly block the gastric proton pump and are taken thirty to sixty minutes before the first meal of the day; long-term use is associated with Clostridioides difficile infection, community-acquired pneumonia, hypomagnesaemia, vitamin B₁₂ deficiency and fractures, so they are prescribed at the lowest effective dose. Histamine-2 receptor antagonists (famotidine) are weaker and useful for breakthrough symptoms. Antacids neutralise acid already present, work in minutes, and must be separated from other medications by one to two hours; aluminium salts constipate, magnesium salts cause diarrhoea, and magnesium-containing antacids are avoided in renal impairment.

A hiatal hernia is herniation of stomach through the diaphragmatic hiatus. The common sliding (type I) hernia moves the gastroesophageal junction upward and simply worsens reflux. The uncommon paraesophageal (type II) hernia lets the fundus roll up beside the esophagus, where it may become incarcerated or strangulated — a surgical emergency signalled by severe chest or epigastric pain, retching without vomiting and inability to pass a nasogastric tube. Antireflux surgery (Nissen fundoplication, often laparoscopic) wraps the fundus around the distal esophagus. Teach these patients that early dysphagia and gas-bloat are expected, that they should avoid carbonated beverages and straws, chew thoroughly, and understand that they may be unable to belch or vomit — persistent nausea needs a call, not a home remedy.

Peptic ulcer disease and Helicobacter pylori

Ulcers form when aggressive factors overwhelm mucosal defence. Two aggressors account for nearly all of them. Helicobacter pylori is a spiral, urease-producing bacterium that colonises gastric mucus, neutralises its microenvironment with ammonia and provokes chronic inflammation. NSAIDs and aspirin inhibit cyclooxygenase-1, cutting the prostaglandins that maintain mucus, bicarbonate and mucosal blood flow — which is why an enteric coating does not protect the stomach; the injury is systemic, not topical. Corticosteroids, smoking, alcohol and severe physiological stress (the stress-related mucosal injury of ventilated or coagulopathic ICU patients) compound the risk. Zollinger-Ellison syndrome, a gastrin-secreting tumour, produces multiple refractory ulcers and is the rare exception.

Location shapes the story. Duodenal ulcers are more common, occur with normal or high acid output, and produce burning epigastric pain two to three hours after eating and often at one or two in the morning; food or antacids relieve it, and weight is stable or increased. Gastric ulcers occur with normal or low acid output and defective mucosa, produce pain thirty to sixty minutes after eating that food makes worse, and lead to anorexia and weight loss; they are more common after age fifty and, unlike duodenal ulcers, may be malignant, so gastric ulcers are biopsied and followed to healing. Diagnosis uses endoscopy with biopsy plus H. pylori testing by urea breath test, stool antigen or biopsy urease test. Both breath and stool testing require holding proton pump inhibitors for two weeks and antibiotics and bismuth for four weeks beforehand, or the test will be falsely negative.

Eradication uses combination therapy for fourteen days, most often bismuth quadruple therapy: a proton pump inhibitor plus bismuth subsalicylate plus metronidazole plus tetracycline. Teach three things. First, finish the entire course — partial treatment breeds resistance and the ulcer returns. Second, bismuth turns the stool and tongue black; that is harmless and is not melena, but the patient must know the difference. Third, metronidazole with alcohol produces a disulfiram-like reaction of flushing, vomiting and tachycardia, so no alcohol during therapy and for three days after. Sucralfate forms a physical barrier over the ulcer base and must be given on an empty stomach, one hour before meals and at bedtime, separated from other drugs and antacids. Misoprostol restores prostaglandin for high-risk NSAID users and is absolutely contraindicated in pregnancy because it induces uterine contractions.

Gastric surgery, gastric cancer and dumping syndrome

Gastric adenocarcinoma is insidious: vague epigastric discomfort, early satiety, anorexia, unexplained weight loss and iron-deficiency anaemia that appear only after the tumour is advanced. Risk rises with H. pylori infection, atrophic gastritis, pernicious anaemia, heavy salt-preserved and smoked food intake, smoking and a family history. Endoscopy with biopsy is definitive; CT and endoscopic ultrasound stage it. Treatment is surgical resection (partial or total gastrectomy) with chemotherapy, and the nursing focus is nutritional. After any gastrectomy the patient loses intrinsic factor and therefore cannot absorb vitamin B₁₂ from the diet — lifelong parenteral or high-dose oral B₁₂ replacement is required, and failure to teach that produces a preventable megaloblastic anaemia with irreversible neuropathy years later. Iron, calcium and folate deficiencies also follow.

Whenever the pylorus is bypassed or removed — gastrectomy, gastrojejunostomy, and also Roux-en-Y gastric bypass — hyperosmolar chyme dumps into the jejunum. Early dumping syndrome occurs fifteen to thirty minutes after eating: the osmotic load pulls fluid into the lumen, producing cramping, borborygmi, nausea, urgent diarrhoea, and simultaneously reduces circulating volume, producing tachycardia, palpitations, diaphoresis, dizziness and pallor. Late dumping occurs one and a half to three hours after eating: the rapid glucose bolus triggers excessive insulin release and the patient becomes hypoglycaemic, with sweating, shakiness, confusion and weakness. Teach small, frequent meals; high protein and moderate fat; low simple carbohydrate; fluids between meals rather than with them; and lying down or reclining for twenty to thirty minutes after eating to slow gastric emptying — the opposite of reflux teaching, which is exactly why students confuse the two.

After bariatric surgery specifically, the emergency to recognise is an anastomotic leak, typically in the first days: sustained heart rate above 120, restlessness or a sense of impending doom, fever, left shoulder pain, and increasing abdominal or back pain. Tachycardia in a fresh bariatric patient is a leak until proven otherwise — notify the surgeon rather than medicating for anxiety. Routine post-gastric-surgery care includes keeping the nasogastric tube patent but never repositioning or irrigating it without a specific order (the tip sits at a fresh suture line), monitoring drainage that should change from bloody to yellow-green within the first day, early ambulation, and slow advancement from sips of clear liquid to small soft meals.

Section 3Inflammatory and Infectious Disorders of the Bowel

Appendicitis and peritonitis

Appendicitis begins with obstruction of the appendiceal lumen by a fecalith, lymphoid hyperplasia or, in older adults, a tumour. Mucus continues to be secreted behind the obstruction, pressure rises, venous drainage fails, bacteria invade the wall and the appendix becomes ischaemic and eventually perforates. That sequence explains the classic migration of pain: distention of a hollow viscus produces vague periumbilical visceral pain with anorexia and nausea, and once inflammation reaches the parietal peritoneum the pain moves to a sharp, focal point at McBurney point, one-third of the way from the right anterior superior iliac spine to the umbilicus. Look for rebound tenderness, guarding, pain on coughing or heel-strike, Rovsing sign (right-lower-quadrant pain when the left lower quadrant is pressed), a low-grade fever of 99–101 °F and a white blood cell count of 10,000–18,000/mm³ (normal 5,000–10,000/mm³); a count above 20,000/mm³ suggests perforation.

Nursing care before surgery is a list of prohibitions, and each one has a reason. Nothing by mouth. No heat to the abdomen — vasodilation accelerates rupture. No enemas or laxatives — increased peristalsis and pressure accelerate rupture. Position of comfort is usually semi-Fowler with knees flexed. Give IV fluids and antibiotics as ordered, and monitor closely. The single most important observation: if severe pain suddenly stops, the appendix has likely ruptured and released the pressure; a brief calm is followed by diffuse pain, rigidity, rising fever and tachycardia. That sudden relief is a red flag, not good news, and it warrants immediate notification. Definitive management is appendectomy, usually laparoscopic; perforated cases may need drain placement and several days of antibiotics.

Peritonitis is the common endpoint of perforation from any cause — ruptured appendix or diverticulum, perforated ulcer, ischaemic bowel, anastomotic leak, or peritoneal dialysis catheter contamination. Bacteria and chemical irritants inflame a membrane with enormous surface area, so fluid shifts into the peritoneal cavity (third spacing), circulating volume falls, and sepsis follows. Findings: severe constant abdominal pain, board-like rigidity, rebound tenderness, absent bowel sounds, shallow rapid breathing because deep breaths hurt, the patient lying still with knees flexed, fever, tachycardia and hypotension. Treatment is broad-spectrum antibiotics, aggressive fluid resuscitation, nasogastric decompression, NPO status, analgesia and surgical source control. Nursing priorities follow ABC and perfusion: oxygen, fluids, hourly urine output, serial lactate and blood cultures before antibiotics whenever that does not delay them.

Diverticular disease

Diverticulosis is the presence of small herniations of mucosa through weak points in the colonic muscular wall, overwhelmingly in the sigmoid colon where luminal pressure is highest. It is a disease of low dietary fibre and ageing; more than half of adults over sixty have it, and most never know. It becomes clinically important two ways. It is the most common cause of brisk painless lower gastrointestinal bleeding in older adults, because a diverticulum sits directly over a penetrating arteriole. And it can inflame.

Diverticulitis occurs when a diverticulum becomes obstructed and micro-perforates. The patient reports steady left-lower-quadrant pain (the mirror image of appendicitis), with fever, leukocytosis, nausea and a change in bowel habit. The diagnostic study is CT of the abdomen and pelvis with contrast. Note carefully what is contraindicated during the acute phase: colonoscopy and barium enema, because insufflation or contrast pressure can convert a contained micro-perforation into a free one. Colonoscopy is done six to eight weeks after recovery to exclude cancer, which can mimic diverticulitis exactly.

Mild uncomplicated cases are managed at home with clear liquids and often oral antibiotics; more ill patients are admitted for bowel rest, IV fluids and IV antibiotics covering gut flora (commonly ciprofloxacin plus metronidazole, or a beta-lactam/beta-lactamase inhibitor). Teach the diet sequence and the reason: low-fibre or clear liquids during the flare to rest the colon, then advance to a high-fibre diet (25–35 grams daily) with generous fluids once inflammation resolves, to prevent recurrence. The old instruction to avoid nuts, seeds, popcorn and corn has been abandoned — evidence does not support it. Complications requiring surgery include abscess, free perforation with peritonitis, obstruction from stricture, and fistula — a colovesical fistula announces itself with pneumaturia and fecaluria, which the patient may describe only as “bubbles when I urinate” unless you ask directly.

Inflammatory bowel disease, celiac disease, irritable bowel syndrome and Clostridioides difficile

Inflammatory bowel disease is immune-mediated chronic inflammation in a genetically susceptible host. Distinguishing its two forms is worth more test points than almost anything else in this chapter, and the distinction is anatomical: how much of the bowel and how deep.

Both share extraintestinal manifestations — arthritis, erythema nodosum, uveitis, aphthous ulcers, primary sclerosing cholangitis — and both cause weight loss, fatigue, iron-deficiency anaemia, hypoalbuminaemia (normal albumin 3.5–5.0 g/dL) and electrolyte loss. Useful labs include CBC, C-reactive protein, erythrocyte sedimentation rate, albumin, iron studies, vitamin B₁₂ and fecal calprotectin, which is elevated in inflammatory bowel disease and normal in irritable bowel syndrome. Colonoscopy with biopsy establishes the diagnosis; CT or MR enterography maps small-bowel Crohn disease.

Drug therapy is stepwise by mechanism. Aminosalicylates (mesalamine, sulfasalazine) deliver topical anti-inflammatory effect to the mucosa and are the backbone for mild ulcerative colitis; sulfasalazine is a sulfonamide, so ask about sulfa allergy, expect orange-yellow discoloration of urine and skin, and supplement folic acid because absorption is impaired. Corticosteroids induce remission in flares and are tapered, never used for maintenance because of osteoporosis, hyperglycaemia, infection and adrenal suppression. Immunomodulators (azathioprine, 6-mercaptopurine, methotrexate) are steroid-sparing and require serial CBC and liver function monitoring; methotrexate demands folate supplementation and reliable contraception. Biologics — anti-tumour necrosis factor agents such as infliximab and adalimumab, plus vedolizumab and ustekinumab — are potent immunosuppressants; before the first dose the patient must be screened for latent tuberculosis and hepatitis B, and during therapy live vaccines are avoided and any fever is treated as potentially serious. Antidiarrhoeals are used cautiously and are contraindicated in a severe flare because slowing the colon can precipitate toxic megacolon.

Celiac disease is an immune reaction to gluten that flattens small-intestinal villi, producing diarrhoea, steatorrhoea, bloating, weight loss, iron and folate deficiency anaemia, osteoporosis and the intensely itchy vesicular rash dermatitis herpetiformis. Diagnosis uses tissue transglutaminase IgA antibodies drawn while the patient is still eating gluten, confirmed by duodenal biopsy. The only treatment is lifelong strict elimination of wheat, barley and rye; teach label reading, cross-contamination in shared toasters and fryers, and that rice, corn, quinoa and certified uncontaminated oats are safe. Irritable bowel syndrome, by contrast, is a disorder of gut-brain interaction with normal structure and normal labs: recurrent abdominal pain related to defecation with altered stool form or frequency, no bleeding, no weight loss, no nocturnal symptoms. Management is dietary (soluble fibre, a trial of a low-FODMAP plan), stress reduction, antispasmodics such as dicyclomine, and agents targeted to the predominant pattern. Any alarm feature — bleeding, anaemia, weight loss, onset after age fifty, nocturnal diarrhoea — means it is not irritable bowel syndrome and requires workup.

Clostridioides difficile infection follows disruption of normal flora by antibiotics — classically clindamycin, fluoroquinolones and cephalosporins — allowing a spore-forming anaerobe to release toxins A and B that inflame the colon. Risk rises with age over sixty-five, hospitalisation, tube feeding and proton pump inhibitor use. The patient has frequent watery, foul-smelling stools, cramping, fever and leukocytosis that can be striking (a white count above 15,000/mm³ is a severity marker), with rising creatinine and falling albumin in severe disease. Diagnosis is stool nucleic acid amplification and toxin testing on liquid stool only; do not send formed stool and do not send a test of cure. Treatment is oral vancomycin or fidaxomicin; recurrent disease may be treated with faecal microbiota transplantation. The nursing actions that matter most are infection control: contact precautions in a private room, dedicated equipment, cleaning with a sporicidal bleach agent, and handwashing with soap and water — alcohol-based gel does not kill spores. Discontinue antidiarrhoeals, replace fluid and potassium (normal 3.5–5.0 mEq/L), and review whether the inciting antibiotic and the proton pump inhibitor can be stopped.

Section 4Obstruction, Ischaemia and Colorectal Cancer

Mechanical obstruction and paralytic ileus

Obstruction is either mechanical (something blocks the lumen) or functional (the bowel stops moving). In mechanical obstruction, gas and fluid accumulate above the blockage; the bowel distends, secretes more fluid, absorbs less, and litres of extracellular fluid are sequestered in the lumen. That third spacing produces hypovolaemia, electrolyte loss and, if pressure exceeds capillary perfusion pressure, strangulation — ischaemic bowel that necroses, perforates and seeds peritonitis. Adhesions from prior surgery cause most small-bowel obstructions; hernias and Crohn strictures follow. In the large bowel, colorectal cancer, volvulus and diverticular stricture dominate.

Assessment is serial and quantitative: vital signs, abdominal girth at a marked line, bowel sounds, character and volume of emesis and nasogastric output, strict intake and output, daily weight, and electrolytes — especially potassium (3.5–5.0 mEq/L), sodium (135–145 mEq/L) and chloride, all of which fall with prolonged suction and vomiting. Abdominal CT identifies the level, cause and any ischaemia; plain films show dilated loops with air-fluid levels. Non-strangulating adhesive obstruction is often managed conservatively: NPO, nasogastric tube to low intermittent suction, isotonic fluid replacement with potassium once urine output is adequate, analgesia, and serial examination. Volvulus may be reduced endoscopically; cancer, strangulation, closed-loop obstruction and failure of conservative therapy go to the operating room.

Escalate immediately for fever, tachycardia, rising or persistent pain that becomes constant rather than colicky, localised tenderness with rebound, rigidity, a rising white count or lactate, hypotension, or bloody nasogastric or rectal output. Those signal strangulation or perforation. Paralytic ileus, by contrast, is usually a post-operative or metabolic problem: manage the cause. Replace potassium, minimise opioids in favour of multimodal analgesia, get the patient walking, and consider chewing gum, which has good evidence for shortening post-operative ileus. Mesenteric ischaemia deserves its own mention because it is missed: an older adult with atrial fibrillation or atherosclerosis who has severe pain out of proportion to a soft, benign-feeling abdomen, often with a rising lactate, may have an occluded mesenteric artery. That combination is an emergency.

Colorectal cancer, screening and stoma creation

Most colorectal cancers arise from adenomatous polyps over roughly ten years, which is why screening works — removing a polyp prevents a cancer. Risk factors include age, a personal or family history of colorectal cancer or adenomas, inflammatory bowel disease of long duration, hereditary syndromes (familial adenomatous polyposis, Lynch syndrome), obesity, physical inactivity, smoking, heavy alcohol and a diet high in processed and red meat and low in fibre. For average-risk adults, screening now begins at age 45 and continues to 75: colonoscopy every ten years, or a faecal immunochemical test annually, or stool DNA testing every three years, or CT colonography every five years. A positive non-invasive test always requires a diagnostic colonoscopy.

Manifestations depend on side. Right-sided tumours present with occult bleeding and iron-deficiency anaemia, fatigue and vague pain, because stool there is liquid and the lumen is wide. Left-sided and rectal tumours present with a change in bowel habit, narrowed “pencil” stools, tenesmus, hematochezia and obstruction. Any unexplained iron-deficiency anaemia in an adult over fifty is colorectal cancer until proven otherwise. Colonoscopy with biopsy confirms; CT of the chest, abdomen and pelvis stages the disease by the TNM system, in which the depth the tumour has invaded through the bowel wall (T), the number of positive regional lymph nodes (N) and the presence of distant metastasis (M, most often liver or lung) together determine stage and prognosis; carcinoembryonic antigen (CEA, usually less than about 3 ng/mL in a non-smoker) is not a screening test but is used to monitor for recurrence after resection. Treatment combines surgical resection with chemotherapy and, for rectal cancer, radiation. Nursing preparation for colonoscopy is its own teaching moment: clear liquids with nothing red or purple, the full bowel preparation solution taken as scheduled even though it is unpleasant, and arrangements for a driver because of sedation.

When bowel is resected, a stoma may be created — temporary to protect a distal anastomosis, or permanent when the rectum is removed. Output depends on location. An ileostomy begins draining within 24 hours, produces 500–1,000 mL daily of liquid to pasty effluent rich in sodium and potassium and containing digestive enzymes that excoriate skin instantly; those patients dehydrate easily and must not take enteric-coated or extended-release tablets, which pass through unabsorbed. A descending or sigmoid colostomy produces formed stool on a semi-predictable schedule. Assess the stoma every shift: it should be pink to beefy red, moist and slightly raised, with mild oedema for the first week. A pale stoma suggests anaemia; a dusky, purple, dark blue or black stoma means ischaemia and must be reported immediately. Report also a stoma that retracts below skin level, prolapses, bleeds beyond a small ooze, or produces no output with distention and cramping — that is obstruction.

Older-adult variation. Older adults with obstruction or peritonitis often lack fever and leukocytosis, and delirium may be the presenting sign. They are more likely to have a large-bowel obstruction from cancer, more likely to be on anticholinergics, calcium channel blockers and opioids that cause ileus, and less able to tolerate the fluid shifts of third spacing. Do not accept “he is just confused today” in a patient who has not passed stool or flatus for three days and has a tympanic, distended abdomen.

Section 5Nutrition, Elimination and the Post-operative Gastrointestinal Patient

Nasogastric tubes and enteral nutrition

A nasogastric tube does one of two things: it takes contents out (decompression for obstruction, ileus or post-operative distention, usually a double-lumen Salem sump on low intermittent suction with the blue air vent kept above the level of the stomach and never clamped) or it puts nutrition in (a small-bore feeding tube). To insert, place the patient in high Fowler position, measure from the tip of the nose to the earlobe to the xiphoid process, mark the tube, lubricate with water-soluble gel, advance along the floor of the nostril, and have the patient flex the chin toward the chest and sip water as you pass the tube — chin flexion closes the airway and opens the esophagus. Stop and withdraw for coughing, choking, gasping or a change in phonation.

Verification is where patients are harmed. Radiographic confirmation is required before the first use of any newly placed blind feeding tube — auscultating an air bolus is not acceptable practice and cannot distinguish stomach from lung. After confirmation, mark the exit point at the nostril, document the external length, and before every feeding and medication and at least every four hours during continuous feeding, verify by checking that the marked length is unchanged and by aspirating gastric contents, which should be grassy-green, tan or bloody with a pH of 5.5 or less; small-bowel aspirate is typically golden and above 6, and respiratory secretions are also above 6. Any doubt means stop and re-image. Never reposition or irrigate a tube placed at surgery near a fresh anastomosis without an explicit order.

Enteral feeding is preferred over parenteral whenever the gut works, because it maintains mucosal integrity and reduces infection. The dominant risk is aspiration: keep the head of bed elevated 30–45 degrees during feeding and for at least 30–60 minutes after intermittent feeds, hold feeding for procedures requiring the patient to lie flat, and provide oral care every four hours. Flush with 30 mL of water before and after each medication, between medications and every four hours during continuous feeding to maintain patency. Give liquid formulations when available; never crush enteric-coated or extended-release tablets, and never mix medications together in the syringe. Monitor gastric residual volumes per facility policy — a single elevated value is not a reason to stop feeding, but a residual above 500 mL together with distention, vomiting or discomfort means hold the feeding and notify. Diarrhoea during tube feeding is usually caused by sorbitol-containing liquid medications, antibiotics, hyperosmolar formula or C. difficile, not by the formula itself; investigate before you stop the nutrition.

Constipation, diarrhoea and the drugs that treat them

Constipation is not a diagnosis; it is a symptom of low fibre, low fluid, immobility, ignored urges, opioids, anticholinergics, iron, calcium channel blockers, hypothyroidism, hypokalaemia or obstruction. Assess the patient’s baseline pattern rather than a textbook number, and screen for the emergency masquerading as constipation: a faecal impaction presents with paradoxical liquid stool leaking around a hard mass, abdominal distention, anorexia and, in an older adult, confusion or urinary retention. Non-drug therapy comes first — 25–35 grams of fibre daily, 1.5–2 litres of fluid unless restricted, activity, and honouring the urge, ideally after breakfast when the gastrocolic reflex is strongest.

Know laxatives by mechanism. Bulk-forming agents (psyllium, methylcellulose) draw water into stool and must be taken with a full glass of fluid or they can obstruct. Osmotic agents (polyethylene glycol, lactulose, magnesium citrate) hold water in the lumen; magnesium products are avoided in renal impairment. Stimulants (senna, bisacodyl) increase peristalsis; do not crush enteric-coated bisacodyl and do not take it within one hour of milk or antacids, which dissolve the coating and cause gastric irritation. Stool softeners (docusate) are surfactants and are weak on their own. For opioid-induced constipation, a stimulant plus softener is started prophylactically with the opioid, and peripherally acting mu-antagonists such as methylnaltrexone are available when that fails.

Diarrhoea threatens volume and potassium before it threatens anything else. Assess frequency, volume, blood, recent antibiotics, travel, tube feeding and new medications; check orthostatic vital signs, mucous membranes, urine output, potassium, sodium and creatinine. Loperamide and diphenoxylate slow transit but are contraindicated in suspected C. difficile, in bloody diarrhoea with fever and in severe colitis, because retaining toxin risks toxic megacolon. Antiemetics have their own cautions: ondansetron prolongs the QT interval, promethazine is a vesicant that causes severe tissue injury and is given deeply and dilutely if at all, and metoclopramide carries a black-box warning for tardive dyskinesia and should not be used beyond twelve weeks. Protect perineal skin with a barrier cream and cleanse gently; incontinence-associated dermatitis is a preventable injury.

The post-operative gastrointestinal patient and discharge teaching

Modern enhanced-recovery practice has changed post-operative abdominal care: routine nasogastric tubes are avoided, clear liquids often begin the day of surgery, multimodal analgesia limits opioids, and patients are out of bed the first evening. Your surveillance targets three complications. Ileus — distention, no flatus, absent sounds — is managed with ambulation, potassium repletion, opioid reduction and gum chewing. Anastomotic leak — classically around post-operative day five to seven — presents with fever, tachycardia, increasing rather than decreasing pain, purulent or feculent drain output and peritoneal signs; it is a surgical emergency. Surgical-site and intra-abdominal infection presents with fever, wound erythema and drainage, or a persistent leukocytosis. Wound evisceration — viscera protruding through a separated incision — is handled by placing the patient supine with knees flexed, covering the viscera with sterile saline-moistened gauze, keeping them NPO and calling the surgeon immediately; never attempt to replace the bowel.

Discharge teaching should be specific enough to act on. Every gastrointestinal patient goes home knowing the red flags: fever above 100.4 °F, vomiting that prevents fluids, severe or worsening abdominal pain, a rigid abdomen, no bowel movement or flatus with distention, black tarry or bloody stools, dizziness on standing, and incision redness, warmth or drainage. Ostomy patients additionally need to know to report output above roughly 1,000–1,500 mL a day from an ileostomy or no output for several hours with cramping, to chew high-residue foods (nuts, popcorn, corn, mushrooms, celery, raw cabbage) thoroughly to prevent blockage, to replace fluid and salt in hot weather or illness, and where their supplies and their ostomy nurse are. Reflux and ulcer patients need the medication timing, the NSAID conversation and the follow-up endoscopy date. Inflammatory bowel disease patients on biologics need to know to report fever and to keep vaccinations current with live vaccines avoided.

Delegation reminder. The unlicensed assistive personnel may empty and measure an established ostomy pouch, record output, assist with ambulation and hygiene, and take vital signs on a stable patient. The LPN/LVN may perform routine appliance changes on a healed stoma, administer most enteral and oral medications, reinforce teaching you have started and monitor a predictable patient. The registered nurse assesses the stoma and the abdomen, verifies feeding-tube placement decisions, initiates blood and parenteral nutrition, evaluates response, teaches the new ostomy patient and manages anyone whose condition is changing.

Words worth knowing

HEPATOBILIARY AND PANCREATIC DISORDERS

The liver, gallbladder and pancreas sit quietly in the right upper quadrant and the epigastrium doing work no machine fully replaces — manufacturing albumin and clotting factors, clearing ammonia and bilirubin, metabolising nearly every drug you will ever hang, emulsifying fat and digesting protein. When they fail, they fail loudly and in patterns you can predict. The cirrhotic patient bleeds because the liver stopped making factor VII; he is confused because his gut is making ammonia his liver cannot clear; his belly is tight because portal pressure is pushing fluid into the peritoneum and his albumin is too low to pull it back. The patient with acute pancreatitis is hypotensive not because he is bleeding but because activated enzymes turned his retroperitoneum into a third space. Learn the mechanism once and the assessment findings, the laboratory values and the nursing priorities all fall out of it. This chapter teaches those mechanisms and then teaches you what to do first.

Section 1The Liver, the Biliary Tree and What the Numbers Mean

What the liver actually does — and what breaks when it stops

Group the liver’s jobs into four buckets and every finding in this chapter becomes predictable. Synthesis: the liver makes albumin, which holds fluid inside the vessel, and clotting factors I, II, V, VII, IX and X. Metabolism: it converts ammonia from gut protein breakdown into urea, stores and releases glucose, and biotransforms drugs through the cytochrome P450 system. Excretion: it conjugates bilirubin from senescent red cells and dumps it into bile. Storage and immune surveillance: it banks glycogen, iron, and the fat-soluble vitamins A, D, E and K, while Kupffer cells filter portal blood coming straight from the gut.

Now reverse each one. Lose synthesis and you get hypoalbuminaemia with oedema and ascites, plus a rising INR and a patient who bruises from a blood-pressure cuff. Lose metabolism and ammonia climbs, the patient becomes confused, blood glucose swings unpredictably, and every sedative you give lasts twice as long. Lose excretion and bilirubin backs up: yellow sclerae, dark tea-coloured urine, clay-coloured stools, and intractable pruritus from bile salts in the skin. Lose storage and vitamin K deficiency compounds the coagulopathy. Nothing in liver failure is arbitrary.

The liver has enormous reserve — it can lose a large fraction of functioning mass before laboratory values move — which is exactly why chronic liver disease is often silent until it is advanced. Your assessment must therefore be deliberate: skin and sclerae in natural light, palms for palmar erythema, chest and shoulders for spider angiomas, abdomen for distension, flank dullness and a fluid wave, hands held out for asterixis (the flapping, non-rhythmic loss of wrist extension), and the legs for pitting oedema. In darker-skinned patients look for jaundice in the sclerae, the hard palate and the palms, not in the general skin tone.

Jaundice: reading the colour

Bilirubin is the breakdown product of haem. Unconjugated (indirect) bilirubin is fat-soluble and travels bound to albumin; the hepatocyte conjugates it with glucuronic acid, making it water-soluble (direct) so it can be excreted in bile. Jaundice becomes visible when total bilirubin exceeds roughly 2 to 3 mg/dL, with a normal total of 0.3 to 1.2 mg/dL and a direct fraction of 0.1 to 0.3 mg/dL.

Where the problem sits tells you which fraction rises. Prehepatic jaundice — haemolysis, a transfusion reaction, a large resolving haematoma — overwhelms conjugation, so indirect bilirubin rises while stool and urine stay normal in colour. Intrahepatic jaundice — hepatitis, cirrhosis, drug injury — damages the cell that conjugates and excretes, so both fractions rise. Posthepatic or obstructive jaundice — a stone in the common bile duct, a pancreatic head tumour — blocks the exit, so conjugated bilirubin refluxes into blood. Because conjugated bilirubin is water-soluble it spills into urine (dark, tea-coloured, and it foams yellow) while none reaches the bowel (clay-coloured, pale stools). That triad — yellow skin, dark urine, pale stool — is obstruction until proved otherwise.

The liver panel is really two panels

Students memorise “LFTs” as a block and then cannot interpret them. Split them. The hepatocellular enzymes ALT (7 to 56 U/L) and AST (10 to 40 U/L) leak out of injured hepatocytes; ALT is more liver-specific because AST also lives in heart and skeletal muscle. Values in the thousands mean acute hepatocyte death — viral hepatitis, ischaemic hepatitis (shock liver) or paracetamol/acetaminophen toxicity. An AST-to-ALT ratio above 2:1 with only modest elevations classically points to alcohol-related liver disease.

The cholestatic enzymes alkaline phosphatase (30 to 120 U/L) and GGT (roughly 8 to 60 U/L) rise when bile flow is obstructed. Alkaline phosphatase also comes from bone, so a rise in both ALP and GGT localises the problem to the biliary tree; a rise in ALP with a normal GGT points to bone. Neither group of enzymes measures function — they measure damage. The true function tests are albumin (3.5 to 5.0 g/dL), which reflects synthesis over the preceding weeks, INR (0.8 to 1.1) and prothrombin time (11 to 12.5 seconds), which reflect synthesis over the preceding hours to days, and total bilirubin, which reflects excretion. A patient whose enzymes are falling while INR climbs is not improving — he is running out of hepatocytes.

Imaging, biopsy and severity scoring

Right upper quadrant ultrasound is the first-line study for almost every hepatobiliary complaint: it is cheap, portable, radiation-free, and it detects gallstones, duct dilation, ascites and coarse hepatic echotexture. CT with contrast stages tumours, defines pancreatic necrosis and finds abscesses. MRCP images the ducts non-invasively; ERCP does the same but can also remove a stone or place a stent, at the cost of an invasive procedure with a real risk of post-procedure pancreatitis. Transient elastography (FibroScan) measures stiffness and increasingly replaces biopsy for staging fibrosis.

If a percutaneous liver biopsy is ordered, the nursing care is a small examination all by itself. Before: verify consent, check platelets and INR (many facilities require platelets above 50,000/mm³ and INR below 1.5), type and screen, hold anticoagulants as ordered, keep the patient NPO. During: the patient exhales and holds the breath at end-expiration so the diaphragm stops moving. After: position the patient on the right side with a rolled towel against the costal margin for two hours to tamponade the puncture site, bed rest for the ordered interval, and monitor vital signs frequently for the classic complications — haemorrhage (tachycardia, falling blood pressure, rising abdominal pain), bile peritonitis and pneumothorax (sudden dyspnoea, pleuritic pain).

Two scores drive real decisions. Child-Pugh classes A, B and C are built from bilirubin, albumin, INR, ascites and encephalopathy. MELD (bilirubin, INR, creatinine and sodium) is a pure number used to rank patients on the transplant list — sicker patients score higher and are transplanted sooner. Knowing that creatinine sits inside MELD explains why nephrotoxic drugs and careless diuresis in a cirrhotic patient are not minor errors.

Section 2Viral Hepatitis and Acute Liver Failure

The hepatitis alphabet, sorted by how it reaches the patient

Five viruses, two routes. A and E travel by the faecal-oral route — contaminated food, water and shellfish, poor hand hygiene, and in the case of E often contaminated drinking water in resource-limited settings. Neither becomes chronic in a patient with an intact immune system (hepatitis E can persist in the profoundly immunocompromised, such as a transplant recipient, but that is the exception). B, C and D travel in blood and body fluids — needles, sharps injuries, tattoos and piercings with unsterile equipment, sexual contact, and for B, perinatal transmission. All three can become chronic and all three can end in cirrhosis and hepatocellular carcinoma.

Hepatitis A has an incubation of roughly 15 to 50 days and is preventable with a two-dose vaccine six months apart; it is most contagious in the two weeks before jaundice appears, which is why outbreaks are traced backwards through food handlers. Hepatitis B has a longer incubation, 45 to 160 days, and becomes chronic in about 5 percent of infected adults but in up to 90 percent of infants infected perinatally — the reason the birth dose of vaccine matters so much. Hepatitis C rarely produces an acute illness anyone notices; roughly three-quarters of those infected develop chronic infection, and it remains a leading indication for liver transplant. Hepatitis D is a defective virus that can only infect a person who already carries hepatitis B surface antigen, so preventing B prevents D. Hepatitis E is usually self-limited but carries a mortality approaching 20 percent in the third trimester of pregnancy.

Hepatitis B serology without tears

Three results answer almost every question. HBsAg (surface antigen) means the virus is present — the patient is infected and infectious right now; persistence beyond six months defines chronic infection. Anti-HBs (surface antibody) means immunity, either from resolved infection or from vaccination. Anti-HBc (core antibody) means the patient has actually encountered the wild virus at some point; the IgM subtype indicates recent or acute infection. Vaccination produces anti-HBs alone, so a nurse with anti-HBs positive and anti-HBc negative is vaccinated, while anti-HBs plus anti-HBc positive means natural resolved infection. HBeAg is a marker of high viral replication and high infectivity.

Clinically, hepatitis moves through three phases. The prodromal (preicteric) phase brings malaise, anorexia, nausea, low-grade fever, myalgia, right upper quadrant discomfort and often a distaste for cigarettes or food — nonspecific enough to be mistaken for influenza. The icteric phase brings jaundice, dark urine, pale stools, pruritus and tender hepatomegaly. The convalescent phase can drag on for weeks to months with fatigue that patients find demoralising because they “look fine.”

Nursing care, prevention and exposure management

Care in acute viral hepatitis is largely supportive: rest balanced against activity as tolerated, small frequent high-calorie meals with the largest meal in the morning when nausea is least, adequate fluids, and absolute avoidance of alcohol and of hepatotoxic drugs. Antiemetics are given cautiously and phenothiazines are avoided where possible because of cholestatic potential. Teach the patient with hepatitis A about scrupulous hand hygiene, not preparing food for others, and not sharing utensils; teach the patient with hepatitis B or C not to share razors, toothbrushes or needles, to use barrier protection, and never to donate blood, organs or semen.

Occupational exposure is a chapter you may live rather than read. After a needlestick, wash the site with soap and water immediately, report it at once, and let occupational health test the source and the exposed worker. For hepatitis B, an unvaccinated or non-immune worker receives HBIG plus the vaccine series, ideally within 24 hours and no later than seven days after percutaneous exposure. There is no post-exposure prophylaxis for hepatitis C — the protocol is baseline and serial testing, with early direct-acting antiviral treatment if seroconversion occurs. Standard precautions handle all of the blood-borne types; contact precautions are added for hepatitis A only when the patient is incontinent or nappy-dependent.

Acute liver failure and the paracetamol problem

Acute (fulminant) liver failure is the rapid loss of hepatic function with coagulopathy (INR of 1.5 or greater) and encephalopathy in a patient with no prior liver disease. In North America the single most common cause is acetaminophen (paracetamol) toxicity, often unintentional — a patient taking a prescription opioid-acetaminophen combination plus an over-the-counter cold preparation plus a sleep aid, none of which he recognises as containing the same drug. The maximum for a healthy adult is 4 g in 24 hours; in chronic liver disease, malnutrition or regular alcohol use, 2 g or less per day is safer.

The mechanism is worth knowing because it explains the antidote. Most acetaminophen is glucuronidated safely; a minority is oxidised to the toxic metabolite NAPQI, which glutathione neutralises. In overdose, glutathione stores are exhausted and NAPQI destroys centrilobular hepatocytes. N-acetylcysteine replenishes glutathione and is dramatically effective when started within 8 hours of ingestion, though it is still given later. It is dosed by weight, typically starting with a 150 mg/kg intravenous loading dose per protocol; the oral form smells of rotten eggs and is far better tolerated chilled, in juice, through a straw.

Nursing priorities in acute liver failure are ABC first and neurological status second. Grade III to IV encephalopathy threatens the airway — a patient who cannot protect it needs intubation, not another dose of lactulose. Monitor glucose hourly or per protocol because a failing liver cannot mobilise glycogen and profound hypoglycaemia is common. Watch for cerebral oedema, the leading cause of death: elevate the head of bed 30 degrees, keep the neck midline, cluster care, and minimise suctioning and other stimulation. Avoid sedatives if humanly possible; they are metabolised by the organ that has stopped working. Transplant evaluation is not a last resort here — it is an early call.

Section 3Cirrhosis, Portal Hypertension and Their Complications

From injury to fibrosis to portal hypertension

Repeated hepatocyte injury — from alcohol, chronic hepatitis B or C, metabolic dysfunction-associated steatotic liver disease (formerly NAFLD), autoimmune disease, haemochromatosis or biliary obstruction — activates hepatic stellate cells, which lay down collagen. Over years the architecture is replaced by regenerative nodules separated by fibrous bands. Two things follow. First, functioning hepatocyte mass falls, producing the synthetic and metabolic failures of Section 1. Second, and more mechanically, blood coming from the entire gut through the portal vein can no longer flow easily through the stiff liver. Portal pressure rises.

Trace that pressure and you have the whole clinical picture. Blood backs up into the spleen, which enlarges and sequesters platelets, producing thrombocytopenia. It backs up into collateral veins that were never designed for the volume — the submucosal veins of the oesophagus and stomach become varices, the periumbilical veins become caput medusae, the rectal veins become haemorrhoids. Hydrostatic pressure in the splanchnic bed, combined with low oncotic pressure from hypoalbuminaemia, pushes fluid into the peritoneum as ascites. Splanchnic vasodilation lowers effective arterial volume, activating the renin-angiotensin-aldosterone system, which retains sodium and water — making the ascites worse and diluting serum sodium. And portal blood carrying gut-derived ammonia now shunts around the liver instead of through it, producing hepatic encephalopathy.

Assessment reflects all of it: jaundice, spider angiomas, palmar erythema, gynaecomastia and testicular atrophy in men (the failing liver cannot metabolise oestrogen), muscle wasting with a protuberant abdomen, ecchymoses, Dupuytren contracture, foetor hepaticus, asterixis and, in men and women alike, a striking loss of temporal muscle mass. Do not be reassured by a blood pressure that looks acceptable on paper; cirrhotic patients often run baseline systolics in the 90s because of splanchnic vasodilation, so a reading of 100/60 that you would call normal in anyone else may already represent significant volume loss in this patient. Compare every pressure with that patient’s own baseline and follow the trend — a falling systolic with a climbing heart rate and a narrowing pulse pressure warns you of bleeding well before the absolute number looks alarming.

Ascites and spontaneous bacterial peritonitis

Ascites is managed in a fixed order. First, sodium restriction to about 2,000 mg per day — this is the intervention patients most often sabotage, usually unknowingly, through canned soup, deli meat, condiments and restaurant food. Fluid restriction is added only when serum sodium falls below roughly 125 mEq/L. Second, diuretics: spironolactone (an aldosterone antagonist, which addresses the actual mechanism) paired with furosemide, classically in a 100 mg to 40 mg ratio to keep potassium balanced. Monitor potassium closely — spironolactone raises it, furosemide lowers it — along with sodium and creatinine. Target weight loss is about 0.5 kg per day without peripheral oedema and up to 1 kg per day with oedema; faster diuresis precipitates renal injury and encephalopathy.

Third, paracentesis for tense or refractory ascites. Have the patient void immediately beforehand to reduce bladder puncture risk, position upright or in high Fowler, measure abdominal girth at a marked point and obtain a weight before and after, and monitor for hypotension during and after drainage. When more than 5 litres are removed, intravenous albumin of roughly 6 to 8 g per litre removed is given to prevent post-paracentesis circulatory dysfunction. TIPS (transjugular intrahepatic portosystemic shunt) is reserved for refractory cases; it reliably lowers portal pressure and just as reliably worsens encephalopathy, because it shunts ammonia-laden blood past the liver by design.

Spontaneous bacterial peritonitis is the infection of ascitic fluid without a perforation, and it is the complication students miss. The classic presentation — fever, diffuse abdominal pain, rebound tenderness — is frequently absent. In many patients the only sign is new or worsening confusion, a rising creatinine, or unexplained hypotension. Diagnosis is by diagnostic paracentesis showing an ascitic fluid polymorphonuclear count of 250 cells/mm³ or more. Treatment is a third-generation cephalosporin such as cefotaxime or ceftriaxone plus intravenous albumin (1.5 g/kg on day 1 and 1 g/kg on day 3) to protect the kidneys, followed by lifelong prophylaxis. A SAAG (serum-ascites albumin gradient) of 1.1 g/dL or greater confirms that the ascites is from portal hypertension rather than from malignancy or infection of the peritoneum itself.

Oesophageal varices: the bleed that kills

Varices are thin-walled submucosal veins under high pressure. When one ruptures the patient can lose litres in minutes, and the coagulopathy and thrombocytopenia of cirrhosis mean the bleeding does not stop on its own. Presentation is haematemesis (bright red or coffee-ground), melaena, tachycardia, hypotension and altered mental status.

Priorities are pure ABC. Airway first — a patient vomiting blood with encephalopathy will aspirate; suction is at the bedside and intubation is often required before endoscopy. Then two large-bore intravenous lines (18 gauge or larger), type and crossmatch, volume resuscitation and blood products with a restrictive transfusion target (generally haemoglobin around 7 g/dL, because over-transfusion raises portal pressure and re-triggers bleeding). Pharmacologically, octreotide reduces splanchnic blood flow — a 50 mcg bolus followed by a 50 mcg/hr infusion for 3 to 5 days — and prophylactic ceftriaxone is given because bacterial infection follows variceal bleeding with depressing regularity and worsens outcomes. Definitive control is endoscopic variceal band ligation within 12 hours. Balloon tamponade with a Sengstaken-Blakemore or Minnesota tube is a rescue bridge only, with scissors taped at the head of the bed for airway obstruction if the gastric balloon migrates.

Prevention matters more than rescue. Patients with known varices take a nonselective beta blocker — propranolol, nadolol or carvedilol — titrated to a resting heart rate of about 55 to 60, which lowers portal pressure. Cardioselective agents such as metoprolol do not work for this. Teach the patient to avoid NSAIDs and aspirin, to avoid straining and heavy lifting (Valsalva raises portal pressure), to treat constipation, to chew thoroughly and avoid coarse or sharp foods, and to seek care immediately for vomiting blood or black tarry stools.

Hepatic encephalopathy and hepatorenal syndrome

Hepatic encephalopathy runs a spectrum from a subtle reversal of sleep-wake cycle and slowed handwriting (grade I), through lethargy and disorientation with asterixis (grade II), to marked confusion and somnolence but rousable (grade III), to coma (grade IV). Serial mental-status assessment is the single most important nursing observation on a cirrhotic patient, and the change from grade II to grade III is an airway decision.

Lactulose is first-line. It is a nonabsorbable disaccharide that acidifies the colon, converting ammonia (NH₃) to ammonium (NH₄⁺), which cannot cross back into blood, and it purges it out as an osmotic laxative. Titrate to two to three soft stools per day — too few and the patient stays encephalopathic, too many and he becomes dehydrated and hypokalaemic, which paradoxically worsens encephalopathy. It can be given orally, by nasogastric tube or as a retention enema. Rifaximin 550 mg twice daily is a minimally absorbed antibiotic that reduces ammonia-producing gut flora and is added to prevent recurrence. Note that serum ammonia correlates poorly with clinical severity: treat the patient, not the number. And modern practice does not restrict protein — these patients are catabolic and need 1.2 to 1.5 g/kg/day, ideally with a late evening snack to shorten the overnight fast.

Hepatorenal syndrome is functional kidney failure in advanced liver disease: intense renal vasoconstriction in response to splanchnic vasodilation, with structurally normal kidneys. It is marked by a rising creatinine, oliguria, and a very low urine sodium (below 10 mEq/L) that does not correct with volume. It is precipitated by over-diuresis, large-volume paracentesis without albumin, NSAIDs, aminoglycosides and contrast. Treatment is albumin plus vasoconstrictors such as terlipressin or midodrine with octreotide, but the definitive treatment is liver transplant. Prevention is nursing work: protect these kidneys.

Section 4Gallbladder and Biliary Disorders

Stones form, and then stones move

The gallbladder stores and concentrates bile and contracts in response to cholecystokinin when fat reaches the duodenum. Cholelithiasis develops when bile becomes supersaturated with cholesterol, when the gallbladder empties sluggishly, or when excess bilirubin forms pigment stones (as in haemolysis or cirrhosis). The classic risk profile is remembered as the four Fs — female, fair, fat, forty — and it is worth extending: pregnancy and oestrogen therapy, rapid weight loss or bariatric surgery, prolonged fasting or total parenteral nutrition, diabetes, and Native American or Hispanic ancestry all raise risk.

Whether the patient has symptoms depends entirely on whether a stone moves. Stones sitting in the gallbladder are often silent. A stone that lodges in the cystic duct during contraction produces biliary colic: severe, steady right upper quadrant or epigastric pain radiating to the right shoulder or scapula, typically 30 minutes to a few hours after a fatty meal, often with nausea and vomiting, resolving when the stone falls back. There is no fever and no leucocytosis, because nothing is inflamed yet. A stone that lodges in the common bile duct is choledocholithiasis and now obstructs bile drainage for the liver and, because the pancreatic duct joins at the ampulla, potentially for the pancreas as well — jaundice, dark urine, clay stools, and gallstone pancreatitis.

Acute cholecystitis and ascending cholangitis

Acute cholecystitis is what happens when the stone does not fall back: the obstructed gallbladder distends, its wall becomes inflamed and oedematous, and bacteria colonise the stagnant bile. Now the pain is persistent rather than colicky, there is fever, leucocytosis with a white count typically 12,000 to 20,000/mm³, guarding, and a positive Murphy sign — the patient stops inspiration abruptly when you palpate under the right costal margin. Ultrasound shows a thickened gallbladder wall, pericholecystic fluid and stones. Untreated it progresses to gangrene and perforation. Acalculous cholecystitis, seen in critically ill, ventilated or TPN-dependent patients without stones, is easy to miss and carries a higher mortality.

Ascending cholangitis is infection of the obstructed biliary tree and it is a surgical and infectious emergency. Charcot triad — fever with rigors, jaundice and right upper quadrant pain — identifies it. When hypotension and altered mental status are added, you have Reynolds pentad, meaning septic shock, and the patient needs blood cultures, broad-spectrum antibiotics, aggressive fluid resuscitation and urgent biliary decompression by ERCP. Do not wait for the fever to declare itself in an older adult: in a patient over 75 the first and sometimes only sign of cholangitis is new confusion or a fall, with a normal or even low temperature and a white count that has not budged.

Procedures and the nursing care around them

Laparoscopic cholecystectomy is the standard, usually same-day or one-night stay. Post-operatively, the finding students find surprising is referred right shoulder pain from residual carbon dioxide irritating the diaphragm. Treat it with early ambulation, position changes, a left side-lying knee-to-chest position and analgesia, and reassure the patient it resolves in 24 to 48 hours — but do not dismiss shoulder pain accompanied by fever, rising abdominal pain, tachycardia or bile-stained drainage, which suggests a bile leak or duct injury. Encourage incentive spirometry: the incisions sit right under the diaphragm, splinting is instinctive, and atelectasis is the commonest complication.

An open cholecystectomy may leave a T-tube in the common bile duct. Keep the collection bag below the level of the gallbladder to prevent reflux, never irrigate or clamp it without an order, expect 300 to 500 mL of bile-coloured drainage in the first 24 hours declining thereafter, and report drainage exceeding 500 mL per day or an abrupt stop. When the tube is clamped before removal (often before and after meals), watch for pain, nausea and chills, which mean bile is not draining into the duodenum. Return of brown stool colour confirms bile is reaching the bowel.

ERCP deserves its own teaching. Keep the patient NPO beforehand, verify consent and allergies, and afterwards keep the patient NPO until the gag reflex returns. The complication to watch for is post-ERCP pancreatitis: new or worsening epigastric pain radiating to the back, nausea and a rising lipase in the hours after the procedure. Perforation and bleeding are rarer but real. Report new severe abdominal pain, fever or vomiting immediately.

Teaching the patient going home

After cholecystectomy the patient no longer stores bile — bile drips continuously into the duodenum instead of arriving in a bolus. Most people tolerate a normal diet within weeks, but for the first four to six weeks advise smaller, lower-fat meals and gradual reintroduction of fatty foods; loose stools are common early and usually settle. Teach incision care, the signs of infection, and the specific reasons to call: fever above 38.3 degrees Celsius (101 degrees Fahrenheit), worsening rather than improving pain, persistent vomiting, jaundice, dark urine or clay-coloured stools. No heavy lifting for the interval the surgeon specifies. For patients managed without surgery, teach the low-fat diet and the pattern of pain that means the stone has moved into the duct.

Section 5Acute and Chronic Pancreatitis and Pancreatic Cancer

Acute pancreatitis: the gland digests itself

The pancreas secretes amylase and lipase in fully active form, but it manufactures its proteases as inactive precursors — zymogens such as trypsinogen, chymotrypsinogen and proelastase — which are normally activated only after they reach the duodenum. In acute pancreatitis, trypsinogen is activated inside the gland, and that premature activation triggers a cascade that converts the remaining zymogens and begins autodigestion. Lipase digests fat, proteases digest protein and vessel walls, and the resulting inflammation causes massive capillary leak. Two causes account for most cases: gallstones obstructing the ampulla, and alcohol. Others include hypertriglyceridaemia (usually above 1,000 mg/dL), hypercalcaemia, ERCP, abdominal trauma, and drugs such as azathioprine, valproic acid, thiazides, sulfonamides and some HIV medications.

Every classic manifestation follows from the mechanism. Pain is severe, boring, epigastric or left upper quadrant, radiating straight through to the back — the pancreas is retroperitoneal — and is characteristically worse supine and relieved by leaning forward or curling into a knee-chest position. Nausea and vomiting that does not relieve the pain, abdominal distension and diminished bowel sounds from a reactive ileus, and low-grade fever are usual. Hypotension and tachycardia reflect third spacing: litres of plasma sequestered in the retroperitoneum and peritoneum, producing hypovolaemic shock with no visible blood loss. Enzymatic fat necrosis binds calcium (saponification), causing hypocalcaemia — look for Chvostek and Trousseau signs, perioral tingling and, in severe cases, tetany or dysrhythmias. Haemorrhagic pancreatitis may produce Cullen sign (periumbilical ecchymosis) or Grey Turner sign (flank ecchymosis), late and ominous findings.

Diagnosis requires two of three: characteristic pain, lipase or amylase at least three times the upper limit of normal, and imaging findings. Lipase (normal roughly 0 to 160 U/L) is preferred because it is more pancreas-specific, rises within 4 to 8 hours and stays elevated 8 to 14 days; amylase (normal roughly 30 to 110 U/L) rises and falls faster and is elevated in many non-pancreatic conditions. Note firmly that the height of the enzyme does not indicate severity — severity is judged by organ failure, by scoring systems such as BISAP or Ranson criteria, and by CT findings of necrosis. Supporting labs include a rising haematocrit from haemoconcentration, rising BUN, leucocytosis, hyperglycaemia (islet cell injury), low calcium (normal 8.6 to 10.2 mg/dL) and elevated ALT above roughly 150 U/L, which strongly suggests a gallstone cause.

Managing the acute attack

There is no drug that stops pancreatitis. Management is supportive and the nursing contribution is enormous. Fluid resuscitation is the single most important early intervention: lactated Ringer’s at roughly 5 to 10 mL/kg/hr initially, titrated to a urine output of at least 0.5 mL/kg/hr, a falling BUN and a normalising haematocrit. More is not better — over-resuscitation causes pulmonary oedema and abdominal compartment syndrome — so this is goal-directed, not maximal, and the nurse’s hourly output and respiratory assessment drive the titration.

Pain control is aggressive and usually opioid-based, frequently by patient-controlled analgesia. Older texts warned that morphine causes sphincter of Oddi spasm; the evidence does not show worse outcomes, and untreated pain has real consequences including splinting and atelectasis. Many programmes and facilities still prefer hydromorphone or fentanyl — follow your protocol, and know why the question is asked. Position the patient side-lying with knees flexed and the head of bed elevated, which relieves pain and improves ventilation.

Nutrition has changed and students are often taught the old answer. Prolonged NPO with total parenteral nutrition is no longer standard. In mild pancreatitis, early oral feeding with a low-fat diet within 24 hours as tolerated improves outcomes; in severe disease, enteral feeding by nasogastric or nasojejunal tube within 24 to 72 hours is preferred over parenteral because it preserves gut mucosal integrity and lowers infection rates. A nasogastric tube to suction is used for ileus, intractable vomiting or distension — not routinely. Alcohol and smoking cessation counselling begins during the admission, not at discharge.

Complications define the mortality. Local: pancreatic pseudocyst (a fluid collection that may present as a palpable epigastric mass with persistent pain and a persistently elevated amylase, and may rupture or bleed), infected necrosis (fever and clinical deterioration at 7 to 14 days, requiring CT-guided aspiration and antibiotics), abscess, and fistula. Systemic: hypovolaemic shock, acute respiratory distress syndrome (the reason a rising respiratory rate and falling oxygen saturation in a pancreatitis patient is never “just pain”), acute kidney injury, disseminated intravascular coagulation, hypocalcaemia and hyperglycaemia.

Chronic pancreatitis and enzyme replacement

Repeated or continuous injury — most often alcohol, and increasingly genetic and autoimmune causes — replaces functional acini with fibrosis and calcification. The pancreas is a gland with both exocrine and endocrine roles, so chronic destruction produces two separate failures. Exocrine insufficiency means fat and protein are not digested: steatorrhoea (bulky, greasy, foul-smelling stools that float and are hard to flush), weight loss despite adequate intake, and deficiency of the fat-soluble vitamins A, D, E and K. Endocrine insufficiency means islet cell loss and diabetes, which is brittle because glucagon-producing cells are lost alongside beta cells, making hypoglycaemia both more likely and harder to counter-regulate. Chronic pain is the third pillar and is often the hardest problem, with a genuine risk of opioid dependence.

Diagnosis rests on imaging — CT or MRCP showing calcifications, a dilated or beaded duct and atrophy — because enzymes may be normal or even low in a burned-out gland. A faecal elastase-1 test confirms exocrine insufficiency. Management is enzyme replacement, glucose control, pain management, nutritional support with fat-soluble vitamin supplementation, and absolute abstinence from alcohol and tobacco.

Pancreatic enzyme replacement therapy teaching is precise and highly testable. Take it with every meal and every snack, not before or after — the enzymes must mix with food to work. Swallow enteric-coated capsules whole; do not crush or chew them, because gastric acid destroys the enzyme. If the patient cannot swallow capsules, the microspheres may be sprinkled on a small amount of an acidic soft food such as applesauce and swallowed immediately without chewing. Do not mix with milk or other alkaline foods. Wipe the lips and rinse the mouth after dosing, since residual enzyme irritates skin and mucosa. Acid suppression with a proton pump inhibitor is often added to protect the enzyme. Evaluate effectiveness by weight gain and by the disappearance of steatorrhoea — the stool is the outcome measure.

Pancreatic cancer

Adenocarcinoma of the pancreatic head is the classic presentation and it announces itself, when it announces itself at all, with painless progressive jaundice as the tumour compresses the common bile duct: yellow sclerae, dark urine, clay stools and relentless pruritus, accompanied by anorexia and marked weight loss. A palpable, non-tender distended gallbladder in a jaundiced patient (Courvoisier sign) suggests malignant obstruction rather than stones. New-onset diabetes in an older adult with weight loss deserves suspicion. Migratory thrombophlebitis and unexplained venous thromboembolism are recognised paraneoplastic clues. CA 19-9 is used to follow treatment response, not to screen. Risk factors include smoking, chronic pancreatitis, diabetes, obesity and family history.

Surgical resection by pancreaticoduodenectomy (the Whipple procedure) — removal of the pancreatic head, duodenum, gallbladder, distal common bile duct and often part of the stomach, with reconstruction — is the only curative option and is possible in a minority of patients. Post-operative nursing is high acuity: multiple drains and often a biliary stent, monitoring for anastomotic leak (fever, rising drain amylase, increasing pain), delayed gastric emptying, haemorrhage, glucose instability and infection. For unresectable disease, care is palliative — biliary stenting to relieve jaundice and pruritus, enzyme replacement, aggressive pain management including coeliac plexus block, nutritional support and early involvement of palliative care.

Words worth knowing

Renal and Urinary Disorders

The kidneys are the quietest organs on your assignment and the least forgiving. They hold sodium and water within a few percent of target, keep potassium inside a window barely one and a half milliequivalents wide, excrete the daily acid load, activate vitamin D, and signal the marrow to make red cells — and they do all of it without producing a single symptom you can see from the doorway. When they fail, the failure announces itself somewhere else: in a peaked T wave on the monitor, in crackles at the bases, in a confused eighty‑two‑year‑old who was oriented yesterday, in a creatinine that crept from 0.9 to 1.4 while everyone was watching the surgical site. This chapter teaches you to read those distant signals, to separate the kidney that is under‑perfused from the kidney that is injured from the kidney that is merely obstructed, and to know which of your four patients needs you first.

Section 1How the Kidney Works and How You Assess It

The nephron in one page

Each kidney holds roughly one million nephrons, and each nephron begins with a tuft of capillaries — the glomerulus — sitting inside a cup called Bowman capsule. Blood arrives under pressure through the afferent arteriole and leaves through the narrower efferent arteriole. That deliberate bottleneck is what drives filtration: about 180 litres of plasma are pushed across the glomerular membrane every day. The membrane is a size and charge filter. Water, electrolytes, glucose, urea and creatinine cross freely; albumin and red cells should not. When you see protein or blood in the urine, the filter itself has been damaged.

What follows is reclamation. The proximal tubule takes back roughly two‑thirds of the filtered sodium and water plus essentially all of the glucose, amino acids and bicarbonate. The loop of Henle builds the medullary concentration gradient that makes concentrated urine possible — and it is the site loop diuretics block. The distal tubule and collecting duct are where fine control happens: aldosterone drives sodium reabsorption in exchange for potassium and hydrogen ion, and antidiuretic hormone opens water channels so water follows. Of the 180 litres filtered, only about 1 to 2 litres leave as urine.

Three hormonal jobs matter enormously in disease. First, renin: when renal perfusion falls, the juxtaglomerular cells release renin, which starts the cascade ending in angiotensin II (vasoconstriction, efferent arteriole constriction to preserve filtration) and aldosterone (sodium and water retention). Second, erythropoietin: peritubular cells sense oxygen delivery and tell the marrow to make red cells. Third, activation of vitamin D: the kidney performs the final hydroxylation that produces calcitriol, without which the gut cannot absorb calcium. Remember those three and the anemia, hypertension and bone disease of chronic kidney disease stop being a list to memorise and become consequences you can predict.

Reading the numbers: creatinine, BUN and eGFR

Serum creatinine (roughly 0.6 to 1.2 mg/dL; about 0.7 to 1.3 in men and 0.6 to 1.1 in women) is the workhorse. Creatinine is a waste product of muscle metabolism produced at a fairly steady rate and cleared almost entirely by filtration, so it rises when filtration falls. Two cautions. It is insensitive early — roughly half of function can be lost before creatinine leaves the normal range — and it depends on muscle mass. A frail 80‑year‑old woman with a creatinine of 1.1 mg/dL may have lost more than half her filtration. Never call a creatinine “normal” in an older or cachectic patient without looking at the estimated GFR.

Blood urea nitrogen (10 to 20 mg/dL) reflects filtration too, but it is contaminated by everything else that affects urea: dehydration, high protein intake, gastrointestinal bleeding, steroids and catabolic states all raise it, while liver failure and malnutrition lower it. That contamination is actually useful. A BUN‑to‑creatinine ratio above 20 to 1 points toward a prerenal cause, because a dry kidney reabsorbs urea avidly along with sodium and water while creatinine keeps moving. A ratio near 10 or 15 to 1 with both values rising suggests intrinsic damage.

Estimated GFR is calculated from creatinine, age and sex, and it is the number that actually drives clinical decisions: staging, drug dosing, contrast decisions and referral for dialysis planning. Normal is above 90 mL/min/1.73 m². Before you give any renally cleared drug — enoxaparin, gabapentin, metformin, vancomycin, many antibiotics — look at the calculated clearance, not the creatinine. One caveat matters at the bedside: eGFR is normalised to body surface area, so for weight‑sensitive drugs such as enoxaparin pharmacy dose‑adjusts from the Cockcroft‑Gault creatinine clearance, which falls far faster than eGFR in a small, low‑weight older adult.

Urine as data

Urine output is the cheapest renal monitor in the hospital, and it is often delegated to unlicensed personnel and then never looked at. The adult threshold to know is 0.5 mL/kg/hr. For a 70 kg patient that is 35 mL per hour, or roughly 210 mL over a six‑hour shift segment. Oliguria is less than 400 mL in 24 hours (or output under 0.5 mL/kg/hr for six hours); anuria is less than 100 mL in 24 hours and should make you think obstruction or catastrophic vascular event until proven otherwise. Pair intake and output with a daily weight taken at the same time, on the same scale, in the same clothing: one kilogram equals approximately one litre of fluid, and weight is far more reliable than an intake and output record that nobody charted at lunch.

The urinalysis tells you where the injury lives. Specific gravity normally ranges 1.005 to 1.030; a high value with concentrated dark urine suggests a dry patient whose tubules still work, while a fixed value near 1.010 (the specific gravity of plasma) suggests tubules that have lost the ability to concentrate at all. Protein should be absent to trace; persistent proteinuria means glomerular disease. The urine albumin‑to‑creatinine ratio categorises albuminuria as A1 (under 30 mg/g), A2 (30 to 300 mg/g) or A3 (over 300 mg/g), and A2 or higher predicts progression.

Casts are cylindrical moulds of the tubule and they are close to diagnostic. Muddy brown granular casts mean acute tubular necrosis. Red blood cell casts mean glomerulonephritis — blood is coming through the filter, not from a stone or a catheter. White blood cell casts mean infection or inflammation inside the kidney, that is pyelonephritis or interstitial nephritis, rather than a bladder infection. Hyaline casts are usually benign and appear with dehydration or exercise.

Imaging, biopsy and the aging kidney

Renal ultrasound is first‑line and answers the single most urgent structural question: is there hydronephrosis, meaning obstruction? It uses no contrast and no radiation, needs no preparation, and can be done at the bedside. Non‑contrast helical CT is the gold standard for stones. CT with iodinated contrast and coronary angiography carry a risk of contrast‑associated AKI, which typically shows a creatinine rise within 48 to 72 hours; prevention is isotonic intravenous fluid before and after, holding other nephrotoxins, and using the smallest contrast volume possible. Metformin is held at the time of contrast when eGFR is under 30, and restarted after 48 hours once renal function is confirmed stable.

Percutaneous kidney biopsy is how glomerular disease is diagnosed. It is a bleeding procedure into a highly vascular organ. Before: check coagulation studies, hemoglobin, type and screen, and confirm consent and held anticoagulants. After: bed rest lying supine with pressure over the site for four to six hours, vital signs on a tapering schedule, serial hemoglobin, and inspection of every urine specimen. Gross hematuria that persists beyond the first few voids, flank pain, hypotension or a falling hemoglobin means bleeding — notify immediately. Teach the patient to avoid heavy lifting and strenuous activity for about two weeks.

Age changes everything you have just read. Nephron number falls steadily from about age 40, renal blood flow declines, the concentrating and diluting ability narrows, and the thirst response blunts. The practical consequences on your floor: an older adult becomes prerenal after one day of poor intake and a dose of furosemide, tolerates a nephrotoxin far worse than a 30‑year‑old, and carries a “normal” creatinine that hides real impairment. Add polypharmacy and the older adult is the patient in whom AKI is both most likely and most likely to be missed.

Section 2Acute Kidney Injury

Three doors into the same room

Acute kidney injury is an abrupt decline in filtration, defined by a creatinine rise of at least 0.3 mg/dL within 48 hours, a creatinine at least 1.5 times baseline within seven days, or urine output under 0.5 mL/kg/hr for six hours. It complicates a large fraction of hospital admissions and carries real mortality. The classification is not academic: prerenal injury is fixed with volume, postrenal injury is fixed with drainage, and intrarenal injury is mostly supported while the tubules heal.

Prerenal AKI is a perfusion problem in a structurally normal kidney — roughly two‑thirds of cases. Causes are anything that lowers effective renal blood flow: hemorrhage, vomiting and diarrhea, aggressive diuresis, burns, sepsis with vasodilation, heart failure with poor forward flow, and cirrhosis. Drugs contribute directly. NSAIDs constrict the afferent arteriole and shut the tap; ACE inhibitors and ARBs dilate the efferent arteriole and drop filtration pressure. Either is tolerated in a well‑perfused patient and dangerous in a dry one. The classic dangerous combination on a med‑surg floor is an ACE inhibitor plus a diuretic plus an NSAID in a patient who has been nothing by mouth — sometimes called the triple whammy.

Intrarenal (intrinsic) AKI is damage to the tissue itself. The most common form is acute tubular necrosis, produced either by prolonged ischemia — prerenal injury that was not corrected — or by nephrotoxins: aminoglycosides, vancomycin, amphotericin B, cisplatin, iodinated contrast, and pigment loads from rhabdomyolysis (myoglobin, tea‑coloured urine, creatine kinase often in the thousands to tens of thousands) or hemolysis. Acute interstitial nephritis is usually an allergic reaction to a drug — proton pump inhibitors, beta‑lactams, sulfonamides — and may come with rash, fever and eosinophilia. Acute glomerulonephritis is inflammation of the filter: post‑streptococcal disease appears one to three weeks after pharyngitis or three to six weeks after skin infection, with tea‑coloured urine, red cell casts, hypertension, periorbital edema, an elevated ASO titre and a low complement C3. Nephrotic syndrome is the other glomerular pattern — proteinuria over 3.5 g per 24 hours, albumin under 3.0 g/dL, massive edema, hyperlipidemia and a hypercoagulable state from urinary loss of antithrombin.

Postrenal AKI is obstruction: benign prostatic hyperplasia, bilateral stones, tumour, retroperitoneal fibrosis, a clotted or kinked catheter. It is the least common cause and the most rewarding to find, because relieving the obstruction often restores function completely if it is caught early. Any patient who abruptly stops making urine deserves a bladder scan and a look at the catheter before anyone reaches for fluids.

One caveat governs that whole table. FeNa and urine sodium are interpretable only in a patient who has not had a diuretic. A loop or thiazide diuretic forces natriuresis, so a volume‑depleted prerenal patient who received furosemide within roughly the previous 24 hours characteristically shows a urine sodium above 40 mEq/L and a FeNa above 2% — the intrarenal pattern — and filing that patient under acute tubular necrosis means withholding the volume they actually need. Since “aggressive diuresis” and “a diuretic in a patient who was already dry” are among the commonest prerenal causes on a med‑surg floor, this is not a rare exception. When a diuretic has been given, use the fractional excretion of urea instead: under about 35% suggests a prerenal state, because urea reabsorption is not blocked by these drugs. Note too that FeNa can read under 1% despite genuine intrinsic injury in contrast nephropathy, pigment nephropathy from rhabdomyolysis, hepatorenal syndrome and acute glomerulonephritis. No single index outranks the bedside picture, the medication record and the response to a fluid challenge.

The four phases and what each one costs you

Onset (initiation) runs from the insult to the first fall in urine output — hours to days — and it is the only window in which the injury can often be reversed. This is when your assessment matters most: the falling output, the rising creatinine, the hypotensive episode nobody escalated.

Oliguric phase typically lasts one to three weeks, and urine output falls below 400 mL per day. This is the dangerous phase. Everything the kidney was supposed to excrete accumulates: potassium climbs, phosphorus climbs, hydrogen ion climbs (metabolic acidosis with a bicarbonate under 22 mEq/L), water accumulates producing hypertension, edema, jugular venous distension, crackles and dilutional hyponatremia, and urea climbs toward uremia. The single most lethal problem here is hyperkalemia. Nursing care is fluid restriction, strict intake and output, daily weights, dietary potassium and phosphorus restriction, and vigilant medication review.

Diuretic phase begins when tubules start recovering filtration before they recover concentrating ability. Output can reach 3 to 5 litres a day and occasionally 10. Now the risk inverts: hypovolemia, hypotension, hypokalemia and hyponatremia. Patients who survived the oliguric phase are lost here when nobody notices that a patient putting out 400 mL an hour is being under‑replaced. Monitor electrolytes at least daily and replace fluid and potassium as ordered — and note that replacement potassium is never given as an intravenous push or bolus under any circumstance: it is always diluted, infused on a pump at a controlled rate, and given with the patient monitored.

Recovery may take up to twelve months, and function may not return fully. A patient who has had AKI carries a permanently higher risk of chronic kidney disease, which is a teaching point at discharge: avoid NSAIDs, stay hydrated, and get renal function rechecked.

Management and the hyperkalemia emergency

Medical management is cause‑directed. Prerenal injury gets isotonic crystalloid and, in shock, vasopressors to restore a mean arterial pressure that perfuses the kidney. Postrenal injury gets drainage. Intrinsic injury gets removal of the offending agent, careful fluid balance, and dose adjustment of every renally cleared drug. Loop diuretics do not treat AKI and do not improve survival — they manage volume in a patient who still makes urine. Renal replacement therapy is started for the indications summarised by AEIOU: refractory Acidosis, Electrolyte disturbance (chiefly hyperkalemia), Intoxications, fluid Overload unresponsive to diuretics, and Uremic complications such as pericarditis, encephalopathy or bleeding.

Hyperkalemia is the emergency you will actually face. Potassium above 5.5 mEq/L in an oliguric patient is urgent; above 6.0 with ECG changes is a code waiting to happen. ECG evolution is orderly: tall peaked T waves first, then a flattened or absent P wave and a prolonged PR interval, then a widening QRS that blends into a sine wave and then asystole or ventricular fibrillation. The nursing sequence is: recognise, place the patient on continuous cardiac monitoring, obtain a 12‑lead ECG, notify the provider, hold all potassium sources (intravenous fluids with potassium, potassium‑sparing diuretics, ACE inhibitors and ARBs, salt substitutes, dietary potassium), and prepare the drugs below in the correct order.

Remember the concept that separates a passing student from a safe nurse: step 1 protects the myocardium without lowering the potassium by a single point, and steps 2 through 4 only buy time by hiding potassium inside cells. The potassium is still in the body and it will come back out. Nothing is finished until step 5 or 6 has actually removed it, and the potassium is rechecked.

Section 3Chronic Kidney Disease and End‑Stage Renal Disease

Staging and the two diseases that cause most of it

Chronic kidney disease is abnormality of kidney structure or function present for more than three months. Diabetes causes roughly 40% of cases in the United States and hypertension another 25% or so; glomerulonephritis, polycystic kidney disease and repeated AKI account for much of the rest. The mechanism of progression is common to all of them: as nephrons are lost, the survivors hyperfilter to compensate, that hyperfiltration scars them, and the disease becomes self‑sustaining. This is exactly why treatment aims at lowering intraglomerular pressure rather than at any specific original insult.

Albuminuria is staged alongside GFR because it independently predicts progression and cardiovascular death: A1 is under 30 mg/g, A2 is 30 to 300 mg/g, A3 is above 300 mg/g. A patient at G2 with A3 is at higher risk than a patient at G3a with A1. When a student asks why we test urine on a patient whose creatinine is normal, this is the answer.

What uremia does to every system

Cardiovascular disease is what actually kills most patients with CKD, long before they reach dialysis. Volume overload plus renin activation plus vascular calcification produces hypertension, left ventricular hypertrophy and accelerated atherosclerosis. Late uremia adds pericarditis: a friction rub, pleuritic chest pain relieved by leaning forward, and a risk of tamponade — muffled heart tones, hypotension, jugular venous distension. That is an urgent dialysis indication, not a wait‑until‑morning finding.

Hematologic. Anemia comes from erythropoietin deficiency, shortened red cell survival, iron deficiency and blood loss in the dialyser. It is normocytic and normochromic. Uremia also causes platelet dysfunction, so these patients bruise, ooze from puncture sites and bleed from the gut with a normal platelet count. Treatment is iron repletion first — check transferrin saturation and ferritin — then an erythropoiesis‑stimulating agent titrated to a hemoglobin of about 10 to 11 g/dL. Do not chase a normal hemoglobin: higher targets increase stroke, thrombosis and death.

CKD mineral and bone disorder follows a predictable chain. The failing kidney cannot excrete phosphorus, so phosphorus rises; phosphorus binds calcium and the kidney can no longer activate vitamin D, so calcium falls; low calcium and high phosphorus drive the parathyroids to secrete PTH continuously; PTH pulls calcium out of bone. The result is renal osteodystrophy — weak bones, fractures, bone pain — plus soft‑tissue and vascular calcification and intractable itching. Treatment is dietary phosphorus restriction, phosphate binders given with meals (calcium acetate, sevelamer, lanthanum — a binder given between meals binds nothing), active vitamin D, and calcimimetics such as cinacalcet, which lower PTH but can cause hypocalcemia.

Metabolic and neurologic. Bicarbonate falls below 22 mEq/L because the kidney cannot excrete acid or regenerate bicarbonate; chronic acidosis worsens bone disease and muscle wasting and is treated with oral sodium bicarbonate. Potassium retention worsens as GFR falls under about 20. Uremic encephalopathy brings fatigue, poor concentration, sleep reversal, asterixis, and in older adults it commonly presents as delirium. Peripheral neuropathy causes restless legs and burning feet. Gastrointestinal effects include anorexia, metallic taste, nausea, uremic fetor and gastritis with bleeding risk. Integumentary findings are a sallow grey‑yellow tone, severe pruritus and uremic frost in extreme cases. Sexual dysfunction, infertility and immune suppression round out a genuinely miserable syndrome.

Slowing it down: drugs, diet and teaching

Four drug classes carry the evidence. ACE inhibitors and ARBs dilate the efferent arteriole, lowering intraglomerular pressure and albuminuria. Expect and tolerate a creatinine rise of up to about 30% after starting; a larger rise, or a potassium above 5.5 mEq/L, means hold and call. Never combine an ACE inhibitor with an ARB. SGLT2 inhibitors (dapagliflozin, empagliflozin) now slow progression in both diabetic and non‑diabetic CKD with albuminuria; a small acute dip in eGFR after starting is expected and is not injury; teach genital hygiene because of mycotic infections, watch for volume depletion, and know that euglycemic diabetic ketoacidosis is a rare but real adverse effect. Finerenone, a non‑steroidal mineralocorticoid receptor antagonist, adds benefit in diabetic CKD — monitor potassium closely. Statins address the cardiovascular risk that is the true cause of death. Blood pressure control — usually a target near 130/80 mmHg or lower, individualised — and glycemic control remain foundational.

Nutrition is a nursing responsibility as much as a dietitian’s. Before dialysis, protein is moderately restricted (roughly 0.6 to 0.8 g/kg/day) to reduce the nitrogenous load; once on hemodialysis, protein needs increase to about 1.0 to 1.2 g/kg/day because amino acids are lost into the dialysate. This reversal is a favourite examination item. Sodium is limited to under 2 g/day, potassium to roughly 2 to 3 g/day, phosphorus to 800 to 1000 mg/day — which means teaching patients to avoid dark colas, processed cheese, and anything with “phos” on the ingredient list, since additive phosphorus is almost completely absorbed. Fluid is commonly restricted to about 1000 mL plus the previous day’s urine output. Teach patients to spread fluid across the day, use ice chips (counted as half their volume), sugar‑free hard candy and frequent mouth care for thirst.

Discharge teaching priorities: take blood pressure and record it, weigh daily and report a gain of more than 2 kg (about 4 to 5 pounds) in a day or 2.5 kg between dialysis treatments, take phosphate binders with the first bite of every meal and snack, never take NSAIDs or magnesium‑ or aluminium‑containing antacids without asking, check with the pharmacist before any new drug or herbal product, get the influenza, COVID‑19, pneumococcal and hepatitis B vaccines, and protect the non‑dominant arm for future access even before dialysis is needed.

Section 4Dialysis, Access and Transplantation

Hemodialysis and protecting the access

In hemodialysis, blood is pumped from the patient through a dialyser containing thousands of semipermeable fibres while dialysate flows in the opposite direction on the other side of the membrane. Solutes move by diffusion down their concentration gradients — urea, creatinine and potassium out of the blood; bicarbonate and calcium in as prescribed. Water is removed separately by ultrafiltration, a pressure gradient set by the amount of fluid the patient needs to lose to reach the prescribed “dry weight.” A typical outpatient schedule is three to four hours, three times a week. Anticoagulation, usually heparin, keeps the circuit from clotting and is a bleeding consideration afterward.

Access determines survival. An arteriovenous fistula is a surgical anastomosis of the patient’s own artery and vein, usually in the non‑dominant forearm. It has the lowest infection rate and longest patency but needs to mature — typically at least six weeks and often two to three months — before it can be cannulated. An AV graft uses synthetic tubing, is usable in about two to three weeks, and clots and infects more often. A tunnelled central venous catheter works immediately but carries the highest infection and central stenosis risk and is the least desirable long‑term choice.

Assessing and protecting a fistula is a nursing skill you must be able to perform without prompting. Palpate for a thrill — a buzzing vibration — and auscultate for a bruit — a swishing sound — at least every shift and any time the patient reports a change. Absence of both means the access has clotted, and that is an urgent call: a fistula can sometimes be salvaged within hours. On the access extremity: no blood pressure cuffs, no venipuncture, no intravenous lines, no restraints, no tight clothing or jewellery, and no sleeping on that arm. Post a sign at the bedside. Also assess distal circulation for steal syndrome — a cool, pale, painful, numb hand distal to the access means the fistula is diverting blood from the extremity.

Around a treatment: weigh before and after (the difference is fluid removed), check whether antihypertensives should be held to prevent intradialytic hypotension, and know which of the patient’s medications are dialysable and therefore scheduled after the run — many antibiotics, water‑soluble vitamins and some antiepileptics. Afterward, assess for hypotension, dizziness, cramps, bleeding from needle sites and the post‑dialysis weight. Dialysis disequilibrium syndrome occurs mainly during the first treatments in a very uremic patient: urea is cleared from blood faster than from brain, water follows the osmotic gradient into brain tissue, and the patient develops headache, nausea, restlessness, confusion and, at worst, seizures. Slow or stop the treatment and notify immediately.

Peritoneal dialysis

Peritoneal dialysis uses the patient’s own peritoneum as the membrane. Warmed dextrose‑based dialysate is instilled through a permanent abdominal catheter (fill), left in place for a prescribed dwell during which solutes diffuse into it and water follows the osmotic pull of the dextrose, and then drained out by gravity (drain). It can be done manually four or five times a day or by a cycler overnight. Its advantages are autonomy, no needles, gentler fluid shifts and a more liberal diet; its disadvantages are the daily discipline it demands, protein loss, hyperglycemia and weight gain from absorbed dextrose, and hernia formation.

The nursing essentials: use strict aseptic technique at every connection, warm the dialysate with a dry warmer or heating pad and never in a microwave, record fill and drain volumes precisely, and weigh the patient after draining. Effluent should be clear and pale yellow. Cloudy effluent is peritonitis until proven otherwise — often with abdominal pain, rebound tenderness and fever — and requires a specimen for cell count, Gram stain and culture, followed by intraperitoneal antibiotics. If outflow is less than inflow, check for a kinked or clamped line, constipation (the most common and most overlooked cause), fibrin in the catheter, and reposition the patient before assuming catheter failure. Peritoneal dialysis is contraindicated with extensive abdominal adhesions, recent abdominal surgery or an unrepaired hernia.

Continuous therapies and transplantation

Continuous renal replacement therapy removes solute and fluid slowly and continuously over 24 hours in the intensive care unit. Because volume is removed gradually, it is far better tolerated by the hemodynamically unstable septic or post‑operative patient than intermittent hemodialysis. It usually requires anticoagulation of the circuit — regional citrate is now preferred over systemic heparin and demands monitoring of ionised calcium — along with one‑to‑one nursing and hourly balance calculation; electrolytes and phosphorus fall and need replacement.

Kidney transplantation offers the best survival and quality of life. The graft is placed in the iliac fossa — palpable and tender if rejecting — and the native kidneys are usually left in place. In the immediate post‑operative period, monitor urine output hourly; a well‑functioning living‑donor graft may produce enormous volumes, and replacement is usually ordered as a percentage of output. Falling urine output, a rising creatinine, fever, weight gain, hypertension and tenderness over the graft suggest rejection, and every one of those is a call to the transplant team.

Immunosuppression is lifelong and non‑negotiable. Calcineurin inhibitors (tacrolimus, cyclosporine) require trough monitoring and are themselves nephrotoxic; antimetabolites (mycophenolate) cause gastrointestinal upset and marrow suppression and are teratogenic; corticosteroids bring hyperglycemia, bone loss and mood change. The composite risk is infection and malignancy. Teach hand hygiene, avoidance of sick contacts, no live vaccines, sun protection and annual skin examination, and above all that a missed dose is never trivial — the graft can be lost in days. A low‑grade fever in a transplant patient is a serious finding, not a nuisance.

Section 5Infection, Obstruction and the Lower Urinary Tract

Urinary tract infection, pyelonephritis and CAUTI

Bacteria — most often Escherichia coli from the perineum — ascend the short female urethra into the bladder. Cystitis produces dysuria, urgency, frequency, suprapubic pain and cloudy, malodorous urine, sometimes with hematuria; fever is usually absent. Urinalysis shows positive leukocyte esterase and nitrites, more than 10 white cells per high‑power field and bacteria; a culture with 100,000 colony‑forming units per millilitre confirms it. Always obtain the culture before the first antibiotic dose. Uncomplicated cystitis is treated with nitrofurantoin (avoid when creatinine clearance is under about 30 mL/min, because it will not concentrate in the urine), trimethoprim‑sulfamethoxazole or fosfomycin. Phenazopyridine relieves burning, turns urine and tears bright orange, will permanently stain contact lenses, is limited to about two days, and is not an antibiotic — patients who stop the antibiotic because the burning stopped are a recurring problem.

Pyelonephritis is infection of the kidney itself: fever above 38.5°C, chills, flank pain, costovertebral angle tenderness, nausea and vomiting on top of lower tract symptoms, with white cell casts in the urine. It requires systemic antibiotics — ceftriaxone or a fluoroquinolone, intravenously if the patient is vomiting or unstable — along with hydration and analgesia. The danger is urosepsis: hypotension, tachycardia, tachypnea, altered mental status, rising lactate. Infection behind an obstruction is a urologic emergency; antibiotics alone will not fix it and the tract must be drained, often with a ureteral stent or a percutaneous nephrostomy.

Catheter‑associated urinary tract infection is the most common preventable hospital infection and it is largely nursing‑controlled. Prevent it by inserting a catheter only when genuinely indicated, using sterile technique, maintaining a closed drainage system, keeping the bag below the level of the bladder and off the floor, securing the tubing to prevent traction and dependent loops, performing daily perineal hygiene with soap and water, and — the intervention with the largest effect — reviewing daily whether the catheter can come out and removing it as soon as possible. Never irrigate routinely, never disconnect the system to obtain a specimen (use the sampling port after disinfecting it), and never raise the bag above the bladder during transfers.

Older adults deserve a paragraph of their own. Classic dysuria may be absent; instead you see new confusion, a fall, incontinence in a previously continent patient, anorexia or simply “not herself.” Fever may be blunted, so a temperature of 37.8°C in an 85‑year‑old can be significant. At the same time, asymptomatic bacteriuria is common in the elderly and should not be treated — a positive culture in a patient with no symptoms does not explain a delirium, and treating it drives resistance and Clostridioides difficile. The safe nursing stance is to work up the confused older adult fully rather than blaming the urine reflexively. Teach prevention: adequate fluids, front‑to‑back wiping, voiding after intercourse, cotton underwear, avoiding douches and prolonged retention.

Urolithiasis

Stones form when solutes supersaturate the urine, most often because of low fluid intake. About 75 to 80% are calcium oxalate or calcium phosphate. Uric acid stones form in acidic urine and are radiolucent. Struvite stones form only in the presence of urease‑producing organisms such as Proteus, grow into large staghorn calculi and are always infection‑associated. Cystine stones are rare and genetic. The pain — renal colic — is sudden, severe, wave‑like flank pain radiating to the groin or testicle or labia, with a patient who cannot lie still, plus nausea, vomiting, hematuria and often urinary frequency once the stone reaches the ureterovesical junction. Non‑contrast CT confirms it.

Management for a stone under about 5 mm is expulsive: aggressive fluids, analgesia with an NSAID such as ketorolac (used cautiously and briefly, and avoided if renal function is impaired) with opioids as needed, an antiemetic, and tamsulosin to relax ureteral smooth muscle. Strain every urine and send any recovered fragment for analysis — that analysis determines the whole prevention plan. Larger or obstructing stones need extracorporeal shock wave lithotripsy, ureteroscopy with laser fragmentation, or percutaneous nephrolithotomy. After lithotripsy, teach that bruising over the flank and hematuria for several days are expected, that fragments may pass for weeks, and that fluids and straining continue.

Retention, obstruction, incontinence and hematuria

Benign prostatic hyperplasia is near‑universal with age and produces obstructive symptoms (hesitancy, weak stream, straining, incomplete emptying, dribbling) and irritative ones (frequency, urgency, nocturia). Alpha‑1 blockers such as tamsulosin relax the bladder neck and work within days — teach to take at bedtime and rise slowly because of orthostatic hypotension, and to tell any eye surgeon about the drug because of intraoperative floppy iris syndrome. 5‑alpha reductase inhibitors such as finasteride shrink the gland but take up to six months to work, lower PSA by roughly half (so the laboratory must know), and must not be handled by anyone who is or may become pregnant because of teratogenicity. After transurethral resection of the prostate, expect continuous bladder irrigation; keep the outflow pink to light red, increase the irrigation rate if it darkens or clots appear, and remember to subtract irrigant from output when charting.

Acute urinary retention presents as suprapubic pain and distension with an inability to void, and in the older adult sometimes as agitation alone. It is also produced by drugs: anticholinergics, antihistamines, opioids, tricyclics and some decongestants. Confirm with a bladder scanner before catheterising — that is the assessment step students most often skip. A post‑void residual above roughly 150 to 200 mL is abnormal. Older teaching directed clamping the catheter after 500 to 1000 mL; current evidence supports complete drainage in most adults, so follow your facility policy, and in either case monitor for post‑obstructive diuresis, hypotension and electrolyte loss afterward.

Incontinence is not a normal part of aging and is worth naming precisely, because the treatment differs. Stress incontinence leaks with cough, laugh or lift and responds to pelvic floor (Kegel) exercises and weight loss. Urge incontinence is a sudden overwhelming need from detrusor overactivity, treated with bladder training and timed voiding, then a beta‑3 agonist (mirabegron — monitor blood pressure) or an antimuscarinic such as oxybutynin, which is best avoided in older adults because of dry mouth, constipation, retention and confusion. Overflow incontinence is constant dribbling from a chronically full bladder, usually obstruction or a neurogenic bladder, and is managed by relieving the obstruction or by intermittent catheterisation. Functional incontinence means the urinary tract works but the patient cannot reach the toilet — the intervention is a bedside commode, a call light within reach, accessible clothing and scheduled toileting, not a catheter.

Finally, one symptom deserves its own alarm. Painless gross hematuria is bladder cancer until proven otherwise, particularly in a smoker over 50. It is often intermittent, so patients dismiss it when it stops. Diagnosis is by cystoscopy with biopsy. Superficial disease is treated by transurethral resection with intravesical therapy such as BCG; teach patients to sit to void for six hours after instillation, to add bleach to the toilet and let it stand, and to wash hands thoroughly. Patients with a urinary diversion or ileal conduit need stoma teaching, expectation that mucus in the urine is normal, and lifelong follow‑up.

Words worth knowing

Shock, Trauma and Emergency Care

Every disorder in the preceding thirteen chapters can end in the same place: cells that are not getting enough oxygen to make enough ATP. That is shock, and it does not care whether the insult began in the heart, the gut, the bloodstream or the roadway. What makes shock frightening to a new graduate is that the patient often looks acceptable right up until the moment they do not — because the young, healthy body compensates brilliantly and then fails all at once. What makes it learnable is that the compensations are predictable, the haemodynamic fingerprints of each shock type are distinct, and the interventions are protocolised. This chapter teaches the common pathway and the four stages, then the low-flow shocks, then the distributive shocks and the sepsis Hour-1 bundle, then the trauma primary and secondary survey, and finally the triage and resuscitation logic that governs an emergency department or a rapid response call on your floor. Learn the mechanism and the manifestations follow.

Section 1Shock: One Common Pathway, Four Stages

The cellular event that defines shock

Shock is inadequate tissue perfusion relative to metabolic demand. The blood pressure is a downstream number; the actual event is that a cell somewhere is not receiving enough oxygen to run oxidative phosphorylation. When mitochondria cannot use oxygen as the terminal electron acceptor, the cell switches to anaerobic glycolysis, which yields two molecules of ATP per glucose instead of roughly thirty-two. Lactate accumulates as the by-product. That is why serum lactate is the single most useful laboratory marker of shock, and why a rising lactate in a patient whose blood pressure looks fine should worry you more than a normal lactate in a patient who is hypotensive.

With ATP scarce, the sodium-potassium ATPase pump fails. Sodium and water move into the cell, the cell swells, the lysosomal membranes leak, and calcium floods the cytosol. Cell membranes lose integrity and intracellular contents spill into the interstitium, which drives capillary leak, interstitial oedema and further impairment of oxygen diffusion. This is why shock is self-perpetuating: the tissue damage caused by hypoperfusion worsens the hypoperfusion. Every hour of untreated shock makes the next hour harder, which is the entire justification for time-based bundles.

Oxygen delivery to the tissues is the product of cardiac output and arterial oxygen content. Cardiac output is heart rate times stroke volume, and stroke volume depends on preload, afterload and contractility. Arterial oxygen content depends overwhelmingly on haemoglobin and its saturation. Any shock state is a failure of one of those terms: not enough volume returning (preload), not enough pump (contractility), not enough vessel tone or too much (afterload and maldistribution), or not enough haemoglobin to carry the oxygen. Once you can name which term has failed, the treatment is nearly self-evident.

The four stages, read off the patient

In the initial stage, cardiac output has fallen, cells have gone anaerobic, and lactate has begun to rise, but there are no reliable clinical signs. The vital signs are normal. You detect this stage only by a laboratory value or by knowing the mechanism — the patient who has just vomited two litres of blood is in shock whether or not the monitor agrees.

The compensatory stage is where nursing assessment earns its keep. Baroreceptors in the carotid sinus and aortic arch sense the fall in mean arterial pressure and unleash the sympathetic nervous system. Heart rate and contractility rise. Peripheral arterioles constrict, shunting blood from skin, gut and kidney to heart and brain. The renin-angiotensin-aldosterone system and antidiuretic hormone conserve sodium and water. The result is a patient with a normal or even elevated blood pressure, a narrowed pulse pressure (the diastolic rises as vasoconstriction increases), tachycardia, cool and clammy skin, delayed capillary refill, a urine output falling below 0.5 mL/kg/hr, hypoactive bowel sounds and — the finding students consistently undervalue — restlessness, anxiety or confusion from cerebral hypoxia. Hyperventilation blows off carbon dioxide and produces an early respiratory alkalosis. In the compensatory stage the patient is fully salvageable, and this is where the diagnosis should be made.

In the progressive stage, compensation is exhausted. The mean arterial pressure falls below the level that autoregulates cerebral and coronary flow. Prolonged vasoconstriction has ischaemised the capillary beds; the precapillary sphincters relax while the postcapillary ones remain constricted, so fluid pools and leaks into the interstitium. Lactic acidosis overtakes the earlier respiratory alkalosis. Organs begin to declare themselves: crackles and hypoxaemia as acute respiratory distress syndrome develops, oliguria progressing to anuria with a rising creatinine, ileus and possible translocation of gut bacteria, hepatic dysfunction with rising bilirubin and ammonia, and disseminated intravascular coagulation with simultaneous bleeding and clotting. The patient becomes lethargic. This stage requires intensive care.

The refractory or irreversible stage is defined by unresponsiveness — the blood pressure no longer responds to escalating vasopressors and fluids, multiple organ dysfunction syndrome is established, and mortality approaches certainty. Recognising this stage matters clinically for goals-of-care conversations, not for further escalation.

The haemodynamic fingerprints

There are four functional categories of shock, and they are separated by three questions: is there enough volume in the tank (preload), is the pump working (cardiac output), and are the pipes appropriately constricted (systemic vascular resistance)? Central venous pressure of 2 to 8 mmHg and pulmonary artery wedge pressure of 6 to 12 mmHg estimate preload. Cardiac output of 4 to 8 L/min and cardiac index of 2.5 to 4.0 L/min/m² describe the pump. Systemic vascular resistance of 800 to 1200 dynes·s·cm⁻⁵ describes the pipes. Mixed venous oxygen saturation of 60 to 80 percent (or central venous saturation around 70 percent) tells you how much oxygen the tissues are extracting.

Three of the four categories look alike at the bedside — cold, clamped-down, tachycardic — because the body compensates for low flow the same way regardless of cause. Distributive shock is the odd one out: the problem is vasodilatation, so the patient may be warm, flushed and bounding early on, with a high cardiac output and a paradoxically high venous oxygen saturation because the cells cannot extract the oxygen being delivered. If you remember only one distinction, remember warm versus cold.

General principles that apply to every shock state

Regardless of type, the goals are the same: restore oxygen delivery, support the failing organ systems and treat the cause. Give supplemental oxygen and secure the airway if the patient cannot protect it or cannot maintain oxygenation. Establish two large-bore intravenous lines — 18 gauge or wider, and 16 gauge or wider in trauma, remembering that a lower gauge number means a wider catheter — because flow through a catheter increases with the fourth power of the radius and falls with length; a short fat peripheral line delivers volume faster than a long central line. Position the patient supine with legs elevated only if it does not compromise breathing; the old Trendelenburg position is no longer recommended because it impairs diaphragmatic excursion and does not reliably improve cardiac output.

The mean arterial pressure target for most adults is at least 65 mmHg, calculated as the systolic plus twice the diastolic, divided by three. Track urine output hourly — below 0.5 mL/kg/hr (roughly 30 mL/hr in an average adult) is renal hypoperfusion until proven otherwise. Trend lactate: a lactate that clears by 10 to 20 percent over the first several hours of resuscitation predicts survival better than any single blood pressure reading. Keep the patient warm, because hypothermia impairs coagulation and shifts the oxyhaemoglobin curve. And treat pain and anxiety, but with the smallest effective doses, because sedatives and opioids blunt the very sympathetic tone that is holding the pressure up.

Section 2Hypovolaemic, Cardiogenic and Obstructive Shock

Hypovolaemic shock: not enough in the tank

Hypovolaemic shock follows loss of intravascular volume, either as whole blood (haemorrhagic) or as plasma and water (non-haemorrhagic: vomiting, diarrhoea, diuresis in diabetic ketoacidosis, burns, third spacing in pancreatitis or bowel obstruction). Roughly 15 percent of circulating volume can be lost with minimal signs. Beyond that, the sympathetic response becomes visible, and the ATLS haemorrhage classes give a useful mental model, provided you remember that they are a teaching framework rather than a bedside calculator and that older adults, athletes, pregnant patients and anyone on a beta-blocker will violate them.

Diagnostics are less about confirming shock than about finding the bleeding. An initial haemoglobin and haematocrit are often deceptively normal in acute haemorrhage because the patient loses whole blood — the concentration does not change until dilution occurs, so a normal haemoglobin of 14 to 18 g/dL in a man or 12 to 16 g/dL in a woman never excludes major bleeding. More useful are the lactate (normal under 2 mmol/L) and the base deficit from an arterial blood gas: a base deficit worse than negative 6 mEq/L signals significant tissue hypoperfusion. Type and crossmatch immediately. A focused assessment with sonography for trauma (FAST) finds free fluid in the abdomen or pericardium in minutes; computed tomography is for the patient stable enough to travel.

Management is control the source and replace the volume. Warmed isotonic crystalloid — balanced solutions such as lactated Ringer’s are preferred over large volumes of 0.9 percent sodium chloride, which produces a hyperchloraemic metabolic acidosis — is given as an initial bolus of about one litre in adults, but the patient who does not respond, or who responds and then deteriorates, needs blood, not more saline. Transfuse packed red blood cells with fresh frozen plasma and platelets in a balanced ratio approaching 1:1:1 under a massive transfusion protocol. Give tranexamic acid within three hours of traumatic injury — 1 g intravenously over 10 minutes followed by 1 g over 8 hours — because after three hours it may increase harm. In penetrating trauma without head injury, permissive hypotension (a systolic around 80 to 90 mmHg) until surgical control is deliberate, since raising the pressure pops fresh clot. That rule reverses in traumatic brain injury, where a single episode of hypotension doubles mortality and systolic pressure should be kept at or above 100 to 110 mmHg.

Nursing priorities: two large-bore lines and a fluid warmer, blood products through a filtered set with normal saline only (never lactated Ringer’s in the same line as blood, and never dextrose), vital signs every 5 to 15 minutes, hourly urine output, continuous cardiac monitoring for the hypocalcaemia and hyperkalaemia of massive transfusion, and active warming. Watch the ionised calcium: citrate in banked blood chelates calcium, and an ionised calcium below 4.5 mg/dL prolongs coagulation and depresses contractility.

Cardiogenic shock: the pump has failed

Cardiogenic shock is the failure of the heart to eject enough blood despite adequate filling. The commonest cause is extensive anterior myocardial infarction with loss of more than 40 percent of the left ventricle, but it also follows acute valvular rupture, ventricular septal rupture, myocarditis, end-stage cardiomyopathy, drug toxicity and sustained dysrhythmia. Physiologically it is a vicious circle: reduced cardiac output lowers coronary perfusion pressure, which worsens myocardial ischaemia, which further reduces output. Diagnostic criteria are a systolic pressure under 90 mmHg for at least 30 minutes or the need for support to maintain it, a cardiac index under 2.2 L/min/m², and a pulmonary artery wedge pressure above 15 mmHg.

The findings are those of forward failure plus backward congestion: cool mottled extremities, weak thready pulses, altered mentation, oliguria, and simultaneously jugular venous distension, an S3 gallop, bilateral crackles and frothy pink sputum. Troponin I is elevated (normal under 0.04 ng/mL), B-type natriuretic peptide is high, the electrocardiogram shows the infarct, and the echocardiogram gives you the ejection fraction and the mechanical complication. Chest radiograph shows pulmonary oedema.

Management is emergent revascularisation — percutaneous coronary intervention is the definitive therapy and door-to-balloon time drives survival. Pharmacologically, the balance is delicate. Inotropes such as dobutamine (a beta-1 agonist, 2 to 20 mcg/kg/min) increase contractility but also myocardial oxygen demand and can cause tachydysrhythmias and hypotension through beta-2 vasodilatation. Milrinone, a phosphodiesterase-3 inhibitor, is an inodilator that is renally cleared and accumulates in kidney injury. Norepinephrine is the preferred vasopressor because it raises coronary perfusion pressure with fewer dysrhythmias than dopamine. Diuretics reduce preload only once perfusion is adequate. Mechanical circulatory support — intra-aortic balloon pump or a percutaneous ventricular assist device — bridges the patient to revascularisation or recovery.

The nursing trap in cardiogenic shock is the fluid bolus. A hypotensive patient triggers the reflex to hang fluid, but this ventricle is already overfilled; a bolus will produce flash pulmonary oedema. Assess for crackles, jugular venous distension and an S3 before giving volume to any hypotensive patient. Keep the head of the bed elevated, cluster care to reduce myocardial oxygen demand, monitor titrated drips through a central line with a dedicated lumen, and check the balloon pump insertion site limb for pulse, colour, temperature and sensation every hour.

Obstructive shock: a mechanical block

In obstructive shock, the heart and the volume are adequate but something physically impedes filling or ejection. Three diagnoses matter most, and all three are fixed by relieving the obstruction — a needle, a tube, a drain or clot-dissolving therapy — never by another fluid bolus.

Cardiac tamponade is blood or fluid in the pericardial sac compressing the ventricles. Beck’s triad is hypotension, jugular venous distension and muffled heart sounds; add pulsus paradoxus (a fall in systolic pressure of more than 10 mmHg on inspiration), a narrow pulse pressure and electrical alternans on the electrocardiogram. Bedside echocardiography confirms it. Treatment is pericardiocentesis or a surgical pericardial window. Tension pneumothorax is air trapped under pressure that collapses the lung and shifts the mediastinum, kinking the great vessels. Findings are absent breath sounds and hyperresonance on the affected side, tracheal deviation away from the affected side (a late sign), jugular venous distension, severe respiratory distress and hypotension. This is a clinical diagnosis — do not wait for a radiograph. Treatment is immediate needle decompression with a large-bore catheter in the fifth intercostal space just anterior to the midaxillary line (or the traditional second intercostal space at the midclavicular line), followed by chest tube thoracostomy. Massive pulmonary embolism obstructs the pulmonary arterial circulation, so right ventricular afterload rises abruptly, the right ventricle dilates and fails, and left ventricular filling collapses — producing sudden dyspnoea, pleuritic chest pain, hypoxaemia, jugular venous distension and right heart strain; management is systemic thrombolysis or catheter-directed therapy plus anticoagulation.

Section 3Distributive Shock: Sepsis, Anaphylaxis and Neurogenic Injury

Sepsis and septic shock

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. The insult is usually a bacterial cell wall component — endotoxin from gram-negative organisms, peptidoglycan from gram-positive — that triggers a massive release of inflammatory mediators including tumour necrosis factor, interleukin-1 and nitric oxide. Nitric oxide causes profound arteriolar vasodilatation, which drops systemic vascular resistance. Endothelial injury causes capillary leak, so intravascular volume moves into the interstitium and the patient becomes relatively hypovolaemic despite total body fluid overload. Simultaneously the coagulation cascade activates, generating microthrombi that plug capillaries, while consumption of clotting factors produces bleeding — disseminated intravascular coagulation. Mitochondrial dysfunction means the cells cannot use the oxygen even where it arrives, which is why the mixed venous oxygen saturation runs high.

Septic shock is the subset of sepsis in which circulatory and cellular abnormalities are profound enough to substantially increase mortality: clinically, a patient who requires vasopressors to maintain a mean arterial pressure of at least 65 mmHg and has a serum lactate above 2 mmol/L despite adequate fluid resuscitation. Hospital mortality exceeds 40 percent.

Early findings are the warm phase: fever above 38.3°C or hypothermia below 36°C, tachycardia, tachypnoea, warm flushed skin, bounding pulses, a widened pulse pressure and confusion. Late findings are the cold phase, indistinguishable from other shock. Screen with an early warning score, and remember that new confusion, a respiratory rate of 22 or higher, or a systolic pressure of 100 mmHg or less in a patient with suspected infection is a red flag. Laboratory findings include a white cell count above 12,000/mm³ or below 4000/mm³ or more than 10 percent immature bands (normal 5000 to 10,000/mm³), a procalcitonin above 0.5 ng/mL, a platelet count falling below 150,000/mm³, a rising creatinine above 0.6 to 1.2 mg/dL baseline, a bilirubin above 1.2 mg/dL, an INR above 1.5 (normal 0.8 to 1.1) and a lactate above 2 mmol/L.