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Cardiac Physical Examination in the Cardiac Intensive Care Unit


Common Misconceptions

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    The physical examination in the Cardiac Intensive Care Unit (CICU) no longer contributes to achieving optimal patient outcomes in the era of ubiquitous laboratory testing and imaging.

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    There is a single normal value for blood pressure.

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    Elevated jugular venous pressure and jugular venous distention are synonymous terms.

Vital Signs

Respiration

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    The respiratory effort, rate, and pattern should be assessed in both ventilated and nonventilated patients.

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    Accessory muscle use is common with pulmonary edema, chronic obstructive pulmonary disease (COPD), asthma exacerbations, and pneumonia.

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    With acute tachypnea (a respiratory rate > 25 breaths/min), an immediate assessment should be performed to distinguish peripheral cyanosis (dusky or bluish tinge to the fingers and toes without mucosal or buccal changes) from central cyanosis (associated with a bluish tinge to the lips or mucosa under the tongue) (see below).

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    Tachypnea, when secondary to hypoxia, should nearly always be associated with a reflex tachycardia.

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    When tachypnea is present with a history of orthopnea, it suggests pulmonary edema, pleural effusion, or both.

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    Hypopnea is defined as less than 10 shallow or slow breaths per minute. It may be caused by severe cardiopulmonary failure, sepsis, central nervous system (CNS) depressants (e.g., sedative-hypnotics, narcotics, and alcohol), or CNS disease (e.g., cerebrovascular accident, meningitis).

Breathing patterns can reveal underlying pathology ( Table 1.1 ).

Table 1.1
Breathing Patterns
Respiratory Pattern Consider Eponym/Classification
Deep and rapid Diabetic ketoacidosis Kussmaul respiration
Snoring with episodic apnea Obstructive sleep apnea
Waxing and waning tachypnea/hypopnea alternating with apnea Oversedation Cheyne-Stokes breathing
Heart failure
Severe CNS process
Respiratory failure
Renal disease (uremia)
Irregularly irregular (yet equal) breaths alternating with periods of apnea Damage to the medulla oblongata (intracranial disease) Biot breathing
Completely irregular breaths (pauses with escalating periods of apnea) Severe damage to the medulla oblongata Ataxic respiration
No breaths or occasional gasps Severe cardiovascular or neurologic disease Agonal breathing
CNS , Central nervous system.

Pulse

The pulse should be assessed bilaterally for presence, rate, volume, contour, and regularity. An initial examination should always contain a description of the radial and carotid arteries, in addition to the brachial, femoral, popliteal, and pedal pulses.

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    A discrepancy in bilateral upper extremity pulses (especially with decreases in rate or volume on the left side) raises the possibility of aortic dissection, subclavian narrowing secondary to atherosclerosis, or congenital webs.

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    Aortic dissection is suggested by a pulse deficit, focal neurologic signs, and mediastinal widening on the chest radiograph.

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    Diminished lower extremity pulses are consistent with coarctation of the aorta or atherosclerotic disease of the abdominal aorta and/or the arterial supply of the lower extremities.

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    Pulsus alternans is a pulse with alternately strong and weak beats.

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    In patients with normal heart rates, pulsus alternans indicates severe left ventricular (LV) dysfunction.

When tachycardia (heart rate > 100 beats/min) is present, the regularity of the rhythm offers important diagnostic clues.

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    Regular rhythm rates between 125 beats/min and 160 beats/min suggest sinus tachycardia, the presence of atrial flutter with 2 : 1 block, or ventricular tachycardia.

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    Intermittent cannon A waves in the neck veins are highly sensitive, whereas a changing intensity of the first heart sound (S 1 ) is highly specific for the detection of ventricular tachycardia.

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    Atrial flutter may be accompanied by rapid undulations in the jugular venous pulse (flutter waves or F waves).

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    Detection of an irregular tachycardia suggests atrial fibrillation, atrial premature beats, or ventricular premature contractions.

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    In atrial fibrillation, assessment of the apical rate (counting heartbeats via auscultation) is more accurate than counting the radial pulse, accounting for a “pulse deficit.”

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    Bradycardia (heart rate < 50 beats/min) in a patient with fatigue, mental status changes, or evidence of impaired peripheral perfusion or pulmonary congestion raises the possibility of pharmacologic toxicity (i.e., digoxin, β-blockers, or calcium channel blockers), hypothermia (owing to hypothyroidism or exposure), or an atrioventricular nodal or ventricular escape rhythm that occurs with complete heart block or sick sinus syndrome.

Appreciation of the pulse volume and contour is also informative ( Table 1.2 ). Irregular rhythms are classified as either regularly irregular , in which the irregular beat can be anticipated at a fixed interval, or irregularly irregular , in which the irregular beat occurs without predictability.

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    A regularly irregular pulse commonly occurs with second-degree atrioventricular block (either Mobitz I or II, depending on whether the PR interval is constant or lengthening before the dropped beat) or with interpolated ventricular premature beats.

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    On the physical examination, the PR interval can be visualized as the distance between the a wave and c wave on the jugular venous pulse.

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    This distance, before and after the dropped beat, can be diagnostic when the electrocardiogram is unable to differentiate between Mobitz type I and Mobitz type II second-degree block.

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    When an interpolated ventricular premature beat is present, it may be accompanied by a weakened pulse (owing to inadequate ventricular filling) that occurs at a fixed interval from the regular pulse.

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    An irregularly irregular pulse implies that the examiner cannot anticipate when the next beat will occur; it may be caused by ventricular premature beats, atrial premature beats, multifocal atrial tachycardia, or atrial fibrillation.

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    Although ventricular premature beats and atrial fibrillation are associated with a pulse deficit (in which the auscultated apical rate is greater than the palpable radial pulse), the impulse that follows a ventricular premature beat should be stronger.

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    If the beat following a ventricular premature beat is diminished (Brockenbrough sign), hypertrophic cardiomyopathy or severe LV dysfunction should be considered.

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    No pulse deficit (or compensatory pause) should be present with atrial premature beats or multifocal atrial tachycardia.

Table 1.2
Pulse Characteristics
Pulse Description Consider
Bounding Septic shock, hyperthyroidism, chronic AR
Weak and thready Severe LV dysfunction, hypovolemia, severe MR, complete heart block, pericardial effusion
Slow rising and weak Severe AS
Alternating between strong and weak LV dysfunction, pericardial tamponade
Double tap (pulsus bisferiens) Hypertrophic cardiomyopathy, AS with AR
AR , Aortic regurgitation; AS , aortic stenosis; LV , left ventricular; MR , mitral regurgitation.

Blood Pressure

There is no rigid definition of “normal” blood pressure. Adequate blood pressure varies by patient and clinical status, but is generally believed to consist of a mean perfusion pressure of at least 60 mm Hg and the absence of end-organ hypoperfusion.

In patients with LV systolic dysfunction, hypotension may be caused by volume depletion from overly aggressive diuresis or because of volume overload.

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    The presence of tachycardia with orthostatic hypotension (a blood pressure decrease of > 20 mm Hg systolic or > 10 mm Hg diastolic when the patient is assessed first in the supine position and then again after 2 minutes with the patient standing or sitting with legs dangling) is consistent with volume depletion.

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    The differential diagnosis of hypotension includes factors that reduce systemic vascular resistance (e.g., infection, inflammation, adrenal insufficiency, anesthetic agents, atrioventricular malformations, and vascular insufficiency), stroke volume (e.g., hypovolemia; aortic stenosis; severe mitral regurgitation; ventricular arrhythmias; and LV dysfunction owing to infarction, ischemia, or a cardiomyopathy), and heart rate (e.g., heart block or pharmacologic bradycardia).

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    A pulsus paradoxus (a > 10 mm Hg decrease in systolic blood pressure occurring at end expiration with the patient breathing normally ) can occur with cardiac tamponade (very sensitive when occurring with tachycardia, jugular venous distention, and an absent y descent), constrictive pericarditis (occurring with jugular venous distention that persistently augments with inspiration, a pericardial knock, hepatomegaly, and an exaggerated y descent), severe hypertension, pulmonary embolism, COPD, and severe obesity.

The pulse pressure (systolic blood pressure – diastolic blood pressure) may be normal, narrow, or wide.

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    A narrow pulse pressure may be present with the decreased stroke volume of hypovolemia, tachycardia, severe aortic or mitral stenosis, pericardial constriction, or cardiac tamponade.

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    With appropriate clinical suspicion, a narrow pulse pressure has high sensitivity and specificity to predict a cardiac index less than 2.2 L/min/m 2 when the pulse pressure divided by the systolic pressure is less than 0.25.

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    A wide pulse pressure (> 60 mm Hg) can be seen with hyperthermia, but may also suggest severe chronic aortic regurgitation or highoutput heart failure from severe anemia, thyrotoxicosis, atrioventricular malformation, sepsis, vitamin B 1 deficiency, or Paget disease.

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