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- Vital Signs
- Chest Inspection and Palpation
- Cardiac Auscultation
- Abdominal and Extremity Examination
- Resources In This Article
Complete examination of all systems is essential to detect peripheral and systemic effects of cardiac disorders and evidence of noncardiac disorders that might affect the heart. Examination includes the following:
Vital sign measurement
Pulse palpation and auscultation
Chest inspection, percussion, auscultation, and palpation
Cardiac percussion, palpation, and auscultation
Lung examination (see page Evaluation of the Pulmonary Patient : Auscultation)
Extremity and abdomen examination
BP is measured in both arms and, for suspected congenital cardiac disorders or peripheral vascular disorders, in both legs. The bladder of an appropriately sized cuff encircles 80% of the limb’s circumference, and the bladder’s width is 40% of the circumference. The first sound heard as the Hg column falls is systolic pressure; disappearance of the sound is diastolic pressure (5th-phase Korotkoff sound). Up to a 15 mm Hg pressure differential between the right and left arms is normal; a greater differential suggests a vascular abnormality (eg, dissecting thoracic aorta) or a peripheral vascular disorder. Leg pressure is usually 20 mm Hg higher than arm pressure. Ankle-brachial index (ratio of ankle to arm systolic BP) is normally > 1. A Doppler probe may be used to measure the ankle BP if the pedal pulses are not easily palpable.
Heart rate and rhythm are assessed by palpating the carotid or radial pulse or by cardiac auscultation if arrhythmia is suspected; some heartbeats during arrhythmias may be audible but do not generate a palpable pulse.
Respiratory rate, if abnormal, may indicate cardiac decompensation or a primary lung disorder. The rate increases in patients with heart failure or anxiety and decreases or becomes intermittent in the moribund. Shallow, rapid respirations may indicate pleuritic pain.
Temperature may be elevated by acute rheumatic fever or cardiac infection (eg, endocarditis). After MI, low grade fever is very common. Other causes are sought only if fever persists > 72 h.
Normally during inspiration, systolic arterial BP can decrease as much as 10 mm Hg, and pulse rate increases to compensate. A greater decrease in systolic BP or weakening of the pulse during inspiration is considered pulsus paradoxus. Pulsus paradoxus occurs in
BP decreases during inspiration because negative intrathoracic pressure increases venous return and hence right ventricular (RV) filling; as a result, the interventricular septum bulges slightly into the left ventricular (LV) outflow tract, decreasing cardiac output and thus BP. This mechanism (and the drop in systolic BP) is exaggerated in disorders that cause high negative intrathoracic pressure (eg, asthma) or that restrict RV filling (eg, cardiac tamponade, cardiomyopathy) or outflow (eg, pulmonary embolism).
Pulsus paradoxus is quantified by inflating a BP cuff to just above systolic BP and deflating it very slowly (eg, ≤ 2 mm Hg/heartbeat). The pressure is noted when Korotkoff sounds are first heard (at first, only during expiration) and when Korotkoff sounds are heard continuously. The difference between the pressures is the “amount” of pulsus paradoxus.
Major peripheral pulses in the arms and legs are palpated for symmetry and volume (intensity); elasticity of the arterial wall is noted. Absence of pulses may suggest an arterial disorder (eg, atherosclerosis) or systemic embolism. Peripheral pulses may be difficult to feel in obese or muscular people. The pulse has a rapid upstroke, then collapses in disorders with a rapid runoff of arterial blood (eg, arteriovenous communication, aortic regurgitation). The pulse is rapid and bounding in thyrotoxicosis and hypermetabolic states; it is slow and sluggish in myxedema. If pulses are asymmetric, auscultation over peripheral vessels may detect a bruit due to stenosis.
Observation, palpation, and auscultation of both carotid pulses may suggest a specific disorder (see Table: Carotid Pulse Amplitude and Associated Disorders). Aging and arteriosclerosis lead to vessel rigidity, which tends to eliminate the characteristic findings. In very young children, the carotid pulse may be normal, even when severe aortic stenosis is present.
Auscultation over the carotid arteries can distinguish murmurs from bruits. Murmurs originate in the heart or great vessels and are usually louder over the upper precordium and diminish toward the neck. Bruits are higher-pitched, are heard only over the arteries, and seem more superficial. An arterial bruit must be distinguished from a venous hum. Unlike an arterial bruit, a venous hum is usually continuous, heard best with the patient sitting or standing, and is eliminated by compression of the ipsilateral internal jugular vein.
Carotid Pulse Amplitude and Associated Disorders
The peripheral veins are observed for varicosities, arteriovenous malformations (AVMs) and shunts, and overlying inflammation and tenderness due to thrombophlebitis. An AVM or a shunt produces a continuous murmur (heard on auscultation) and often a palpable thrill (because resistance is always lower in the vein than in the artery during systole and diastole).
The neck veins are examined to estimate venous wave height and waveform. Height is proportional to right atrial pressure, and waveform reflects events in the cardiac cycle; both are best observed in the internal jugular vein.
The jugular veins are usually examined with the patient reclining at 45°. The top of the venous column is normally just below the clavicles (upper limit of normal: 4 cm above the sternal notch in a vertical plane). The venous column is elevated in heart failure, volume overload, cardiac tamponade, constrictive pericarditis, tricuspid stenosis, superior vena cava obstruction, or reduced compliance of the RV. If such conditions are severe, the venous column can extend to jaw level, and its top can be detected only when the patient sits upright or stands. The venous column is low in hypovolemia.
Normally, the venous column can be briefly elevated by firm hand pressure on the abdomen (hepatojugular or abdominojugular reflux); the column falls back in a few seconds (maximum 3 respiratory cycles or 15 sec) despite continued abdominal pressure (because a compliant RV increases its stroke volume via the Frank-Starling mechanism). However, the column remains elevated (> 3 cm) during abdominal pressure in disorders that cause a dilated and poorly compliant RV or in obstruction of RV filling by tricuspid stenosis or right atrial tumor.
Normally, the venous column falls slightly during inspiration as lowered intrathoracic pressure draws blood from the periphery into the vena cava. A rise in the venous column during inspiration (Kussmaul sign) occurs typically in chronic constrictive pericarditis, right ventricular MI, and COPD, and usually in heart failure and tricuspid stenosis.
Jugular vein waves (see Figure: Normal jugular vein waves.) can usually be discerned clinically but are better seen on the screen during central venous pressure monitoring.
Normal jugular vein waves.
The a waves are increased in pulmonary hypertension and tricuspid valve stenosis. Giant a waves (Cannon waves) are seen in atrioventricular dissociation when the atrium contracts while the tricuspid valve is closed. The a waves disappear in atrial fibrillation and are accentuated when RV compliance is poor (eg, in pulmonary hypertension or pulmonic stenosis). The v waves are very prominent in tricuspid regurgitation. The x descent is steep in cardiac tamponade. When RV compliance is poor, the y descent is very abrupt because the elevated column of venous blood rushes into the RV when the tricuspid valve opens, only to be stopped abruptly by the rigid RV wall (in restrictive myopathy) or the pericardium (in constrictive pericarditis).
Chest contour and any visible cardiac impulses are inspected. The precordium is palpated for pulsations (determining apical impulse and thus cardiac situs) and thrills.
Chest deformities, such as shield chest and pectus carinatum (a prominent birdlike sternum), may be associated with Marfan syndrome (which may be accompanied by aortic root or mitral valve disease) or Noonan syndrome. Rarely, a localized upper chest bulge indicates aortic aneurysm due to syphilis. Pectus excavatum (depressed sternum) with a narrow anteroposterior chest diameter and an abnormally straight thoracic spine may be associated with hereditary disorders involving congenital cardiac defects (eg, Turner syndrome, Noonan syndrome) and sometimes Marfan syndrome.
A central precordial heave is a palpable lifting sensation under the sternum and anterior chest wall to the left of the sternum; it suggests severe RV hypertrophy (RVH). Occasionally, in congenital disorders that cause severe RVH, the precordium visibly bulges asymmetrically to the left of the sternum.
A sustained thrust at the apex (easily differentiated from the less focal, somewhat diffuse precordial heave of RVH) suggests LV hypertrophy (LVH). Abnormal focal systolic impulses in the precordium can sometimes be felt in patients with a dyskinetic ventricular aneurysm. An abnormal diffuse systolic impulse lifts the precordium in patients with severe mitral regurgitation. The lift occurs because the left atrium expands, causing anterior cardiac displacement. A diffuse and inferolaterally displaced apical impulse is found when the LV is dilated and hypertrophied (eg, in mitral regurgitation).
Location of thrills (palpable buzzing sensation present with particularly loud murmurs) suggests the cause (see Table: Location of Thrills and Associated Disorders).
Location of Thrills and Associated Disorders
A sharp impulse at the 2nd intercostal space to the left of the sternum may result from exaggerated pulmonic valve closure in pulmonary hypertension. A similar early systolic impulse at the cardiac apex may represent closure of a stenotic mitral valve; opening of the stenotic valve sometimes can be felt at the beginning of diastole. These findings coincide with an augmented 1st heart sound and an opening snap of mitral stenosis, heard on auscultation.
Auscultation of the heart requires excellent hearing and the ability to distinguish subtle differences in pitch and timing. Hearing-impaired health care practitioners can use amplified stethoscopes. High-pitched sounds are best heard with the diaphragm of the stethoscope. Low-pitched sounds are best heard with the bell. Very little pressure should be exerted when using the bell. Excessive pressure converts the underlying skin into a diaphragm and eliminates very low-pitched sounds.
The entire precordium is examined systematically, typically beginning over the apical impulse with the patient in the left lateral decubitus position. The patient rolls supine, and auscultation continues at the lower left sternal border, proceeds cephalad with auscultation of each interspace, then caudad from the right upper sternal border. The clinician also listens over the left axilla and above the clavicles. The patient sits upright for auscultation of the back, then leans forward to aid auscultation of aortic and pulmonic diastolic murmurs or pericardial friction rub.
Major auscultatory findings include
Heart sounds are brief, transient sounds produced by valve opening and closure; they are divided into systolic and diastolic sounds.
Murmurs are produced by blood flow turbulence and are more prolonged than heart sounds; they may be systolic, diastolic, or continuous. They are graded by intensity (see Table: Heart Murmur Intensity) and are described by their location and when they occur within the cardiac cycle.
Rubs are high-pitched, scratchy sounds often with 2 or 3 separate components; during tachycardia, the sound may be almost continuous.
The clinician focuses attention sequentially on each phase of the cardiac cycle, noting each heart sound and murmur. Intensity, pitch, duration, and timing of the sounds and the intervals between them are analyzed, often providing an accurate diagnosis. A diagram of the major auscultatory and palpatory findings of the precordium should be routinely drawn in the patient’s chart each time the patient’s cardiovascular system is examined (see Figure: Diagram of physical findings in a patient with aortic stenosis and mitral regurgitation.). With such diagrams, findings from each examination can be compared.
Diagram of physical findings in a patient with aortic stenosis and mitral regurgitation.
Systolic sounds include the following:
S1 and the 2nd heart sound (S2, a diastolic heart sound) are normal components of the cardiac cycle, the familiar “lub-dub” sounds.
S1 occurs just after the beginning of systole and is predominantly due to mitral closure but may also include tricuspid closure components. It is often split and has a high pitch. S1 is loud in mitral stenosis. It may be soft or absent in mitral regurgitation due to valve leaflet sclerosis and rigidity but is often distinctly heard in mitral regurgitation due to myxomatous degeneration of the mitral apparatus or due to ventricular myocardial abnormality (eg, papillary muscle dysfunction, ventricular dilation).
Clicks occur only during systole; they are distinguished from S1 and S2 by their higher pitch and briefer duration. Some clicks occur at different times during systole as hemodynamics change. Clicks may be single or multiple.
Clicks in congenital aortic or pulmonic stenosis are thought to result from abnormal ventricular wall tension. These clicks occur early in systole (very near S1) and are not affected by hemodynamic changes. Similar clicks occur in severe pulmonary hypertension. Clicks in mitral or tricuspid valve prolapse, typically occurring in mid to late systole, are thought to result from abnormal tension on redundant and elongated chordae tendineae or valve leaflets.
Clicks due to myxomatous degeneration of valves may occur any time during systole but move toward S1 during maneuvers that transiently decrease ventricular filling volume (eg, standing, Valsalva maneuver). If ventricular filling volume is increased (eg, by lying supine), clicks move toward S2, particularly in mitral valve prolapse. For unknown reasons, characteristics of the clicks may vary greatly between examinations, and clicks may come and go.
S1 splitting is normal in many patients and is thought to be caused by mitral valve closure followed by an aortic ejection sound.
High pulmonary artery pressures may dilate the pulmonary artery, stretching the valve ring and causing a click when taut cusps open rapidly.
Diastolic sounds include the following:
Unlike systolic sounds, diastolic sounds are low-pitched; they are softer in intensity and longer in duration. Except for S2, these sounds are usually abnormal in adults, although an S3 may be physiologic up to age 40 and during pregnancy.
S2 occurs at the beginning of diastole, due to aortic and pulmonic valve closure. Aortic valve closure normally precedes pulmonic valve closure unless the former is late or the latter is early. Aortic valve closure is late in left bundle branch block or aortic stenosis; pulmonic valve closure is early in some forms of preexcitation phenomena. Delayed pulmonic valve closure may result from increased blood flow through the RV (eg, in atrial septal defect of the common secundum variety) or complete right bundle branch block. Increased RV flow in atrial septal defect also abolishes the normal respiratory variation in aortic and pulmonic valve closure, producing a fixed split S2. Left-to-right shunts with normal RV volume flow (eg, in membranous ventricular septal defects) do not cause fixed splitting. A single S2 may occur when the aortic valve is regurgitant, severely stenotic, or atretic (in truncus arteriosus when there is a common valve).
Sound is that of paradoxical splitting, ie, S1-P2-A2 at rest (“out”) and S1-S2 with inspiration (“in”). Left bundle branch block delays aortic valve closure, so that split is audible at rest; inspiration decreases intrathoracic pressure, drawing more blood into the right ventricle and postponing pulmonic valve closure until it is superimposed on A2 and splitting becomes inaudible.
Sound is that of wide splitting, ie, S1-A2-P2 at rest (“out”) with an even wider A2-P2 interval with inspiration (“in”). Right bundle branch block delays pulmonic valve closure so that S2 splitting becomes audible at rest. Inspiration decreases intrathoracic pressure, drawing more blood into the right ventricle and postponing pulmonic valve closure even more, so that the normal split becomes wider.
Sound is that of fixed S2 splitting, ie, S1-A2-P2 at rest (“out”) and with inspiration (“in”). Splitting is fixed because the volume of flow through the right ventricle is increased, eliminating the normal delay in closure of the pulmonic valve associated with inspiration.
Sound is that of S1-A2-OS with a relatively long A2-OS interval. The opening snap, most commonly caused by mitral stenosis, is thought to be caused by abrupt downward bulging (snapping) of the anterior leaflet as left ventricular pressure drops below left atrial pressure during diastole. A2-OS can be distinguished from a split S2 by dynamic maneuvers (OS intensity increases with inspiration, A2-OS interval widens with standing), a triple S2 (ie, A2-P2-OS), and a louder volume at the apex.
S3 occurs in early diastole, when the ventricle is dilated and noncompliant. It occurs during passive diastolic ventricular filling and usually indicates serious ventricular dysfunction in adults; in children, it can be normal, sometimes persisting even to age 40. S3 also may be normal during pregnancy. RV S3 is heard best (sometimes only) during inspiration (because negative intrathoracic pressure augments RV filling volume) with the patient supine. LV S3 is best heard during expiration (because the heart is nearer the chest wall) with the patient in the left lateral decubitus position.
S4 is produced by augmented ventricular filling, caused by atrial contraction, near the end of diastole. It is similar to S3 and heard best or only with the bell of the stethoscope. During inspiration, RV S4 increases and LV S4 decreases. S4 is heard much more often than S3 and indicates a lesser degree of ventricular dysfunction, usually diastolic. S4 is absent in atrial fibrillation (because the atria do not contract) but is almost always present in active myocardial ischemia or soon after MI. S3, with or without S4, is usual in significant systolic LV dysfunction; S4 without S3 is usual in diastolic LV dysfunction.
A summation gallop occurs when S3 and S4 are present in a patient with tachycardia, which shortens diastole so that the 2 sounds merge. Loud S3 and S4 may be palpable at the apex when the patient is in the left lateral decubitus position.
A diastolic knock occurs at the same time as S3, in early diastole. It is not accompanied by S4 and is a louder, thudding sound, which indicates abrupt arrest of ventricular filling by a noncompliant, constricting pericardium.
An opening snap may occur in early diastole in mitral stenosis or, rarely, in tricuspid stenosis. Mitral opening snap is very high pitched, brief, and heard best with the diaphragm of the stethoscope. The more severe mitral stenosis is (ie, the higher the left atrial pressure), the closer the opening snap is to the pulmonic component of S2. Intensity is related to the compliance of the valve leaflets: The snap sounds loud when leaflets remain elastic, but it gradually softens and ultimately disappears as sclerosis, fibrosis, and calcification of the valve develop. Mitral opening snap, although sometimes heard at the apex, is often heard best or only at the lower left sternal border.
Timing of the murmur in the cardiac cycle correlates with the cause (see Table: Etiology of Murmurs by Timing); auscultatory findings correlate with specific heart valve disorders. Various maneuvers (eg, inspiration, Valsalva, handgrip, squatting, amyl nitrate inhalation) can modify cardiac physiology slightly, making differentiation of causes of heart murmur possible (see Table: Maneuvers That Aid in Diagnosis of Murmurs).
Etiology of Murmurs by Timing
Maneuvers That Aid in Diagnosis of Murmurs
All patients with heart murmurs are evaluated by chest x-ray and ECG. Most require echocardiography to confirm the diagnosis, determine severity, and track severity over time. Usually, a cardiac consultation is obtained if significant disease is suspected.
Systolic murmurs may be normal or abnormal. They may be early, mid, or late systolic, or holosystolic (pansystolic). Systolic murmurs may be divided into ejection, regurgitant, and shunt murmurs.
Ejection murmurs are due to turbulent forward flow through narrowed or irregular valves or outflow tracts (eg, due to aortic or pulmonic stenosis). They are typically mid systolic and have a crescendo-diminuendo character that usually becomes louder and longer as flow becomes more obstructed. The greater the stenosis and turbulence, the longer the crescendo phase and the shorter the diminuendo phase.
Systolic ejection murmurs may occur without hemodynamically significant outflow tract obstruction and thus do not necessarily indicate a disorder. In normal infants and children, flow is often mildly turbulent, producing soft ejection murmurs. The elderly often have ejection murmurs due to valve and vessel sclerosis.
During pregnancy, many women have soft ejection murmurs at the 2nd intercostal space to the left or right of the sternum. The murmurs occur because a physiologic increase in blood volume and cardiac output increases flow velocity through normal structures. The murmurs may be greatly exaggerated if severe anemia complicates the pregnancy.
The 6th beat in this illustration is a ventricular premature beat (VPB). The 7th beat illustrates post-VPB potentiation of the murmur due to increased left ventricular filling during the post-VPB compensatory pause.
The murmur becomes audible only with inspiration (“in”) because inspiration decreases intrathoracic pressure, drawing more blood into the right ventricle and increasing right ventricular outflow.
This holosystolic mitral regurgitation murmur maintains the same intensity throughout systole and extends from S1 to S2.
The murmur of a ventricular septal defect is similar to that of mitral regurgitation but is louder at the left lower sternal border than at the apex.
Regurgitant murmurs represent retrograde or abnormal flow (eg, due to mitral regurgitation, tricuspid regurgitation, or ventricular septal defects) into chambers that are at lower resistance. They are typically holosystolic and tend to be louder with high-velocity, low-volume regurgitation or shunts and softer with high-volume regurgitation or shunts. Late systolic murmurs, which may or may not be preceded by a click, are typical of mitral valve prolapse or papillary muscle dysfunction. Various maneuvers are usually required for more accurate diagnosis of timing and type of murmur (see Table: Maneuvers That Aid in Diagnosis of Murmurs).
Shunt murmurs may originate at the site of the shunt (eg, patent ductus arteriosus, ventricular septal defects) or result from altered hemodynamics remote from the shunt (eg, pulmonic systolic flow murmur due to an atrial septal defect with left-to-right shunt).
Diastolic murmurs are always abnormal; most are early or mid diastolic, but they may be late diastolic (presystolic). Early diastolic murmurs are typically due to aortic or pulmonic regurgitation. Mid diastolic (or early to mid diastolic) murmurs are typically due to mitral or tricuspid stenosis. A late diastolic murmur may be due to rheumatic mitral stenosis in a patient in sinus rhythm.
A mitral or tricuspid murmur due to an atrial tumor or thrombus may be evanescent and may vary with position and from one examination to the next because the position of the intracardiac mass changes.
Continuous murmurs occur throughout the cardiac cycle. They are always abnormal, indicating a constant shunt flow throughout systole and diastole. They may be due to various cardiac defects (see Table: Etiology of Murmurs by Timing). Some defects produce a thrill; many are associated with signs of RVH and LVH. As pulmonary artery resistance increases in shunt lesions, the diastolic component gradually decreases. When pulmonary and systemic resistance equalize, the murmur may disappear.
Patent ductus arteriosus murmurs are loudest at the 2nd intercostal space just below the medial end of the left clavicle.Aorticopulmonary window murmurs are central and heard at the 3rd intercostal space level. Murmurs of systemic arteriovenous fistulas are best heard directly over the lesions; those of pulmonic arteriovenous fistulas and pulmonary artery branch stenosis are more diffuse and heard throughout the chest.
The murmur of patent ductus arteriosus is classically continuous and machine-like in character. It may be accompanied by an S3 and a mitral diastolic flow murmur when left-sided volumes are large.
Friction rubs are frequently described as creaking or scratching but may sound like more common murmurs. This rub is triphasic, with a soft systolic component and 2 louder components in quick succession during early diastole.
When circulation is increased, as occurs during pregnancy, anemia, and hyperthyroidism, a continuous venous hum is often heard in the right supraclavicular fossa; this venous hum also occurs normally in children. The sound generated by increased flow in a dilated internal mammary artery (mammary souffle), may be mistaken for a continuous cardiac murmur. Mammary souffle is typically heard best over the breast at the level of the right and/or left 2nd or 3rd intercostal space and, although often classified as continuous, is usually louder during systole.
A pericardial friction rub is caused by movement of inflammatory adhesions between visceral and parietal pericardial layers. It is a high-pitched or squeaking sound; it may be systolic, diastolic and systolic, or triphasic (when atrial contraction accentuates the diastolic component during late diastole). The rub sounds like pieces of leather squeaking as they are rubbed together. Rubs are best heard with the patient leaning forward or on hands and knees with breath held in expiration.
The abdomen and extremities are examined for signs of fluid overload, which may occur with heart failure as well as noncardiac disorders (eg, renal, hepatic, lymphatic).
In the abdomen, significant fluid overload manifests as ascites (see page Ascites). Marked ascites causes visible abdominal distention, which is tense and nontender to palpation, with shifting dullness on abdominal percussion and a fluid wave. The liver may be distended and slightly tender, with a hepatojugular reflux (see page Neck veins) present.
In the extremities (primarily the legs), fluid overload is manifest as edema (see page Edema), which is swelling of soft tissues due to increased interstitial fluid. Edema may be visible on inspection, but modest amounts of edema in very obese or muscular people may be difficult to recognize visually. Thus, extremities are palpated for presence and degree of pitting (visible and palpable depressions caused by pressure from the examiner’s fingers, which displaces the interstitial fluid). The area of edema is examined for extent, symmetry (ie, comparing both extremities), warmth, erythema, and tenderness. With significant fluid overload, edema may also be present over the sacrum, genitals, or both.
Tenderness, erythema, or both, particularly when unilateral, suggests an inflammatory cause (eg, cellulitis or thrombophlebitis). Nonpitting edema is more suggestive of lymphatic or vascular obstruction than fluid overload.
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