Download Relationship of Heart Sounds to Acceleration of Blood Flow

Relationship of Heart Sounds to
Acceleration of Blood Flow
By Thomas E. Piemme, M.D., G. Octo Barnett, M.D., and
Lewis Dexter, M.D.
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• After more than 100 years of observation,
no universal agreement exists regarding the
precise nature of the cause of the familiar
transient heart sounds. Most arguments for
specific cause are based on the demonstration
of an association in time between the sound
and some other pressure or flow-related
event, i.e., valve closure, chordae tensing, etc.
There would appear to be two chief reasons
for the existing disagreement.
In the first place there has been too often
a failure to appreciate the physics of the system under investigation. This has led to errors
in interpretation. No portion of the interdependent cardiohemic system may vibrate independently.1 Thus, a purely valvular cause
of transient heart sounds is difficult to conceive. A realistic approach would seem to result from a consideration of those forces
which set into vibratory motion the system of
blood, heart walls, and valves. Such forces
are associated with acceleration and deceleration of blood flow.2 Acceleration of blood flow
is provided by the force of ventricular (or
atrial) contraction per unit mass of blood. De-
From the Departments of Medicine, Peter Bent
Brigham Hospital and Harvard Medical School, Boston, Massachusetts.
Supported in part by grants from the Life Insurance Medical Research Fund, and Grants HE-00450,
HTS-5234, and HTS-5550 from the National Heart
Institute, U. S. Public Health Service, and the American Heart Association.
During this work Dr. Piemme held a Research
Fellowship of the American Heart Association.
Dr. Bamett is an Established Investigator of the
American Heart Association.
Presented in part at the Forty-seventh Annual
Meeting of the Federation of American Societies for
Experimental Biology, Atlantic City, New Jersey,
April 15, 1963. (Federation Proc. 22: 642, 1963.)
Accepted for publication September 7, 1965.
Circulation Research, Vol. XV111, March 1966
celeration of blood flow occurs in the presence
of impedance exceeding the forces promoting
forward flow. Heart walls, and tension within
elastic vascular structures, as well as heart
valves, contribute to total impedance. Some,
but not all, of these factors have been taken
into account in consideration of the origin of
cardiac sound.3
A second cause of disagreement has been
the fact that instrumentation frequently used
for the recording of events of the cardiac
cycle (for the purpose of time comparison)
has been inadequate to the task. All recording
systems contain some time delay in the registration of the observed physical event. Such
time delays in any study of the origin of heart
sounds assume major importance inasmuch as
events of the cardiac cycle to which audible
pressure phenomena have been attributed
follow so rapidly upon one another, especially
at the onset of ventricular contraction, as to
fall within the time delay of many transducerrecorder systems. Instrumentation for the registration of cardiac sound is reasonably precise, but instrumentation used for the
recording of functions against which sound
has been compared (e.g., pressure) is notoriously deficient for this purpose.45 The recording of jugular and venous pulse tracings involves, quite apart from instrument delay, a
delay in pulse wave transmission from the
heart to the transducer site. Whenever events,
occurring within 20 to 40 milliseconds of one
another, are being compared, the instrumentation for their registration must introduce a
time delay of not greater than a few milliseconds.
The purpose of this communication is to
relate the application of suitable high frequency response instrumentation to the investigation of the time relationships of cardiac
303
PIEMME, BARNETT, DEXTER
304
transient sounds to pressure and flow events
of the cardiac cycle.
Methods
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Simultaneous recordings have been made of intravascular and intracardiac pressures, aortic
blood flow and acceleration, the electrocardiogram, and intracardiac sound in healthy anesthetized dogs.
Intracardiac and aortic pressure were measured with the Dallons-Telco* variable inductance
microtransducer, a catheter-tip manometer with
a frequency response that has been demonstrated
in this laboratory to have a relatively constant
ratio of output to input amplitude to well over
500 cycles/sec. The maximum time lag which
could be introduced by this transducer would be
on the order of less than 2 milliseconds. Access to
the left ventricle and left atrium was gained by
retrograde passage from the left carotid artery.
Aortic pressures were obtained with the cathetermanometer located fluoroscopically within 2 cm
of the aortic valve.
Intracardiac "sound" was obtained from the
Dallons-Telco amplifier by filtering frequencies
below 40 cycles/sec from the pressure output
and amplifying the result. This is an integral
part of the apparatus as obtained from the company. These higher frequency pressure transients,
altered in their passage through the tissues by
damping, and by the natural frequencies of intervening structures, appear on the chest wall,
and are translated by the auditory mechanism
into recognizable sound. That such recording of
intracardiac "sound" is comparable in time with
phonocardiographically recorded sound transients
has been demonstrated.0
Aortic blood flow was obtained from the root
of the aorta with the Medicon K-2000t electromagnetic flowmeter. The amplifier employs a 400
cycles/sec carrier wave frequency. Circuit computations reveal a maximum phase lag of 6 to 8
milliseconds when the amplifier is used in the unfiltered position. Following placement of the flowmeter probe, the chest was closed and the lung
reinflated before any observations were made.
Electronic differentiation of aortic flow velocity
was used to measure acceleration. Differentiation
of left ventricular pressure was occasionally done
to detect subtle changes in slope not discernible by
inspection of the tracing. Time derivatives were
obtained with the use of the Philbrick P-2 differ*Dallons Laboratories, Inc., 5066 Santa Monica
Blvd., Los Angeles, California.
tMedicon, 2800 North Figueroa Street, Los Angeles, California.
ential operational amplifier* with a resistancecapacitance network chosen so that the accuracy
of computation was in error by less than 5% of all
frequencies out to 150 cycles/sec. The time lag
introduced by this computation was less than
1 millisecond.
The electrocardiogram was monitored from a
modified lead i with electrodes placed in the
axillae. Care was taken to reduce the resistance
between electrodes to less than 500 ohms. Where
necessary, subcutaneous contact was made.
Some recordings were made on an Electronicsfor-Medicinet electron beam photographic recorder, others on a Sanborn model 350t directwriter. In the latter case a 60 cycle filter was
occasionally used in the recording of sound and
flow. Since identical circuits were employed when
these functions were being compared with one
another, there was no time delay introduced into
the recording of one that was not identically
introduced into the recording of the other. It was
therefore possible to make a valid time comparison of the events occurring in the two different
parameters.
The above instrumentation is reasonably precise. In every situation, careful attention was
paid to any possible time delay that could be
introduced by the transducer, amplifiers, computing elements, filtering devices, or the recording equipment. Direct comparison of recorded
events within the constraints of the known time
delays is valid.
Once control observations were made, many
of the animals were given infusions of isoproterenol (0.4 /lig/ml at 2 to 3 ml/min) or methoxamine (40 yug/ml at 2 to 3 ml/min) to determine, respectively, the effects of high flow and
high resistance on the comparative timing of
events of the cardiac cycle.
Results
FIRST HEART SOUND
The first heart sound was found to contain two major components, often separated
by a discernible silent period. The separation
of the two components was a function of the
duration of isometric ventricular contraction.
The first major component was seen to occur
simultaneously with the onset of isometric
ventricular contraction and the occurrence of
•Philbrick Researches, Inc., 127 Clarendon Street,
Boston, Massachusetts.
fElectronics-for-Medicine, Inc., 30 Virginia Road,
White Plains, New York.
tSanborn Instrument Company, Waltham, Massachusetts.
Circulation Research, Vol. XVIII, March 1966
HEART SOUNDS AND ACCELERATION OF BLOOD FLOW
305
Ao Pressure
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FIGURE 1
Comparison of sound with pressure events on the left side of the heart. Left: comparison of
sound with central aortic and left atrial pressures. The first component of the first sound (lt)
occurs synchronously with an aortic presystolic wave (arrow) and a complex atrial "c-wave."
Right: comparison of sound with left ventricular diastolic and central aortic pressures. The
first major component of the first sound is written during early ventricular isometric contraction.
Reflection of the atrial "a-wave" in the left ventricle is clearly seen, occurring earlier. All
pressure, as well as sound, recorded with the Dallons-Telco transducer. Time lines are 0.04
sec apart. Electronics-f or-Medicine recording.
the left atrial "c-wave" (fig. 1). The form of
the atrial "c-wave" was not always as classically described, but was frequently biphasic
and, on occasion, even more complex. There
occurred at this time a distinct positive, or
biphasic, wave in the central aorta. This wave
was invariably present, even in one animal in
the face of atrial fibrillation (fig. 2) and,
therefore, could not possibly have been due
to atrial contraction as has often been thought.
The presence of simultaneous low frequency pressure waves in the aorta and left
atrium together with the first component of
the first heart sound led to an inquiry as to
whether a similar low frequency event might
not be present in the left ventricle, but obscured by the rapidly rising intraventricular
CircuUiio* RtsMrcb, Vol. XVIII, Mirch
1966
pressure. Accordingly, the left ventricular
pressure was differentiated (fig. 3), revealing
the presence of a subtle change in slope in
early isometric ventricular contraction. This
was present in all cases. It is not discernible
by mere inspection of the undifferentiated
pressure trace, since its amplitude is sufficiently low, and its "frequency" sufficiently high,
to be hidden within the width of the rapidly
rising electron beam inscription.
The second major component of the first
heart sound began concomitantly with the
rise of aortic pressure, and the onset of aortic
blood flow. It peaked with peak acceleration
of aortic blood flow, and ended just prior to
maximum instantaneous flow. A comparison
of sound with central aortic flow and pres-
306
PIEMME, BARNETT, DEXTER
EKG
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FIGURE 2
Central aortic and left atrial pressures in the presence of atrial fibrillation in the dog. Atrial
"c-wace" and small aortic presystolic wave (arrow) persist. Recording conditions as in figure 1.
sure is shown in figure 4. Direct comparison
of sound with flow and acceleration of flow
(first time derivative) is shown in figure 5.
Recording was made with the pressure-sound
transducer located within the lumen of the
flowmeter probe, less than 2 cm above the
aortic valve ring.
SECOND HEART SOUND
The second heart sound began at that time
during systole when instantaneous flow, which
had been gradually declining, suddenly began a rapid descent to below baseline. It
thus began with the onset of the rapid deceleration phase, while forward flow was still
going on. Comparison of sound with aortic flow
and its derivative are shown in figure 6 under
control conditions, under conditions of high
flow induced by isoproterenol, and under conditions of low flow and increased peripheral
resistance induced by methoxamine. In each
case the sound began with the onset of rapid
deceleration, and peaked synchronously with
peak deceleration. Later components, usually
lesser in magnitude, were timed with the
short period of reversal of aortic blood flow
as the aortic valves closed, and with deceleration of pulmonary arterial flow. The onset
of the second heart sound occurred approximately 25 milliseconds before the nadir of
aortic flow, the latter being the point at which
the aortic valves presumably close (figs. 4, 5,
and 6). Such a time interval is clearly outside
the maximum time delay of sound, flow, or
acceleration recording.
The fundamental components of the second
heart sound here recorded are on the order of
30 to 60 cycles/sec. It should be remembered
that filtering circuits discriminated against
higher frequencies of sound which were,
nevertheless, concomitantly present. It is obvious, however, that there is significant energy
at this effective band-pass, and that much of
CinuUticn Rtsttrcb,
Vol. XVIII, Msrcb 1966
307
HEART SOUNDS AND ACCELERATION OF BLOOD FLOW
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Cti«.3)
FIGURE 3
Demonstration of the subtle change in slope of the left ventricular pressure in early isometric
contraction. Upper trace is a recording of left ventricular pressure. Lower trace is the first
time derivative of the signal. Distinct notching near the peak of the derivative is evidence
of the presence of higher frequencies of pressure not seen upon inspection of the rapidly
changing left ventricular pressure. The notch represents roughly a maximum change in the
steepness of the slope of 20%, with instability persisting for less than 20 milliseconds. It is
not surprising, therefore, that such information is not readily seen in the undifferentiated trace.
this energy occurs before the end of forward
aortic flow. Furthermore, the magnitude of
this early sound transient is roughly proportional to the magnitude of flow.
DIASTOLIC HEART SOUNDS
Third and fourth heart sounds are rarely
heard in adult man in the absence of pathology. Similarly, they could not be recorded
from the central aorta of the dog under normal conditions of pressure and flow. The
administration of methoxamine, however, resulted in the production of a fourth heart
sound that appeared simultaneously with the
left atrial "a-wave" and a low frequency pressure wave recordable from the central aorta
(fig. 7). The onset of heart failure and elevaCircuUtiou Rtittrcb,
Vol. XVIII, Mtrcb
1966
tion of left ventricular end diastolic pressure
with methoxamine, alone or in combination
with dextran infusion, resulted in the appearance of a protodiastolic third heart sound and
a new diastolic wave appearing in the aorta at
the time of rapid ventricular filling (fig. 8).
Discussion
In a previous communication from this laboratory,7 the concept was presented of the
heart as a second order mechanical system to
account for the presence of distinct diastolic
low frequency pressure transients appearing
in the central aorta. The heart represents a
distributed mass of fluid-filled muscle rather
loosely suspended from the great vessels within the sleeve of the pericardium. These ele-
PIEMME, BARNETT, DEXTER
308
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FIGURE 4
Pressure, sound, and flow recorded from the central aorta. Sound and flow recorded with
60-cycle filter permitting only dominant frequencies of sound to appear. Second major component of the first heart sound is seen to occur during early ventricular ejection. The onset of the
second sound occurs 30 milliseconds before the nadir of flow reversal is inscribed. Sanborn
350 direct-writer recording.
ments of mass, elastance, and resistance are
constantly changing as blood flows in and
out of the system. Should parts of the system
be underdamped, oscillations would occur in
the presence of an applied force. Oscillatory
displacement of the system would further
result in transient counterforces of induced
pressure within the fluid chambers. Such
transients would be complex wave-forms with
frequency and amplitude spectra that are a
function of the mass at the instant of displacement, the "spring" of suspension, and the
resistance offered by the myocardium, pericardium, and surrounding mediastinal structures. The lower frequencies might be seen
superimposed upon otherwise smooth intracardiac pressure functions, recorded via sufficiently sensitive transducers. The higher
frequencies, recordable from within the chambers, would be translated through surround-
ing tissues to the chest wall, identifiable as
external sound.
A number of observations appear to fit the
above concept. That the system is underdamped, and oscillates at moderate frequencies
(less than 60 cycles/sec), is seen in tracings
of slit- and electro-kymography.8"10 The response of such instruments discriminates
against higher frequencies. That similar frequency oscillations are reflected in induced
counterpressures within the chambers has
been shown in this laboratory.7 Further, these
oscillations are seen at expected times of
force inputs: isometric ventricular contraction,
atrial contraction, and rapid ventricular filling.
That vibration of the heart at higher (audible) frequencies does indeed occur is witnessed by the fact that we hear sound at all
from the heart. Whatever the source within
the heart, vibrations of the chest wall imply
OrcmUtim Rtiurcb,
Vol. XVIII, AUrcb 1966
HEART SOUNDS AND ACCELERATION OF BLOOD FLOW
309
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FIGURE S
Sound compared with flow (bottom) and the derivative of flow (top). Onset and end of forward
acceleration phase* bracketed in middle complex. The association of a major portion of the
sound w,th aortic blood flow acceleration is apparent. Recording conditions as ,n figured
vibration of intervening structures, including
blood and heart wall.
Rushmer1 emphasized the concept of acceleration and deceleration of blood flow as
forces sufficient to induce sound. McKusick11
states: It is . . . "probably most accurate to
think of sounds such as the first and second
sound, and the mitral 'opening snap,' as hydrostatic pressure transients produced by the
abrupt interruption of the momentum of local
flow. . . . Whether abrupt acceleration, as
CircmUiion R,st*,cb,
Vol. XVIII, M.rcb
1966
with valve opening, can produce sound is less
convincingly demonstrated, but clinical experience would suggest it can." Thus, McKusick felt that most, if not all, sounds were
the product of abrupt changes in local flow.
The observations related here extend the
above concept, and lend weight to it.
FIRST HEART SOUND
For many years two schools of thought
existed, attributing the first heart sound, re-
PIEMME, BARNETT, DEXTER
310
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FIGURE 6
Sound compared with flow (bottom) and the derivative of flow (top), under control conditions,
under conditions of high flow (isoproterenol) and under conditions of increased peripheral
resistance (methoxamine). Bracketing in each panel identifies onset of rapid deceleration, and
peak deceleration, of aortic blood flow. In each instance, these events time respectively with
the onset and peak of the second heart sound. The second sound begins 25, 20 and 30 milliseconds before the nadir of flow reversal under the three respective conditions. Such an event
cannot be accounted for by phase lags in the systems (see text). Note that later components
of the first sound increase as absolute magnitude of acceleration increases with increased flow
(isoproterenol), and decrease with decrease of acceleration with high peripheral resistance
(methoxamine). The latter effect is striking. Recording conditions as in figure 4.
spectively, to muscular contraction of the
ventricle, and to closure of the A-V valves.12
Any significant muscular contribution was,
however, firmly excluded by the experiments
of Dock.18 Orias and Braun-Menendez,14 supported by others,18-10 then proposed that
the first heart sound was comprised of four
components: (1) initial vibrations due to
atrial contraction, (2) a major component due
to closure of the A-V valves, (3) a major component due to opening of the semilunar valves,
and (4) terminal vibrations, perhaps due to
accelerating aortic flow.
In spite of much support for initial vibrations of atrial origin 17, 18 many authors
disagreed,19"22 calling attention to the fact
that such initial vibrations persist in the
presence of atrial fibrillation. The dispute
was resolved with the discovery that under
unusual pathological circumstances (e.g., arterial hypertension and decompensated aortic
stenosis) the fourth heart sound did indeed
move into the first heart sound,28"25 but that
under normal circumstances atrial contraction
played no part in the origin of the first heart
sound.
There is general agreement, then, that the
first major component of the first heart sound,
including initial vibrations, is a result of
forces set in motion during isometric ventricCircmUtion Rtstrcb,
Vol. XVIII, hUrcb 1966
HEART SOUNDS AND ACCELERATION OF BLOOD FLOW
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FIGURE 7
Effect of the pressor agent, methoxamine, upon the aortic pressure trace, and upon sound. A
fourth heart sound appears, coincident with a distinct wave in the aorta in late diastole
(arrow) in the presence of augmented atrial contraction. Electronics-for-Medicine recording.
tut*
FIGURE 8
Effect of left ventricular failure upon the aortic pressure trace. Three distinct waves (a, b
and c) are seen during diastole in the central aorta, timing respectively with rapid ventricular
filling, atrial contraction, and isometric ventricular contraction. Corresponding heart sounds
are numbered. Failure was induced by sustained infusion of norepinephrine following administration of chloralose in a large volume of fluid.
Circulation RtsHtcb,
Vol. XVIII, M.rcb
1966
311
312
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ular contraction, and a seemingly obvious
result of valve closure. Great doubt, however,
has been shed on a valve closure mechanism
by the accumulating evidence 2827 that the
A-V valves have at this point in time been
already closed by inertial forces resulting
from atrial contraction. This mechanism, first
proposed in 1912,28 is hemodynamically persuasive.
One is left then with the concept, alluded
to by others,1'11 that isometric ventricular
contraction induces a ballooning of the apposed valve curtains toward the atria. As
these curtains are stretched to their elastic
limit, flow in this direction is suddenly decelerated. If the present hypothesis is correct,
this would result in the first component of the
first heart sound, as well as low frequency
pressure transients in all chambers of the
heart. Figure 1 shows such a wave in the left
atrium (the "c-wave") and in the aorta (the
presystolic wave). Indeed, simultaneously occurring waves may be demonstrated in all
chambers of the heart.7
Even less agreement exists regarding the
second major component of the first heart
sound. Previous recording methods have not
clearly revealed whether the second major
component occurred before, during, or after
the instant of aortic valve opening. Thus, it
has been thought by some to be due to valve
opening,14"10'20 by others to be due to systolic ejection,30 and by still others to be due to
asynchronous closure of the A-V valves.31"38
Results presented here show clearly that
the second major component of the first heart
sound occurs at the time of ejection of blood
from the ventricle, a time too late to be accounted for by any asynchronous closure
mechanism. Although there may be asynchronism of mitral and tricuspid valve closure,
the time difference is probably so slight that
both contribute to the first major component.
The widening of the gap between first and
second components in bundle branch block
has been used as an argument for asynchronous closure of the two valves, but this widening may be as readily explained by delay of
ejection following the onset of depolarization
PIEMME, BARNETT, DEXTER
in bundle branch block. In fact, any process
lengthening isometric ventricular contraction
would be expected to produce a widening
and splitting of the two components of the
first sound.
That aortic flow acceleration bears a direct
time correspondence to the second component
of the first sound is clear from figures 4 and 5.
Careful inspection of figure 6 shows that, as
the magnitude of acceleration decreases in
the face of high peripheral resistance (secondary to methoxamine infusion), the magnitude of the second major component of the
first heart sound decreases accordingly. The
reverse obtains with isoproterenol. Acceleration is a function of change in force, and
greater acceleration implies increased force.
This force would therefore be expected to be
associated with a proportional increase in
pressure transients in all frequency ranges.
Acceleration of pulmonary arterial flow may
contribute to the sound as well, but, since the
duration of right ventricular ejection is longer,
acceleration of flow in the pulmonary artery
need be much less than that in the aorta. Such
low pressure chambers are low energy producing and, consequently, must have much
less influence on sound than would the high
energy systemic chambers.
SECOND HEART SOUND
There has been no disagreement with the
concept of the origin of the second heart
sound. It has been thought to be due to asynchronous closure of the semilunar valves,
aortic closure preceding pulmonic closure under normal conditions.37-38 This has been
reinforced by the clinical observation that
high flow in either circuit delays closure of
the respective valve and, correspondingly,
widens or narrows the gap between the two
components. Some observers have felt that
terminal vibrations may be due to tricuspid
and mitral valve opening.39
The precise physical mechanism for the
occurrence of the second sound was thought
by Rushmer1 to be due to impedance to back
flow as the semilunar valves abruptly closed.
McKusick11 has agreed with this concept.
If the reversal of aortic and pulmonic flow
Circulation Research, Vol. XVIII, March 1966
HEART SOUNDS AND ACCELERATION OF BLOOD FLOW
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may be invoked to account for the origin of
the second heart sound, then by similar argument forward deceleration should result in
the production of sound. Indeed, the magnitude of forward deceleration (and associated
force) is considerably greater than that of
reverse deceleration, the mass of blood acting
over a longer distance and at higher velocity.
The evidence presented here shows clearly
that the second sound begins at the onset of
the phase of rapid deceleration of forward
aortic flow. Furthermore, the first major component peaks with peak deceleration and ends
with the nadir of flow reversal. This would
appear to be strong evidence for a causal relationship, and is consistent with physical
considerations. The remaining component is
probably due to similar behavior of pulmonic
flow.
That the onset of the sound earlier than has
been thought is not due to artifact produced
by the presence of the flowmeter probe is indicated by the consistent relationship of the
sound to aortic pressure with or without the
probe in place. In two dogs, simultaneous
measurement of aortic and pulmonic pressures
with the probe in place has confirmed that
aortic valve closure preceded pulmonic valve
closure in these preparations.
DIASTOLIC HEART SOUNDS
Under normal conditions of pressure, flow,
and volume within the cardiac chambers,
impedance to flow from atrium to ventricle
may not result in sufficiently rapid deceleration to produce significant high frequency
oscillations. This would certainly be true
should ventricular relaxation be an active
process, literally "sucking" blood into the
ventricles.40 However, increased end diastolic
volume and/or pressure, or disease restricting
left ventricular filling (e.g., constrictive pericarditis), could result in augmentation (or
change in character) of impedance to flow,
giving rise to forces quite capable of displacing the system sufficiently to result in resonant
motion. Further, the primary alteration of the
volume-elastic characteristic in disease is a
loss of compliance. Such loss of damping must
Circulation Research, Vol. XVIII, March 1966
313
predispose to ringing as a result of whatever
increased forces are present.
As demonstrated here, left ventricular failure in the dog gave rise to both a third heart
sound and an associated low frequency pressure transient within the ascending aorta.
Indeed, the entire concept (and the evidence
shown here) would appear to be supported
by demonstrations of Lewis,8 Lewis and
Dock,9 and Brady and Taubman10 that most
normal adults have smooth outward motion
of the ventricular border during early diastole,
while children and patients with protodiastolic gallops demonstrate a sharp inflection
with notching, as recorded by kymograms.
This is certainly suggestive evidence for oscillation of the system, resulting in the observed
pressure transients, including sound.
The etiology of the fourth heart sound may
be similarly argued. The atrium and ventricle
during atrial contraction act as a single chamber. Under the influence of a pressure
gradient, blood flows from the atrium into an
already distended ventricle. As the elastic
limit of the musculature is reached, the rate
of flow will be suddenly changed, the deceleration again resulting in an oscillation of all
chambers and a coincident pressure transient.
Both Kincaid-Smith and Barlow,24 and Weitzman41 have agreed that, although the appellation "atrial sound" is frequently attached to
this phenomenon, it probably originates in
the ventricle as a filling sound. More to the
point, it originates from all participating resonant chambers.
Although the present communication contributes no evidence regarding the "opening
snap" or the systolic ejection click, there is
no reason to believe their origin is not on the
same basis. The concept of valvular "snapping"
in mitral stenosis is seriously damaged by the
realization that "opening snaps" are commonly
heard in left atrial myxoma. The hemodynamics of the two diseases are identical. Blood
enters the left ventricle in early diastole at
high velocity under a very large pressure
gradient, and is impeded in the one instance
by the elastic limit of the deformed mitral
valve, in the other instance by mechanical
314
PIEMME, BARNETT, DEXTER
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obstruction by the atrial tumor. Indeed, the
authors believe that all transient cardiovascular sound has the same principle of origin.
The hypothesis presented here is consistent
with the physics of sound production, and the
observed behavior of the cardiovascular system. To say that valve closure is responsible
for the origin of sound is to stop short of the
essential point. Valve closure does indeed result in the production of sound, but only by
providing a barrier to local flow. Furthermore,
the concentration on valvular mechanisms as
manufacturers of sound forces one to seek
explanations for other sounds (third and
fourth heart sounds) that are almost certainly
not valvular in origin. Abrupt changes in
momentum of flow, i.e., acceleration and
deceleration of flow velocity, must set the
heart in motion. This oscillatory motion is
associated with a spectrum of induced pressure frequencies that will continue until the
system is brought to rest through damping.
Should one doubt that acceleration and deceleration of flowing fluids can be responsible
for sound production, he need only enter an
old house, and abruptly turn on and off the
water faucets. The resultant noise can be impressive.
Summary
A concept has been presented that abrupt
acceleration or deceleration of blood flow is
associated with an energy source sufficient
to displace the mass of the heart, and that,
consequently, this mass will oscillate at a sum
of frequencies that are a function of chamber
mass and restoring forces. Induced pressure
transients may be observed in all chambers,
the lower frequencies appearing on conventional pressure tracings, the higher frequencies as intracardiac sound.
Using high frequency response instrumentation in dogs, intravascular sound has been
compared with pressure and flow events
throughout the cardiac cycle.
(1) The first component of the first heart
sound occurs during early isometric ventricular contraction and is associated with lower
frequency pressure transients that may be
recorded from all chambers of the heart. The
left atrial "c-wave" is one of these transients.
(2) The second component of the first
heart sound occurs during ventricular ejection,
and appears to be a function of acceleration
of aortic blood flow.
(3) The second heart sound begins significantly before aortic valve closure, while
forward flow is still going on, and is proportional to the magnitude of deceleration of
blood flow.
(4) The third heart sound appears only
in the presence of left ventricular failure at
the time of rapid ventricular filling, and is
associated with a low frequency wave recordable from the central aorta. The production of these transients is presumed to be
deceleration of inflow as the limits of ventricular relaxation are reached.
(5) A fourth sound arises coincident with
pressure transients in other chambers as atrial
systole further distends the left ventricle.
It is proposed that acceleration and deceleration of blood flow is a sufficient and necessary condition for the origin of cardiovascular
sound transients.
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Relationship of Heart Sounds to Acceleration of Blood Flow
Thomos E. Piemme, G. Octo Barnett and Lewis Dexter
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Circ Res. 1966;18:303-315
doi: 10.1161/01.RES.18.3.303
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