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Clinical Examination of the Heart
Clinical Examination of the Heart JOHN R. BLAKE, M.D.* WALTER T. GOODALE, M.D.**
RECENT advances in treatment of heart disease have stimulated interest in a more accurate technique of cardiac examination. The all-important early detection of significant heart disease must start in the physician's office even before the use of electrocardiograms, x-rays, or exercise tolerance tests. Ten years of clinical experience, correlated directly with findings at cardiac catheterization and surgical exploration, has provided a sound basis for more accurate and informative cardiac physical examination. This paper will review some often neglected signs on inspection and palpation, and emphasize principles and highlights of auscultation. The timing of heart sounds and murmurs will receive particular attention. Most cardiologists agree that a consistent technique of examination and a properly fitting stethoscope are first essentials in cardiac physical diagnosis. Both diaphragm and bell type chest pieces must be used for adequate cardiac auscultation. The diaphragm is essential to best hear high-pitched murmurs and sounds but will often miss low-pitched murmurs. The latter are detected with the bell piece applied lightly to the skin. All maneuvers are most effectively carried out by examining the patient from the right side. This also provides an optimally comfortable position for the examiner. The light should pass across the chest uniformly to enable one to see small but significant precordial pulsations. Patients with dextrocardia are most readily examined from the left side.
INSPECTION AND PALPATION
Inspection and palpation together provide a rapid, reliable method of evaluating left, right and combined ventricular hypertrophy. This is a From the Medical Clinic, Peter Bent Brigham Hospital, and the Department of Medicine, H arvard Medical School, Boston, Massachusetts.
* Research Fellow in Medicine (Card1·ology) , Harvard Medical School; Assistant in Medicine, Peter Bent Brigham Hospital.
** Senior Associate in Medicine, Peter Bent Brigham Hospital; Cardiologist, Adolescent Unit, Children's Medical Center, and Clinical Associate in Medicine, Harvard M edical School. 1215
John R. Blake, Walter T. Goodale
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3
Sounds
Ca'fotid
ERG Fig. 121. The normal jugular and carotid pulse waves. The jugular venous pulse consists essentially of two positive waves (a and v) and two negative waves (x and y). Tne a wave is seen just before the first sound and is due to right atrial systole. It disappears in atrial fibrillation. The x descent is due to downward movement of the atrial floor during ventricular systole and to relaxation of the atrium. The c wave interrupts the x descent and is due mainly to transmitted pulsation from the carotid artery.2 The v wave represents rising right atrial pressure due to obstruction of blood flow during ventricular systole. At the summit of the v wave the tricuspid valve opens, and subsequent emptying of the right atrium produces the y descent.
valuable and a neglected procedure, as emphasized by Harrison. 1 In minimal or combined ventricular hypertrophy the electrocardiogram and x-ray are much less rel1·able than simple physical examination. Left ventricular hypertrophy appears as a forceful, localized apical systolic thrust. It is often accompanied by a systolic retraction of the skin in the interspace just above and medial to the apex, producing the typical "rocking" apical impulse. In left ventricular hypertrophy the impulse mayor may not be to the left of the normal outer limit. More important, is the strong thrusting character of the impulse. It lifts the fingers and is obviously increased in force. Right ventricular hypertrophy produces a diffuse lifting impulse along the left sternal border, and is frequently associated with a systolic retraction at the apex. The latter results from displacement and rotation of the left ventricle posteriorly by the enlarged right ventricle. It should be emphasized that inspection and palpation are more accurate in establishing ventricular hypertrophy than the laborious attempt to outline the heart by percussion. Inspection of the jugular venous pulse is an extremely useful way to study dynamic events in the right atrium, tricuspid valve and right ventricle. Its importance has been well emphasized by Wood. 2 The normal jugular pulse is seen best when the patient is lying with the head slightly elevated. The most conspicuous event in normals is a collapse of
Clinical Examination of the Heart
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COMPLETE HEART BLOCK
SOUNDS JUGULAR PULSE
EKG L Fig. 122. In complete heart block isolated a waves occur in the jugular pulse with each atrial contraction. Cannon a waves occur when the right atrium contracts against a closed tricuspid valve (when the P wave of the electrocardiogram falls between the QRS complex and the T wave).
the full vein occurring in early systole; this immediately follows the small positive a wave of atrial systole. The collapse wave is exaggerated whenever the right ventricular stroke volume is high, as on exercise or in atrial septal defect. With right ventricular failure the neck veins become distended, even with the patient sitting upright. (See Fig. 121.) The hepatojugular reflex is useful in detecting subclinical congestive failure. Firm pressure on the liver or right costal margin produces obvious distention of the neck veins when borderline right ventricular failure is present. Tricuspid regurgitation will produce a prominent v wave which may begin earlier than normal and will replace the systolic collapse with a positive pulsation. Giant a waves (presystolic in timing) are due to powerful right atrial contraction and increased resistance to right ·ventricular filling. They are seen in severe pulmonary stenosis, marked pulmonary hypertension, tricuspid stenosis, and tricuspid atresia. Sometimes combined inspection and palpation is necessary to avoid confusing a hyperactive carotid pulse with a giant venous a wave. Particularly large a waves, called cannon a waves, will occur in complete heart block whenever the right atrium contracts against a closed tricuspid valve (Le., during ventricular systole) (Fig. 122). The carotid arterial pulse should be inspected routinetly during any clinical examination of the heart. This pulse will help differentiate systole from diastole since it immediately follows the first sound. The causes of an accentuated carotid pulse include aortic insufficiency, aneurysm, hypertensive arteriosclerotic disease, and coarctation of the aorta. A weak carotid pulsation suggests aortic stenosis or a reduced left ventricular ejection (e.g., congestive heart failure). (See Fig. 121.) A thrill over the carotid artery is most commonly a transmitted mur-
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mur from the aortic or pulmonary valve. A murmur from either valve sets up vibrations in the entire great vessel system, since the walls of the aorta and pulmonary artery are immediately adjacent at the point where the murmurs are produced. There is nothing specific diagnostically about which side of the neck shows the maximum thrill or transmission of a valvular murmur. Carotid artery thrills may also be produced by rapid flow through tortuous, sclerotic vessels or through an enlarged, overactive thyroid gland. Differences in rate between carotid arterial and jugular venous pulses will be noted in atrial flutter or varying degrees of A-V block. PERCUSSION
Percussion is of limited value compared with combined inspection and palpation. For example, with right ventricular hypertrophy the right ventricle enlarges forward and to the left, tending to displace the left ventricle posteriorly. This makes percussion of the left border nonspecific and often inaccurate. However, percussion may be useful in establishing the heart border if the heart is hypodynamic, or in detecting massive pericardial effusion. Marked dilatation of the main pulmonary artery and ascending aorta may be apparent on light percussion in the second and third interspaces. But a faint systolic ripple in these areas often proves to be a more reliable sign. While a straight left cardiac border sometimes indicates left atrial enlargement, significant left atrial enlargement occurs posteriorly and to the right against the esophagus, and cannot be outlined by percussion. The right border, if detected at all, usually represents the right atrium. In severe combined valvular disease it may represent the right ventricle. AUSCULTATION
There are two basic rules of auscultation: (1) Auscultation should always be combined with inspection and palpation, sometimes simultaneously. (2) One must concentrate selectively on each specific event in the cardiac cycle in all pertinent areas. This has been emphasized by Levine and Harvey.3 For example, the apex and lower left sternal border are optimal areas for evaluating the first heart sound, since it is produced by mitral and tricuspid valve closure. The second sound is best analyzed in the third and second left interspaces where both of its components (aortic and pulmonary valve closure) are well heard. The First Heart Sound
A thorough understanding of the normal heart sounds is essential in the evaluation of more complex auscultatory findings. To differentiate the first and second sounds it is useful to remember that the carotid pulse immediately follows the first sound. If timing is difficult due to
Third heart sound or protodiastolic gallop.
Fig. 123. The heart sounds.
tachycardia, the heart may be slowed by carotid sinus pressure. Another useful maneuver in clarifying the normal sounds is to listen first in the pulmonary area where the second sound defines itself best. If hypertrophy is present on inspection, the most useful way of timing systole and diastole is to watch the motion of the stethoscope during auscultation. (See Fig. 123.) The first heart sound occurs with the onset of ventricular systole and is produced by closure of the mitral and tricuspid valves. Splitting of the first sound at the apex and tricuspid area is a normal finding in many people and is due to slight asynchrony of valve closure. The intensity of the first sound depends chiefly on the position of the valve cusps at the instant the ventricles contract. Atrial systole forces the valve leaflets wide open and when the atrium relaxes the leaflets float into apposition. The loudest first sound is produced when the P-R interval is short (0.14 second or less) and the leaflets are wide open at the time the ventricles contract. When the P-R interval is long (0.22 second or more) the cusps will have floated toward each other before the ventricles contract and their final closure will result in a fainter sound. This relationship is best illustrated in patients with complete A-V block, where the constantly changing P-It interval causes variable intensity of the first sound. The importance of the first heart sound in the differential diagnosis of paroxysmal rapid heart action has been stressed by Levine and Harvey.3 The loud first sound of mitral stenosis results from two factors. First, the high left atrial pressure keeps the mitral cusps open until the very end of diastole. Second, fibrotic changes in the mitral valve leaflets alter
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them in such a way that they tense more abruptly with ventricular contraction, producing a louder, higher-pitched sound. A loud first sound in the pulmonary area has a different significance and is frequently heard in patients with mild or moderate pulmonary valvular stenosis. The Second Heart Sound
The second heart sound is due to aortic and pulmonary valve closure· It is best heard along the left sternal border at the third interspace in close proximity to the anatomical location of these valves but may be heard in all areas. The difference in transmission of the aortic versus the pulmonary component is great. The pulmonary component is normally heard well only in the second and third left interspaces. On the other hand, aortic valve closure is well heard in the second right interspace, over the carotid artery, and at the apex, as well as in the second and third left interspaces. Thus the second sound in the second and third left interspaces is made up both by aortic and pulmonary components.. Standard textbooks on physical diagnosis define the aortic area as the second right intercostal space and the pulmonary area as the second left intercostal space. Actually, pulmonary valve closure is usually best heard in the third left intercostal space, and the pulmonary area would best be redefined in this location. On the basis of listening in the aortic and pulmonary areas students are taught to determine whether "P2 is louder than A 2" or vice versa. Such a concept is unphysiological because aortic valve closure contributes to the second sound heard in the pulmonary area. A loud second sound heard in the pulmonary area may indicate loud closing of the aortic valve or loud closing of the pulmonary valve. Therefore it is misleading to say that "P 2 is accentuated" unless one can determine that the pulmonary component rather than the aortic component is the loud one. Usually an accentuated aortic closure sound is most marked in the second right interspace. This area is closest to the ascending aorta, where the "tambour" A2 of systemic hypertension is typically produced. Careful auscultation reveals that the second sound in the pulmonary area normally is split. The first element is aortic valve closure (because of earlier left ventricular contraction and higher pressures in the aorta than in the pulmonary artery) and the second element is pulmonary. Inspiration causes wider splitting of the second sound because of increased right ventricular filling and prolonged right ventricular systole which delay the second component. Right bundle branch block produces wide splitting of the basal second sound because of the delayed pulmonary closure. Inspiration will further widen this splitting. Left bundle branch block produces delay in aortic valve closure. The normal order of valve closure may be reversed if left bundle branch block is severe. This
Clinical Examination of the Heart BASAL
NORMAL A
INSPIRATION
2 ND
SOUND
RBBB
LBBS
·A
I I P
EXPIRATION
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A
I I I I P
p
Fig. 124. Effect of respiration on splitting of the basal second sound. Inspiration further delays pulmonary valve closure (P) and widens the splitting in normals and in right bundle branch block. In left bundle branch block, where normal order of valve closure may be reversed, the delay of pulmonary closure with inspiration narrows the splitting.
can be detected clinically because inspiration, which delays pulmonary closure, will now cause the splitting to narrow rather than widen (Fig. 124.) Pulmonary stenosis causes prolongation of right ventricular systole and a mechanical delay in closure of the pulmonary valve. This results in wide splitting of the second sound. This splitting may be obscured on auscultation because the late pulmonary element tends to be very faint and the aortic element may be obscured by the loud systolic murmur (Fig. 125). Wide splitting of the second sound is typical of atrial septal defect. This is caused by the electrical delay from right bundle branch block combined with the mechanical delay from increased right ventricular stroke volume. In mitral regurgitation wide splitting of the second sound can occur from early closure of the aortic valve. Because of the double route of left ventricular ejection, systole is shortened and aortic closure occurs prematurely. Marked accentuation of pulmonary valve closure producing a palpable second sound in the pulmonary area is one of the most reliable clinical signs of pulmonary hypertension. As pulmonary vascular resistance rises the pulmonary valve closes earlier, causing a narrower splitting of the second sound. It is a common misconception that pulmonary hypertension causes widn splitting of the basal second sound. This confusion arises when the
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PULMONIC
PULM
aur.
STENOSIS
aur.
CAROTID _ _-.
J.MACN. ST251 Fig. 125. Wide splitting of the second sound in pulmonic stenosis is due to marked delay in pulmonary valve closure (P). Aortic valve closure CA) is identified by the dicrotic notch in the carotid artery pulse. Continuation of the pulmonic systolic murmur past aortic valve closure may be misinterpreted as an early diastolic murmur. An auricular sound (aur.), also known as a presystolic gallop or loud fourth heart sound, is present.
opening snap of mitral stenosis-audible often at the base-is mistaken for the second component of a split second sound. Actually one can usually detect the narrow splitting of the second sound in addition to the transmitted opening snap in mitral stenosis. The second sound at the apex is normally single and is due to aortic valve closure. Narrow splitting of the apical second sound is due to transmission of the pulmonary element and almost invariably indicates pulmonary hypertension. Diastolic Sounds
The physiological third heart sound is heard in the great majority of children and about 50 per cent of young adults. It is soft and low-pitched, best heard at the apex, and becomes louder during inspiration. It is loudest after exercise or when the subject lies on the left side. It occurs in early diastole and is produced by the rapid inflow of blood into the ventricles after opening of the A-V valves. The third sound is accentuated by any condition which produces rapid left ventricular filling such as mitral regurgitation, ventricular septal defect, patent ductus arteriosus, and left ventricular failure. It may become loud and prolonged enough to be termed a "diastolic rumble. " Very delicate and precise localization with the bell stethoscope may be necessary to detect a diastolic rumble. The fourth heart sound is related to atrial contraction and is usually inaudible in normal hearts with normal A-V conduction. When the P-R interval is prolonged or third degree heart block exists, atrial sounds will become audible and are sometimes double,
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Gallop Rhythnt
The term "gallop rhythm" Jlas been used to describe the cadence produced by the addition of all extra sound to the two sounds normally heard. Since this rhythm was often noted in patients with heart disease, the term became synonymous with heart failure in the minds of many clinicians. It has become clear, however, that protodiastolic and presystolic gallop sounds are basically much the same as the normal third and fourth heart sounds respectively, but are named differently depending on the circumstances in which they are heard. A protodiastolic gallop, also knoWn as an early diastolic gallop, a ventricular gallop, or a third heart sound gallop, has essentially the same timing and characteristics as the physiological third heart sound. It is probably produced by vibrations set up in the chordae tendineae or A-V valves due to tensing and partial reclosure of the valves as the ventricle fills. This sound is associated with early or frank ventricular failure but is also common in mitral regurgitation, as mentioned above, because of the increased volume of blood in the left atrium rapidly entering the left ventricle in early diastole. A presystolic gallop, also known as an atrial gallop or fourth heart sound gallop, occurs just before the first heart sound and is the pathological counterpart of the normal fourth heart sound. Its mechanism is less well understood but it is probably related to a brief re-tensing of the A-V valves at the end of atrial systole. It is best heard along the left sternal border or at the apex and is audible in some patients with hypertension or recent myocardial infarction, and in conditions producing right atrial hypertrophy. In contrast to the protodiastolic gallop, the presystolic gallop is not usually associated with congestive heart failure. When the heart rate increases and diastole is shortened, a protodiastolic gallop may become superimposed on a presystolic gallop producing a loud "summation" gallop. In such an instance, slowing the heart by carotid sinus pressure will separate the two gallop sounds. (See Fig. 123.) Opening Snap
The opening snap of the mitral valve is a characteristic finding in mitral valvular disease and its recognition by auscultation is of great importance. It must be differentiated from the second component of a split second sound and from a third heart sound. A few simple clues will permit one to make this differentiation at the bedside. The opening snap occurs perceptibly later than the second component of a split second sound. A split second sound is loudest at the pulmonary area whereas the opening snap is best heard medial to the apex or at the lower left sternal border. The interval between the two parts of a split second sound will vary with respiration~ but the interval between a
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second sound and an opening snap (2-0S interval) will not. When atrial fibrillation is present the 2-0S interval will change from beat to beat depending on the length of the preceding diastole. Following a short diastole the opening snap will occur closer to the second sound, and after a long diastole the opening snap will occur later. Splitting of the second sound does not show this variation in atrial fibrillation. In most patients with opening snaps, careful auscultation at the lower left sternal border will reveal both a split second sound and the opening snap. A third heart sound or protodiastolic gallop occurs later than an opening snap, is lower in pitch, and is best heard at the apex. (See Fig. 123.) Murmurs
Murmurs are heard both in healthy individuals and in patients with heart disease. The following aspects of each murmur should be noted: (1) timing, (2) intensity, (3) quality and (4) transmission. On the basis of this type of analysis, one may secure information not obtainable by any other method. 4 Timing can be systolic, diastolic or continuous. Diastolic murmurs should be further characterized as early or late (presystolic). Intensity is graded 1 to 6. A grade 1 murmur is the faintest that can be heard on careful auscultation, and a grade 6 murmur is one which can be heard even with the stethoscope removed from the chest wall. Grades 2 to 5 correspond to slight, moderate, loud, and very loud. The area of maximum intensity should also be noted. The quality of a murmur depends mainly on its pitch (high, low, medium) and its configuration. The configuration of a murmur refers to its "shape" and includes crescendo, plateau, decrescendo and diamond shaped (crescendo-decrescendo). Quality is further characterized by more subjective terms such as blowing, harsh and rumbling. Thus a murmur of aortic stenosis might be described as "a grade 3, medium-pitched, harsh, diamond-shaped systolic murmur, transmitted to the neck vessels." Systolic murmurs are frequently heard in normal individuals, especially in children and adolescents. The term "functional murmur" has led to much confusion, because in a sense all murmurs are an expression of function. Furthermore, there is a tendency to regard faint murmurs as "functional" or benign and very loud murmurs as ominous. The fallacy of this reasoning is readily apparent when one considers the grade 5 systolic murmur from a small, insignificant ventricular septal defect, and the very faint murmurs of pulmonary atresia or very severe mitral stenosis. In view of these difficulties, one should first describe a murmur accurately and then, with the help of other clinical and laboratory information, decide whether or not it is significant. 4 The murmurs of mitral or tricuspid regurgitation start with the first sound, and extend throughout systole at the same intensity or slightly decrescendo. They are characteristically high-pitched and blowing, and
Clinical Examination of the Heart
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are poorly transmitted. On the other hand, the murmurs of aortic and pulmonary stenosis are harsh and diamond shaped (i.e., beginning slightly after the first sound, rising to a peak near midsystole, and tapering off before the second sound). They are well transmitted to the neck and over the precordium. At times the murmur of aortic stenosis will be louder at the apex than at the base. This could lead to an erroneous diagnosis of mitral regurgitation unless one recognized the diamond shape of the murmur in both areas. The systolic murmur of ventricular septal defect is usually plateau but sometimes accentuated in midsystole. It is best heard in the third or fourth left interspace. Despite its loudness (grade 3 to 6) and its transmission over the precordium, it is poorly transmitted to the neck. In contrast to systolic murmurs, diastolic murmurs almost invariably indicate structural heart disease. The diastolic murmurs of mitral stenosis and regurgitation will be discussed in the next section. The diastolic murmur of tricuspid stenosis has the same quality as that of mitral stenosis but is usually best heard at the lower left sternal border. Another differential point is that tricuspid murmurs become louder during inspiration and fainter during expiration. Mitral murmurs will either remain unchanged during respiration or become slightly fainter during inspiration. Short diastolic murmurs, aptly termed "prolonged third heart sounds," are commonly heard in the mitral or tricuspid areas in patients with congenital heart disease and a left-to-right shunt. In atrial septal defect with a shunt from left atrium to right atrium the murmur is produced by increased tricuspid valve flow and right ventricular filling; in ventricular septal defect and patent ductus arteriosus the left-to-right shunt occurs distal to the tricuspid valve and the murmur is produced by increased mitral valve flow and left ventricular filling. These murmurs simulate the early diastolic rumble of mitral stenosis. The Austin Flint murmur is a presystolic murmur at the apex in patients with aortic regurgitation. By auscultation this murmur is identical with the presystolic murmur of mitral stenosis, but these patients do not have mitral stenosis demonstrable at autopsy. The murmur is probably due to deflection of the anterior leaflet of the mitral valve by the regurgitant blood stream, producing a relative mitral stenosis. It can be differentiated from the murmur of organic mitral stenosis by the absence of an opening snap and the absence of a snapping first heart sound. The basal diastolic murmur of aortic regurgitation is very difficult to differentiate from the murmur of pulmonary regurgitation (Graham Steell murmur). Although in aortic regurgitation the murmur may be well heard in the second right interspace, both murmurs are usually IIlaximal along the left sternal border. Differentiation must usually be
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made by inference based on evidence of aortic valve disease versus evidence of pulmonary hypertension. A continuous murmur is one which persists through systole and into diastole without interruption. This murmur is typical of shunts between vessels and is found in patent ductus arteriosus and arteriovenous fistula. In patent ductus the murmur begins after the first sound, is loudest at the end of systole, envelops the second sound, and decreases in diastole. It is best heard in the second left interspace, often well away from the sternum, and tends to radiate up and outward over the left upper chest. The following conditions produce murmurs closely resembling those of patent ductus: aortic-pulmonary window, high ventricular septal defect with aortic regurgitation, ruptured sinus of Valsalva, anomalous pulmonary veins, coronary A-V fistula, and the shunt created by a Blalock or Potts operation for tetralogy of Fallot. Other "continuous" murmurs include the thyroid bruit of hyperthyroidism, venous hums, and murmurs from collateral circulation. The dilated intercostal collaterals in coarctation of the aorta are best heard over the posterior chest. Bronchial collaterals in pulmonary atresia or severe stenosis produce a continuous murmur over a wide area, but maximal over the right upper lobe bronchus. In "atypical patent ductus," progressive pulmonary hypertension with increasing vascular resistance eliminates first the diastolic and finally the systolic components of the murmur as the left-to-right shunt is eliminated and finally reversed. MITRAL STENOSIS AND MITRAL REGURGITATION
The auscultatory findings in pure mitral stenosis and in pure mitral regurgitation are well defined. However, in many patients these two lesions are combined. Since marked insufficiency requires a different approach to mitral surgery, it is very important to determine the predominant lesion. A snapping first sound and an opening snap strongly favor predominant mitral stenosis. An apical pansystolic murmur obscuring the first sound is typical of mitral regurgitation, but the loudness of the murmur is not a reliable indication of the amount of regurgitation. Many patients with predominant mitral stenosis may have systolic murmurs of variable intensity with only an insignificant degree of regurgitation. If right heart failure or tricuspid disease is present, a systolic murmur produced by tricuspid regurgitation may be falsely attributed to mitral insufficiency. A well-developed third heart sound strongly favors predominant mitral regurgitation. The character of the apical diastolic murmur is helpful in differentiating these lesions. In mitral stenosis the diastolic murmur begins with or shortly after the opening snap and tends to be prolonged throughout most of diastole. If normal sinus rhythm is present there is often a presystolic crescendo murmur. This presystolic accentuation is usually
Clinical Examination of the Heart
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absent with atrial fibrillation, and it may disappear during congestive heart failure even when sinus rhythm is present. When mitral stenosis is complicated by significant mitral regurgitation, a large proportion of the left ventricular output is ejected into the left atrium during systole. In predominant mitral insufficiency, regurgitant flow may be two or three times as great as forward flow out the aortic valve. This results in a larger forward flow across the mitral valve during early diastole which in itself produces a "relative" mitral stenosis. It also leads to dilatation of the left ventricle and the mitral annulus so that a vicious cycle is set up producing more regurgitation. On auscultation, patients with mitral regurgitation will have apical diastolic murmurs, sometimes very loud because of the turbulence set up by greatly increased mitral valve flow in early diastole. However, there are two features which distinguish the apical diastolic murmurs of mitral regurgitation: Ca) They are initiated by a loud component, often a thrill, corresponding in time with the third heart sound and rapid ventricular filling. Cb) They tend to be shorter in duration because ventricular filling takes place more rapidly than in predominant mitral stenosis. Although an opening snap is generally a reliable sign of mitral stenosis, a few patients with predominant regurgitation show opening snaps. This is not so surprising when one considers that these patients have a high early diastolic pressure gradient across the mitral valve which is one of the major factors in the genesis of the opening snap. We have also recorded opening snaps in ruptured mitral chordae tendineae and in myxoma of the left atrium. In mitral stenosis with advanced valvular fibrosis and calcification the first sound becomes faint and the opening snap may disappear. In general, the tighter the valve and the lower the mitral valve flow, the softer will be the mitral murmurs. Stenosis of the mitral, aortic or pulmonary valves may be so severe that flow is reduced below the range necessary to produce murmurs. Finally, inspection and palpation are always useful in distinguishing tight mitral stenosis from predominant mitral regurgitation. These bedside observations are often more accurate than x-ray or electrocardiography. If there are no signs of left ventricular hypertrophy by the criteria mentioned previously, and obvious right ventricular hypertrophy is present, significant mitral regurgitation can be ruled out. Combined ventricular hypertrophy may be seen in tight mitral stenosis if systemic hypertension, aortic valvular disease, or marked coronary insufficiency is also present. CONCLUSION
The bedside cardiac examination provides important diagnostic information when auscultation is coordinated with careful inspection and palpation.
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Whereas percussion of heart borders is grossly inaccurate, palpation of the precordial impulses furnishes a simple and reliable indication of ventricular hypertrophy. In minimal or combined ventricular hypertrophy the electrocardiogram and x-ray are much less reliable than simple physical examination. Correlation of physical findings with cardiac catheterization and surgical exploration has provided the basis for reappraisal of certain timehonored concepts regarding clinical examination of the heart. REFERENCES 1. Harrison, T. R.: Palpation of the Precordial Impulses. Stanford M. Bull. 13: 385, 1955. 2. Wood, P.: Disea5es of the Heart and Circulation. 2nd Ed., London, Eyre & Spottiswoode, 1956. 3. Levine, S. A. and Harvey, W. P.: Clinical Auscultation of the Heart. Philadelphia, W. B. Saunders Co., 1949. 4. N adas, A. S.: Pediatric Cardiology. Philadelphia, W. B. Saunders Co., 1957.
3560 J Street Sacramento, California (Dr. Blake)
RECENT advances in treatment of heart disease have stimulated interest in a more accurate technique of cardiac examination. The all-important early detection of significant heart disease must start in the physician's office even before the use of electrocardiograms, x-rays, or exercise tolerance tests. Ten years of clinical experience, correlated directly with findings at cardiac catheterization and surgical exploration, has provided a sound basis for more accurate and informative cardiac physical examination. This paper will review some often neglected signs on inspection and palpation, and emphasize principles and highlights of auscultation. The timing of heart sounds and murmurs will receive particular attention. Most cardiologists agree that a consistent technique of examination and a properly fitting stethoscope are first essentials in cardiac physical diagnosis. Both diaphragm and bell type chest pieces must be used for adequate cardiac auscultation. The diaphragm is essential to best hear high-pitched murmurs and sounds but will often miss low-pitched murmurs. The latter are detected with the bell piece applied lightly to the skin. All maneuvers are most effectively carried out by examining the patient from the right side. This also provides an optimally comfortable position for the examiner. The light should pass across the chest uniformly to enable one to see small but significant precordial pulsations. Patients with dextrocardia are most readily examined from the left side.
INSPECTION AND PALPATION
Inspection and palpation together provide a rapid, reliable method of evaluating left, right and combined ventricular hypertrophy. This is a From the Medical Clinic, Peter Bent Brigham Hospital, and the Department of Medicine, H arvard Medical School, Boston, Massachusetts.
* Research Fellow in Medicine (Card1·ology) , Harvard Medical School; Assistant in Medicine, Peter Bent Brigham Hospital.
** Senior Associate in Medicine, Peter Bent Brigham Hospital; Cardiologist, Adolescent Unit, Children's Medical Center, and Clinical Associate in Medicine, Harvard M edical School. 1215
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3
Sounds
Ca'fotid
ERG Fig. 121. The normal jugular and carotid pulse waves. The jugular venous pulse consists essentially of two positive waves (a and v) and two negative waves (x and y). Tne a wave is seen just before the first sound and is due to right atrial systole. It disappears in atrial fibrillation. The x descent is due to downward movement of the atrial floor during ventricular systole and to relaxation of the atrium. The c wave interrupts the x descent and is due mainly to transmitted pulsation from the carotid artery.2 The v wave represents rising right atrial pressure due to obstruction of blood flow during ventricular systole. At the summit of the v wave the tricuspid valve opens, and subsequent emptying of the right atrium produces the y descent.
valuable and a neglected procedure, as emphasized by Harrison. 1 In minimal or combined ventricular hypertrophy the electrocardiogram and x-ray are much less rel1·able than simple physical examination. Left ventricular hypertrophy appears as a forceful, localized apical systolic thrust. It is often accompanied by a systolic retraction of the skin in the interspace just above and medial to the apex, producing the typical "rocking" apical impulse. In left ventricular hypertrophy the impulse mayor may not be to the left of the normal outer limit. More important, is the strong thrusting character of the impulse. It lifts the fingers and is obviously increased in force. Right ventricular hypertrophy produces a diffuse lifting impulse along the left sternal border, and is frequently associated with a systolic retraction at the apex. The latter results from displacement and rotation of the left ventricle posteriorly by the enlarged right ventricle. It should be emphasized that inspection and palpation are more accurate in establishing ventricular hypertrophy than the laborious attempt to outline the heart by percussion. Inspection of the jugular venous pulse is an extremely useful way to study dynamic events in the right atrium, tricuspid valve and right ventricle. Its importance has been well emphasized by Wood. 2 The normal jugular pulse is seen best when the patient is lying with the head slightly elevated. The most conspicuous event in normals is a collapse of
Clinical Examination of the Heart
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COMPLETE HEART BLOCK
SOUNDS JUGULAR PULSE
EKG L Fig. 122. In complete heart block isolated a waves occur in the jugular pulse with each atrial contraction. Cannon a waves occur when the right atrium contracts against a closed tricuspid valve (when the P wave of the electrocardiogram falls between the QRS complex and the T wave).
the full vein occurring in early systole; this immediately follows the small positive a wave of atrial systole. The collapse wave is exaggerated whenever the right ventricular stroke volume is high, as on exercise or in atrial septal defect. With right ventricular failure the neck veins become distended, even with the patient sitting upright. (See Fig. 121.) The hepatojugular reflex is useful in detecting subclinical congestive failure. Firm pressure on the liver or right costal margin produces obvious distention of the neck veins when borderline right ventricular failure is present. Tricuspid regurgitation will produce a prominent v wave which may begin earlier than normal and will replace the systolic collapse with a positive pulsation. Giant a waves (presystolic in timing) are due to powerful right atrial contraction and increased resistance to right ·ventricular filling. They are seen in severe pulmonary stenosis, marked pulmonary hypertension, tricuspid stenosis, and tricuspid atresia. Sometimes combined inspection and palpation is necessary to avoid confusing a hyperactive carotid pulse with a giant venous a wave. Particularly large a waves, called cannon a waves, will occur in complete heart block whenever the right atrium contracts against a closed tricuspid valve (Le., during ventricular systole) (Fig. 122). The carotid arterial pulse should be inspected routinetly during any clinical examination of the heart. This pulse will help differentiate systole from diastole since it immediately follows the first sound. The causes of an accentuated carotid pulse include aortic insufficiency, aneurysm, hypertensive arteriosclerotic disease, and coarctation of the aorta. A weak carotid pulsation suggests aortic stenosis or a reduced left ventricular ejection (e.g., congestive heart failure). (See Fig. 121.) A thrill over the carotid artery is most commonly a transmitted mur-
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mur from the aortic or pulmonary valve. A murmur from either valve sets up vibrations in the entire great vessel system, since the walls of the aorta and pulmonary artery are immediately adjacent at the point where the murmurs are produced. There is nothing specific diagnostically about which side of the neck shows the maximum thrill or transmission of a valvular murmur. Carotid artery thrills may also be produced by rapid flow through tortuous, sclerotic vessels or through an enlarged, overactive thyroid gland. Differences in rate between carotid arterial and jugular venous pulses will be noted in atrial flutter or varying degrees of A-V block. PERCUSSION
Percussion is of limited value compared with combined inspection and palpation. For example, with right ventricular hypertrophy the right ventricle enlarges forward and to the left, tending to displace the left ventricle posteriorly. This makes percussion of the left border nonspecific and often inaccurate. However, percussion may be useful in establishing the heart border if the heart is hypodynamic, or in detecting massive pericardial effusion. Marked dilatation of the main pulmonary artery and ascending aorta may be apparent on light percussion in the second and third interspaces. But a faint systolic ripple in these areas often proves to be a more reliable sign. While a straight left cardiac border sometimes indicates left atrial enlargement, significant left atrial enlargement occurs posteriorly and to the right against the esophagus, and cannot be outlined by percussion. The right border, if detected at all, usually represents the right atrium. In severe combined valvular disease it may represent the right ventricle. AUSCULTATION
There are two basic rules of auscultation: (1) Auscultation should always be combined with inspection and palpation, sometimes simultaneously. (2) One must concentrate selectively on each specific event in the cardiac cycle in all pertinent areas. This has been emphasized by Levine and Harvey.3 For example, the apex and lower left sternal border are optimal areas for evaluating the first heart sound, since it is produced by mitral and tricuspid valve closure. The second sound is best analyzed in the third and second left interspaces where both of its components (aortic and pulmonary valve closure) are well heard. The First Heart Sound
A thorough understanding of the normal heart sounds is essential in the evaluation of more complex auscultatory findings. To differentiate the first and second sounds it is useful to remember that the carotid pulse immediately follows the first sound. If timing is difficult due to
Third heart sound or protodiastolic gallop.
Fig. 123. The heart sounds.
tachycardia, the heart may be slowed by carotid sinus pressure. Another useful maneuver in clarifying the normal sounds is to listen first in the pulmonary area where the second sound defines itself best. If hypertrophy is present on inspection, the most useful way of timing systole and diastole is to watch the motion of the stethoscope during auscultation. (See Fig. 123.) The first heart sound occurs with the onset of ventricular systole and is produced by closure of the mitral and tricuspid valves. Splitting of the first sound at the apex and tricuspid area is a normal finding in many people and is due to slight asynchrony of valve closure. The intensity of the first sound depends chiefly on the position of the valve cusps at the instant the ventricles contract. Atrial systole forces the valve leaflets wide open and when the atrium relaxes the leaflets float into apposition. The loudest first sound is produced when the P-R interval is short (0.14 second or less) and the leaflets are wide open at the time the ventricles contract. When the P-R interval is long (0.22 second or more) the cusps will have floated toward each other before the ventricles contract and their final closure will result in a fainter sound. This relationship is best illustrated in patients with complete A-V block, where the constantly changing P-It interval causes variable intensity of the first sound. The importance of the first heart sound in the differential diagnosis of paroxysmal rapid heart action has been stressed by Levine and Harvey.3 The loud first sound of mitral stenosis results from two factors. First, the high left atrial pressure keeps the mitral cusps open until the very end of diastole. Second, fibrotic changes in the mitral valve leaflets alter
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them in such a way that they tense more abruptly with ventricular contraction, producing a louder, higher-pitched sound. A loud first sound in the pulmonary area has a different significance and is frequently heard in patients with mild or moderate pulmonary valvular stenosis. The Second Heart Sound
The second heart sound is due to aortic and pulmonary valve closure· It is best heard along the left sternal border at the third interspace in close proximity to the anatomical location of these valves but may be heard in all areas. The difference in transmission of the aortic versus the pulmonary component is great. The pulmonary component is normally heard well only in the second and third left interspaces. On the other hand, aortic valve closure is well heard in the second right interspace, over the carotid artery, and at the apex, as well as in the second and third left interspaces. Thus the second sound in the second and third left interspaces is made up both by aortic and pulmonary components.. Standard textbooks on physical diagnosis define the aortic area as the second right intercostal space and the pulmonary area as the second left intercostal space. Actually, pulmonary valve closure is usually best heard in the third left intercostal space, and the pulmonary area would best be redefined in this location. On the basis of listening in the aortic and pulmonary areas students are taught to determine whether "P2 is louder than A 2" or vice versa. Such a concept is unphysiological because aortic valve closure contributes to the second sound heard in the pulmonary area. A loud second sound heard in the pulmonary area may indicate loud closing of the aortic valve or loud closing of the pulmonary valve. Therefore it is misleading to say that "P 2 is accentuated" unless one can determine that the pulmonary component rather than the aortic component is the loud one. Usually an accentuated aortic closure sound is most marked in the second right interspace. This area is closest to the ascending aorta, where the "tambour" A2 of systemic hypertension is typically produced. Careful auscultation reveals that the second sound in the pulmonary area normally is split. The first element is aortic valve closure (because of earlier left ventricular contraction and higher pressures in the aorta than in the pulmonary artery) and the second element is pulmonary. Inspiration causes wider splitting of the second sound because of increased right ventricular filling and prolonged right ventricular systole which delay the second component. Right bundle branch block produces wide splitting of the basal second sound because of the delayed pulmonary closure. Inspiration will further widen this splitting. Left bundle branch block produces delay in aortic valve closure. The normal order of valve closure may be reversed if left bundle branch block is severe. This
Clinical Examination of the Heart BASAL
NORMAL A
INSPIRATION
2 ND
SOUND
RBBB
LBBS
·A
I I P
EXPIRATION
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A
I I I I P
p
Fig. 124. Effect of respiration on splitting of the basal second sound. Inspiration further delays pulmonary valve closure (P) and widens the splitting in normals and in right bundle branch block. In left bundle branch block, where normal order of valve closure may be reversed, the delay of pulmonary closure with inspiration narrows the splitting.
can be detected clinically because inspiration, which delays pulmonary closure, will now cause the splitting to narrow rather than widen (Fig. 124.) Pulmonary stenosis causes prolongation of right ventricular systole and a mechanical delay in closure of the pulmonary valve. This results in wide splitting of the second sound. This splitting may be obscured on auscultation because the late pulmonary element tends to be very faint and the aortic element may be obscured by the loud systolic murmur (Fig. 125). Wide splitting of the second sound is typical of atrial septal defect. This is caused by the electrical delay from right bundle branch block combined with the mechanical delay from increased right ventricular stroke volume. In mitral regurgitation wide splitting of the second sound can occur from early closure of the aortic valve. Because of the double route of left ventricular ejection, systole is shortened and aortic closure occurs prematurely. Marked accentuation of pulmonary valve closure producing a palpable second sound in the pulmonary area is one of the most reliable clinical signs of pulmonary hypertension. As pulmonary vascular resistance rises the pulmonary valve closes earlier, causing a narrower splitting of the second sound. It is a common misconception that pulmonary hypertension causes widn splitting of the basal second sound. This confusion arises when the
John R. Blake, Walter T. Goodale
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PULMONIC
PULM
aur.
STENOSIS
aur.
CAROTID _ _-.
J.MACN. ST251 Fig. 125. Wide splitting of the second sound in pulmonic stenosis is due to marked delay in pulmonary valve closure (P). Aortic valve closure CA) is identified by the dicrotic notch in the carotid artery pulse. Continuation of the pulmonic systolic murmur past aortic valve closure may be misinterpreted as an early diastolic murmur. An auricular sound (aur.), also known as a presystolic gallop or loud fourth heart sound, is present.
opening snap of mitral stenosis-audible often at the base-is mistaken for the second component of a split second sound. Actually one can usually detect the narrow splitting of the second sound in addition to the transmitted opening snap in mitral stenosis. The second sound at the apex is normally single and is due to aortic valve closure. Narrow splitting of the apical second sound is due to transmission of the pulmonary element and almost invariably indicates pulmonary hypertension. Diastolic Sounds
The physiological third heart sound is heard in the great majority of children and about 50 per cent of young adults. It is soft and low-pitched, best heard at the apex, and becomes louder during inspiration. It is loudest after exercise or when the subject lies on the left side. It occurs in early diastole and is produced by the rapid inflow of blood into the ventricles after opening of the A-V valves. The third sound is accentuated by any condition which produces rapid left ventricular filling such as mitral regurgitation, ventricular septal defect, patent ductus arteriosus, and left ventricular failure. It may become loud and prolonged enough to be termed a "diastolic rumble. " Very delicate and precise localization with the bell stethoscope may be necessary to detect a diastolic rumble. The fourth heart sound is related to atrial contraction and is usually inaudible in normal hearts with normal A-V conduction. When the P-R interval is prolonged or third degree heart block exists, atrial sounds will become audible and are sometimes double,
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Gallop Rhythnt
The term "gallop rhythm" Jlas been used to describe the cadence produced by the addition of all extra sound to the two sounds normally heard. Since this rhythm was often noted in patients with heart disease, the term became synonymous with heart failure in the minds of many clinicians. It has become clear, however, that protodiastolic and presystolic gallop sounds are basically much the same as the normal third and fourth heart sounds respectively, but are named differently depending on the circumstances in which they are heard. A protodiastolic gallop, also knoWn as an early diastolic gallop, a ventricular gallop, or a third heart sound gallop, has essentially the same timing and characteristics as the physiological third heart sound. It is probably produced by vibrations set up in the chordae tendineae or A-V valves due to tensing and partial reclosure of the valves as the ventricle fills. This sound is associated with early or frank ventricular failure but is also common in mitral regurgitation, as mentioned above, because of the increased volume of blood in the left atrium rapidly entering the left ventricle in early diastole. A presystolic gallop, also known as an atrial gallop or fourth heart sound gallop, occurs just before the first heart sound and is the pathological counterpart of the normal fourth heart sound. Its mechanism is less well understood but it is probably related to a brief re-tensing of the A-V valves at the end of atrial systole. It is best heard along the left sternal border or at the apex and is audible in some patients with hypertension or recent myocardial infarction, and in conditions producing right atrial hypertrophy. In contrast to the protodiastolic gallop, the presystolic gallop is not usually associated with congestive heart failure. When the heart rate increases and diastole is shortened, a protodiastolic gallop may become superimposed on a presystolic gallop producing a loud "summation" gallop. In such an instance, slowing the heart by carotid sinus pressure will separate the two gallop sounds. (See Fig. 123.) Opening Snap
The opening snap of the mitral valve is a characteristic finding in mitral valvular disease and its recognition by auscultation is of great importance. It must be differentiated from the second component of a split second sound and from a third heart sound. A few simple clues will permit one to make this differentiation at the bedside. The opening snap occurs perceptibly later than the second component of a split second sound. A split second sound is loudest at the pulmonary area whereas the opening snap is best heard medial to the apex or at the lower left sternal border. The interval between the two parts of a split second sound will vary with respiration~ but the interval between a
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second sound and an opening snap (2-0S interval) will not. When atrial fibrillation is present the 2-0S interval will change from beat to beat depending on the length of the preceding diastole. Following a short diastole the opening snap will occur closer to the second sound, and after a long diastole the opening snap will occur later. Splitting of the second sound does not show this variation in atrial fibrillation. In most patients with opening snaps, careful auscultation at the lower left sternal border will reveal both a split second sound and the opening snap. A third heart sound or protodiastolic gallop occurs later than an opening snap, is lower in pitch, and is best heard at the apex. (See Fig. 123.) Murmurs
Murmurs are heard both in healthy individuals and in patients with heart disease. The following aspects of each murmur should be noted: (1) timing, (2) intensity, (3) quality and (4) transmission. On the basis of this type of analysis, one may secure information not obtainable by any other method. 4 Timing can be systolic, diastolic or continuous. Diastolic murmurs should be further characterized as early or late (presystolic). Intensity is graded 1 to 6. A grade 1 murmur is the faintest that can be heard on careful auscultation, and a grade 6 murmur is one which can be heard even with the stethoscope removed from the chest wall. Grades 2 to 5 correspond to slight, moderate, loud, and very loud. The area of maximum intensity should also be noted. The quality of a murmur depends mainly on its pitch (high, low, medium) and its configuration. The configuration of a murmur refers to its "shape" and includes crescendo, plateau, decrescendo and diamond shaped (crescendo-decrescendo). Quality is further characterized by more subjective terms such as blowing, harsh and rumbling. Thus a murmur of aortic stenosis might be described as "a grade 3, medium-pitched, harsh, diamond-shaped systolic murmur, transmitted to the neck vessels." Systolic murmurs are frequently heard in normal individuals, especially in children and adolescents. The term "functional murmur" has led to much confusion, because in a sense all murmurs are an expression of function. Furthermore, there is a tendency to regard faint murmurs as "functional" or benign and very loud murmurs as ominous. The fallacy of this reasoning is readily apparent when one considers the grade 5 systolic murmur from a small, insignificant ventricular septal defect, and the very faint murmurs of pulmonary atresia or very severe mitral stenosis. In view of these difficulties, one should first describe a murmur accurately and then, with the help of other clinical and laboratory information, decide whether or not it is significant. 4 The murmurs of mitral or tricuspid regurgitation start with the first sound, and extend throughout systole at the same intensity or slightly decrescendo. They are characteristically high-pitched and blowing, and
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are poorly transmitted. On the other hand, the murmurs of aortic and pulmonary stenosis are harsh and diamond shaped (i.e., beginning slightly after the first sound, rising to a peak near midsystole, and tapering off before the second sound). They are well transmitted to the neck and over the precordium. At times the murmur of aortic stenosis will be louder at the apex than at the base. This could lead to an erroneous diagnosis of mitral regurgitation unless one recognized the diamond shape of the murmur in both areas. The systolic murmur of ventricular septal defect is usually plateau but sometimes accentuated in midsystole. It is best heard in the third or fourth left interspace. Despite its loudness (grade 3 to 6) and its transmission over the precordium, it is poorly transmitted to the neck. In contrast to systolic murmurs, diastolic murmurs almost invariably indicate structural heart disease. The diastolic murmurs of mitral stenosis and regurgitation will be discussed in the next section. The diastolic murmur of tricuspid stenosis has the same quality as that of mitral stenosis but is usually best heard at the lower left sternal border. Another differential point is that tricuspid murmurs become louder during inspiration and fainter during expiration. Mitral murmurs will either remain unchanged during respiration or become slightly fainter during inspiration. Short diastolic murmurs, aptly termed "prolonged third heart sounds," are commonly heard in the mitral or tricuspid areas in patients with congenital heart disease and a left-to-right shunt. In atrial septal defect with a shunt from left atrium to right atrium the murmur is produced by increased tricuspid valve flow and right ventricular filling; in ventricular septal defect and patent ductus arteriosus the left-to-right shunt occurs distal to the tricuspid valve and the murmur is produced by increased mitral valve flow and left ventricular filling. These murmurs simulate the early diastolic rumble of mitral stenosis. The Austin Flint murmur is a presystolic murmur at the apex in patients with aortic regurgitation. By auscultation this murmur is identical with the presystolic murmur of mitral stenosis, but these patients do not have mitral stenosis demonstrable at autopsy. The murmur is probably due to deflection of the anterior leaflet of the mitral valve by the regurgitant blood stream, producing a relative mitral stenosis. It can be differentiated from the murmur of organic mitral stenosis by the absence of an opening snap and the absence of a snapping first heart sound. The basal diastolic murmur of aortic regurgitation is very difficult to differentiate from the murmur of pulmonary regurgitation (Graham Steell murmur). Although in aortic regurgitation the murmur may be well heard in the second right interspace, both murmurs are usually IIlaximal along the left sternal border. Differentiation must usually be
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made by inference based on evidence of aortic valve disease versus evidence of pulmonary hypertension. A continuous murmur is one which persists through systole and into diastole without interruption. This murmur is typical of shunts between vessels and is found in patent ductus arteriosus and arteriovenous fistula. In patent ductus the murmur begins after the first sound, is loudest at the end of systole, envelops the second sound, and decreases in diastole. It is best heard in the second left interspace, often well away from the sternum, and tends to radiate up and outward over the left upper chest. The following conditions produce murmurs closely resembling those of patent ductus: aortic-pulmonary window, high ventricular septal defect with aortic regurgitation, ruptured sinus of Valsalva, anomalous pulmonary veins, coronary A-V fistula, and the shunt created by a Blalock or Potts operation for tetralogy of Fallot. Other "continuous" murmurs include the thyroid bruit of hyperthyroidism, venous hums, and murmurs from collateral circulation. The dilated intercostal collaterals in coarctation of the aorta are best heard over the posterior chest. Bronchial collaterals in pulmonary atresia or severe stenosis produce a continuous murmur over a wide area, but maximal over the right upper lobe bronchus. In "atypical patent ductus," progressive pulmonary hypertension with increasing vascular resistance eliminates first the diastolic and finally the systolic components of the murmur as the left-to-right shunt is eliminated and finally reversed. MITRAL STENOSIS AND MITRAL REGURGITATION
The auscultatory findings in pure mitral stenosis and in pure mitral regurgitation are well defined. However, in many patients these two lesions are combined. Since marked insufficiency requires a different approach to mitral surgery, it is very important to determine the predominant lesion. A snapping first sound and an opening snap strongly favor predominant mitral stenosis. An apical pansystolic murmur obscuring the first sound is typical of mitral regurgitation, but the loudness of the murmur is not a reliable indication of the amount of regurgitation. Many patients with predominant mitral stenosis may have systolic murmurs of variable intensity with only an insignificant degree of regurgitation. If right heart failure or tricuspid disease is present, a systolic murmur produced by tricuspid regurgitation may be falsely attributed to mitral insufficiency. A well-developed third heart sound strongly favors predominant mitral regurgitation. The character of the apical diastolic murmur is helpful in differentiating these lesions. In mitral stenosis the diastolic murmur begins with or shortly after the opening snap and tends to be prolonged throughout most of diastole. If normal sinus rhythm is present there is often a presystolic crescendo murmur. This presystolic accentuation is usually
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absent with atrial fibrillation, and it may disappear during congestive heart failure even when sinus rhythm is present. When mitral stenosis is complicated by significant mitral regurgitation, a large proportion of the left ventricular output is ejected into the left atrium during systole. In predominant mitral insufficiency, regurgitant flow may be two or three times as great as forward flow out the aortic valve. This results in a larger forward flow across the mitral valve during early diastole which in itself produces a "relative" mitral stenosis. It also leads to dilatation of the left ventricle and the mitral annulus so that a vicious cycle is set up producing more regurgitation. On auscultation, patients with mitral regurgitation will have apical diastolic murmurs, sometimes very loud because of the turbulence set up by greatly increased mitral valve flow in early diastole. However, there are two features which distinguish the apical diastolic murmurs of mitral regurgitation: Ca) They are initiated by a loud component, often a thrill, corresponding in time with the third heart sound and rapid ventricular filling. Cb) They tend to be shorter in duration because ventricular filling takes place more rapidly than in predominant mitral stenosis. Although an opening snap is generally a reliable sign of mitral stenosis, a few patients with predominant regurgitation show opening snaps. This is not so surprising when one considers that these patients have a high early diastolic pressure gradient across the mitral valve which is one of the major factors in the genesis of the opening snap. We have also recorded opening snaps in ruptured mitral chordae tendineae and in myxoma of the left atrium. In mitral stenosis with advanced valvular fibrosis and calcification the first sound becomes faint and the opening snap may disappear. In general, the tighter the valve and the lower the mitral valve flow, the softer will be the mitral murmurs. Stenosis of the mitral, aortic or pulmonary valves may be so severe that flow is reduced below the range necessary to produce murmurs. Finally, inspection and palpation are always useful in distinguishing tight mitral stenosis from predominant mitral regurgitation. These bedside observations are often more accurate than x-ray or electrocardiography. If there are no signs of left ventricular hypertrophy by the criteria mentioned previously, and obvious right ventricular hypertrophy is present, significant mitral regurgitation can be ruled out. Combined ventricular hypertrophy may be seen in tight mitral stenosis if systemic hypertension, aortic valvular disease, or marked coronary insufficiency is also present. CONCLUSION
The bedside cardiac examination provides important diagnostic information when auscultation is coordinated with careful inspection and palpation.
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Whereas percussion of heart borders is grossly inaccurate, palpation of the precordial impulses furnishes a simple and reliable indication of ventricular hypertrophy. In minimal or combined ventricular hypertrophy the electrocardiogram and x-ray are much less reliable than simple physical examination. Correlation of physical findings with cardiac catheterization and surgical exploration has provided the basis for reappraisal of certain timehonored concepts regarding clinical examination of the heart. REFERENCES 1. Harrison, T. R.: Palpation of the Precordial Impulses. Stanford M. Bull. 13: 385, 1955. 2. Wood, P.: Disea5es of the Heart and Circulation. 2nd Ed., London, Eyre & Spottiswoode, 1956. 3. Levine, S. A. and Harvey, W. P.: Clinical Auscultation of the Heart. Philadelphia, W. B. Saunders Co., 1949. 4. N adas, A. S.: Pediatric Cardiology. Philadelphia, W. B. Saunders Co., 1957.
3560 J Street Sacramento, California (Dr. Blake)