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The cardiac examination proper should commence with inspection of the chest, which can best be accomplished with the examiner standing at the side or foot of the bed or examining table. Respirations--their frequency, regularity, and depth--as well as the relative effort required during inspiration and exhalation, should be noted. Simultaneously, one should search for cutaneous abnormalities, such as spider nevi (seen in hepatic cirrhosis and Osler-Weber-Rendu disease). Dilation of veins on the anterior chest wall with caudal flow suggests obstruction of the superior vena cava, whereas cranial flow occurs in patients with obstruction of the inferior vena cava. Precordial prominence is most striking if cardiac enlargement developed before puberty, but may also be present, although to a lesser extent, in patients in whom cardiomegaly developed in adult life, after the period of thoracic growth. (54) (55)
A heavy muscular thorax, contrasting with less developed lower extremities, may occur in coarctation of the aorta, in which collateral arteries may be visible in the axillae and along the lateral chest wall. The upper portion of the thorax exhibits symmetrical bulging in children with stiff lungs in whom the inspiratory effort is increased. A "shield chest" is a broad chest in which the angle between the manubrium and the body of the sternum is greater than normal and is associated with widely separated nipples; shield chest is frequently observed in the Turner and Noonan syndromes. Careful note should be made of other deformities of the thoracic cage, such as kyphoscoliosis, which may be responsible for cor pulmonale (Chap. 47) ; ankylosing spondylitis, sometimes associated with aortic regurgitation (Chap. 56) ; and pectus carinatum (pigeon chest), which may be associated with Marfan syndrome but does not directly affect cardiovascular function.
Pectus excavatum, a condition in which the sternum is displaced posteriorly, is commonly observed in Marfan syndrome, homocystinuria, Ehlers-Danlos syndrome, Hunter-Hurler syndrome, and a small fraction of patients with mitral valve prolapse. This thoracic deformity rarely compresses the heart or elevates the systemic and pulmonary venous pressures, and the signs of heart disease are more
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These should be looked for on the entire chest but specifically in the regions of the cardiac apex, the left parasternal region, and the third left and second right intercostal spaces. Prominent pulsations in these areas suggest enlargement of the left ventricle, right ventricle, pulmonary artery, and aorta, respectively. A thrusting apex exceeding 2 cm in diameter suggests left ventricular enlargement; systolic retraction of the apex may be visible in constrictive pericarditis. Normally, cardiac pulsations are not visible lateral to the midclavicular line; when present there, they signify cardiac enlargement unless there is thoracic deformity or congenital absence of the pericardium. Shaking of the entire precordium with each heartbeat may occur in patients with severe valvular regurgitation, large left-to-right shunts, especially patent ductus arteriosus, complete AV block, hypertrophic obstructive cardiomyopathy, and various hyperkinetic states (Chap. 15) . Aortic aneurysms may produce visible pulsations of one of the sternoclavicular joints of the right anterior thoracic wall.
Pulsations of the heart and great arteries that are transmitted to the chest wall are best appreciated when the examiner is positioned on the right side of a supine patient. In order to palpate the movements of the heart and great arteries, the examiner should use the fingertips or the area just proximal thereto. Precordial movements should be timed by using the simultaneously palpated carotid pulse or auscultated heart sounds. (58) (59) (60) The examination should be carried out with the chest completely exposed and elevated
The apex beat, also referred to as the cardiac impulse and the apical thrust, is normally produced by left ventricular contraction and is the lowest and most lateral point on the chest at which the cardiac impulse can be appreciated and is normally above the anatomic apex (Fig. 2-10B) (Figure Not Available) . Although the apex beat may also be the point of maximal impulse (PMI), this is not necessarily the case, because the pulsations produced by other structures, e.g., an enlarged right ventricle, a dilated pulmonary artery, or an aneurysm of the aorta, may be more powerful than the apex beat. Normally the left ventricular impulse is medial and superior to the intersection of the left midclavicular line and the fifth intercostal space and is palpable as a single, brief outward motion. Although it may not be palpable in the supine position in as many as half of all normal subjects more than 50 years of age, the left ventricular impulse can usually be felt in the left lateral decubitus position. Displacement of the apex beat lateral to the midclavicular line or more than 10 cm lateral to the midsternal line is a sensitive but not specific indicator of left ventricular enlargement. However, when the patient is in the left lateral decubitus position a palpable apical impulse that has a diameter of more than 3 cm is an accurate sign of left ventricular enlargement. (61) Thoracic deformities--particularly scoliosis, straight back, and pectus excavatum--can result in the lateral displacement of a normal-sized heart.
The patient should be examined both supine and then in the left lateral decubitus position. The examination should be carried out with both the fingertips and the distal metacarpals. The subxiphoid region, which allows palpation of the right ventricle, should be examined with the tip of the index finger during held inspiration.
The apex cardiogram, which reflects the movement of the chest wall, represents the pulsation of the entire left ventricle. Its contour differs from what is perceived on palpation of the apex or what is recorded by the kinetocardiogram, a device in which the motion of specific points on the chest wall is recorded relative to a fixed point in space (62) and which therefore presents a more faithful graphic registration of the movements of the palpating finger on the chest wall.
During isovolumetric contraction, the heart normally rotates counterclockwise (as one faces the patient), and the lower anterior portion of the left ventricle strikes the anterior chest wall, causing a brief outward motion followed by medial retraction of the adjacent chest wall during ejection (Fig. 2-11) (Figure Not Available) . The segment of the left ventricle responsible for the apex beat is usually medial to the actual cardiac apex identified on radiological or angiographic examination. For timing purposes it is useful to correlate pulsations while simultaneously listening to heart sounds; a convenient way to do this is to correlate the observed motion of the stethoscope, placed lightly at the apex, with the auscultatory events.
The peak outward motion of the left ventricular impulse is brief and occurs simultaneously with, or just after, aortic valve opening; then the left ventricular apex moves inward. In asthenic persons, in patients with mild left ventricular enlargement, and in subjects with a normal left ventricle but an augmented stroke volume, as occurs in anxiety and other hyperkinetic states, and in mitral or aortic regurgitation, the cardiac impulse may be overactive but with a normal contour; i.e., the outward thrust during systole is exaggerated in amplitude, but it is not sustained during ejection.
With moderate or severe left ventricular concentric hypertrophy, the outward systolic thrust persists throughout ejection, often lasting up to the second heart sound (Fig. 2-11) (Figure Not Available) , and this motion is accompanied by retraction of the left parasternal region. This rocking motion can often be appreciated by placing the index finger of one hand on the apex beat and that of the other hand in the parasternal region and by observing the simultaneous outward motion of the former with retraction of the latter. The left ventricular heave or lift, which is more prominent in concentric hypertrophy than in left ventricular dilatation without volume overload, is characterized by a sustained outward movement of an area that is larger than the normal apex; i.e., it is more than 2 to 3 cm in diameter. In patients with left ventricular enlargement the systolic impulse is displaced laterally and downward into the sixth or seventh interspaces. In patients with ischemic heart disease a sustained apex beat is usually associated with a reduced ejection fraction. (63)
In patients with volume overload and/or sympathetic stimulation, the left ventricular impulse is hyperkinetic, i.e., it is brisker and larger than normal. It is hypokinetic in patients with reduced stroke volume, especially in acute myocardial infarction of dilated cardiomyopathy.
This produces a larger-than-normal area of pulsation of the left ventricular apex. Alternatively, it may produce a sustained systolic bulge several centimeters superior to the left ventricular impulse. In left ventricular pressure overload with normal ventricular function, the left ventricular impulse is prolonged and forceful. In patients with left ventricular dyskinesia, as occurs in acute myocardial ischemia following myocardial infarction, or left ventricular aneurysm, there may be two distinct impulses separated from each other by several centimeters; alternatively, a mid- or late systolic bulge may be palpated. In mitral stenosis there may be a brief prominent apical tap owing to an accentuated first sound, which must be distinguished from the apical thrust of the left ventricle.
A double systolic outward thrust of the left ventricle is characteristic of patients with hypertrophic obstructive cardiomyopathy (Fig. 2-12) who also often exhibit a typical presystolic cardiac expansion, thus resulting in three separate outward movements of the chest wall during each cardiac cycle. (46) In aortic regurgitation the apex exhibits a prominent outward thrust that may be followed by medial systolic retraction of the anterior chest wall as a consequence of the large stroke volume that evacuates the thorax during systole.
Constrictive pericarditis (as well as nonconstricting adherent pericarditis) is characterized by systolic retraction of the chest, particularly of the ribs in the left axilla (Broadbent s sign). This inward movement results from interference with the descent of the base of the heart and the compensatory exaggerated motion of the free wall of the left ventricle during ventricular ejection. (64) When left ventricular filling is very rapid during early diastole, outward movement of the chest wall may be particularly prominent and mistaken for systole, but it is usually accompanied by a third heart sound (see p. 35) . A hypokinetic apical impulse is associated with a variety of low cardiac output states, including those secondary to hypovolemia, constrictive pericarditis, and pericardial effusion.
The outward motion of the apex characteristic of rapid left ventricular diastolic filling is most readily palpated with the patient in the left lateral decubitus position and in full exhalation. The outward motion is accentuated when the inflow of blood into the left ventricle is accelerated, as occurs, for example, in mitral regurgitation, when the volume of the left ventricle is increased or its function is impaired. (55) This motion is the mechanical equivalent of and occurs simultaneously with a third heart sound. Prominent early diastolic left ventricular filling in constrictive pericarditis may be palpable.
When the atrial contribution to ventricular filling is augmented, as occurs in patients with reduced left ventricular compliance associated with concentric left ventricular hypertrophy, myocardial ischemia, and myocardial fibrosis, a presystolic pulsation (usually accompanying a fourth heart sound) is palpable, resulting in a double outward movement of the left ventricular impulse. This presystolic expansion is most readily discernible during exhalation, when the patient is in the left lateral decubitus position, and it can be confirmed by detecting the motion of the stethoscope placed over the left ventricular impulse or by observing the motion of an X mark over the left ventricular impulse. Presystolic expansion of the left ventricle can be enhanced by sustained handgrip, and is usually associated with marked elevation of left ventricular end-diastolic (rather than early diastolic) pressure. In contrast to prominence of early diastolic filling, in patients without ischemic
Figure 2-10 (Figure Not Available) A, Palpation of the anterior wall of the right ventricle
by applying the
tips of three fingers in the third, fourth, and fifth
interspaces, left sternal edge (arrows), during full held exhalation. Patient
is supine with the trunk elevated 30 degrees. B,
Subxiphoid
palpation of the inferior wall of the right ventricle (RV) with the relative
position of the abdominal aorta (Ao) shown by the arrow. C,
The bell of the stethoscope is applied to the cardiac apex while the patient
lies in a partial left lateral decubitus position. The thumb
of the examiner s free left hand is used to palpate the carotid artery for
timing purposes. D, The soft, high-frequency
early diastolic
murmur of aortic regurgitation or pulmonary hypertensive regurgitation is
best
elicited by applying the stethoscopic diaphragm very
firmly to the mid-left sternal edge. The patient leans forward with breath
held in full exhalation. E, Palpation of
the left ventricular
impulse with a fingertip (arrow). The patient s trunk is 30 degrees above
the
horizontal. The examiner s right thumb palpates the carotid
pulse for timing purposes. F, Palpation of
the liver. The patient is
supine with knees flexed to relax the abdomen. The flat of the
examiner s right hand is placed on the right upper quadrant just below the
expected inferior margin of the liver; the left hand is applied
diametrically opposite.
(From Perloff, J. K.: Physical Examination of the Heart and Circulation.
2nd
ed. Philadelphia, W. B. Saunders
Company, 1990.)
Figure 2-11 (Figure Not Available) Schematic diagrams of normal hyperdynamic and sustained left ventricular
impulse. Heart
sounds are also illustrated. A, Normal apex
cardiogram. The a
wave, related to ventricular filling during atrial
systole, usually does not exceed 15 per cent of the total height. E point
usually coincides with the beginning of
left ventricular ejection. Following E point, there is a gradual inward
movement, explaining the brief duration of
the normal left ventricular impulse. The O point approximately coincides
with
the mitral valve opening. B,
Hyperdynamic left ventricular impulse is usually seen in left ventricular
volume overloaded conditions such as
primary mitral regurgitation and aortic regurgitation. Left ventricular
ejection fraction is usually normal. Increased
amplitude of a wave may be associated with
palpable a waves, which
are usually associated with
increased left ventricular end-diastolic pressure. Accentuated rapid filling
wave is frequently associated with
audible S3
. C, Sustained left
ventricular impulse (outward movement
continued during ejection phase) is usually
seen in the presence of decreased ejection fraction or when the left ventricle
is markedly hypertrophied
(S4
= atrial sound; S1
= first heart sound;
A2
, = aortic component of the second
heart sound; a
= a wave; E
= E
point beginning of ejection; OM = outward
movement; O
= O point; RFW = rapid filling wave.)
(From Chatterjee,
K.: Bedside evaluation of the heart: The physical examination. In
Chatterjee, K., et al. (eds.): Cardiology: An
Illustrated Text/Reference. Philadelphia, J. B. Lippincott, 1991, pp.
3.11-3.51.)
Figure 2-12 Apex cardiogram in hypertrophic obstructive cardiomyopathy. The
a wave (A) is exaggerated in height, being
18 per cent
of the entire amplitude of the apexcardiogram (H), and has an unusually
rapid upstroke that culminates in a sharp peak, coinciding with
the fourth heart sound (4). The systolic phase of the apexcardiogram
has a bifid appearance with a prominent late systolic hump. The
saddle-shaped decline in midsystole coincides in time with the systolic
murmur and carotid pulse deformity, which, in turn, are related to the
obstruction occasioned by the systolic anterior motion of the mitral
valve.
(From Craige, E., and Smith, D.: Heart sounds. In Braunwald, E.
(ed.): Heart Disease: A Textbook of Cardiovascular Medicine. 3rd
ed. Philadelphia,
W. B. Saunders Company, 1988, p. 59.)
Normally, neither this chamber, nor its motion, is palpable. A palpable anterior systolic movement (replacing systolic retraction) in the left parasternal region (Fig. 2-10A) (Figure Not Available) , best felt by the proximal palm or fingertips, and with the patient supine, usually represents right ventricular enlargement or hypertrophy. (65) In the absence of associated left ventricular enlargement, the right ventricular impulse is accompanied by reciprocal systolic retraction of the apex. In patients with pulmonary emphysema, even an enlarged right ventricle is not readily palpable at the left sternal edge but is better appreciated in the subxiphoid region. Exaggerated motion of the entire parasternal area, i.e., a hyperdynamic impulse with normal contour, usually reflects increased right ventricular contractility due to augmented stroke volume, as occurs in patients with atrial septal defect or tricuspid regurgitation, whereas a sustained left parasternal outward thrust reflects right ventricular hypertrophy due to pressure overload, as occurs in pulmonary hypertension or pulmonic stenosis. With marked right ventricular enlargement, this chamber occupies the apex because the left ventricle is displaced posteriorly.
When both ventricles are enlarged, both the left parasternal and the apical areas may rise with systole, but an area of systolic retraction between them can usually be appreciated. In patients with emphysema or obesity, an enlarged right ventricle is detected most readily in the subxiphoid region by palpating the epigastrium and pointing the fingers upward. With marked isolated right ventricular enlargement, the right ventricle may form the cardiac apex, and should not be confused with those of left or biventricular enlargement. When acute myocardial ischemia or myocardial infarction causes dyskinetic movement of the ventricular septum, there may be a transient left parasternal impulse not caused by right ventricular enlargement.
Pulmonary hypertension and/or increased pulmonary blood flow frequently produce a prominent systolic pulsation of the pulmonary trunk in the second intercostal space just to the left of the sternum. This pulsation is often associated with a prominent left parasternal impulse, reflecting right ventricular enlargement, or hypertrophy and a palpable shock synchronous with
An enlarged left atrium or a large posterior left ventricular aneurysm can make right ventricular pulsations more prominent by displacing the right ventricle anteriorly against the left parasternal area, and in severe mitral regurgitation an expanding left atrium may be responsible for marked left parasternal movement, even in the absence of right ventricular hypertrophy. The systolic bulging of the left atrium, which is transmitted through the right ventricle, commences and terminates after the left ventricular thrust. Movement imparted by the systolic expansion of the left atrium can be appreciated by placing the index finger of one hand at the left ventricular apex and the index finger of the other in the left parasternal region in the third intercostal space; the movement of the latter finger begins and ends slightly later than that of the former. Although this difference in timing may be difficult to appreciate on palpation, particularly when the heart rate is rapid, recordings of chest wall motion in severe chronic mitral regurgitation demonstrate a delayed fall in the left lower precordium compared with the cardiac apex. Outward movement of the chest wall that is more marked to the right than to the left of the sternum is usually due to aneurysm of the aorta or to marked enlargement of the right atrium in the presence of tricuspid regurgitation. Occasionally, a giant left atrium is palpable in the right hemithorax. The left atrial appendage is sometimes visible and palpable in the third left intercostal space.
Enlargement or aneurysm of the ascending aorta or aortic arch may cause visible or palpable systolic pulsations of the right or left sternoclavicular joint; and may also cause a systolic impulse in the suprasternal notch or the first or second right intercostal space. (1)
Valve closure, if abnormally forceful or if normal in a patient with a thin chest wall, can be appreciated as a tapping sensation. A palpable sound occurs most prominently in the second left intercostal space in patients with pulmonary hypertension (pulmonic valve closure), in the second right intercostal space in patients with systemic hypertension (aortic valve closure), and at the cardiac apex in patients with mitral stenosis (mitral valve closure). Occasionally, in congenital aortic stenosis, aortic ejection sounds can be palpated at the cardiac apex; ejection sounds originating in a dilated aorta or pulmonary artery can sometimes be felt at the base of the heart. (61) Prominent third and fourth heart sounds are often palpable as diastolic movements at the cardiac apex. In patients with mitral stenosis an opening snap may be palpated at the apex.
The flat of the hand or the fingertips usually best appreciate thrills, vibratory sensations which are palpable manifestations of loud, harsh murmurs having low-frequency to medium components. (66) Because the vibrations must be quite intense before they are felt, far more information can be obtained from the auscultatory than from the palpatory features of heart murmurs. High-pitched murmurs such as those produced by valvular regurgitation, even when loud, are not usually associated with thrills.
Palpation is far more helpful than is percussion in determining cardiac size. However, in the absence of an apical beat, as in patients with pericardial effusion, or in some patients with dilated cardiomyopathy, heart failure, and marked displacement of a hypokinetic apical beat, the left border of the heart can be outlined by means of percussion. Also, percussion of dullness in the right lower parasternal area may, in some instances, aid in the detection of a greatly enlarged right atrium. Percussion aids materially in determining visceral situs, i.e., in ascertaining the side on which the heart, stomach, and liver are located. When the heart is in the right chest but the abdominal viscera are located normally, congenital heart disease is usually present. When both the heart and abdominal viscera are in the opposite side of the chest (situs inversus), congenital heart disease is uncommon.
The modern binaural stethoscope is a well-crafted, airtight instrument with earpieces selected for comfort, with metal tubing joined to single flexible 12-inch-long, thick-walled rubber tubing (internal diameter of 1/8 inch) and with dual chest pieces--diaphragm for high frequencies, bell for low or lower frequencies--designed so that the examiner can readily switch from one chest piece to the other. (67) (68) When the bell is applied with just enough pressure to form a skin seal, low frequencies are accentuated; when the bell is pressed firmly, the stretched skin becomes a diaphragm, damping low frequencies. Variable pressure with the bell provides a range of frequencies from low to medium.
Cardiac auscultation is best accomplished in a quiet room with the patient comfortable and the chest fully exposed. Percussion
Figure 2-13 (Figure Not Available) Maximal intensity and radiation of six isolated systolic
murmurs. HCM = hypertrophic cardiomyopathy; MI = mitral
incompetence;
Pulm = pulmonary; VSD = ventricular septal defect.
(From
Barlow, J. B.: Perspectives on the Mitral Valve. Philadelphia, F. A.
Davis, 1987, p. 140.)
Information derived from auscultation benefits not only from knowledge of the cardiac situs, but also from identification of palpable and visible movements of the ventricles. During auscultation, the examiner is generally on the patient s right; three positions are routinely employed: left lateral decubitus (assuming left thoracic heart), supine, and sitting. Auscultation should begin by applying the stethoscope to the cardiac apex with the patient in the left lateral decubitus position (Fig. 2-14) . If tachycardia makes identification of the first heart sound difficult, timing can be established, with few exceptions, by simultaneous palpation of the carotid artery with the thumb of the free left hand (Fig. 2-14) . Once the first heart sound is identified, analysis then proceeds by systematic, methodical, sequential attention to early, mid, and late systole, the second heart sound, then early, mid, and late diastole (presystole), returning to the first heart sound. When auscultation at the apex has been completed, the patient is turned into the supine position. Each topographic area--lower to upper left sternal edge interspace by interspace and then the right base--is interrogated using the same systematic sequence of analysis.
Assessment of pitch or frequency ranging from low to moderately high can be achieved by variable pressure of
Figure 2-14 The bell
of the stethoscope is applied to the cardiac
apex while the patient lies in a left lateral decubitus position. The
thumb of the examiner s free left hand palpates the carotid artery
(arrow) for timing purposes.
Heart sounds are relatively brief, discrete auditory vibrations of varying intensity (loudness), frequency (pitch), and quality (timbre). The first heart sound identifies the onset of ventricular systole, and the second heart sound identifies the onset of diastole. These two auscultatory events establish a framework within which other heart sounds and murmurs can be placed and timed. (1)
The basic heart sounds are the first, second, third, and fourth sounds (Fig. 2-15A) . Each of these events can be normal or abnormal. Other heart sounds are, with few exceptions, abnormal, either intrinsically so or iatrogenic (e.g., prosthetic valve sounds, pacemaker sounds). A heart sound should first be characterized by a simple descriptive term that identifies where in the cardiac cycle the sound occurs. Accordingly, heart sounds within the framework established by the first and second sounds are designated as "early systolic, mid-systolic, late systolic," and "early diastolic, mid-diastolic, late diastolic (presystolic)" (Fig. 2-15B) . (2) The next step is to draw conclusions based upon what a sound so identified represents. An early systolic sound might be an ejection sound (aortic or pulmonary) or an aortic prosthetic sound. Mid- and late systolic sounds are typified by the click(s) of mitral valve prolapse but occasionally are "remnants" of pericardial rubs. Early diastolic sounds are represented by opening snaps (usually mitral), early third heart sounds (constrictive pericarditis, less commonly mitral regurgitation), the opening of a mechanical inflow prosthesis, or the abrupt seating of a pedunculated mobile atrial myxoma ("tumor plop"). Mid-diastolic sounds are generally third heart sounds or summation sounds (synchronous occurrence of third and fourth heart sounds). Late diastolic or presystolic sounds are almost always fourth heart sounds, rarely pacemaker sounds.
Figure 2-15 A, The basic heart sounds consist of the first heart
sound (S1
), the second heart sound (S2
), the third heart
sound
(S3
), and
the fourth heart sound (S4
). B,
Heart sounds within the
auscultatory
framework established by the first heart sound (S1
) and the second
heart sound (S2
). The additional heart sounds are designated
descriptively
as early systolic (ES), midsystolic (MS), late systolic (LS), early
diastolic (ED), mid-diastolic (MD), and late diastolic (LD) or
presystolic. C,
Upper tracing illustrates a low-frequency fourth heart sound
(S4
), and the lower tracing illustrates a split first heart sound
(S1
), the
two components of which are of the same quality.
The first heart sound consists of two major components (Fig. 2-15C) . The initial component is most prominent at the cardiac apex when the apex is occupied by the left ventricle. (69) The second component, if present, is normally confined to the lower left sternal edge, is less commonly heard at the apex, and is seldom heard at the base. The first major component is associated with closure of the mitral valve and coincides with abrupt arrest of leaflet motion when the cusps--especially the larger and more mobile anterior mitral cusp--reach their fully closed positions (maximal cephalad systolic excursion into the left atrium). The origin of the second major component of the first heart sound has been debated but is generally assigned to closure of the tricuspid valve based upon an analogous line of reasoning. (70) Opening of the semilunar valves with ejection of blood into the aortic root or pulmonary trunk usually produces no audible sound in the normal heart, although phonocardiograms sometimes record a low-amplitude sound following the mitral and tricuspid components and coinciding with the maximal opening excursion of the aortic cusps. (1) In complete right bundle branch block the first heart sound is widely split as a result of delay of the tricuspid component. (71) In complete left bundle branch block, the first heart sound is single as a result of delay of the mitral component. (72)
Because the two major audible components of the first heart sound are believed to originate in the closing movements of the atrioventricular valves, the quality of the two components (pitch) is similar (Fig. 2-15C) . When the first heart sound is split, its first component is normally the
Figure 2-16 Upper tracing, Phonocardiogram and
electrocardiogram (lead 2) from a 12-year-old girl with
congenital complete heart block. The first heart sound
(S1
) varies from soft (long P-R interval) to loud (short
P-R interval). There is a grade 2/6 vibratory midsystolic
murmur (SM). A soft fourth heart sound (arrow) follows
the second P wave. Lower tracing, Phonocardiogram
and electrocardiogram from a 15-year-old boy
with congenital complete heart block. Arrows point to
independent P waves. The first heart sound (S1
) varies
from loud to soft depending upon the P-R interval. The
short diastolic murmurs (DM) are especially prominent
when atrial contraction (P wave) coincides with and
reinforces the rapid filling phase (shortly after the T
wave).
Aortic or pulmonary ejection sounds are the most common early systolic sounds. (76) "Ejection sound" is preferred to the term ejection "click," with the latter designation best reserved for the mid- to late systolic clicks of mitral valve prolapse (see p. 1032) . Ejection sounds coincide with the fully opened position of the relevant semilunar valve, as in congenital aortic valve stenosis (Fig. 2-17A) or bicuspid aortic valve in the left side of the heart, or pulmonary valve stenosis (Fig. 2-18) in the right side of the heart. (75) (77) Ejection sounds are relatively high frequency events, and depending upon intensity, have a pitch similar to that of the two major components of the first heart sound. An ejection sound originating in the aortic valve (congenital aortic stenosis or bicuspid aortic valve) or in the pulmonary valve (congenital pulmonary valve stenosis) indicates that the
Figure 2-17 A, Phonocardiogram over the left ventricular impulse
in a patient with mild congenital bicuspid aortic valve stenosis. The
aortic ejection sound (E) is louder than the first heart sound
(S1
). A2
= Aortic component of the second heart sound.
B, Left
ventriculogram
(LV) in another patient with congenital aortic valve stenosis. The
cephalad systolic doming of the stenotic valve (arrows) produces the
ejection sound.
Pulmonary ejection sounds often selectively and distinctively decrease in intensity during normal inspiration (Fig. 2-19A) . The mechanism responsible for respiratory variation of a pulmonary ejection sound is most convincing in the setting of typical pulmonary valve stenosis. (78) An inspiratory increase in right atrial contractile force is transmitted into the right ventricle and onto the ventricular surface of the mobile stenotic valve, moving its cusps upward before the onset of ventricular contraction. Cephalad excursion of the valve during ventricular systole is therefore diminished, accounting for the inspiratory decrease in intensity of the ejection sound. This mechanism cannot apply to the respiratory variation of a pulmonary ejection sound associated
Figure 2-18 A, Phonocardiogram in the second left intercostal
space of a patient with congenital pulmonary valve stenosis. The
ejection sound (E) is obvious during exhalation (EXP) but disappears
entirely during casual inhalation (INSP). The pulmonary component of
the second heart sound (P2
) is delayed and soft. SM = Systolic
murmur;
S1
= first heart sound. B, Right
ventriculogram (RV) in
another
patient with pulmonary valve stenosis. The cephalad systolic doming
of the mobile stenotic valve (arrow) produces the pulmonary
ejection sound. There is post-stenotic dilatation of the pulmonary
trunk (PT).
Figure 2-19 Phonocardiograms from an 11-year-girl with Fallot s
tetralogy and pulmonary atresia. The upper tracing from the second
right intercostal space (2RICS) shows an aortic ejection sound (E) that
is prominent during exhalation (EXP) but absent during inspiration
(INSP). The lower tracing from the left midchest shows a continuous
murmur of aortopulmonary collaterals. The second heart sound is
necessarily single and is represented by the aortic component
(A2
). S1
= First heart sound.
Figure 2-20 (Figure Not Available) Composite of the
principal auscultatory and phonocardiographic
manifestations of
pulmonary hypertension.
(From
Perloff, J. K.: Auscultatory and
phonocardiographic manifestations
of pulmonary hypertension. Prog.
Cardiovasc. Dis. 9:303, 1967.)
Figure 2-21 (Figure Not Available) Postural maneuvers that affect the
click(s) and late systolic murmur (SM) of mitral valve
prolapse. A change from supine to sitting or standing
causes the click to become earlier and the murmur
longer although softer. Conversely, squatting delays the
timing of the click, and the murmur becomes shorter
but louder.
(From Devereux, R., Perloff, J. K., Reichek,
N., and Josephson, M.: Mitral valve prolapse. Circulation
54:3, 1976, by permission of the American Heart
Association.)
Early systolic sounds accompany mechanical prostheses in the aortic location, especially the Starr-Edwards ball-incage valve, less so with a tilting disc valve such as the Bjork-Shiley. Early systolic sounds do not occur with bioprosthetic valves (tissue valves) in either the aortic or pulmonary location.
Far and away the most common mid- to late systolic sound(s) are associated with mitral valve prolapse (2) (79) (80) (see p. 1029) . The term "click" is appropriate because these mid- to late systolic sounds are of relatively high frequency and often, but not invariably, "clicking." Mid- to late systolic clicks of mitral valve prolapse coincide with maximal systolic excursion of a prolapsed leaflet (or scallop(s) of the posterior leaflet) into the left atrium and are ascribed to sudden tensing of the redundant leaflet(s) and elongated chordae tendinae. Variability epitomizes mitral systolic clicks, which from time-to-time may be replaced by a cluster of discrete late systolic "crackles." Physical or pharmacological interventions that reduce left ventricular volume, such as the Valsalva maneuver, or a change in position from squatting to standing (Fig. 2-21) (Figure Not Available) causes the click(s) to occur earlier in systole. (79) (80) (81) (82) Conversely, physical or pharmacological interventions that increase left ventricular volume, such as squatting (Fig. 2-21) (Figure Not Available) or sustained hand grip, serve to delay the timing of the click(s). Multiple clicks are thought to arise from asynchronous tensing of different
On rare occasions, a pericardial friction rub leaves in its wake mid- to late systolic sounds--remnants of rubs--that persist after disappearance of the systolic phase of the rub. Carl Potain, in 1894, commented upon "small, short clicking sounds, well localized and such that one can scarcely attribute them to anything except the tensing of a pericardial adhesion." (83)
Respiratory splitting of the second heart sound was described by Potain in 1866, (84) and Leatham called the second heart sound the "key to auscultation of the heart." (85) The first component of the second heart sound is designated "aortic" and the second "pulmonary." (86) (87) Each component coincides with the dicrotic incisura of its great arterial pressure pulse (Fig. 2-22) . (69) Inspiratory splitting of the second heart sound is due chiefly to a delay in the pulmonary component, less to earlier timing of the aortic component. (88) During inspiration, the pulmonary arterial dicrotic incisura moves away from the descending limb of the right ventricular pressure pulse because of an inspiratory increase in capacitance of the pulmonary vascular bed, delaying the pulmonary component of the second heart sound. (89) Exhalation has the opposite effect. The earlier inspiratory timing of the aortic component of the second heart sound is attributed to a transient reduction in left ventricular volume coupled with unchanged impedance (capacitance) in the systemic vascular bed. Normal respiratory variations in the timing of the second heart sound are therefore ascribed principally to the variations in impedance characteristics (capacitance) of the pulmonary vascular bed, not to an inspiratory increase in right ventricular volume as originally proposed. (69) (85) When an increase in capacitance of the pulmonary bed is lost because of a rise in pulmonary vascular resistance, inspiratory splitting of the second heart sound narrows and, if present at all, reflects an increase in right ventricular ejection time and/or earlier timing of the aortic component. (2)
The frequency compositions of the aortic and pulmonary components of the second heart sound are similar, but their normal amplitudes differ appreciably, reflecting the differences in systemic (aortic) and pulmonary arterial closing
Figure 2-22 Tracings from a 28-year-old woman with an uncomplicated
ostium secundum atrial septal defect. In the second left interspace
(2LICS), the pulmonary component (P2
) of a widely split second
heart sound is synchronous with the dicrotic notch (DN) of the pulmonary
arterial pressure pulse. (S1
= First heart sound; SM =
midsystolic murmur). In the lower tracing, the aortic component (A2
)
of the widely split second heart sound is synchronous with the dicrotic
notch of the carotid arterial pulse (CAR).
| NORMAL SPLITTING |
| DELAYED PULMONIC CLOSURE |
| Delayed electrical activation of the right ventricle |
| Complete RBBB (proximal type) |
| Left ventricular paced beats |
| Left ventricular ectopic beats |
| Prolonged right ventricular mechanical systole |
| Acute massive pulmonary embolus |
| Pulmonary hypertension with right heart failure |
| Pulmonic stenosis with intact septum (moderate to severe) |
| Decreased impedance of the pulmonary vascular bed (increased hang-out) |
| Normotensive atrial septal defect |
| Idiopathic dilatation of the pulmonary artery |
| Pulmonic stenosis (mild) |
| Atrial septal defect, postoperative (70%) |
| EARLY AORTIC CLOSURE |
| Shortened left ventricular mechanical systole (LVET) |
| Mitral regurgitation |
| Ventricular septal defect |
|
|
| REVERSED SPLITTING |
| DELAYED AORTIC CLOSURE |
| Delayed electrical activation of the left ventricle |
| Complete LBBB (proximal type) |
| Right ventricular paced beats |
| Right ventricular ectopic beats |
| Prolonged left ventricular mechanical systole |
| Complete LBBB (peripheral type) |
| Left ventricular outflow tract obstruction |
| Hypertensive cardiovascular disease |
| Arteriosclerotic heart disease |
| Chronic ischemic heart disease |
| Angina pectoris |
| Decreased impedance of the systemic vascular bed (increased hang-out) |
| Poststenotic dilatation of the aorta secondary to aortic stenosis or insufficiency |
| Patent ductus arteriosus |
| EARLY PULMONIC CLOSURE |
| Early electrical activation of the right ventricle |
| Wolff-Parkinson-White syndrome, type B |
| RBBB = right bundle-branch block; LVET = left ventricular ejection time; LBBB = left bundle-branch block. |
| Modified from Shaver, J. A., and O Toole, J. D.: The second heart sound: Newer concepts. Parts 1 and 2. Mod. Concepts Cardiovasc. Dis. 46:7 and 13, 1977. |
Three general categories of abnormal splitting are recognized: (1) persistently single, (2) persistently split (fixed or nonfixed), and (3) paradoxically split (reversed). When the second heart sound remains single throughout the respiratory cycle, one component is absent or the two components are persistently synchronous. The most common cause of a single second heart sound is inaudibility of the pulmonary component in older adults with increased anteroposterior chest dimensions. In the setting of congenital heart disease, a single second heart sound due to absence of the pulmonary component is a feature of pulmonary atresia (Fig. 2-18) , severe pulmonary valve stenosis, dysplastic pulmonary valve or complete transposition of the great arteries (pulmonary component inaudible because of the posterior position of the pulmonary trunk). (75) Conversely, a single second heart sound due to inaudibility of the aortic component occurs when the aortic valve is immobile (severe calcific aortic stenosis) or atretic (aortic atresia). A single second sound due to persistent synchrony of its two components is a feature of Eisenmenger s complex, in which the aortic
Both components of the second heart sound are sometimes inaudible at all precordial sites. This is likely to be so in older adults in whom fibrocalcific changes limit mobility of the aortic valve, whereas the pulmonary component is inaudible because of a large anteroposterior chest dimension (see above).
A single semilunar valve, as in truncus arteriosus, does not necessarily generate what is judged on auscultation to be a single second heart sound. Instead, the second sound may be perceived as "split" because of asynchronous closure of the unequal cusps of a quadricuspid valve. (75) In systemic or pulmonary hypertension, the duration of a single loud second heart sound may be sufficiently prolonged and slurred (reduplicated) to encourage the mistaken impression of splitting.
This term applies when the two components remain audible (or recordable) during both inspiration and exhalation. Persistent splitting may be due to a delay in the pulmonary component, as in simple complete right bundle branch block (69) or to early timing of the aortic component, as occasionally occurs in mitral regurgitation. (90) Normal directional changes in the interval of the split (greater with inspiration, lesser with exhalation) in the presence of persistent audibility of both components defines the split as persistent but not fixed.
This term applies when the interval between the aortic and pulmonary components is not only wide and persistent, but remains unchanged during the respiratory cycle. (69) Fixed splitting is an auscultatory hallmark of uncomplicated ostium secundum atrial septal defect. The aortic and pulmonary components are widely separated during exhalation and exhibit little or no change in the degree of splitting during inspiration or with the Valsalva maneuver. The wide splitting is caused by a delay in the pulmonary component because a marked increase in pulmonary vascular capacitance prolongs the interval between the descending limbs of the pulmonary arterial and right ventricular pressure pulses ("hangout"), and therefore delays the pulmonary incisura and the pulmonary component of the second heart sound (Fig. 2-22) . The capacitance (impedance) of the pulmonary bed is appreciably increased, so there is little or no additional increase during inspiration and little or no inspiratory delay in the pulmonary component of the second sound. Phasic changes in systemic venous return during respiration in atrial septal defect are associated with reciprocal changes in the volume of the left-to-right shunt, minimizing respiratory variations in right ventricular filling. The net effect is the characteristic wide fixed splitting of the two components of the second heart sound. (75)
This term refers to a reversed sequence of semilunar valve closure, the pulmonary component (P2 ) preceding the aortic component (A2 ). (69) Common causes of paradoxical splitting are complete left bundle branch block (91) or a right ventricular pacemaker, both of which are associated with initial activation of the right side of the ventricular septum, and delayed activation of the left ventricle owing to transseptal (right-to-left) depolarization. (92) When the second heart sound splits paradoxically, its two components separate during exhalation and become single (synchronous) during inspiration. Inspiratory synchrony is achieved as the two components fuse because of a delay in the pulmonary component, less to earlier timing of the aortic component.
Assessment of intensity requires that both components be compared when heard simultaneously at the same site. The relative softness of the normal pulmonary component is responsible for its localization in the second left intercostal space, whereas the relative loudness of the normal aortic component accounts for its audibility at all precordial sites (see earlier). (2) An increase in intensity of the aortic component of the second sound occurs with systemic hypertension. The intensity of the aortic component also increases when the aorta is closer to the anterior chest wall owing to root dilatation or transposition of the great arteries, or when an anterior pulmonary trunk is small or absent, as in pulmonary atresia (Fig. 2-18) . (75)
A loud pulmonary component of the second heart sound (Fig. 2-20) (Figure Not Available) and (Fig. 2-23A) is a feature of pulmonary hypertension, and the loudness is enhanced by dilatation of a hypertensive pulmonary trunk. Graham Steell, in describing the auscultatory signs of pulmonary hypertension, remarked that "... extreme accentuation of the pulmonary second sound is always present, the closure of the pulmonary semilunar valve being generally perceptible to the hand placed over the pulmonary area, as a sharp thud." (93) An accentuated pulmonary component can be transmitted to the mid or lower left sternal edge, and when very loud, throughout the precordium to the apex and right base. A loud pulmonary component in the second left interspace may obscure a closely preceding aortic component. In this eventuality, auscultation at other precordial sites often identifies the transmitted but attenuated pulmonary component and allows detection of splitting. A moderate increase in loudness of the pulmonary component of the second heart sound sometimes occurs in the absence of pulmonary hypertension when the pulmonary trunk is dilated, as with idiopathic dilatation or ostium secundum atrial septal defect, or when there is a decrease in anteroposterior chest dimensions (loss of thoracic kyphosis) that places the pulmonary trunk closer to the chest wall. (94)
The opening snap of rheumatic mitral stenosis is the best known early diastolic sound (Fig. 2-23B) . The term "snap" was introduced in 1908 by W. S. Thayer as the English equivalent to the "claquement d ouverture" of Rouches. (95) The diagnostic value derived from the pitch, loudness, and
Figure 2-23 A, Tracings from a 32-year-old woman with an ostium
secundum atrial septal defect, pulmonary hypertension, and a
small right-to-left shunt. In the second left intercostal space (2LICS),
the first heart sound is followed by a prominent pulmonary ejection
sound (E). The second sound remains split. The pulmonary component
(P2
) is very loud and is transmitted to the apex. (CAR = Carotid
pulse). B, Phonocardiogram recorded in the
left lateral decubitus
position
over the left ventricular impulse in a patient with pure rheumatic
mitral stenosis. The first heart sound (S1
) is loud. The second
heart
sound (S2
) is followed by an opening snap (OS). There is a mid-diastolic
murmur (MDM). The prominent presystolic murmur (PM) goes
up to the subsequent loud first heart sound.
The timing of the opening snap (OS) relative to the aortic component of the second heart sound (A2 ) has important physiological meaning. (2) A short A2 -OS interval generally reflects the high left atrial pressure of severe mitral stenosis. However, in older subjects with systolic hypertension, mitral stenosis of appreciable severity can occur without a short A2 -OS interval because the elevated left ventricular systolic pressure takes longer to fall below the left atrial pressure. In the presence of atrial fibrillation, the A2 -OS interval varies inversely with cycle length, because (all else being equal) the higher the left atrial pressure (short cycle length), the earlier the stenotic valve opens and vice versa.
Early diastolic sounds are not confined to the opening snap of rheumatic mitral stenosis. In 1842, Dominic Corrigan, in a presentation to the Pathological Society of Dublin, described a "very loud bruit de frappement" in a patient with chronic constrictive pericarditis. (98) In French, "frapper" means "to knock," implying that Corrigan s "bruit de frappement" was what has come to be known as the pericardial "knock" of chronic constrictive pericarditis. (99) The term "knock" has also been applied to an early diastolic sound in pure severe mitral regurgitation with reduced left ventricular compliance. Both Corrigan s "pericardial knock" and the "knock" of mitral regurgitation are rapid filling sounds that are early and loud because a high-pressure atrium rapidly decompresses across an unobstructed AV valve into a recipient ventricle whose compliance is impaired.
Early diastolic sounds are sometimes caused by atrial myxomas. (100) The generation of such a sound, called a tumor "plop," requires a mobile myxoma attached to the atrial septum by a long stalk. The "plop" is believed to result from abrupt diastolic seating of the tumor within the right or left AV orifice. (100)
An early diastolic sound is generated by the opening movement of a mechanical prosthesis in the mitral location. This opening sound is especially prominent with a ball-in-cage prosthesis (Starr-Edwards) and less prominent with a tilting disc prosthesis (Bjork-Shiley).
Mid-diastolic sounds are, for all practical purposes, either normal or abnormal third heart sounds, and most if not all late diastolic or presystolic sounds are fourth heart sounds (Fig. 2-24) . Each sound coincides with its relevant diastolic filling phase. (101) In sinus rhythm, the ventricles receive blood during two filling phases (Fig. 2-24) . The first phase occurs when ventricular pressure drops sufficiently to allow the AV valve to open; blood then flows from atrium into ventricle. This flow coincides with the y descent of the atrial pressure pulse (Fig. 2-24) and is designated the "rapid filling phase," accounting for about 80 per cent of normal ventricular filling. The rapid filling phase is not a passive event in which the recipient ventricle merely expands in response to augmented inflow volume. Rather, ventricular relaxation is an active, complex, energy-dependent process.
Figure 2-24 Atrial pressure pulse showing the a wave and x descent,
and the v wave and y descent. The fourth heart sound (S4
)
coincides with the phase of ventricular filling following atrial
contraction. The
third heart sound (S3
) coincides with the y descent (the
phase of rapid ventricular filling). S1
= First heart sound;
S2
= second
heart sound.
The sound generated during the rapid filling phase is called the third heart sound (Fig. 2-24) . (102) The second filling phase--diastasis--is variable in duration, usually accounting for less than 5 per cent of ventricular filling. The third phase of diastolic filling is in response to atrial contraction, which accounts for about 15 per cent of normal ventricular filling. The sound generated during the atrial filling phase is called the fourth heart sound (Fig. 2-24) . Third and fourth heart sounds occur within the recipient ventricle as that chamber receives blood. Potain in 1876 attributed the third heart sound to sudden cessation of distention of the ventricle in early diastole, and he attributed the fourth heart sound to "... the abruptness with which the dilatation of the ventricle takes place during the presystolic period, a period which corresponds to the contraction of the auricle." (103) On both counts, he was not far from the mark.
The addition of either a third or a fourth heart sound to the cardiac cycle produces a triple rhythm. If both third and fourth heart sounds are present, a quadruple rhythm is produced. When diastole is short or the PR interval long, third and fourth heart sounds occur synchronously to form a summation sound. (2)
Children and young adults often have normal (physiological) third heart sounds but do not have normal fourth heart sounds. (104) Normal third heart sounds sometimes persist beyond age 40 years, especially in women. (105) After that age, however, especially in men, the third heart sound is likely to be abnormal. (106) Fourth heart sounds are sometimes heard in healthy older adults without clinical evidence of heart disease, particularly after exercise. (107) Such observations have led to the conclusion, still debated, that these fourth heart sounds are normal for age.
Because a fourth heart sound requires active atrial contribution to ventricular filling, the sound disappears when coordinated atrial contraction ceases, as in atrial fibrillation. When the atria and ventricles contract independently as in complete heart block (Fig. 2-16) , fourth heart sounds or summation sounds occur randomly in diastole because the relationship between the P wave and the QRS of the electrocardiogram is random. Third and fourth heart sounds are events of ventricular filling, so obstruction of an AV valve, by impeding ventricular inflow, removes one of the prime preconditions for the generation of these filling sounds. Accordingly, the presence of a third or fourth heart sound implies an unobstructed (or relatively unobstructed) AV orifice on the side of the heart in which the sound originates. Right ventricular third or fourth heart sounds often respond selectively and distinctively to respiration, becoming more prominent during inspiration. (2) The inspiratory increase in right atrial flow is converted into an inspiratory
Third and fourth heart sounds, either normal or abnormal, are relatively low-frequency events that vary considerably in intensity (loudness), that originate in either the left or right ventricle, and that are best elicited when the bell of the stethoscope is applied with just enough pressure to provide a skin seal. Left ventricular third and fourth heart sounds should be sought over the left ventricular impulse so identified with the patient in the left lateral decubitus position. Right ventricular third and fourth heart sounds should be sought over the right ventricular impulse (lower left sternal edge, occasionally subxiphoid) with the patient supine. An understanding of these simple principles sets the stage for bedside detection. The same principles can be used with advantage to distinguish a fourth heart sound preceding a single first heart sound from splitting of the two components of the first heart sound (Fig. 2-15C) . The two components of the first heart sound are similar in frequency (pitch) although not in intensity (loudness), but differ in pitch from a preceding fourth heart sound. Selective pressure with the bell of the stethoscope enhances these distinctions.
Audibility of third heart sounds is improved by isotonic exercise that augments venous return and mid-diastolic AV flow. A few sit-ups usually suffice to produce the desired increase in venous return and acceleration in heart rate that increase the rate and volume of AV flow. Venous return can be increased by simple passive raising of both legs with the patient supine. The heart rate is also transiently increased by vigorous coughing. Left ventricular fourth heart sounds, especially in patients with ischemic heart disease, can be induced or augmented when resistance to left ventricular discharge is increased by sustained handgrip (isometric exercise, see later).
In the presence of sinus tachycardia, atrial contraction may coincide with the rapid filling phase, making it impossible
Figure 2-25 Tracings from an 18-year-old man with primary pulmonary
hypertension. A, The phonocardiogram from
the fourth left
intercostal space (4LICS) shows a fourth heart sound (S4
). The
jugular
venous pulse (JVP) exhibits a prominent a
wave. (S1
= First
heart
sound; S2
= second heart sound). B,
The increased force of
right atrial
contraction, reflected in the large jugular venous a wave, results in
presystolic distention (arrow) of the right ventricle (RV).
The normal third heart sound is believed to be caused by sudden limitation of longitudinal expansion of the left ventricular wall during early diastolic filling. (108) (109) (110) (111) The majority of abnormal third heart sounds are generated by altered physical properties of the recipient ventricle and/or an increase in the rate and volume of AV flow during the rapid filling phase of the cardiac cycle. (112) Abnormal fourth heart sounds occur when augmented atrial contraction generates presystolic ventricular distention (an increase in end-diastolic segment length) so that the recipient chamber can contract with greater force. (113) (114) Typical substrates are the left ventricular hypertrophy of aortic stenosis or systemic hypertension in the left side of the heart, (115) or the right ventricular hypertrophy of pulmonary stenosis or pulmonary hypertension in the right side of the heart (Fig. 2-25) . (113) Fourth heart sounds are also common in ischemic heart disease and are almost universal during angina pectoris or acute myocardial infarction because the atrial "booster pump" is needed to assist the relatively stiff ischemic ventricle.
A variation on the theme is the presystolic pacemaker sound. (116) A pacemaker electrode in the apex of the right ventricle may produce a presystolic sound that is relatively high-pitched and clicking and therefore different in pitch from a fourth heart sound. The presystolic pacemaker sound is believed to be extracardiac, resulting from contraction of chest wall muscle following spread of the electrical impulse from the pacemaker site. (116) (117)
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