“Where is the pain?”

“How long have you had the pain?”

“Do you have recurrent episodes of pain?”

“What is the duration of the pain?”

“How often do you get the pain?”

“What do you do to make it better?”

“What makes the pain worse? Breathing? Lying flat? Moving your arms or neck?”

“How would you describe the pain?¹ Burning? Pressing? Crushing? Dull? Aching? Throbbing? Knifelike? Sharp? Constricting? Sticking?”

“Does the pain occur at rest? With exertion? After eating? When moving your arms? With emotional strain? While sleeping? During sexual intercourse?”

“Is the pain associated with shortness of breath? Palpitations? Nausea or vomiting? Coughing? Fever? Coughing up blood? Leg pain?”

“How long have you had palpitations?”

“Do you have recurrent attacks?” If so, “How frequently do they occur?”

“When did the current attack begin?”

“How long did it last?”

“What did it feel like?”

“Did any maneuvers or positions stop it?”

“Did it stop abruptly?”

“Could you count your pulse during the attack?”

“Can you tap out on the table what the rhythm was like?”

“Have you noticed palpitations after strenuous exercise? On exertion? While lying on your left side? After a meal? When tired?”

“During the palpitations, have you ever fainted? Had chest pain?”

“Was there an associated flush, headache, or sweating associated with the palpitations?”²

“Have you noticed an intolerance to heat? Cold?”

“What kind of medications are you taking?”

“Do you take any medications for your lungs?”

“Are you taking any thyroid medications?”

“Have you ever been told that you had a problem with your thyroid?”

“How much tea, coffee, chocolate, or cola sodas do you consume a day?”

“Do you smoke?” If yes, “What do you smoke?”

“Do you drink alcoholic beverages?”

“Did you notice that after the palpitations you had to urinate?”³

“How was your previous attack terminated?”

“How often do you get the attacks?”

“Are you able to terminate them?” If so, “How?”

“Have you ever been told that you have Wolff-Parkinson-White syndrome?”⁴

“What were you doing just before you fainted?”

“Have you had recurrent fainting spells?” If so, “How often do you have these attacks?”

“Was the fainting sudden?”

“Did you lose consciousness?”

“In what position were you when you fainted?”

“Was the fainting preceded by any other symptom? Nausea? Chest pain? Palpitations? Confusion? Numbness? Hunger?”

“Did you have any warning that you were going to faint?”

“Did you have any black, tarry bowel movements after the faint?”

“How long have you been tired?”

“Did the fatigue start suddenly?”

“Do you feel tired all day? In the morning? In the evening?”

“When do you feel least tired?”

“Do you feel more tired at home than at work?”

“Is the fatigue relieved by rest?”

“When was the swelling first noted?”

“Are both legs swollen equally?”

“Did the swelling appear suddenly?”

“Is the swelling worse at any time of the day?”

“Does it disappear after a night’s sleep?”

“Does elevation of your feet reduce the swelling?”

“What kind of medications are you taking?”

“Is there a history of kidney, heart, or liver disease?”

“Do you have shortness of breath?” If so, “Which came first, the edema or the shortness of breath?”

“Do you have pain in the legs?”

“Do you have any ulcers on your legs?”

“Are you taking oral contraceptives?”

“Is the edema associated with menstrual changes?”

Are xanthomata present? Tendon xanthomata are stony-hard, slightly yellowish masses that are commonly found on the extensor tendons of the fingers and are pathognomonic for familial hypercholesterolemia. The Achilles tendon and plantar tendons of the soles are also common locations for tendon xanthomata. Figure 11-12 shows tendon xanthomata on the extensor surfaces of the fingers of a patient with a total serum cholesterol concentration higher than 450 mg/dL.⁶

Figure 11-13 shows multiple tuberous xanthomata of the hand of another patient. This patient had primary biliary cirrhosis and extremely elevated cholesterol levels. Primary biliary cirrhosis is a rare, progressive, and often fatal liver disease occurring mostly in women. Pruritus is a common symptom. Xanthomata develop in approximately 15% to 20% of affected patients and are typically found on the palms, soles, knees, elbows, and hands. The serum cholesterol, usually LDL, is often as high as 1000 to 1500 mg/dL. Antimitochondrial antibody is present in nearly 90% of patients.

Eruptive xanthomata are seen in several familial disturbances of fat metabolism, specifically hyperlipidemia types I and IV. The chest, buttocks, abdomen, back, face, and arms are most commonly affected. Figure 11-14 shows eruptive xanthomata on the abdomen of a patient with uncontrolled diabetes mellitus and hypertriglyceridemia. Eruptive xanthomata on the face of a patient are pictured in Figure 11-15. Eruptive xanthomata result from elevations in plasma triglyceride concentrations, often to levels greater than 1500 mg/dL.⁷ These lesions developed in this patient after excessive alcohol consumption; his serum triglyceride concentrations exceeded 2000 mg/dL. The lesions, frequently found on the abdomen, buttocks, elbows, knees, and back, are small (1 to 3 mm in diameter), yellowish papules on an erythematous base. With reduction in the level of triglycerides, the lesions may recede.

Is a rash present? The presence of erythema marginatum (erythema in which the reddened areas are disc-shaped with raised edges) in a febrile patient is suggestive of acute rheumatic fever.

Are any painful lesions on the fingers or toes present? Osler’s nodes are painful lesions that occur in the tufts of the fingers and toes in patients with infective endocarditis. They are evanescent but are said to occur in 10% to 25% of patients with infective endocarditis.

Inspect the Nails

Frequently, splinter hemorrhages are visible as small, reddish-brown lines in the nail bed. These hemorrhages run from the free margin proximally and are classically associated with infective endocarditis. However, the finding is nonspecific because it is seen in many other conditions, even local trauma to the nail. A nail with splinter hemorrhages in a patient with endocarditis is shown in Figure 11-16.

Inspect the Facies

Abnormalities of the heart may also be associated with peculiarities of the face and head. Supravalvular aortic stenosis, a congenital problem, occurs in association with widely set eyes, strabismus, low-set ears, an upturned nose, and hypoplasia of the mandible. Moon facies and widely spaced eyes are suggestive of pulmonic stenosis. Expressionless facies with puffy eyelids and loss of the outer third of the eyebrow is seen in hypothyroidism. Affected individuals may have a cardiomyopathy. The earlobe crease, or Lichtstein’s sign, is an oblique crease, often bilateral, seen frequently in patients older than 50 years with significant CHD. This sign is shown in Figure 11-17. Although it is a useful sign, there are many false-positive and false-negative findings for this sign to be very reliable.

Inspect the Eyes

The presence of yellowish plaques on the eyelids, called xanthelasma, should raise the suspicion of an underlying hyperlipoproteinemia, even though this lesion is less specific than the xanthoma. Xanthelasma in a patient with hypercholesterolemia is shown in Figure 11-18.

Examination of the eyes may reveal an arcus senilis. An arcus (see Figs. 7-57 and 7-58) seen in a patient younger than 40 years should raise the suspicion of hypercholesterolemia. Opacities in the cornea may be evidence for sarcoidosis, which may be responsible for cor pulmonale or myocardial involvement. Displacement of the lens is frequently seen in patients with Marfan’s syndrome, an important cause of aortic regurgitation (see Fig. 7-74). Conjunctival hemorrhages are commonly seen in infective endocarditis. Hypertelorism, or widely set eyes, is often associated with congenital heart disease, especially pulmonic stenosis and supravalvular aortic stenosis. Retinal evaluation may furnish valuable information about diabetes (see Figs. 7-93 to 7-105), hypertension (see Figs. 7-84 and 7-106 to 7-110), and atherosclerosis. Roth’s spots may develop in patients with infective endocarditis (see Fig. 7-114).

Inspect the Mouth

Have the patient open the mouth widely. Inspect the palate. Is the palate highly arched? A high-arched palate may be associated with congenital heart problems such as mitral valve prolapse.

Are there petechiae on the palate? Infective endocarditis is often associated with palatal petechiae, as seen in Figure 11-19.

Inspect the Neck

Examination of the neck may reveal webbing. Webbing is seen in individuals with Turner’s syndrome,⁸ who may have coarctation of the aorta, and in patients with Noonan’s syndrome.⁹ Pulmonic stenosis is the associated cardiac abnormality in this condition.

Inspect the Chest Configuration

Inspection of the chest often reveals information about the heart. Because the chest and the heart develop at about the same time during embryogenesis, it is not surprising that anything interfering with the development of the chest may interfere with the heart. A pectus excavatum, or caved-in chest, is seen in Marfan’s syndrome and in mitral valve prolapse (see Fig. 10-7). Pectus carinatum, or pigeon breast, is also associated with Marfan’s syndrome (see Fig. 10-8).

Assess the presence of visible cardiac motions.

Inspect the Extremities

Some congenital abnormalities of the heart are associated with abnormalities of the extremities. Patients with atrial septal defects may have an extra phalanx, an extra finger, or an extra toe. Long, slender fingers may be suggestive of Marfan’s syndrome and aortic regurgitation. Short stature, cubitus valgus, and medial deviation of the extended forearm are typical of patients with Turner’s syndrome.

The Principles

Blood pressure can be measured directly with an intraarterial catheter or indirectly with a sphygmomanometer. The sphygmomanometer consists of an inflatable rubber bladder within a cloth cover, a rubber bulb to inflate the bladder, and a manometer to measure the pressure in the bladder. Indirect measurement of blood pressure involves the auscultatory detection of the appearance and disappearance of the Korotkoff sounds over the compressed artery. Korotkoff sounds are low-pitched sounds originating in the vessel that are related to turbulence produced by partially occluding an artery with a blood pressure cuff. Several phases occur in sequence as the occluding pressure drops. Phase 1 occurs when the occluding pressure falls to the systolic blood pressure. The tapping sounds are clear and gradually increase in intensity as the occluding pressure falls. Phase 2 occurs at a pressure approximately 10 to 15 mm Hg lower than that in phase 1 and consists of tapping sounds followed by murmurs.¹⁰

Phase 3 occurs when the occluding pressure falls enough to allow a large amount of volume to cross the partially occluded artery. The sounds are similar to the sounds of phase 2, except that only the tapping sounds are heard. Phase 4 is the abrupt muffling and decreased intensity of the sounds as the pressure approaches the diastolic blood pressure. Phase 5 is the complete disappearance of the sounds. The vessel is no longer compressed by the occluding cuff. Turbulent flow is no longer present.

The normal blood pressure for adults is less than 120 mm Hg systolic and less than 80 mm Hg diastolic. Borderline (prehypertensive) blood pressure is 120 to 139 systolic and 80 to 89 diastolic. When systolic and diastolic blood pressures fall into different categories, the higher category should be used to classify blood pressure level. For the diastolic blood pressure reading, the point of disappearance of the Korotkoff sounds is probably more accurate than the point of muffling. However, if the point of disappearance is more than 10 mm Hg lower than the point of muffling, the point of muffling is probably more accurate. Recording both the point of muffling and disappearance frequently helps in communication. A blood pressure might be recorded as 125/75–65: the systolic blood pressure is 125; the point of muffling is 75; the point of disappearance is 65 (the diastolic blood pressure).

Blood pressure should be recorded only to the nearest 5 mm Hg because there is a ± 3 mm Hg limit of accuracy for all sphygmomanometers. In addition, normal blood pressure changes occur from moment to moment, and measuring to less than 5 mm Hg provides a false sense of accuracy.

Two types of hypertension need to be recognized. White coat hypertension is a common phenomenon (approximately 15–20% of all stage 1 hypertensives) in which the patient’s blood pressure is higher in the doctor’s office than if measured at home or at work. These patients are at low cardiovascular risk. In contrast, masked hypertension is more serious because these individuals have normal blood pressures in the medical facility, but actually have much higher blood pressures throughout the day, indicative of a high risk of CVD. Masked hypertension has been estimated to occur in 10% of the general population.

Determine Blood Pressure by Palpation

Blood pressure assessment is performed with the patient lying comfortably in the supine position. The cuff bladder is centered over the right brachial artery. If the arm is obese, a large adult or thigh cuff should be used. The arm should be slightly flexed, and it should be supported at approximately the level of the heart. To determine the systolic blood pressure adequately and to exclude an error as a result of an auscultatory gap, blood pressure is first assessed by palpation. In this procedure, the right brachial or right radial artery is palpated while the cuff is inflated above the pressure required to obliterate the pulse. The adjustable screw is opened slowly for deflation. The systolic pressure is identified by the reappearance of the brachial pulse. As soon as the pulse is felt, the adjustable screw is opened for rapid deflation. This assessment is demonstrated in Figure 11-20.

Determine Blood Pressure by Auscultation

Blood pressure by auscultation is assessed in the right arm by inflating the cuff to approximately 20 mm Hg above the systolic pressure that was determined by palpation. The diaphragm of the stethoscope should be placed over the artery as close to the edge of the cuff as possible, preferably just under the edge. The cuff is deflated slowly while the Korotkoff sounds are evaluated. The systolic blood pressure, the point of muffling, and the point of disappearance are determined. The systolic blood pressure is the point at which the initial tapping sounds are heard. The technique of determining auscultatory blood pressure is shown in Figure 11-21. If the blood pressure is high, it is useful to measure the blood pressure again at the end of the examination, when the patient may be calmer.

Rule Out Orthostatic Hypotension

Rule Out Supravalvular Aortic Stenosis

Rule Out Coarctation of the Aorta

If the blood pressure is elevated in the arms, determination of the blood pressure in the lower extremities is important for ruling out coarctation of the aorta. The patient is asked to lie on the abdomen while the thigh cuff, which is 6 cm wider than the arm cuff, is placed around the posterior aspect of the midthigh. The stethoscope is placed over the artery in the popliteal fossa. The Korotkoff sounds are determined as in the upper extremity. If a thigh cuff is not available, the regular cuff can be applied to the lower leg with the distal border just at the malleoli. The stethoscope is placed over either the posterior tibial or the dorsalis pedis artery, and the auscultatory blood pressure is taken. A leg systolic blood pressure that is lower than that in the arm should raise suspicion of coarctation of the aorta.

Rule Out Cardiac Tamponade

In the presence of low arterial blood pressure and a rapid and feeble pulse, it is necessary to rule out the presence of cardiac tamponade. A valuable clinical sign suggestive of cardiac tamponade is the presence of a marked paradoxical pulse (also known as a pulsus paradoxus), which is characterized by an exaggeration of the normal inspiratory fall in systolic pressure. There is much confusion about the definition of a normal paradoxical pulse. A normal paradoxical pulse should be defined as the normal fall (approximately 5 mm Hg) in systolic arterial pressure during inspiration. It is the magnitude of the phenomenon that should determine whether the pulsus paradoxus is normal or abnormal.

The technique for assessing the magnitude of a paradoxical pulse is as follows: Have the patient breathe as normally as possible. Inflate the blood pressure cuff until no sounds are heard. Gradually deflate the cuff until sounds are heard in expiration only. Note this pressure. Continue to deflate the cuff slowly until sounds are heard during inspiration. Note this pressure. If the difference in these two pressures exceeds 10 mm Hg, a marked (abnormal) pulsus paradoxus is present; cardiac tamponade may be the cause. Cardiac tamponade results when there is an increase in intrapericardial pressure that interferes with normal diastolic filling. A marked paradoxical pulse is not a specific phenomenon for tamponade because it is also seen in large pericardial effusions, in constrictive pericarditis, and in conditions associated with increased ventilatory effort, such as asthma and emphysema.

• The rate and rhythm of the heart

• The contour of the pulse

• The amplitude of the pulse

Cardiac rate is routinely assessed by the radial pulse. The examiner should stand in front of the patient and grasp both radial arteries. The second, third, and fourth fingers should overlie the radial artery, as shown in Figure 11-22. The examiner should count the pulse for 30 seconds and multiply the number of beats by 2 to obtain the beats per minute. This method is accurate for most regular rhythms. If the patient has an irregularly irregular rhythm, as is found in atrial fibrillation, a pulse deficit may be present. In atrial fibrillation, many impulses bombard the AV node and ventricles. Owing to the varying lengths of diastolic filling periods, some of the contractions may be very weak and unable to produce an adequate pulse wave despite ventricular contraction. A pulse deficit, which is the difference between the apical (precordial) and radial pulses, occurs. In such cases, only auscultation of the heart, not the radial pulse, provides an accurate assessment of the cardiac rate.

Determine the Cardiac Rhythm

When palpating the pulse, carefully evaluate the regularity of the rhythm. The slower the rate, the longer you should palpate. If the rhythm is irregular, is there a pattern to the irregularity?

Cardiac rhythm may be described as regular, regularly irregular, or irregularly irregular. A regularly irregular rhythm is a pulse with an irregularity that occurs in a definite pattern. An irregularly irregular pulse has no pattern.

Electrocardiography is really the best medium for diagnosing the rhythm, but the physical examination may provide some clues. Premature beats may be recognized by the presence of isolated extra beats during a regular rhythm. Bigeminy is a coupled rhythm of beats in pairs. The first beat is the sinus beat, which is followed by a premature, usually ventricular, beat. If the premature beat is very early in the diastolic period, the pulse from this beat may be missed if the examiner evaluates the rhythm by palpation alone. A rhythm that is grossly irregular with no pattern is irregularly irregular and is the pulse in patients with atrial fibrillation.

Palpate the Carotid Artery

Assess the carotid artery pulse by standing at the patient’s right side, with the patient lying on the back. Auscultate the patient’s carotid arteries for bruits first (see Chapter 12, The Peripheral Vascular System). If a bruit is present, do not palpate the carotid artery. If a cholesterol plaque is present, palpation may produce an embolus.

To palpate the carotid artery, place your index and third fingers on the patient’s thyroid cartilage and slip them laterally between the trachea and the sternocleidomastoid muscle. You should be able to feel the carotid pulsations just medial to the sternocleidomastoid muscle. Palpation should be performed low in the neck to avoid pressure on the carotid sinus, which would cause a reflex drop in blood pressure and heart rate. Each carotid artery is evaluated separately. Never press on both carotid arteries at the same time. After the right carotid artery is evaluated, stand in the same position, and place the same fingers back on the patient’s trachea and slip them laterally to the left to feel the left carotid artery. This technique is demonstrated in Figure 11-23.

Evaluate the Characteristics of the Pulse

The carotid artery is used for the assessment of the contour and amplitude of the pulse. Contour is the shape of the wave. It is frequently described as the speed of the upward slope, downward slope, and duration of the wave. Place a hand firmly against the carotid artery until maximal force is felt. At this moment, the wave form should be discernible. The pulse may be described as normal, diminished, increased, or double-peaked. The normal carotid pulse wave is smooth, with the upward stroke steeper and more rapid than the downward stroke. A diminished pulse is a small, weak pulse. The palpating finger feels a gentle pressure rise with a distinct peak. An increased pulse is a large, strong, hyperkinetic pulse. The palpating finger feels an increased rate of rise of the ascending limb of the pulse and a brisk tap at its peak. A double-peaked pulse has a prominent percussion and tidal wave with or without a dicrotic wave. Arterial pulse abnormalities are summarized in Figure 11-24.

Determine the Jugular Wave Forms

To visualize the jugular wave forms, the patient should lie flat without a pillow so that his or her neck is not flexed and does not interfere with the pulsations. The patient’s trunk should be at approximately 25 degrees to the horizontal. The higher the venous pressure, the greater the elevation required; the lower the pressure, the lower the elevation needed. The patient’s head should be turned slightly to the right and slightly down to relax the right sternocleidomastoid muscle. Standing on the patient’s right side, the examiner should place his or her right hand, holding a small pocket flashlight, on the patient’s sternum and shine the light tangentially across the right side of the patient’s neck. Shadows of the pulsations will be cast on the sheet behind the patient. The light and shadows magnify the wave forms. This technique is demonstrated in Figure 11-25. If no wave forms are seen, the angle of elevation of the head of the bed should be reduced. To help identify the wave forms, the examiner can time the cardiac cycle by palpating the cardiac impulse beneath his or her right hand or by feeling the left carotid impulse with his or her left hand. The descents, rather than the waves themselves, tend to be more obvious. If the neck veins are visible at the jaw margin while the patient is seated, the examiner should watch for the wave forms at the angle of the jaw with the patient seated upright.

The jugular pulse must be differentiated from the pulsation of the carotid artery. Table 11-6 lists the most important characteristic differences of these pulses.

Estimate the Jugular Venous Pressure

To assess the pressure in the right side of the heart, it is necessary to establish a reference level. The standard reference is the manubriosternal angle. At any degree of elevation, this position is used to measure the pressure in the jugular venous system and right heart. The patient should be positioned at whatever angle between the supine and upright positions best demonstrates the top of the neck veins. An imaginary horizontal line is then drawn from this height to above the sternal angle. The heart is approximately 5 cm below the sternal angle; thus if the height of the column is 3 cm above the sternal angle, the estimated venous pressure is 3 + 5 cm, or 8 cm water. If the top of the column is 3 cm above the sternal angle, central venous pressure is probably elevated. The specificity of this finding is estimated to be from 93% to 96% (Sankoff & Zidulka, 2008). If there is neck vein distention up to the jaw margin while the patient is seated at 90 degrees, the right atrial pressure usually exceeds 15 mm Hg.¹¹ In Figure 11-26, the neck veins are distended to the angle of the jaw while the patient is seated upright. The patient’s right atrial pressure was 21 mm Hg.

Evaluate the Hepatojugular Reflux

A useful test in assessing high jugular venous pressure is that of the hepatojugular reflux, also known as abdominal compression. By applying pressure over the liver, the examiner can grossly assess right ventricular function. Patients with right ventricular failure have dilated sinusoids in the liver. Pressure on the liver pushes blood out of these sinusoids and into the inferior vena cava and right side of the heart, causing further distention of the neck veins. The procedure is performed with the patient lying in bed, mouth open, breathing normally; this prevents a Valsalva maneuver. The examiner places his or her right hand over the patient’s liver in the right upper quadrant and applies a firm, progressive pressure. Compression is maintained for 10 seconds. The normal response is for the internal and external jugular veins to show a transient increase in distention during the first few cardiac cycles, which is followed by a fall to baseline levels during the later part of the compression. In patients with right ventricular failure or elevated pulmonary artery wedge pressure, the neck veins remain distended during the entire period of compression; this distention diminishes rapidly (at least 4 cm) on sudden release of the compressing hand. If the examination is incorrectly performed with the patient’s mouth closed, a Valsalva maneuver results and produces inaccurate results of the hepatojugular reflux test.

Like most other clinical maneuvers, the hepatojugular reflux test must be performed in a standardized manner. If performed correctly, this test can be of considerable value in the bedside assessment of the patient. The test result correlates best with the pulmonary artery wedge pressure and, as such, is a reflection of increased central blood volume. Ewy (1988) evaluated this test and showed that in the absence of right ventricular failure, a positive test result is suggestive of a pulmonary artery wedge pressure of 15 mm Hg or greater.

Percuss the Heart’s Borders

The technique of percussion is discussed in Chapter 10, The Chest. Percussion of the heart is performed at the third, fourth, and fifth intercostal spaces from the left anterior axillary line to the right anterior axillary line. Normally, there is a change in the percussion note from resonance to dullness approximately 6 cm lateral to the left of the sternum. This dullness is attributable to the presence of the heart.

A percussion dullness distance of greater than 10.5 cm in the left fifth intercostal space has a sensitivity of 91.3% and a specificity of 30.3% for detecting increased left ventricular end-diastolic volume (LVEDV) or left ventricular mass. Percussion dullness of more than 10.5 cm in the fifth intercostal space has a sensitivity of 94.4% and a specificity of 67.2% in detecting cardiomegaly. In patients with a palpable apical impulse of greater than 3 cm in the left decubitus position, the sensitivity of detecting increased LVEDV or left ventricular mass increases to 100% and the specificity is 40%.

The examiner should stand on the right side of the patient, with the bed at a level comfortable for the examiner. Palpation for the PMI is most easily performed with the patient in a sitting position. Only the examiner’s fingertips should be applied to the patient’s chest in the fifth intercostal space, midclavicular line, because they are the most sensitive for assessing localized motion. The PMI should be noted. This technique is demonstrated in Figure 11-27. If the apical impulse is not felt, the examiner should move his or her fingertips in the area of the cardiac apex. The PMI is usually within 10 cm of the midsternal line and is no larger than 2 to 3 cm in diameter. A PMI that is laterally displaced or is felt in two interspaces during the same phase of respiration is suggestive of cardiomegaly.

The PMI is felt in approximately 70% of normal individuals while they are sitting. If it cannot be felt in the sitting position, the patient should be reevaluated while supine and in the left lateral decubitus position. The position of the PMI in the left lateral decubitus position must be assessed with the understanding that the normal cardiac impulse is now shifted slightly to the left. If the patient is in the left lateral decubitus position and the PMI is not laterally displaced, the examiner can suspect that cardiomegaly is not present.

In a patient without conditions predisposing to left ventricular hypertrophy, a palpable apical impulse felt in the left lateral decubitus position that is greater than 3 cm is said to be a specific (91%) and sensitive (92%) indicator of left ventricular enlargement. An apical diameter greater than 3 cm is predictive (86%) of an increased LVEDV. In patients with an apical diameter of less than 3 cm and a normal LVEDV, the negative predictive value is 95%.

The PMI usually corresponds to the left ventricular apex, but in patients with an enlarged right ventricle, the heart is rotated clockwise, as viewed from below, and the PMI may actually be produced by the right ventricle. This rotation turns the left ventricle posteriorly and makes it difficult to palpate. The apical impulse by the right ventricle is diffuse, whereas that of the left ventricle tends to be more localized.

In patients with chronic obstructive lung disease, the overinflation of the lungs displaces the PMI downward and to the right. The PMI in such patients is felt in the epigastric area, at the lower end of the sternum. In patients with chronic obstructive lung disease, a PMI in the normal location is suggestive of cardiomegaly.

Palpate for Localized Motion

The patient should now lie down so that all four main cardiac areas can be palpated. The examiner uses his or her fingertips to assess any localized motion. This technique is demonstrated in Figure 11-28.

The presence of a systolic impulse in the second intercostal space to the left of the sternum is suspect for pulmonary hypertension. This impulse is caused by the closure of the pulmonic valve under increased pressure. The presence of this impulse is suggestive of a dilated pulmonary artery, but it may also be felt in thin individuals without pulmonary hypertension.

Palpate for Generalized Motion

After the chest has been palpated with the fingertips, the examiner uses the proximal portion of his or her hand to palpate for any large area of sustained outward motion, called a heave or lift. The examiner again palpates each of the four main cardiac areas. The technique for assessing heaves is demonstrated in Figure 11-29. The presence of a right ventricular rock, which is a sustained left parasternal impulse associated with lateral retraction, is suggestive of a large right ventricle.

Any condition that increases the rate of ventricular filling during early diastole can produce a palpable impulse that occurs after the main left ventricular impulse. This second impulse in the area of the PMI is usually felt in association with an S₃. Frequently, an S₃ is more easily felt than heard.

The use of a tongue blade or an applicator stick can be helpful to reinforce visually what has been palpated. The tip of the stick is placed directly over the area and held in place by the examiner’s finger. This acts as a fulcrum, and the motions tend to be magnified by the movement of the stick. The technique is demonstrated in Figure 11-30.

Palpate for Thrills

Thrills are the superficial vibratory sensations felt on the skin overlying an area of turbulence. The presence of a thrill indicates a loud murmur. Thrills are best felt by using the heads of your metacarpal bones rather than the fingertips and applying very gentle pressure on the skin. If too much pressure is applied, thrills are not felt. The palpation of thrills is generally of little importance because auscultation reveals the presence of the loud murmur that has produced the thrill. Therefore the finding of a thrill adds little to the diagnosis, but it is an interesting physical sign to alert the examiner as to what will be heard.

The Technique

Proper auscultation requires a quiet area. Every attempt should be made to eliminate extraneous noise from radios, televisions, and so forth. The earpieces of the stethoscope are directed anteriorly or parallel to the direction of the external auditory canal. If the earpieces are put in backward, the openings of the earpieces impinge on the wall of the external canal and lower the intensity of the sounds. The earpieces should fit properly so as to be comfortable but tight enough to exclude external noises.

It is often useful for you to close your eyes when listening to the heart. Sounds that are more difficult to hear sound louder with your eyes closed, because the brain is flooded with all types of sensory input when the eyes are open. The input from the eyes appears to be the most important. The next important sensory input is auditory, which is followed by tactile input. If you eliminate the distraction of visual stimuli, the brain concentrates more on the auditory input, and the sounds become more evident.

As indicated in Chapter 10, The Chest, the bell of the stethoscope should be applied lightly to the skin, whereas the diaphragm should be pressed tightly against the skin. High-pitched sounds, such as valve closure, systolic events, and regurgitant murmurs, are better heard with the diaphragm. Low-pitched sounds, such as gallop rhythms or the murmur of AV stenosis, are better heard with the bell.

It is common in many countries to examine patients through their clothing or a hospital gown. In the United States, however, never listen through any type of clothing.

There are several other pitfalls in auscultation. Make sure that the stethoscope is in good shape: Cracked tubing certainly interferes with good listening. Both the examiner and the patient must be comfortable for the best hearing. An examiner who is straining over the patient and is uncomfortable will want to finish the examination quickly without a proper assessment. Always inspect and palpate before auscultation. Accumulate as much information as possible before listening.

Auscultate the Cardiac Areas

The examiner should be on the right side of the patient while the patient lies flat on the back. If not already at the proper height, the bed should be adjusted so that the examiner is comfortable. The examiner should listen in the aortic, pulmonic, tricuspid, and mitral areas. However, the examiner should not limit auscultation to these areas alone. The examiner should start at any area and move the stethoscope gradually over the precordium from area to area. The areas have been established to provide some degree of standardization.

While listening at the apex and LLSB with the bell, the examiner should determine whether an S₃ or an S₄ is present.

Cardiac murmurs may radiate widely. The examiner should determine where the sounds are loudest or best heard. There are no acoustic walls in the chest. A murmur typically heard at the apex with radiation to the axilla may be heard in the neck, if it is loud enough. The murmur in this example is probably loudest at the apex and axilla.

The Standard Auscultation Positions

The four standard positions for auscultation are shown in Figure 11-31. They are as follows:

All precordial areas are examined while the patient is supine. Using a systematic approach, the examiner starts at either the aortic area or the apex and carefully listens to the heart sounds. After all areas are examined, the patient is then instructed to turn onto the left side. The examiner should now listen at the apex for the low-pitched diastolic murmur of mitral stenosis, which is best heard with the bell of the stethoscope. Then the patient sits upright, and all areas are examined with the diaphragm of the stethoscope. Finally, the patient sits up and leans forward. The patient is asked to exhale and hold his or her breath while the examiner, using the diaphragm, listens for the high-pitched diastolic murmur of aortic regurgitation at the right and left second and third intercostal spaces.

Time the Cardiac Events

To interpret heart sounds accurately, the examiner must be able to time the events of the cardiac cycle. The most reliable way of identifying S₁ and S₂ is to time the sounds by palpating the carotid artery. While the examiner’s right hand is positioning the stethoscope, the left hand is placed on the patient’s carotid artery. This technique is demonstrated in Figure 11-32. The sound that precedes the carotid pulse is the S₁. The S₂ follows the pulse. The carotid, not the radial pulse, must be used. The time delay from S₂ to the radial pulse is significant, and errors in timing will result.

Approach to Careful Auscultation

Until the examiner gains expertise in cardiac examination, heart sounds should be evaluated in the manner suggested in Table 11-7. The examiner should take time in each area before continuing on to the next area. The examiner should listen to several cardiac cycles at each position to be certain of the observations made, which include respiratory effects.

Describe Any Murmurs Present

If a murmur is present, attention should be directed to the following features:

Timing of murmurs as to systole and diastole is paramount. Does the systolic murmur begin with, or after, S₁? Does it end before, with, or after S₂? Does the murmur occupy the entire systolic period? Murmurs occurring throughout systole are termed holosystolic or pansystolic. These murmurs begin with S₁ and end after S₂. A systolic ejection murmur begins after S₁ and ends before S₂. Does the murmur occur only in early systole, midsystole, or late systole? Does the murmur persist throughout the entire diastolic period? Such murmurs are termed holodiastolic.

In which area is the murmur best heard?

The radiation of the murmur can provide a clue as to its cause. Does it radiate to the axilla? The neck? The back?

The intensity of a murmur is graded from I to VI, based on increasing loudness. The following grading system, although antiquated, serves as a means of communicating the intensity of the murmur:

Describe Any Pericardial Rubs

Friction rubs are extracardiac sounds of short duration that have a unique quality similar to the sound of scratching on sandpaper. Rubs may result from irritation of the pleura (i.e., a pleural rub) or of the pericardium (i.e., a pericardial rub). Pericardial rubs typically have three components: one systolic and two diastolic. The systolic component occurs during ejection; the two diastolic components occur during rapid filling and atrial contraction. Pericardial rubs are best heard with the patient sitting while holding breath in expiration. Patients with pericardial rubs commonly have chest pain that is lessened by sitting forward. A rub that disappears while the patient holds the breath originates from the pleura.

The Goals of Auscultation

The goals at the end of auscultation are to be able to describe the following:

Test for Edema

To test for pitting edema, the examiner presses his or her fingers into a dependent area, such as the patient’s shin, for 2 to 3 seconds. If pitting edema is present, the fingers sink into the tissue, and when the fingers are removed, the impression of the fingers remains. This technique is demonstrated in Figure 11-33.

Pitting edema is usually quantified from 1+ to 4+, depending on the depth and how long the indentation persists. The grading for pitting edema is:

In patients who are bedridden, the dependent area is usually the sacrum and not the shins. The examiner should evaluate for edema over the sacrum in these patients. Figure 11-34 illustrates a 4+ sacral edema in a bedridden patient.

• The rate of rise of ventricular pressure

• The condition of the valve

• The position of the valve

• The distance of the heart from the chest wall

Abnormalities of the Intensity of the Second Heart Sound

The conditions that change the intensity of S₂ are the following:

Abnormalities of Splitting of the Second Heart Sound

Normal physiologic splitting of S₂ was discussed in the section, “The Cardiac Cycle.” This section deals with abnormalities of splitting.

Any condition that delays right ventricular systole, either electrically or mechanically, delays P₂ and produces a widened splitting of S₂. Right ventricular emptying is delayed by a right bundle branch block or pulmonic stenosis. The pulmonic component of S₂ is delayed during both inspiration and expiration, and wide splitting of S₂ occurs.

Any condition that shortens left ventricular systole allows A₂ to occur earlier than normal, and wide splitting likewise occurs. Conditions such as mitral regurgitation, ventricular septal defect, and PDA shorten left ventricular systole, and the S₁-A₂ interval is shorter than normal. In these conditions, there is a “double outlet” to the left ventricle, and systole therefore is shorter. In a ventricular septal defect, with a left-to-right shunt, not only is left ventricular systole shorter but also right ventricular systole is prolonged. Both factors are crucial in producing the wide splitting of S₂.

Any condition, either electrical or mechanical, that delays left ventricular emptying produces paradoxical splitting of S₂. Left bundle branch block or aortic stenosis delays left ventricular emptying. These conditions delay the closure of the aortic valve after right ventricular systole and P₂ have occurred. The normal sequence of A₂-P₂ is reversed. During inspiration, P₂ moves normally away from S₁ toward A₂. The split is said to be narrowed. With expiration, P₂ moves normally and approaches S₁; the P₂-A₂ split widens. This widening during expiration is paradoxical. Other conditions, such as left ventricular failure and severe hypertension, delay left ventricular ejection and cause paradoxical splitting of S₂.

Fixed splitting of S₂ is the auscultatory hallmark of an atrial septal defect. In this situation, the split is wide and does not change with respiration. This is because inspiratory increases in venous return to the right atrium normally raise its pressure. During expiration, the right atrial pressure is lower, but the left-to-right atrial shunt keeps the volume in the right atrium constant during respiration; therefore, normal splitting does not occur.

Normal physiologic splitting of the second heart sound and abnormalities of splitting are illustrated in Figure 11-35.