Assessing the Heart and Peripheral Vascular System

Cardiovascular disease is the leading cause of death in this country, and the nurse at the bedside is the person most likely to notice it turning. This chapter teaches the cardiac and peripheral vascular exam the way it is actually performed: where the valve areas sit on the chest wall, how to find the apical impulse with your fingertips, how to tell a jugular pulsation from a carotid one, when to use the bell and when the diaphragm, and how to grade a pulse, an edema and a murmur so the next nurse can tell whether the patient improved. You will learn the four-step order — inspection, palpation, percussion, auscultation — and the single exception to it. You will learn the real numbers: heart rate and blood pressure across the lifespan, capillary refill, ankle-brachial index, the size and location of a normal apical impulse. And you will learn which findings do not wait for morning rounds, because a cold pulseless foot and a new S3 in a patient gaining weight are both clocks that have already started.

Section 1The Pump, the Cycle and the Cardiac Baseline

Chambers, valves and the direction of flow

The heart sits in the mediastinum behind the sternum, roughly two thirds of it to the left of the midline, with its broad base up under the second intercostal spaces and its pointed apex down and to the left at about the fifth intercostal space. That orientation is upside down from how students first picture it, and it matters: the valves closest to the base are the ones you hear best at the top of the chest, and the apex — the tip of the left ventricle — is what taps your fingers low on the left chest wall.

Deoxygenated blood returns from the body through the superior and inferior vena cava into the right atrium, crosses the tricuspid valve into the right ventricle, and is pumped through the pulmonic valve into the pulmonary artery and on to the lungs. Oxygenated blood returns through the four pulmonary veins into the left atrium, crosses the mitral valve into the left ventricle, and is ejected through the aortic valve into the aorta. The tricuspid and mitral valves are the atrioventricular valves; the pulmonic and aortic are the semilunar valves. The left ventricle does the systemic work and is therefore the thickest chamber, which is why it is the chamber you can feel and the chamber that hypertrophies under a lifetime of high blood pressure.

The heart is wrapped in the pericardium, a two-layered sac with a thin film of fluid between the layers. When those layers inflame they scrape against each other and produce a friction rub; when fluid accumulates rapidly between them the ventricles cannot fill, which is cardiac tamponade. The coronary arteries branch off the aorta immediately above the aortic valve and fill during diastole, not systole, which is why a very fast heart rate — by shortening diastole — worsens myocardial ischemia even when nothing else changes.

The cardiac cycle and what makes the sounds

Systole is ventricular contraction and ejection; diastole is ventricular relaxation and filling. Diastole is normally the longer of the two at rest, occupying roughly two thirds of the cycle. The heart sounds are not made by valves opening — opening is silent — but by the abrupt deceleration of blood and the vibration of structures when valves close.

S1, the “lub,” is closure of the mitral and tricuspid valves and marks the beginning of systole. It is lower pitched, slightly longer, and loudest at the apex. S2, the “dub,” is closure of the aortic and pulmonic valves and marks the end of systole. It is higher pitched, shorter, and loudest at the base. The interval between S1 and S2 is systole; the longer interval between S2 and the next S1 is diastole. If you cannot tell which sound is which — and at a rate over about 120 you often cannot — palpate the carotid pulse while you listen: the carotid upstroke coincides with S1.

Two more facts turn this into usable clinical information. First, S2 normally splits during inspiration, because negative intrathoracic pressure increases venous return to the right heart, prolongs right ventricular ejection and delays pulmonic closure behind aortic closure. Physiologic splitting is heard best at the second left intercostal space, appears on inspiration and vanishes on expiration, and is a normal finding, most obvious in children and thin young adults. Splitting that persists through expiration, or that widens on expiration, is not normal. Second, the atria contribute a final “atrial kick” of about 20 to 30 percent of ventricular filling at the very end of diastole. When the atria fibrillate, that kick disappears — which is why patients who go into atrial fibrillation often drop their blood pressure, and why an S4, which is generated by atrial contraction, can never exist in atrial fibrillation.

Precordial landmarks and the auscultatory areas

The five listening areas are not directly over their valves. They are the spots on the chest wall where blood flow carries each valve’s sound most clearly, so you must learn them as surface locations, counted from the sternal angle (angle of Louis) exactly as you learned to count ribs in the chest exam.

A common mnemonic runs All People Enjoy Time Magazine — aortic, pulmonic, Erb’s, tricuspid, mitral — and it tracks the standard base-to-apex sequence. Move in that order or its reverse, but move in an order and use the same one every time. Do not skip from spot to spot; slide the stethoscope in small steps so you do not miss a murmur that lives between two named areas.

The cardiac baseline: rate, rhythm and pressure

The apical pulse is auscultated at the mitral area with the diaphragm and counted for a full 60 seconds whenever the rhythm is irregular, whenever the patient is an infant or young child, and before administering any medication with a heart-rate parameter. Digoxin is the classic example: hold the dose and notify the provider if the apical rate is under 60 in an adult, under 70 in a child or under 90 in an infant, and always follow the parameters actually written in the order.

A pulse deficit is the difference between the apical rate and the radial rate counted over the same minute. It is measured by two clinicians counting simultaneously, or by counting apical then radial back to back if only one nurse is available, and it means that some ventricular contractions are too weak to generate a peripheral pulse. A deficit is common in atrial fibrillation and with frequent premature ventricular contractions, and it is always the apical rate — never the radial — that is the true heart rate.

Pulse pressure is systolic minus diastolic and is normally about 30 to 40 mmHg, up to roughly 50. A narrow pulse pressure suggests reduced stroke volume — hypovolemia, heart failure, aortic stenosis, tamponade. A wide pulse pressure suggests stiff arteries in an older adult, or aortic regurgitation, thyrotoxicosis, anemia or fever. Cuff technique changes the number: the bladder width should be about 40 percent of the arm circumference and the bladder length about 80 percent, the arm must be supported at heart level, and the patient should sit quietly for five minutes with the back supported, feet flat on the floor, legs uncrossed, and should not talk during the measurement. An unsupported back raises the diastolic reading and crossed legs raise the systolic reading. A cuff that is too small or too loose reads falsely high; an arm held below heart level reads falsely high; an arm held above heart level reads falsely low.

Orthostatic vital signs are a cardiovascular test, not a courtesy. Measure blood pressure and heart rate after the patient has been supine at least five minutes, then repeat sitting and again standing at one minute and at three minutes. Orthostatic hypotension is a drop of 20 mmHg or more in systolic pressure, or 10 mmHg or more in diastolic pressure, within three minutes of standing; a compensatory rise in heart rate of 20 beats per minute or more is corroborating. Stay with the patient. If they become dizzy or pale, sit them down and abandon the test — you have your answer.

Section 2Inspecting and Palpating the Precordium and Neck Vessels

Setting up, and the order of the exam

The cardiovascular exam follows the same fixed sequence as the rest of the body: inspection, palpation, percussion, auscultation. The abdomen is the single exception — there you inspect, then auscultate, then percuss, then palpate, because pressing on the abdomen first alters bowel motility and produces falsely absent or falsely hyperactive bowel sounds. Nothing about the heart uses that modified order.

Position matters more here than anywhere else in the physical exam. Begin with the patient supine with the head of the bed at 30 to 45 degrees, chest exposed, room warm, and stand on the patient’s right side if you can. You will use two more positions later: the left lateral decubitus position, which rolls the apex of the heart toward the chest wall and brings out low-pitched apical sounds such as S3, S4 and the rumble of mitral stenosis; and sitting upright and leaning forward, which brings the base of the heart forward and brings out the soft early-diastolic murmur of aortic regurgitation and a pericardial friction rub. Tell the patient what you are doing and drape a female patient so that only the area being examined is uncovered; when breast tissue overlies the apex, ask the patient to lift the breast or displace it upward yourself with the back of your hand.

Inspection and palpation of the precordium

Inspect with tangential light across the chest so that movement casts a shadow. Look for the apical impulse, which is visible in roughly half of adults and in most thin patients and children, and for any other pulsation, lift or retraction. Note the chest wall itself: pectus excavatum can displace the heart, a median sternotomy scar tells you about prior surgery, and a firm rectangular bulge below the left clavicle is a pacemaker or defibrillator generator, which should be documented along with the site’s appearance.

Now palpate. Use the finger pads for pulsations and the ball of the hand at the base of the fingers for the low-frequency buzzing of a thrill. Palpate systematically at the apex, the left lower sternal border, the left and right second intercostal spaces and the epigastrium. The point of maximal impulse, or PMI, is the apical impulse and normally sits at the fifth intercostal space at or just medial to the left midclavicular line. It is small — about 1 to 2 cm across, no more than the size of a quarter, roughly one interspace — it is a brief gentle tap occupying the first half of systole, and it is easiest to feel with the patient rolled to the left side or in full expiration. If you cannot find it, that alone is not abnormal: obesity, a muscular chest wall, emphysema and large breasts all conceal it.

Percussion of the heart is the third step in the sequence, and honesty is owed to students here: it is now rarely performed and has largely been replaced by chest radiography and echocardiography, because percussing the left cardiac border is imprecise and unreliable. It is still taught, and if you perform it you percuss from resonance in the left anterior axillary line medially toward the sternum at the third, fourth and fifth interspaces, listening for the change to dullness, which normally occurs at or medial to the midclavicular line. Cardiac dullness extending well past the midclavicular line suggests cardiac enlargement. Chart what you did and did not perform; do not chart a percussion you skipped.

The neck vessels: carotids and jugular venous pressure

The carotid arteries and internal jugular veins are the two windows onto the heart that sit outside the chest. Assess the carotid arteries one at a time, never both simultaneously — simultaneous compression can reduce cerebral perfusion, and pressure over the carotid sinus can trigger a reflex bradycardia or even asystole in a susceptible patient. Palpate low in the neck, medial to the sternocleidomastoid, below the level of the thyroid cartilage, using light pressure. The normal carotid upstroke is brisk, smooth and symmetric, graded 2+, and it coincides with S1. A weak, slow-rising and delayed upstroke suggests aortic stenosis; a bounding upstroke suggests aortic regurgitation, fever, anemia or hyperthyroidism.

Auscultate the carotids before you palpate them in any patient over about 50, or with known atherosclerosis, hypertension, diabetes, or a history of stroke or transient ischemic attack. Place the bell lightly over each carotid at the angle of the jaw, at the midcervical level and at the base of the neck, and ask the patient to hold their breath briefly so tracheal sounds do not mask what you are listening for. A bruit is a blowing, swishing sound of turbulent flow and requires reporting. Be aware that a bruit does not reliably indicate the degree of stenosis: a tightly narrowed artery may be silent because so little blood is moving through it.

Jugular venous pressure is a direct bedside estimate of right atrial filling pressure and volume status, and it is one of the most useful skills in this chapter. Position the patient at 30 to 45 degrees, turn the head slightly away from the side you are examining, and use tangential lighting. Look for the flickering pulsation of the internal jugular between the two heads of the sternocleidomastoid. Identify the highest point at which the pulsation is visible, then measure the vertical distance in centimeters from that point up from the horizontal plane of the sternal angle. Normal is 3 cm or less above the sternal angle; because the sternal angle sits about 5 cm above the right atrium in any position, that corresponds to a central venous pressure of roughly 8 cm of water or less. A jugular pulsation visible with the patient sitting fully upright at 90 degrees is markedly elevated.

Elevated jugular venous pressure, commonly charted as jugular venous distention, means the right side of the heart cannot handle its returning volume: right-sided heart failure, fluid overload, tricuspid regurgitation, pulmonary hypertension, cardiac tamponade, constrictive pericarditis or tension pneumothorax. Flat neck veins in a patient lying supine suggest the opposite — hypovolemia. Hepatojugular reflux refines the finding: with the patient at 30 to 45 degrees and breathing normally through an open mouth, press firmly over the right upper quadrant for 10 to 15 seconds. A sustained rise in jugular pressure of more than 3 cm that persists throughout the pressure suggests the right ventricle cannot accommodate additional volume. Stop if the patient reports pain.

Section 3Auscultating the Heart: Normal Sounds, Extra Sounds and Murmurs

Technique: bell, diaphragm, position and sequence

Auscultate on bare skin in a quiet room. Clothing and gowns generate rustling that beginners mistake for murmurs and rubs. Warm the endpiece. Then use both sides of the stethoscope deliberately, because they filter different frequencies: the diaphragm, pressed firmly enough to leave a light ring, transmits high-pitched sounds — S1, S2, most murmurs, and friction rubs. The bell, applied lightly enough that it barely dimples the skin, transmits low-pitched sounds — S3, S4 and the diastolic rumble of mitral stenosis. Pressing the bell firmly stretches the skin beneath it into a diaphragm and eliminates exactly the sounds you were trying to hear, which is why so many students never hear an S3.

Go through all five areas with the diaphragm first, then repeat all five with the bell. At every site, listen for one thing at a time rather than trying to hear everything at once. Identify S1, then S2, then the systolic interval between them, then diastole, and only then listen for extra sounds. Note the rate and the rhythm: regular, regularly irregular (a repeating pattern, as in bigeminy or second-degree block) or irregularly irregular (no pattern at all, the hallmark of atrial fibrillation).

Finally, use the two special positions. Roll the patient into the left lateral decubitus position and listen at the apex with the bell — this is where S3, S4 and mitral stenosis appear. Then sit the patient up, ask them to lean forward and exhale fully and hold, and listen along the left sternal border and at the base with the diaphragm — this is where aortic regurgitation and a pericardial friction rub appear. Skipping these two maneuvers is why soft diastolic murmurs get missed on the unit and found in the cath lab.

S1, S2 and normal variation

At the apex, S1 is louder than S2; at the base, S2 is louder than S1. Both should be crisp. Muffled or distant heart sounds occur with obesity, emphysema, a thick chest wall, and — urgently — with pericardial effusion and cardiac tamponade, where muffled sounds join hypotension and jugular distention to form Beck’s triad. An accentuated S1 occurs with tachycardia, fever, anemia, exercise and mitral stenosis; a diminished S1 occurs with first-degree heart block and with mitral regurgitation. Variable S1 intensity from beat to beat is a clue to atrial fibrillation or complete heart block, because the relationship between atrial and ventricular contraction keeps changing.

Physiologic splitting of S2, described earlier, is normal when it appears on inspiration and disappears on expiration at the pulmonic area. Persistent splitting through both phases, fixed splitting that never varies with respiration (classically atrial septal defect) and paradoxical splitting that appears on expiration and disappears on inspiration (left bundle branch block, severe aortic stenosis) are all abnormal and reportable. A nurse is not expected to name the lesion; a nurse is expected to notice that the second sound is doing something it should not and to describe it accurately.

S3, S4, and the other extra sounds

Learn the two gallops by their rhythm, not by their pitch, because a low-pitched sound is hard for a beginner to isolate but a three-beat cadence is not. If the extra beat falls after the “dub” you have S3; if it falls before the “lub” you have S4. Say the mnemonics aloud in your head while you listen. And note the age rule carefully in both directions: an S3 in a 22-year-old athlete or a pregnant patient at 32 weeks may be entirely physiologic, and an S3 in a 68-year-old who has gained four pounds since yesterday is a phone call.

Murmurs: grading them and describing them

A murmur is the sound of turbulent flow — blood forced through a narrowed valve, leaking backward through an incompetent one, moving through an abnormal opening, or simply moving fast through a normal heart. Intensity is graded on the six-point Levine scale, and the grade is always written as a fraction so the reader knows which scale you used: II/VI, not “grade 2.”

Grade IV and above always includes a thrill, so palpation and auscultation cross-check each other: if you graded a murmur IV/VI you should be able to feel it, and if you can feel it, it is at least IV/VI. Beyond intensity, describe six more attributes: timing (systolic or diastolic, and where within the phase), location of maximum intensity, radiation, pitch (high, medium, low), quality (blowing, harsh, rumbling, musical) and what changes it (position, respiration, exercise). A single clinical rule is worth memorizing: most systolic murmurs may be benign, but a diastolic murmur is never innocent and always requires evaluation.

Section 4The Peripheral Vascular Exam

Arteries: pulses, perfusion and the numbers that go with them

Palpate each pulse with the pads of two or three fingers — never the thumb, which has its own pulse strong enough to fool you — using light pressure that you increase only until you feel the maximum impulse. Assess rate, rhythm, amplitude, contour and symmetry, and always compare the two sides. The sites are temporal, carotid, brachial, radial, ulnar, femoral, popliteal, dorsalis pedis and posterior tibial. In infants, use the brachial pulse for the pulse check, not the carotid, and use the femoral to screen for coarctation of the aorta: a femoral pulse that is weaker than the brachial, or delayed behind it, is a classic sign.

Facilities differ: some use a 0 to 3+ scale in which 3+ means bounding. Chart with the scale your facility uses and state it, and describe rather than rely on the number alone. When a pulse is not palpable, obtain a Doppler ultrasound probe and document explicitly: “right dorsalis pedis not palpable, present by Doppler” is a materially different finding from “absent by Doppler.” Mark the location of a Doppler-only pulse with a skin pen so the next nurse finds the same spot.

Two anatomic facts prevent unnecessary alarm and unnecessary reassurance. The dorsalis pedis pulse is congenitally absent or anatomically variant in roughly 2 to 10 percent of healthy people, so an isolated absent dorsalis pedis with a strong posterior tibial and warm pink foot is usually benign. The posterior tibial is rarely absent in healthy adults, and both pedal pulses absent in the same foot is abnormal until proven otherwise.

Capillary refill is assessed by compressing a nail bed until it blanches, holding for about five seconds, releasing and counting until color returns, with the hand or foot held at the level of the heart. Normal is under 2 seconds in children and adults; up to 3 seconds is generally accepted in neonates and in a cold room. Prolonged refill suggests poor perfusion, shock, hypothermia or peripheral arterial disease, and it is a soft sign in older adults with chronically thickened nails. The ankle-brachial index (ABI) is the systolic pressure at the ankle divided by the higher of the two brachial systolic pressures, measured with a Doppler: 1.00 to 1.40 is normal, 0.91 to 0.99 is borderline, 0.90 or less indicates peripheral arterial disease, under 0.40 indicates severe disease with a risk of critical limb ischemia, and a value above 1.40 means the vessels are calcified and non-compressible — a falsely reassuring high number seen in long-standing diabetes and renal disease.

The modified Allen test checks ulnar collateral flow before radial artery puncture or cannulation. Have the patient make a tight fist while you occlude both the radial and ulnar arteries, then have them open the hand, which will look pale. Release the ulnar artery only and watch. Color should return to the entire palm within about 5 to 7 seconds; return taking longer than 15 seconds is abnormal and the radial artery on that side should not be used.

Veins, edema and the two kinds of insufficiency

Inspect the legs with the patient both lying and standing. Note varicosities, which are dilated tortuous superficial veins made obvious by standing; note color, hair distribution, nail thickness, temperature compared side to side using the back of your hand, and any ulceration with its exact location, size in centimeters, border and wound-bed appearance. Measure calf circumference at a marked, reproducible point — conventionally 10 cm below the tibial tuberosity — and record the measurement so the next nurse measures the same place. A difference of more than 3 cm between the calves is one of the criteria used in deep vein thrombosis scoring.

Assess pitting edema by pressing firmly with your thumb for at least five seconds over a bony prominence — the dorsum of the foot, behind the medial malleolus, or over the tibia — then removing your thumb and observing the depth and rebound. In a patient on bed rest, also press over the sacrum, because dependent edema follows gravity and will collect there rather than in the feet.

Edema-grading scales vary between textbooks and facilities, which makes the number alone a weak communication tool. Strengthen it by charting depth in millimeters, the anatomic level to which the edema extends, whether it pits, whether it is unilateral or bilateral, and the rebound time. Non-pitting edema that feels firm or woody is a different problem — lymphedema, chronic venous change or myxedema — and should be described as such rather than forced onto a pitting scale. Daily weight is the most sensitive fluid measure you have: measure at the same time each morning, after voiding, in the same clothing, on the same scale. Each kilogram of gain represents roughly a liter of retained fluid, so a gain of about 1 kilogram, or 2 pounds, in 24 hours or about 2.3 kilograms, 5 pounds, in a week is a reportable threshold in heart failure.

The vascular emergencies

Acute arterial occlusion is memorized as the six Ps: Pain (sudden and severe), Pallor, Pulselessness, Paresthesia, Paralysis and Poikilothermia (the limb takes on room temperature, feeling cold). Pain and pulselessness come first; paresthesia and paralysis are late and signal nerve and muscle death. Pallor is the least reliable of the six in richly pigmented skin — compare the sole, palm and nail beds against the opposite limb, and weigh sudden pain, absent pulses, coolness and numbness far more heavily than color. The limb is generally salvageable for only about six hours, so this is a call-now finding, not an end-of-shift note. The same six Ps drive neurovascular checks after orthopedic surgery, casting or trauma, where they also warn of compartment syndrome — in which the earliest and most reliable sign is pain out of proportion to the injury and pain on passive stretch of the muscle, appearing well before any pulse disappears. A cast that feels tight and a patient asking for more analgesia than the injury explains is an emergency assessment, not a medication question.

Deep vein thrombosis presents as unilateral calf or thigh swelling, warmth, erythema or a dusky discoloration, tenderness along the deep venous course, and sometimes a low-grade fever. Measure and compare calf circumferences and document both numbers. Do not perform Homans sign. Dorsiflexing the foot to elicit calf pain has poor sensitivity and poor specificity, is positive in many patients without thrombosis and negative in many with it, and offers no benefit that justifies manipulating a possibly clotted limb. Assess instead for the constellation of findings, escalate for imaging, and watch for the complication that actually kills: sudden dyspnea, pleuritic chest pain, tachycardia and hypoxemia signaling pulmonary embolism.

Section 5Red Flags, Lifespan Variation, Documentation and Escalation

Findings that mean escalate now

Chest pain is assessed with a structured tool — OPQRST: onset, provocation and palliation, quality, region and radiation, severity on a 0 to 10 scale, and timing. But do not let the absence of classic chest pain reassure you. Women, older adults and people with diabetes frequently present with no chest pain at all: unexplained fatigue, dyspnea, nausea, indigestion, diaphoresis, back, jaw or shoulder discomfort, or simply new confusion may be the entire presentation of an acute coronary syndrome. Diabetic neuropathy blunts the pain signal, and a silent infarction is still an infarction.

Lifespan and skin-tone variation

Infants and children. The apical impulse sits higher and more laterally the younger the child: in an infant and toddler it is at the fourth intercostal space slightly lateral to the midclavicular line, from about age four to six it is at the fourth space at the midclavicular line, and by roughly age seven it has descended to the adult position at the fifth space at or just medial to the midclavicular line. Sinus arrhythmia — heart rate accelerating with inspiration and slowing with expiration — is a normal, healthy finding in children and young adults. Count apically for a full minute. Innocent murmurs are extremely common in childhood; the reassuring features are grade I to II, systolic only, no radiation, marked change with position, and a completely well child with normal growth. The alarming pediatric findings are a diastolic murmur, a murmur with a thrill, cyanosis — which in a darker-skinned infant will show as a gray or ashen tongue, oral mucosa and nail beds rather than a blue tint, so look in the mouth and not only at the skin — poor feeding, diaphoresis with feeds, failure to thrive, hepatomegaly and weak or delayed femoral pulses. Remember that in infants bradycardia is a hypoxia sign, and that in children hypotension is a very late sign of shock — prolonged capillary refill, cool mottled extremities, weak peripheral pulses and tachycardia come first.

Pregnancy. Blood volume rises 30 to 50 percent, cardiac output rises 30 to 50 percent, resting heart rate rises 10 to 20 beats per minute, and systemic vascular resistance falls so that diastolic pressure drops 10 to 15 mmHg in the second trimester before returning to baseline near term. The heart is displaced upward and to the left, so the apical impulse shifts up and laterally. A soft systolic ejection murmur and an S3 are found in most pregnancies and are physiologic. A diastolic murmur is not. From about 20 weeks, position the patient in a left lateral tilt rather than flat supine, because the gravid uterus compresses the inferior vena cava and can drop cardiac output sharply — supine hypotensive syndrome. Dependent edema of the feet and ankles is expected; sudden facial or hand edema with headache or visual change is preeclampsia until proven otherwise.

Older adults. Arteries stiffen, so systolic pressure and pulse pressure rise and isolated systolic hypertension is common. Ventricular compliance falls, so an S4 is a frequent and often benign finding while an S3 remains ominous. A soft systolic murmur from aortic sclerosis is very common. Baroreceptor reflexes blunt, making orthostatic hypotension and falls more likely, especially with diuretics, antihypertensives and after prolonged bed rest. Maximum heart rate and the ability to mount a tachycardia both decline, and a beta blocker will mask the tachycardia of hemorrhage or sepsis entirely — so a “normal” heart rate of 78 in a septic older adult on metoprolol is not reassurance. Peripheral pulses become harder to palpate as vessels calcify, and the presenting sign of a myocardial infarction may be confusion, a fall, weakness or dyspnea rather than pain.

Skin tone. Color changes central to cardiovascular assessment are unreliable when judged only on the outer skin of patients with richly pigmented skin. Assess the oral mucosa, tongue, lips, conjunctivae, palms, soles and nail beds, in natural or full-spectrum light. Central cyanosis appears as a gray or ashen cast to the lips, tongue and oral mucosa rather than a blue tint, and requires roughly 5 g/dL of deoxygenated hemoglobin — so it is a late sign in anyone and may never appear in a profoundly anemic patient. Pallor may present as ashen, gray or yellow-brown rather than white; check the conjunctivae and palmar creases. Erythema, as in cellulitis or phlebitis, may appear violaceous, deep brown or simply darker than surrounding skin, and is often easier to feel than to see — compare warmth, induration and tenderness against the opposite limb, and outline the border with a skin pen and time it so progression is measurable. Dependent rubor and hemosiderin staining are likewise subtler; rely on temperature, pulses, capillary refill and the pattern of hair loss. Finally, remember that pulse oximetry systematically overestimates arterial saturation in patients with darker skin pigmentation, producing occult hypoxemia; when the number looks acceptable but the patient looks unwell, believe the patient.

Charting the cardiovascular exam

Chart what you measured and observed, not what you concluded. Include rate and rhythm with the method used, the location and character of the apical impulse, the sounds at each area, the murmur description with its grade as a fraction, pulses with their grade and whether Doppler was needed, edema with depth and level, capillary refill, temperature and color of the extremities, jugular venous pressure with the head-of-bed angle, and the patient’s own words in quotation marks.

Delegation, scope and the SBAR call

Apply the five rights of delegation: right task, right circumstance, right person, right direction and communication, right supervision and evaluation. The registered nurse may delegate routine data collection on a stable patient, but never delegates assessment, interpretation, teaching, evaluation, or any aspect of care for an unstable or deteriorating patient. Delegating the task never transfers accountability for the outcome.

When a red flag appears, escalate with SBAR. Have the chart, the last two sets of vital signs, the medication list and the most recent laboratory values in front of you before you dial. A worked example: Situation — “This is Priya Raman, RN, on 6 East. I am calling about Mr. Whitfield in room 618, a 71-year-old admitted two days ago with a heart failure exacerbation. He has new orthopnea and his weight is up 1.4 kilograms since yesterday morning.” Background — “He has a history of ischemic cardiomyopathy with an ejection fraction of 30 percent, hypertension and chronic kidney disease. He is on furosemide 40 milligrams IV twice daily, metoprolol and lisinopril. Admission weight was 82.8 kilograms; this morning he is 84.2. Baseline blood pressure has been running around 118 over 70.” Assessment — “Apical rate 104 and regular, blood pressure 102 over 64, respirations 26, SpO2 91 percent on room air rising to 95 percent on 2 liters nasal cannula. He now has an S3 at the apex that was not there yesterday, jugular venous pressure 5 centimeters above the sternal angle at 45 degrees, bilateral pitting edema to mid-calf at 4 millimeters, and fine crackles at both bases that do not clear with cough. He needed three pillows last night instead of one. Urine output has been 20 milliliters an hour for the last four hours. Pedal pulses are 2 plus and both feet are warm.” Recommendation — “I think he is decompensating and I would like him seen now. I am requesting an additional diuretic dose, a basic metabolic panel and BNP, a chest x-ray, and an order for oxygen to keep his saturation above 92 percent. Do you want strict intake and output and a repeat weight this evening? Can you come to the bedside?” Then close the loop: read the orders back, document the time of the call and the response, and reassess after the intervention.

Words worth knowing