Temperature

Because core body temperature is carefully controlled within a narrow range, the detection of hyperthermia or hypothermia offers important clinical clues. Normal oral body temperature is approximately 37° C (98.6° F) with early morning temperatures (approximately 1° C lower) compared with later in the afternoon. By convention, fever is defined as an oral temperature greater than 38° C (>100° F), although it is common practice to consider temperatures greater than 38.4° C (>101.1° F) in hospitalized patients to be clinically significant (albeit without significant data to support this assumption).

Hyperthermia associated with infection (for patients not receiving negative chronotropic agents or with intrinsic cardiac conduction disease) should be accompanied by an increase in the pulse rate of approximately 8.5 beats/min for each 1° C increase in temperature (Liebermeister’s rule).¹ The presence of a factitious fever is suggested by the lack of a similar temperature elevation in voided urine compared with the oral temperature. Although a hot drink can quickly increase oral temperature up to 2° C, 5 minutes later the increase is only 0.3° C.²

The pattern of the fever spikes should also be assessed; patterns include intermittent (returning to normal each day), sustained (with minor daily variation [i.e., <0.3° C] suggesting gram-negative infections or pneumonia), remittent (varying >0.3° C each day but not returning to normal), and relapsing (febrile and afebrile days suggesting the Pel-Ebstein fever of Hodgkin disease, Borrelia infections, or episodic cholangitis caused by a mobile common bile duct stone). Once-daily spikes (quotidian fever) occur with liver abscesses or acute cholangitis, whereas twice-daily spikes (double quotidian fever) suggest gonococcal endocarditis. Prolonged fever despite antibiotic therapy can also occur with connective tissue disorders, drug fever, neoplasm, abscess, or antibiotic-resistant organisms and superinfection.

The presence of hypothermia (oral temperature <35° C (<95° F) requires confirmation. Drinking ice water reduces the oral temperature up to 0.6° C (1° F) for 5 minutes.² False-negative hypothermic readings can also occur with ear temperatures taken in the presence of cerumen and oral temperatures recorded in the presence of tachypnea. Confirmed hypothermia requires the assessment of a patient’s temperature with a rectal thermometer (which averages approximately 0.6° C (1° F) higher than the oral temperature). The differential diagnosis of true hypothermia includes ambient cold exposure, submersion, hypothyroidism, hypoglycemia, sepsis, and adrenal insufficiency. With hypothermia from submersion or exposure, warming to room temperature is necessary for adequate assessment of end-organ and neurologic function.

Respiration

The respiratory effort, rate, and pattern should be assessed in ventilated and nonventilated patients. Accessory muscle use is common with pulmonary edema, chronic obstructive pulmonary disease (COPD), asthmatic exacerbations, and pneumonia. It may be detected visually or by palpation over the sternocleidomastoid or intercostal muscles. 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 hypoxemia (associated with a bluish tinge to the lips or mucosa under the tongue). Peripheral cyanosis may occur with or without hypoxemia, such as in the case of severe peripheral vasoconstriction. This condition is accompanied by cold extremities and compromised capillary refill.

Tachypnea (>25 breaths/min), when secondary to hypoxia, should nearly always be associated with a reflex tachycardia. Although resting tachypnea may occur with cardiopulmonary disease, it may also be present in response to fever, pain, anemia, hyperthyroidism, abdominal distention, respiratory muscle paralysis, obesity, or metabolic acidosis. When tachypnea accompanies chest pain or collapse, acute pulmonary embolism should be included in the differential diagnosis. When tachypnea is present with a history of orthopnea, it suggests the presence of pulmonary edema, pleural effusion or both. When tachypnea is present in a patient being weaned from a ventilator, tachypnea predicts weaning failure.³

Hypopnea is defined as less than 10 shallow or slow breaths per minute. It may be due to severe cardiopulmonary failure, sepsis, central nervous system (CNS) depressants (e.g., sedative-hypnotics, narcotics, and alcohol), or CNS disease (e.g., cerebrovascular accident, meningitis). Hypopnea may also occur secondary to factors that limit inspiration, such as pericarditis or pleuritis, or in the postoperative period.

Breathing patterns can reveal underlying pathology (Table 4-1). Exaggerated deep and rapid respirations were noted by Kussmaul to imply the presence of diabetic ketoacidosis because most causes of hypoxia usually result in shallow and rapid respirations. Apneic episodes with snoring suggest obstructive sleep apnea, a potentially treatable contributor to hypertension and right heart failure. Cheyne-Stokes breathing, in which periods of waxing and waning tachypnea and hyperpnea alternate with apnea, occurs in various cardiac, neurologic, and pulmonary disorders or with simple oversedation. When Cheyne-Stokes breathing occurs in the setting of uremia or heart failure, it portends a poor prognosis. Biot breathing is characterized by irregularly irregular breaths of equal depth that are associated with periods of apnea. It can be seen in patients with intracranial disease affecting the medulla oblongata. More severe damage to the medulla oblongata results in ataxic respiration, the complete irregularity of breathing, with irregular pauses and increasing periods of apnea. As this breathing pattern deteriorates further, it merges with agonal respiration.

Table 4–1 Breathing Patterns

Orthopnea (shortness of breath while supine) is most commonly present in patients with heart failure and pleural effusion, but also can occur with ascites, morbid obesity, and diaphragmatic paralysis. Alternatively, platypnea (shortness of breath when assuming the upright position) suggests the right-to-left shunting that occurs with an atrial septal defect or intrapulmonary shunt. Trepopnea (shortness of breath while lying on one side) occurs with a right pleural effusion or with unilateral lung or diaphragm disease when the healthy lung is down.^4,5

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. This examination is important for patients with hypotension, claudication, arterial insufficiency, or cerebrovascular accident, or after intra-aortic balloon pump insertion. Assessing the pulse for 30 seconds is more accurate than counting for only 15 seconds.⁶

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. If such a discrepancy is present, the examiner should search for evidence of a subclavian steal phenomenon, detected as a decrease in pulse amplitude after raising or exercising the affected arm for approximately 45 seconds (the left side is affected 70% of the time; the reduction in systolic blood pressure is >20 mm Hg 94% of the time).⁷ Aortic dissection is suggested by the presence of a pulse deficit, focal neurologic signs, and mediastinal widening on the chest radiograph.⁸ Diminished lower extremity pulses are consistent with coarctation of the aorta or atherosclerotic disease of the abdominal aorta. Although the detection of low femoral pulse amplitude (or its absence) is crucial for assessing the risk-to-benefit ratio in patients who may require vascular access or device implantation, its diminution or absence after catheterization or intra-aortic balloon pump implantation requires urgent intervention.

When tachycardia (a heart rate >100 beats/min) is present, the regularity of the rhythm offers important diagnostic clues. 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. The presence of intermittent cannon A waves in the neck veins is highly sensitive, whereas a changing intensity of the first heart sound (S₁) is highly specific for the detection of ventricular tachycardia.⁹ Atrial flutter may be accompanied by rapid undulations in the jugular venous pulse (flutter waves or F waves). Because sinus tachycardia may be due to correctable causes, such as hypovolemia, hypoxia, infection, hyperthyroidism, anemia, or anxiety, or may be due to the pathologic adaptation occurring with chronic heart failure or myocardial ischemia, integration of these clinical suspicions with the nature of the underlying rhythm is important. The use of vagal maneuvers may help differentiate the causes of narrow-complex tachycardia.

The Valsalva maneuver, performed by asking the patient to bear down as if “having a bowel movement” or pushing up the abdomen against the examiner’s hand placed on the middle of the abdomen, seems to be more effective than carotid sinus massage, performed by pressing on the neck at the bifurcation of the carotid artery just below the angle of the jaw, at terminating supraventricular tachycardia^10,11 in 50% of cases. Paroxysmal supraventricular tachycardia (nodal re-entry and reciprocating tachycardias) may be interrupted with enhanced vagal tone. Sinus tachycardia, atrial flutter, and atrial fibrillation usually slow only transiently (but may reveal the underlying rhythm), although an abrupt halving of the rate may occur with atrial flutter. Detection of an irregular tachycardia on physical examination suggests atrial fibrillation, atrial premature beats, or ventricular premature contractions. 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.”¹²

Bradycardia (heart rate <50 beats/min) may be appropriate in trained athletes, but should be asymptomatic and associated with a gradual increase in heart rate with exercise.¹³ Detection of a regular-rhythm bradycardia in a patient with fatigue, mental status changes, or evidence of impaired peripheral perfusion or pulmonary congestion raises the possibility of pharmacologic toxicity (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 4-2). Tachycardia with a bounding pulse is present with septic shock (owing to the acute reduction in afterload), hyperthyroidism, or the sudden collapse of the pulse with chronic aortic insufficiency (a water-hammer pulse). Consistent with the presence of chronic aortic insufficiency is the accentuation of the radial pulse when the examiner lifts the whole arm above the patient’s head (Mayne’s sign). A weak and thready pulse may be present with severe left ventricular dysfunction, hypovolemia, severe mitral regurgitation, or complete heart block. A slow rising and weak carotid pulse (pulsus parvus et tardus) is consistent with a diagnosis of severe aortic stenosis, whereas a regular pulse that alternates between weak and strong (pulsus alternans) occurs with left ventricular dysfunction or pericardial tamponade. A “double tap” during systole (pulsus bisferiens) can occur with either hypertrophic cardiomyopathy or the combination of aortic stenosis and aortic insufficiency.^14,15 In the presence of a bisferiens pulse, two soft and rapid sounds can be auscultated with each cardiac cycle as the brachial artery is compressed by a blood pressure cuff proximally.¹⁶

Table 4–2 Pulse Characteristics

Irregular rhythms are classified as either regularly irregular, where the irregular beat can be anticipated at a fixed interval, or irregularly irregular, where the irregular beat occurs without predictability. A regularly irregular pulse commonly occurs with second-degree atrioventricular block (either Mobitz I or II, depending on whether the P–R interval is constant or lengthening before the dropped beat) or with interpolated ventricular premature beats. On the physical examination, the P–R interval can be visualized as the distance between the a wave and c wave on the jugular venous pulse (JVP). This distance, before and after the dropped beat, can be diagnostic when the electrocardiogram is unable to differentiate between Mobitz type I and II second-degree block. 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.

An irregularly irregular pulse implies that the examiner cannot anticipate when the next beat will occur, and may be due to ventricular premature beats, atrial premature beats, multifocal atrial tachycardia, or atrial fibrillation. Although ventricular premature beats and atrial fibrillation are associated with a pulse deficit (where the auscultated apical rate is greater than the palpable radial pulse), the pulse that follows a ventricular premature beat should be stronger. It is clinically relevant to realize that significant numbers of ventricular premature beats can compromise cardiac output. Alternatively, if the beat following a ventricular premature beat is diminished (Brockenbrough sign), hypertrophic cardiomyopathy or severe left ventricular dysfunction should be considered. No pulse deficit (or compensatory pause) should be present with atrial premature beats or multifocal atrial tachycardia. The physician can differentiate atrial premature beats from ventricular premature beats by tapping out the rhythm with his or her hand. Atrial premature beats result in a beat that occurs while the physician’s hand is “up.” Although a ventricular premature beat also occurs with the hand in the “up” position, the pulse resumes on the second down-beat after the compensatory pause.

Blood Pressure

In the ICU, there is no rule defining “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. For accurate assessment, an adequately sized blood pressure cuff must be used (there are lines on all blood pressure cuffs to indicate adequate sizing) and should be correctly situated around the bicep (and not over clothing). A blood pressure obtained with a cuff that is too short or narrow, especially if the patient is obese or has an enlarged upper arm, may result in a factitiously elevated blood pressure.^17,18

Although palpation of pulses is commonly used in emergency situations to estimate systolic blood pressure (i.e., palpation of a radial pulse suggests a minimum systolic blood pressure of 80 mm Hg; a femoral pulse, a blood pressure of at least 70 mm Hg; and a carotid pulse, a blood pressure of at least 60 mm Hg), the overall accuracy of this estimation has been questioned.¹⁹ To obtain the palpable systolic blood pressure, the cuff should first be inflated until the radial pulse is no longer palpable (usually 150 to 200 mm Hg) and then slowly deflated (2 to 3 mm Hg per second) until the pulse returns.

For the auscultatory blood pressure, inflation should be repeated (inflate the cuff to 10 mm Hg above the palpable systolic blood pressure) and listen for the first and fifth (last audible) Korotkoff sounds during slow cuff deflation. The diastolic blood pressure may be difficult, if not impossible, to appreciate in the presence of fever, severe anemia, aortic insufficiency, thyrotoxicosis, vitamin B₁ deficiency, or Paget disease. For patients in atrial fibrillation or with significant ventricular arrhythmias, a relatively accurate blood pressure assessment is obtained by averaging three individual readings.

In patients with left ventricular systolic dysfunction, multiple etiologies of hypotension require assessment during the physical examination. Although hypotension may be caused by overly aggressive diuresis, it may also occur because of volume overload. The presence of a 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. 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 left ventricular dysfunction owing to infarction, ischemia, or a cardiomyopathy), and heart rate (e.g., heart block or pharmacologic bradycardia).

Hypotension without a concomitant increase in the pulse rate (in the absence of medications that can blunt a heart rate response) raises the possibility of autonomic dysfunction. The presence of 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),^20,21 constrictive pericarditis (occurring with jugular venous distention that persistently augments with inspiration, a pericardial knock, hepatomegaly, and an exaggerated y descent),²² severe hypertension, pulmonary embolism, COPD, and severe obesity.

With appropriate clinical scenarios, blood pressure should also be assessed in both arms and one leg. Leg blood pressure can be assessed by placing the blood pressure cuff around the calf and using the dorsalis pedis pulse for auscultation or Doppler interrogation. A systolic blood pressure difference greater than 10 mm Hg between arms suggests aortic dissection, proximal aortic aneurysm, or subclavian artery stenosis. With coarctation of the aorta, arm blood pressures are greater than blood pressures in the legs (this may also be accompanied by underdeveloped lower extremity musculature compared with upper extremity musculature). Leg blood pressure that is more than 15 mm Hg higher than arm blood pressure suggests aortic dissection, aortic insufficiency, or a proximal vasculitis (i.e., giant cell or Takayasu arteritis).

The pulse pressure ([systolic blood pressure − diastolic blood pressure] may also be informative. A low pulse pressure may be present with the decreased stroke volume of hypovolemia, tachycardia, severe aortic or mitral stenosis, pericardial constriction, or cardiac tamponade. With appropriate clinical suspicion, it has a high sensitivity and specificity to predict a cardiac index less than 2.2 L/min/m² when the pulse pressure divided by the systolic pressure is less than 0.25. A wide pulse pressure (>60 mm Hg) can be seen with hyperthermia, but may also suggest greater than moderate chronic aortic insufficiency or high output failure owing to severe anemia, thyrotoxicosis, atrioventricular malformation, sepsis, vitamin B₁ deficiency, or Paget disease. If the wide pulse pressure is present in just one arm, a search for an atrioventricular fistula distal to the site of blood pressure cuff should be undertaken.

Weight

The daily weight is an important vital sign. It often proves to be especially significant for patients in whom volume overload or hypovolemia subsequently complicates the clinical picture. When a weight appears inconsistent with prior weights or the clinical history, the clinician should not hesitate to have the patient reweighed. Noting an increase in weight may be crucial to discern the presence of volume overload in a patient with shortness of breath, whereas loss of weight should occur in patients being diuresed. A weight gain despite the presence of effective diuresis suggests increased fluid intake, either orally or via the intravenous route.