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