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The genesis of diastolic heart sounds
The Genesis of Diastolic Heart Sounds The Sonic Potential of Cardiac Tissues and the Diastolic Sounds from Mitral Prostheses
WILLIAM
DOCK, M.D.
New York, New York
From the Outpatient Clinic, The Veterans Administration Hospital, New York, New York. This study was supported by the Lavinia Dock Trust Fund. Requests for reprints should be addressed to Dr. William Dock, 145 East 16th Street, New York, New York 10003. Manuscript received May 14, 1970.
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The vena cava and the pulmonary vein, as well as the atrioventricular (A-V) valves, emit loud sounds over a wide range of frequencies when tensed, under water, by application of moderate force. Much larger forces are required to elicit low-pitched sounds from the large arteries, strips of atrial or ventricular walls or even from most aneurysms of the left ventricle. Only the A-V valves seem capable of causing the heart sounds heard over the precordium, but the jugular and pulmonic veins could emit the sounds heard above the clavicles or from the esophagus at the level of the left atrium, synchronous with the venous atrial wave. Some ventricular aneurysms could contribute to low-pitched gallop sounds. The diastolic sounds recorded from patients with mitral Starr-Edwards prostheses have the high pitch and brief duration characteristic of the opening and closing sounds of the metal valves, and vary in the same way as third and fourth sounds from normal valves. This proves that third and fourth sounds usually are purely valvular in origin. Rapid ventricular filling, protodiastolic or presystolic, leads to kinetic forces from deceleration in the ventricles adequate to tense the A-V valves or force the ball into the atrial orifice of the prosthesis with sufficient force to evoke loud, high-pitched sounds. Lesser forces yield faint, low-pitched noises. Previous studies [l] showed that the wall of the left ventricle could not be set into audible vibration by sudden tension due to forces many times stronger than those which evoked loud sounds from human A-V valves. This seemed to confirm the theory that heart sounds must be purely valvular in origin [2]. As far as the first sound is concerned this has been conclusively proved by catheter studies on men [3] and horses [4,5], as well as by records of the sounds arising in Starr-Edwards prostheses in the mitral orifice [6,7]. Observations on the loud first sound and loud gallop sounds in patients with ventricular aneurysms, together with recent contributions claiming that diastolic heart sounds must arise in the “ventricular wall” or in a nebulous
The American Journal of Medicino
GENESIS
“cardiohemic” mass, led to a reexamination of the sonic potentialities of various cardiovascular structures. This seemed desirable because better methods of recording sound were now available, notably for the low frequency sounds characteristic of gallops and the high frequency sounds characteristic of Starr-Edwards valves. METHODS To avoid intensification of sounds by resonance, wooden elements used in 1959 [l] were eliminated
the
and was
the Lucite@ tank in which sounds were evoked lined with foam rubber sheets 15 mm thick. A water-
proofed diaphragm-type stethoscope head inside the tank (Figure 1) was connected to a microphone resting on foam rubber outside the tank. The signal from this went to a Sage [8] amplifier and the output in three channels, 20 to 80 cycles per second (cps), 80 to 240 cps and 240 to 2,000 cps, was recorded in millivolts (mv) by a 4 channel Sanborn 964 galvanometer. Gains on the Sage amplifier were always set at 45 degrees from zero, on the Sanborn they varied from 0.5 to 10 mm/mv. Necropsy material provided fresh tissues: superior vena cava, pulmonary artery, aorta, intact mitral and tricuspid valves, walls of atria and ventricles. The annulus of the valves, or one end of the strips of tissue, was fastened with upholsterers’ tacks to a rubber stopper 3 cm in diameter and 1.5 cm thick, held to a 2 kg cube of lead by a lead disc and steel screw. The papillary muscles, or the other end of a strip of tissue, were fastened to a similar rubber stopper by tacks and linen ligatures. This stopper was fastened to a lead rod, 1 by 2 cm, 30 cm long and weighing 400 gm. With the lead cube resting on foam rubber 3 cm thick on the bottom of the water-filled Lucite tank, the valve or tissue could be tensed by raising the rod (Figure 1). A coil mounted on the rod moved in the field of two fixed Alnico magnets, and the induced current was recorded on the fourth channel of the galvanometer. Voltage varies with velocity of motion of the rod, and the square of the peak voltage varies with the maximal force exerted on the tissue or valve.
RESULTS Figures 2 and 3 show how phonocardiograms compare with the records made from isolated tissues. Sound-force ratios are obtained by dividing the sound signal (in mv) by 1 per cent of the square of the velocity signal (mv?). In Table I are the averages of sound-force ratios for various tissues, with the loudest for each in parentheses. In the 1959 study, using a calibrated straingauge and one signal for sound intensity over the range 120 to 5,000 cps, sound to force ratios be-
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came linear at 50,000 to 80,000 dynes [l]. An anterior mitral leaflet and its chordae gave 60 decibels at 100,000 dynes, 80 decibels at 300, 000. With the new system of recording it became evident that low frequency sounds became linear with force at much lower levels than sounds over 240 cps. Only this latter channel was calibrated with an audiometer. A 5 mv signal at 500 cps corresponds with 75 db, 8 mv with 90 db, 12 mv with 110 db. The latter is very loud to the ear; 30 db, which is barely audible, gives a signal of 0.2 mv in the high frequency record. The wide variation of sonic potential of the same structure from different hearts is evident in Table II. Valves No. 1 and 6 came from normal hearts; No. 5 came from a hypertrophied heart with thick chordae and atheromatous anterior cusp. With A-V valves, variation was much greater than with strips of tissue. Obviously there is difficulty in placing papillary muscles so as to permit uniform tensing of chordae. Optimal attachment was approached in heart valve No. 6 but not in No. 1, and other early cases. When using only anterior mitral leaflets [l] the variation from case to case was relatively small when compared with tests on entire valves. The averages given in Table I understate the true sonic potential of the A-V valves as contrasted with the other tissues. In the frequencies below 240 cps, the highest sound-force ratio was noted in strips of superior vena cava, but A-V valves with their delicate chordae gave higher ratios at frequencies over 240 cps. An intact left ventricular wall, from annulus to near the apex, gave no sound when tensed by forces which lifted the 2 kg weight and gave velocity squared values of 8,000 to 9,000 on the sensing system. This is 20 times the force needed to evoke loud sounds from mitral valves. Strips of left ventricles about 4 cm wide and 4 to 6 cm long, centered at the apex (the thinnest part of the wall), yielded sound-force ratios less than 10 per cent of those from strips of superior vena cava of comparable dimensions. Over 240 cps, strips of left ventricle have a sound potential only 1 per cent as great as that of the mitral valve. Pulmonary arterial strips gave sounds 3 to 10 times as loud as those from aortas of the same subjects. One ventricular aneurysm, entirely free of epicardial fat and of muscle, showed sonic potential comparable with that of an A-V valve, but only below 240 cps. The other five aneurysms amounts of residual muscle contained varying and of epicardial fat and their sonic potential
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lOmm/mv
Figure 1. An anterior mitral leaf/et, fastened to rubber stoppers, is tensed by lifting lead rod with attached coil, C, in the field of two magnets, M. Sound is detected by the stethoscope, S, inside the water filled tank and the microphone outside. Wires to galvanometers record sound intensity and velocity of motion of the rod. Figure 3. Right, heart sounds at the apex recorded as in Figure 2. Left, sounds from strip of vena cava; these are as loud as those from A-V valves, and much louder than normal heart sounds. High-pitched sounds are much weaker at apex than just to left of sternum.
averaged about as low as that ventricular wall.
of strips
of right
COMMENTS
MITRAL
Figure 2. Left, heart sounds in three frequency bands, recorded from lead V, area using same stethoscope and connection to microphone as for in vitro records. Center, sounds from an intact mitral valve. Right, sounds from the membranous wall of a ventricular aneurysm. Lower trace gives the electrocardiogram or the velocity of motion of the rod. Sensitivity of galvanometers is given in millimeters per millivolt (mm/mv).
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These observations show that even the thin apical part of the left ventricular wall, in an isolated strip, has about 5 per cent of the sonic potential, at 20 to 240 cps, of the A-V valves or strips of superior vena cava. Over 240 cps this falls to 1 per cent. However, the walls of the few aneurysms of the left ventricle which are free of muscle and of epicardial fat may equal the sound production, below 240 cps, of the valvular structures. For practical purposes, only the A-V valves, the semilunar valves and the great veins can be considered sources of the relatively high-pitched sounds we hear and record with standard phonocardiographs. Although forces available to tense the veins are very small compared with those causing arterial sounds in the chest, or during estimation of b’lood pressure in the brachial artery, we can hear and
The American
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GENESIS
record loud sounds from above the right clavicle [9] which are evoked by the a and even by the v wave of the venous pulse, and, from the esophagus, sounds which atrial systole causes in the pulmonic veins [lo]. The second loud element of the first sound (0.08 to 0.12 second after Q) can be due to the very sharp and strong rise in pressure in the pulmonary artery or the aorta at the start of systolic ejection. Here sonic potential, especially in the aorta, is relatively low but force is great. When sounds are evoked by a sudden rise of pressure in a vein or artery, the force tensing the wall is the difference in internal and external pressure. But pressure differences across the semilunar cusps are trifling at the moment the second heart sound occurs. Until the valve is closed and drawn taut the aorta and pulmonary artery form common chambers with the ventricles, and there is scarcely any gradient during systolic ejection. As pressure falls at the end of systole, blood runs back toward the ventricle until the valve is closed. It is the kinetic energy of the column of blood moving toward the ventricle which tenses the semilunar cusps, not a simple pressure gradient, which is only a few millimeters of mercury at the instant the second sound occurs. The same situation exists at the A-V orifice at the moment the first loud element of the first sound occurs (0.04 to 0.06 second after Q in normal hearts; 0.05 to 0.09 second in mitral stenosis). Pressure is higher in the atrium than in the ventricle before the sound occurs, and the gradient is only a few millimeters of mercury 0.02 second later. The first sound is due to the kinetic energy or momentum of blood moving toward the atrium during isometric rise in intraventricular pressure. If the valve is wide open, due to inflow in early diastole or atrial systole, the first sound will be very loud. If inflow has ended and the A-V valve has moved toward the atrium, the sound will be faint because blood cannot gain much momentum before the A-V valve is tensed. In mitral stenosis, with the valve pushed under high pressure into the ventricle, blood must move a greater distance and gains momentum before the membrane is tensed toward the atrium; in early diastole it produces a snap when tense in the ventricle. To produce sounds in diastole, all the force must come from kinetic energy, since pressure in atria and ventricles is low and the ventricular wall relaxed and flabby. With almost no pressure gradient, blood moves swiftly through wide ori-
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TABLE
OF
Sound-Force
I
DIASTOLIC
Ratios,
Tissue
20-80 cps
Great veins Mitral valves Tricuspids Aneurysmofventricle Pulmonary artery Left atrium Right ventricle Left ventricle Aorta
4.7 (5.2) 3.1 (6.9) 2.2 (2.5) 1.0 (3.5) 0.7 (0.9) 0.3 (0.6) 0.15(0.2) 0.1 (0.14) 0.1 (0.16)
HEART
SOUNDS-DOCK
Calculated
as in Table
II
80-240 cps 240-2,000 cps 8.6 (12.0) 8.5 (17.0) 6.9 (9.5) 2.8 (7.5) 3.3 (4.2) 1.5 (2.3) 0.9 (1.2) 0.35 (0.5) 0.8 (1.2)
3.4 (4.4) 2.4 (4.9) 2.0 (4.1) 0.2 (0.3) 0.3 (0.5) 0.1 (0.15) 0.1 (0.12) 0.03(0.05) O.Ol(O.03)
NOTE: Data based on averages from data derived as in Table II. Great veins includes right pulmonary vein and superior vena cava. Figures in parentheses represent loudest sound-force ratios.
fices into the ventricles. When mitral stenosis is present, no third or fourth sound occurs, thus confirming the view that the energy needed to cause these sounds must be kinetic and due to rapid inflow. Dean [ll], Rushmer [12] and Zaky [13] have presented evidence for the closure of the A-V valves after phases of rapid ventricular filling, and Wong [14] has described reflux of radiopaque media into the left atrium during protodiastole in cases of mitral regurgitation. The protodiastolic apical thrust is unusually forceful in young men with normal hearts and loud third heart sounds [2], as well as in constrictive pericarditis, in which the third sound is louder than the first or second [15, Figure 76-91. These thrusts end sharply, and the apex “retracts” either at or shortly before the third sound. Similar phenomena at the apex accompany the fourth sound and are in patients with ventricular most striking aneurysms. TABLE
II
Data, as in Table I, Derived in Figures 2 and 3.
Data Peak velocity of rod (mv) Force = velocity* Sound intensity (mv) 20-80 cps 80-240 cps 240-2,000 cps Sound-force ratio (S/lo/,F) 20-80 cps 80-240 cps 240-2,000 cps
Valve 1 in Air 20 400 4.0 2.0 0.0
from
Records,
Valve 1 Valve 5 in Water in Water 26 676 19.0 22.0 12.0
25 625 6.0 11.0 2.0
as
Valve 6 in Water 17 289 20.0 48.0 14.0
6.9 0.9 17.0 1.8 0.3 4.9 ~__ NOTE: Data on three hearts, contrasting sound intensity recorded from the same valve in air and then in water, and the intensity recorded from the mitral valve which gave the lowest and from that giving the highest intensity. For each heart, this gives the highest sound-force ratios calculated from a series of 20 to 40 tensings. 1.0 0.5 0.0
2.8 3.2 1.8
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Figure 4. Electrocardiogram ana sounds at apex in man with apical aneurysm, six months after infarc. tion. The low-pitched presystolic (4) occurs in every beat, following apical thrust illustrated top left with R marker from electrocardiogram, and large backward thrust of body in seismocardiogram, upper right. A high-pitched third sound (3) occurs only in first two beats and last beat. Although P-R is 0.20 second, the first sound is very loud, as is usually the case with apical aneurysms. This low-pitched gallop may arise in the aneurysmal membrane, tensed by the jet from atrial systole.
The apical pull-in is due to rounding out the heart, which has been elongated by the jet of blood from the atrium and can resume the spheroid form which has the lowest ratio of surface, or fiber length, to volume. It has been ascribed [16] to pull-in by the chordae tendineae and papillary muscles, stretched taut and causing the third sound. Since both retraction and third sounds occur in patients with resected mitral valves and papillary muscles, and aortic homografts in the mitral orifice, this explanation has been dropped [17,18]. The change in form which causes apical retraction may begin before the third or fourth sound. Blood rebounding from the concave wall of the ventricle may focus on the mitral orifice, and the third or fourth sound may coincide with the start of apical retraction. When the shaking of the body by the heart beat is recorded (seismocardiogram), it is often observed in constrictive pericarditis [19;20; Figure 121, mitral or tricuspid regurgitation, or myocardial failure, that larger forces are registered in diastole, with the third or fourth sounds, than during systolic ejection into the aorta and pulmonary arteries. These hearts fill more swiftly and forcefully than they empty. It is this force which gives the blood the kinetic energy needed to stretch the mitral valve and chordae so sharply that sound is evoked when rapidly moving masses of blood are decelerated. In constrictive pericardi-
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tis and in youths with normal third sounds the mass of blood is not great, but velocity of inflow squared is high. In heart failure or A-V regurgitation the volume of blood is very great. Since the force of inflow is spread over the dilated ventricle, pressure per square centimeter is not great but concentrated on the A-V orifice during rebound from the concave wall, pressure per square centimeter may be much greater. In patients with aneurysms of the left ventricle located in the antero-apical region the sonic properties of the wall are such that part of the first sound and the gallop sounds may arise in the aneurysmal wall. This is tensed at, or slightly before, the tensing of the mitral valve in which the high-pitched elements arise. These usually are strikingly loud [21; Figure 31, but in a few cases, as shown in Figure 4, there may be a loud lowpitched early element in the presystolic gallop, with almost no high-pitched sound. In most cases the wall merely acts as “a thin wall, freely transmitting intracardiac vibrations to the chest wall” [22]. The surprisingly loud presystolic sounds heard and recorded over the jugular veins above the clavicle [9] or recorded from the esophagus at the level of the atrium and pulmonic veins [lo] can be ascribed to sudden tensing of these thinwalled vessels by the relatively small pressure change due to atrial systole. The sonic potential of these veins is so high compared to those in the
The American
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GENESIS
aorta (Table I) that a rise of less than 10 mm Hg in large veins can evoke a sound comparable with that produced by a sudden rise of 100 mm Hg in the femoral artery in a man with the classic “pistol shot” of aortic insufficiency. The facts now known give strong circumstantial evidence for the valvular origin of the third and fourth sounds. Origin in the ventricular wall is highly unlikely, origin in the A-V valves at the observed instant is possible, but still unproved. However, if third and fourth sounds can be recorded in patients with metallic prostheses in their mitral orifices, and are found to have the characteristic high-pitched sound, then there could be no dispute as to the site and mechanism of their origin. Because many patients with mitral disease continue to fibrillate, only protodiastolic sounds could occur, and rapid filling is retarded by the ball. Because most cardiologists do not record sounds with a separate high-pitched channel, prosthetic gallop can easily escape detection, but Hultgren [6] and Dayem [7] recorded faint diastolic sounds in patients with prostheses. Of these only Hultgren’s Figures 6 and 11 and Dayem’s Figure 6 show third and fourth sounds with the sharp highpitched character which permits identification as prosthetic sounds. Since these reports have been ignored in all recent discussions of the genesis of diastolic sounds, they did not carry conviction. Perhaps two recent cases, recorded with a system which brings out the peculiar features of prosthetic sounds, will be more convincing. Figure 5 shows a constantly present presystolic gallop from a Starr-Edwards valve in the mitral orifice and
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Sounds in pulmonic area, eighteen Figure 5. months after insertion of Starr-Edwards valve in mitral orifice. The presystolic gallops (41, the opening (0) and closing (C) sounds all have the loud, sharp, high-pitched “metallic” character of this prosthesis, either mitral or aortic. Note that amplification of sounds over 240 cps is one-fifth as great as in records from a normal heart, Figures 2 and 3.
Figure 6. Sounds medial to apex, three years after insertion of mitral Starr-Edwards prosthesis. The presystolic gallop (4) is loud and highpitched only in sinus beat which follows ventricular ectopic beat, becomes fainter and lower pitched in next beat, then fades to very faint sound recorded in most sinus beats. Accentuation or appearance of presystolic gallop after ectopic beats has often been noted in patients with normal valves.
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Figure 6 shows a loud fourth sound following a ventricular ectopic beat. In both cases the classic sound pattern, recorded from all aortic and mitral valve Starr-Edwards valves as they open and close, are evident in the diastolic sounds. In the second case the sound fades into a faint, lower pitched sound, evident in all the beats recorded in that area and similar to many of the diastolic sounds recorded by Hultgren and Raftery in patients with mitral prostheses. Thus, it is clearly proved that diastolic heart sound can occur in mitral prostheses, that mechanisms do exist for reversing flow and sharply tensing normal valves or forcing the ball in the prosthesis to rebound briefly toward the atrium. That such rebound can occur very swiftly is shown by the sounds of the ectopic beat in Figure 6. Here the closing sound of the ectopic beat is very loud 0.14 second after the previous second sound and only 0.05 second after the opening
sound which signals the start of protodiastolic inflow. Because rapid inflow is interrupted, this closing sound is louder than those of sinus beats with P-R of 0.18 second, whereas the closing sound after the following beat and loud fourth sound is relatively faint. Prosthetic closing sounds thus show the same variation in intensity, in relation to P-R interval, previous second sound or previous gallop sounds, as do those from normal valves. The valvular origin of all heart sounds seems thus to be firmly established, but further study, using suitable recording of sounds to bring out highpitched elements, after exercise, and also with the patient in the left lateral position, is needed to verify this conclusion. The brief reversal of the pressure gradient from atrium to ventricle at the instant the third or fourth sound occurs has been clearly demonstrated in the horse [4; Figure lo] in which these sounds are normally audible.
REFERENCES 1.
2.
Dock W: cardiac
The forces needed to evoke tissues, and the attenuation
sound from of sounds.
Circulation 19: 376, 1959. Lewis JK, Dock W: The origin of heart sounds their variations in myocardial disease. JAMA
13. and
110:
271, 1938. 3.
4.
5.
6.
7.
8.
9. 10.
11.
184
12.
Braunwald E, Morrow AG: Origin of heart sounds as elucidated by analysis of the sequence of cardiodynamic events. Circulation 18: 971, 1958. Patterson DF, Detwiler DK, Glendenning SA: Heart sounds and murmurs in the normal horse. Ann NY Acad Sci 127: 242, 1965. Smetzer DL, Smith CR, Hamlin RL: The fourth heart sound in the equine. Ann NY Acad Sci 127: 306, 1965. Hultgren HN, Hubis H: A phonocardiographic study of patients with the Starr-Edwards mitral valve prosthesis. Amer Heart J 69: 306, 1965. Dayem MKA, Raftery EB: Mechanisms of production of heart sounds based on records of sounds after valve replacement. Amer J Cardiol 18: 837, 1966. Dock W: A simple way to record heart sounds on direct-writing electrocardiographs. JAMA 184: 148, 1963. Dock W: Loud presystolic sounds over jugular veins. Amer J Med 20: 853, 1956. Taquini A: Les bruits cardiaques normaux par voie oesophagienne. CR Sot Biol 127: 534, 1937. Dean AL, Jr: The movements of the mitral cusps in relation to the cardiac cycle. Amer J Physiol 40: 206, 1916.
14.
15.
16.
17. 18.
19.
20. 21.
22.
Rushmer RF: Cardiac Diagnosis, Philadelphia, WB Saunders Co, 1955, p 213. Zaky A, Steinmetz E, Feigenbaum H: Role of atrium in closure of mitral valve in man. Amer J Physiol 217: 1652, 1969. Wong M: Diastolic mitral regurgitation, hemodynamic and angiographic correlation. Brit Heart J 31: 468, 1969. Fowler NO: Pericarditis, The Heart, Arteries and Veins, 2nd ed (Hurst JW and Logue RB, eds), New York, McGraw-Hill Book, 1970, p 1266. Fleming JS: Evidence for a mitral valve origin of the left ventricular diastolic heart sounds. Brit Heart J 29: 192, 1967. Marshall JC, Gibson DG: Origin of third heart sound. Brit Med J 3: 778, 1969. Gianelly RE, Popp RL, Hultgren HN: Heart sounds in patients with homograft mitral valves. Circulation 42: 309, 1970. Scarborough WR, McKusick VA, Baker BM Jr: The ballistocardiogram in constrictive pericarditis before and after pericardiectomy. Bull Johns Hopkins Hosp 90: 42, 1952. Dock W: The three plane ballistocardiogram in heart failure. Amer J Cardiol 3: 384, 1959. Dock W: Signos fisicos de 10s aneurismas ventriculares con insuficiencia cardiaca. Pren Med Argent 53: 341, 1966. Mourdjenis A, Olsen E, Raphael MJ, Mounsey JPD: Clinical diagnosis and prognosis of ventricular aneurysms. Brit Heart J 30: 497, 1968.
The American
Journal
of Medicine
WILLIAM
DOCK, M.D.
New York, New York
From the Outpatient Clinic, The Veterans Administration Hospital, New York, New York. This study was supported by the Lavinia Dock Trust Fund. Requests for reprints should be addressed to Dr. William Dock, 145 East 16th Street, New York, New York 10003. Manuscript received May 14, 1970.
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The vena cava and the pulmonary vein, as well as the atrioventricular (A-V) valves, emit loud sounds over a wide range of frequencies when tensed, under water, by application of moderate force. Much larger forces are required to elicit low-pitched sounds from the large arteries, strips of atrial or ventricular walls or even from most aneurysms of the left ventricle. Only the A-V valves seem capable of causing the heart sounds heard over the precordium, but the jugular and pulmonic veins could emit the sounds heard above the clavicles or from the esophagus at the level of the left atrium, synchronous with the venous atrial wave. Some ventricular aneurysms could contribute to low-pitched gallop sounds. The diastolic sounds recorded from patients with mitral Starr-Edwards prostheses have the high pitch and brief duration characteristic of the opening and closing sounds of the metal valves, and vary in the same way as third and fourth sounds from normal valves. This proves that third and fourth sounds usually are purely valvular in origin. Rapid ventricular filling, protodiastolic or presystolic, leads to kinetic forces from deceleration in the ventricles adequate to tense the A-V valves or force the ball into the atrial orifice of the prosthesis with sufficient force to evoke loud, high-pitched sounds. Lesser forces yield faint, low-pitched noises. Previous studies [l] showed that the wall of the left ventricle could not be set into audible vibration by sudden tension due to forces many times stronger than those which evoked loud sounds from human A-V valves. This seemed to confirm the theory that heart sounds must be purely valvular in origin [2]. As far as the first sound is concerned this has been conclusively proved by catheter studies on men [3] and horses [4,5], as well as by records of the sounds arising in Starr-Edwards prostheses in the mitral orifice [6,7]. Observations on the loud first sound and loud gallop sounds in patients with ventricular aneurysms, together with recent contributions claiming that diastolic heart sounds must arise in the “ventricular wall” or in a nebulous
The American Journal of Medicino
GENESIS
“cardiohemic” mass, led to a reexamination of the sonic potentialities of various cardiovascular structures. This seemed desirable because better methods of recording sound were now available, notably for the low frequency sounds characteristic of gallops and the high frequency sounds characteristic of Starr-Edwards valves. METHODS To avoid intensification of sounds by resonance, wooden elements used in 1959 [l] were eliminated
the
and was
the Lucite@ tank in which sounds were evoked lined with foam rubber sheets 15 mm thick. A water-
proofed diaphragm-type stethoscope head inside the tank (Figure 1) was connected to a microphone resting on foam rubber outside the tank. The signal from this went to a Sage [8] amplifier and the output in three channels, 20 to 80 cycles per second (cps), 80 to 240 cps and 240 to 2,000 cps, was recorded in millivolts (mv) by a 4 channel Sanborn 964 galvanometer. Gains on the Sage amplifier were always set at 45 degrees from zero, on the Sanborn they varied from 0.5 to 10 mm/mv. Necropsy material provided fresh tissues: superior vena cava, pulmonary artery, aorta, intact mitral and tricuspid valves, walls of atria and ventricles. The annulus of the valves, or one end of the strips of tissue, was fastened with upholsterers’ tacks to a rubber stopper 3 cm in diameter and 1.5 cm thick, held to a 2 kg cube of lead by a lead disc and steel screw. The papillary muscles, or the other end of a strip of tissue, were fastened to a similar rubber stopper by tacks and linen ligatures. This stopper was fastened to a lead rod, 1 by 2 cm, 30 cm long and weighing 400 gm. With the lead cube resting on foam rubber 3 cm thick on the bottom of the water-filled Lucite tank, the valve or tissue could be tensed by raising the rod (Figure 1). A coil mounted on the rod moved in the field of two fixed Alnico magnets, and the induced current was recorded on the fourth channel of the galvanometer. Voltage varies with velocity of motion of the rod, and the square of the peak voltage varies with the maximal force exerted on the tissue or valve.
RESULTS Figures 2 and 3 show how phonocardiograms compare with the records made from isolated tissues. Sound-force ratios are obtained by dividing the sound signal (in mv) by 1 per cent of the square of the velocity signal (mv?). In Table I are the averages of sound-force ratios for various tissues, with the loudest for each in parentheses. In the 1959 study, using a calibrated straingauge and one signal for sound intensity over the range 120 to 5,000 cps, sound to force ratios be-
Volume
50.
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1971
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DIASTOLIC
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came linear at 50,000 to 80,000 dynes [l]. An anterior mitral leaflet and its chordae gave 60 decibels at 100,000 dynes, 80 decibels at 300, 000. With the new system of recording it became evident that low frequency sounds became linear with force at much lower levels than sounds over 240 cps. Only this latter channel was calibrated with an audiometer. A 5 mv signal at 500 cps corresponds with 75 db, 8 mv with 90 db, 12 mv with 110 db. The latter is very loud to the ear; 30 db, which is barely audible, gives a signal of 0.2 mv in the high frequency record. The wide variation of sonic potential of the same structure from different hearts is evident in Table II. Valves No. 1 and 6 came from normal hearts; No. 5 came from a hypertrophied heart with thick chordae and atheromatous anterior cusp. With A-V valves, variation was much greater than with strips of tissue. Obviously there is difficulty in placing papillary muscles so as to permit uniform tensing of chordae. Optimal attachment was approached in heart valve No. 6 but not in No. 1, and other early cases. When using only anterior mitral leaflets [l] the variation from case to case was relatively small when compared with tests on entire valves. The averages given in Table I understate the true sonic potential of the A-V valves as contrasted with the other tissues. In the frequencies below 240 cps, the highest sound-force ratio was noted in strips of superior vena cava, but A-V valves with their delicate chordae gave higher ratios at frequencies over 240 cps. An intact left ventricular wall, from annulus to near the apex, gave no sound when tensed by forces which lifted the 2 kg weight and gave velocity squared values of 8,000 to 9,000 on the sensing system. This is 20 times the force needed to evoke loud sounds from mitral valves. Strips of left ventricles about 4 cm wide and 4 to 6 cm long, centered at the apex (the thinnest part of the wall), yielded sound-force ratios less than 10 per cent of those from strips of superior vena cava of comparable dimensions. Over 240 cps, strips of left ventricle have a sound potential only 1 per cent as great as that of the mitral valve. Pulmonary arterial strips gave sounds 3 to 10 times as loud as those from aortas of the same subjects. One ventricular aneurysm, entirely free of epicardial fat and of muscle, showed sonic potential comparable with that of an A-V valve, but only below 240 cps. The other five aneurysms amounts of residual muscle contained varying and of epicardial fat and their sonic potential
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lOmm/mv
Figure 1. An anterior mitral leaf/et, fastened to rubber stoppers, is tensed by lifting lead rod with attached coil, C, in the field of two magnets, M. Sound is detected by the stethoscope, S, inside the water filled tank and the microphone outside. Wires to galvanometers record sound intensity and velocity of motion of the rod. Figure 3. Right, heart sounds at the apex recorded as in Figure 2. Left, sounds from strip of vena cava; these are as loud as those from A-V valves, and much louder than normal heart sounds. High-pitched sounds are much weaker at apex than just to left of sternum.
averaged about as low as that ventricular wall.
of strips
of right
COMMENTS
MITRAL
Figure 2. Left, heart sounds in three frequency bands, recorded from lead V, area using same stethoscope and connection to microphone as for in vitro records. Center, sounds from an intact mitral valve. Right, sounds from the membranous wall of a ventricular aneurysm. Lower trace gives the electrocardiogram or the velocity of motion of the rod. Sensitivity of galvanometers is given in millimeters per millivolt (mm/mv).
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These observations show that even the thin apical part of the left ventricular wall, in an isolated strip, has about 5 per cent of the sonic potential, at 20 to 240 cps, of the A-V valves or strips of superior vena cava. Over 240 cps this falls to 1 per cent. However, the walls of the few aneurysms of the left ventricle which are free of muscle and of epicardial fat may equal the sound production, below 240 cps, of the valvular structures. For practical purposes, only the A-V valves, the semilunar valves and the great veins can be considered sources of the relatively high-pitched sounds we hear and record with standard phonocardiographs. Although forces available to tense the veins are very small compared with those causing arterial sounds in the chest, or during estimation of b’lood pressure in the brachial artery, we can hear and
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GENESIS
record loud sounds from above the right clavicle [9] which are evoked by the a and even by the v wave of the venous pulse, and, from the esophagus, sounds which atrial systole causes in the pulmonic veins [lo]. The second loud element of the first sound (0.08 to 0.12 second after Q) can be due to the very sharp and strong rise in pressure in the pulmonary artery or the aorta at the start of systolic ejection. Here sonic potential, especially in the aorta, is relatively low but force is great. When sounds are evoked by a sudden rise of pressure in a vein or artery, the force tensing the wall is the difference in internal and external pressure. But pressure differences across the semilunar cusps are trifling at the moment the second heart sound occurs. Until the valve is closed and drawn taut the aorta and pulmonary artery form common chambers with the ventricles, and there is scarcely any gradient during systolic ejection. As pressure falls at the end of systole, blood runs back toward the ventricle until the valve is closed. It is the kinetic energy of the column of blood moving toward the ventricle which tenses the semilunar cusps, not a simple pressure gradient, which is only a few millimeters of mercury at the instant the second sound occurs. The same situation exists at the A-V orifice at the moment the first loud element of the first sound occurs (0.04 to 0.06 second after Q in normal hearts; 0.05 to 0.09 second in mitral stenosis). Pressure is higher in the atrium than in the ventricle before the sound occurs, and the gradient is only a few millimeters of mercury 0.02 second later. The first sound is due to the kinetic energy or momentum of blood moving toward the atrium during isometric rise in intraventricular pressure. If the valve is wide open, due to inflow in early diastole or atrial systole, the first sound will be very loud. If inflow has ended and the A-V valve has moved toward the atrium, the sound will be faint because blood cannot gain much momentum before the A-V valve is tensed. In mitral stenosis, with the valve pushed under high pressure into the ventricle, blood must move a greater distance and gains momentum before the membrane is tensed toward the atrium; in early diastole it produces a snap when tense in the ventricle. To produce sounds in diastole, all the force must come from kinetic energy, since pressure in atria and ventricles is low and the ventricular wall relaxed and flabby. With almost no pressure gradient, blood moves swiftly through wide ori-
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TABLE
OF
Sound-Force
I
DIASTOLIC
Ratios,
Tissue
20-80 cps
Great veins Mitral valves Tricuspids Aneurysmofventricle Pulmonary artery Left atrium Right ventricle Left ventricle Aorta
4.7 (5.2) 3.1 (6.9) 2.2 (2.5) 1.0 (3.5) 0.7 (0.9) 0.3 (0.6) 0.15(0.2) 0.1 (0.14) 0.1 (0.16)
HEART
SOUNDS-DOCK
Calculated
as in Table
II
80-240 cps 240-2,000 cps 8.6 (12.0) 8.5 (17.0) 6.9 (9.5) 2.8 (7.5) 3.3 (4.2) 1.5 (2.3) 0.9 (1.2) 0.35 (0.5) 0.8 (1.2)
3.4 (4.4) 2.4 (4.9) 2.0 (4.1) 0.2 (0.3) 0.3 (0.5) 0.1 (0.15) 0.1 (0.12) 0.03(0.05) O.Ol(O.03)
NOTE: Data based on averages from data derived as in Table II. Great veins includes right pulmonary vein and superior vena cava. Figures in parentheses represent loudest sound-force ratios.
fices into the ventricles. When mitral stenosis is present, no third or fourth sound occurs, thus confirming the view that the energy needed to cause these sounds must be kinetic and due to rapid inflow. Dean [ll], Rushmer [12] and Zaky [13] have presented evidence for the closure of the A-V valves after phases of rapid ventricular filling, and Wong [14] has described reflux of radiopaque media into the left atrium during protodiastole in cases of mitral regurgitation. The protodiastolic apical thrust is unusually forceful in young men with normal hearts and loud third heart sounds [2], as well as in constrictive pericarditis, in which the third sound is louder than the first or second [15, Figure 76-91. These thrusts end sharply, and the apex “retracts” either at or shortly before the third sound. Similar phenomena at the apex accompany the fourth sound and are in patients with ventricular most striking aneurysms. TABLE
II
Data, as in Table I, Derived in Figures 2 and 3.
Data Peak velocity of rod (mv) Force = velocity* Sound intensity (mv) 20-80 cps 80-240 cps 240-2,000 cps Sound-force ratio (S/lo/,F) 20-80 cps 80-240 cps 240-2,000 cps
Valve 1 in Air 20 400 4.0 2.0 0.0
from
Records,
Valve 1 Valve 5 in Water in Water 26 676 19.0 22.0 12.0
25 625 6.0 11.0 2.0
as
Valve 6 in Water 17 289 20.0 48.0 14.0
6.9 0.9 17.0 1.8 0.3 4.9 ~__ NOTE: Data on three hearts, contrasting sound intensity recorded from the same valve in air and then in water, and the intensity recorded from the mitral valve which gave the lowest and from that giving the highest intensity. For each heart, this gives the highest sound-force ratios calculated from a series of 20 to 40 tensings. 1.0 0.5 0.0
2.8 3.2 1.8
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Figure 4. Electrocardiogram ana sounds at apex in man with apical aneurysm, six months after infarc. tion. The low-pitched presystolic (4) occurs in every beat, following apical thrust illustrated top left with R marker from electrocardiogram, and large backward thrust of body in seismocardiogram, upper right. A high-pitched third sound (3) occurs only in first two beats and last beat. Although P-R is 0.20 second, the first sound is very loud, as is usually the case with apical aneurysms. This low-pitched gallop may arise in the aneurysmal membrane, tensed by the jet from atrial systole.
The apical pull-in is due to rounding out the heart, which has been elongated by the jet of blood from the atrium and can resume the spheroid form which has the lowest ratio of surface, or fiber length, to volume. It has been ascribed [16] to pull-in by the chordae tendineae and papillary muscles, stretched taut and causing the third sound. Since both retraction and third sounds occur in patients with resected mitral valves and papillary muscles, and aortic homografts in the mitral orifice, this explanation has been dropped [17,18]. The change in form which causes apical retraction may begin before the third or fourth sound. Blood rebounding from the concave wall of the ventricle may focus on the mitral orifice, and the third or fourth sound may coincide with the start of apical retraction. When the shaking of the body by the heart beat is recorded (seismocardiogram), it is often observed in constrictive pericarditis [19;20; Figure 121, mitral or tricuspid regurgitation, or myocardial failure, that larger forces are registered in diastole, with the third or fourth sounds, than during systolic ejection into the aorta and pulmonary arteries. These hearts fill more swiftly and forcefully than they empty. It is this force which gives the blood the kinetic energy needed to stretch the mitral valve and chordae so sharply that sound is evoked when rapidly moving masses of blood are decelerated. In constrictive pericardi-
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tis and in youths with normal third sounds the mass of blood is not great, but velocity of inflow squared is high. In heart failure or A-V regurgitation the volume of blood is very great. Since the force of inflow is spread over the dilated ventricle, pressure per square centimeter is not great but concentrated on the A-V orifice during rebound from the concave wall, pressure per square centimeter may be much greater. In patients with aneurysms of the left ventricle located in the antero-apical region the sonic properties of the wall are such that part of the first sound and the gallop sounds may arise in the aneurysmal wall. This is tensed at, or slightly before, the tensing of the mitral valve in which the high-pitched elements arise. These usually are strikingly loud [21; Figure 31, but in a few cases, as shown in Figure 4, there may be a loud lowpitched early element in the presystolic gallop, with almost no high-pitched sound. In most cases the wall merely acts as “a thin wall, freely transmitting intracardiac vibrations to the chest wall” [22]. The surprisingly loud presystolic sounds heard and recorded over the jugular veins above the clavicle [9] or recorded from the esophagus at the level of the atrium and pulmonic veins [lo] can be ascribed to sudden tensing of these thinwalled vessels by the relatively small pressure change due to atrial systole. The sonic potential of these veins is so high compared to those in the
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GENESIS
aorta (Table I) that a rise of less than 10 mm Hg in large veins can evoke a sound comparable with that produced by a sudden rise of 100 mm Hg in the femoral artery in a man with the classic “pistol shot” of aortic insufficiency. The facts now known give strong circumstantial evidence for the valvular origin of the third and fourth sounds. Origin in the ventricular wall is highly unlikely, origin in the A-V valves at the observed instant is possible, but still unproved. However, if third and fourth sounds can be recorded in patients with metallic prostheses in their mitral orifices, and are found to have the characteristic high-pitched sound, then there could be no dispute as to the site and mechanism of their origin. Because many patients with mitral disease continue to fibrillate, only protodiastolic sounds could occur, and rapid filling is retarded by the ball. Because most cardiologists do not record sounds with a separate high-pitched channel, prosthetic gallop can easily escape detection, but Hultgren [6] and Dayem [7] recorded faint diastolic sounds in patients with prostheses. Of these only Hultgren’s Figures 6 and 11 and Dayem’s Figure 6 show third and fourth sounds with the sharp highpitched character which permits identification as prosthetic sounds. Since these reports have been ignored in all recent discussions of the genesis of diastolic sounds, they did not carry conviction. Perhaps two recent cases, recorded with a system which brings out the peculiar features of prosthetic sounds, will be more convincing. Figure 5 shows a constantly present presystolic gallop from a Starr-Edwards valve in the mitral orifice and
OF
DIASTOLIC
HEART
SOUNDS-DOCK
Sounds in pulmonic area, eighteen Figure 5. months after insertion of Starr-Edwards valve in mitral orifice. The presystolic gallops (41, the opening (0) and closing (C) sounds all have the loud, sharp, high-pitched “metallic” character of this prosthesis, either mitral or aortic. Note that amplification of sounds over 240 cps is one-fifth as great as in records from a normal heart, Figures 2 and 3.
Figure 6. Sounds medial to apex, three years after insertion of mitral Starr-Edwards prosthesis. The presystolic gallop (4) is loud and highpitched only in sinus beat which follows ventricular ectopic beat, becomes fainter and lower pitched in next beat, then fades to very faint sound recorded in most sinus beats. Accentuation or appearance of presystolic gallop after ectopic beats has often been noted in patients with normal valves.
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GENESIS
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HEART SOUNDS-DOCK
Figure 6 shows a loud fourth sound following a ventricular ectopic beat. In both cases the classic sound pattern, recorded from all aortic and mitral valve Starr-Edwards valves as they open and close, are evident in the diastolic sounds. In the second case the sound fades into a faint, lower pitched sound, evident in all the beats recorded in that area and similar to many of the diastolic sounds recorded by Hultgren and Raftery in patients with mitral prostheses. Thus, it is clearly proved that diastolic heart sound can occur in mitral prostheses, that mechanisms do exist for reversing flow and sharply tensing normal valves or forcing the ball in the prosthesis to rebound briefly toward the atrium. That such rebound can occur very swiftly is shown by the sounds of the ectopic beat in Figure 6. Here the closing sound of the ectopic beat is very loud 0.14 second after the previous second sound and only 0.05 second after the opening
sound which signals the start of protodiastolic inflow. Because rapid inflow is interrupted, this closing sound is louder than those of sinus beats with P-R of 0.18 second, whereas the closing sound after the following beat and loud fourth sound is relatively faint. Prosthetic closing sounds thus show the same variation in intensity, in relation to P-R interval, previous second sound or previous gallop sounds, as do those from normal valves. The valvular origin of all heart sounds seems thus to be firmly established, but further study, using suitable recording of sounds to bring out highpitched elements, after exercise, and also with the patient in the left lateral position, is needed to verify this conclusion. The brief reversal of the pressure gradient from atrium to ventricle at the instant the third or fourth sound occurs has been clearly demonstrated in the horse [4; Figure lo] in which these sounds are normally audible.
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2.
Dock W: cardiac
The forces needed to evoke tissues, and the attenuation
sound from of sounds.
Circulation 19: 376, 1959. Lewis JK, Dock W: The origin of heart sounds their variations in myocardial disease. JAMA
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Braunwald E, Morrow AG: Origin of heart sounds as elucidated by analysis of the sequence of cardiodynamic events. Circulation 18: 971, 1958. Patterson DF, Detwiler DK, Glendenning SA: Heart sounds and murmurs in the normal horse. Ann NY Acad Sci 127: 242, 1965. Smetzer DL, Smith CR, Hamlin RL: The fourth heart sound in the equine. Ann NY Acad Sci 127: 306, 1965. Hultgren HN, Hubis H: A phonocardiographic study of patients with the Starr-Edwards mitral valve prosthesis. Amer Heart J 69: 306, 1965. Dayem MKA, Raftery EB: Mechanisms of production of heart sounds based on records of sounds after valve replacement. Amer J Cardiol 18: 837, 1966. Dock W: A simple way to record heart sounds on direct-writing electrocardiographs. JAMA 184: 148, 1963. Dock W: Loud presystolic sounds over jugular veins. Amer J Med 20: 853, 1956. Taquini A: Les bruits cardiaques normaux par voie oesophagienne. CR Sot Biol 127: 534, 1937. Dean AL, Jr: The movements of the mitral cusps in relation to the cardiac cycle. Amer J Physiol 40: 206, 1916.
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Rushmer RF: Cardiac Diagnosis, Philadelphia, WB Saunders Co, 1955, p 213. Zaky A, Steinmetz E, Feigenbaum H: Role of atrium in closure of mitral valve in man. Amer J Physiol 217: 1652, 1969. Wong M: Diastolic mitral regurgitation, hemodynamic and angiographic correlation. Brit Heart J 31: 468, 1969. Fowler NO: Pericarditis, The Heart, Arteries and Veins, 2nd ed (Hurst JW and Logue RB, eds), New York, McGraw-Hill Book, 1970, p 1266. Fleming JS: Evidence for a mitral valve origin of the left ventricular diastolic heart sounds. Brit Heart J 29: 192, 1967. Marshall JC, Gibson DG: Origin of third heart sound. Brit Med J 3: 778, 1969. Gianelly RE, Popp RL, Hultgren HN: Heart sounds in patients with homograft mitral valves. Circulation 42: 309, 1970. Scarborough WR, McKusick VA, Baker BM Jr: The ballistocardiogram in constrictive pericarditis before and after pericardiectomy. Bull Johns Hopkins Hosp 90: 42, 1952. Dock W: The three plane ballistocardiogram in heart failure. Amer J Cardiol 3: 384, 1959. Dock W: Signos fisicos de 10s aneurismas ventriculares con insuficiencia cardiaca. Pren Med Argent 53: 341, 1966. Mourdjenis A, Olsen E, Raphael MJ, Mounsey JPD: Clinical diagnosis and prognosis of ventricular aneurysms. Brit Heart J 30: 497, 1968.
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