EDITORIALS

The Main Heart Sounds as Vibrationsof the

Cardiohemic System: Old Controversy and New Facts
ALDO A. LUISADA, MD, and FRANCESCO PORTALUPPI, MD

The Controversy and the Facts

Most of the energy involved in the heart beat results in

the creation of pressure gradients in the different
chambers of the heart and in the great vessels. Pressure
gradients are responsible for the motions of certain
cardiac structures and the progression of the blood mass
along the vascular trees, and the generation of mechanical vibrations. The latter are caused by groups of
molecules that are alternately compressed and rarified
by the energy source, and have measurable wave-like
properties with regard to position and time. The branch
of physics that deals with them is called acoustics.

Although there is general agreement about considering the lower frequencies as an expression of cardiac
dynamics (displacement, velocitv and acceleration of
the various parts of the cardiohemic system), numerous
controversies have arisen in the last 25 years in regard
to the role of the cardiac valves in the production of the
heart sounds.
Important findings published in the last 25 years
allow us to take a definite stand with regard to the
valve/sound relation. Some of the early investigators
believed that sounds were produced by the forceful
closure of the valves, while later, to reconcile different
facts that had been demonstrated, other investigators
believed that valve closure was silent but that valve
tension, which immediately follows the former, was the
cause of the heart sounds.
The first finding that refuted valve closure as a factor
of sound was reported by Edler et al,i Pohost et al2 and
Wexler et al3 for the mitral valve, and Thubrikar et al4
for the aortic valve. They showed that the leaflets of the
mitral and the cusps of the aortic valves do not close
uniformly and at the same time. Often, 1 leaflet or cusp
closes slightly before the other (or the others) and even
different parts of the same leaflet do not close at the
same time. Obviously, the demonstration of this complex mechanism does not favor the hypothesis of sound
created by the closure of a valve.
Another important finding, reported by Wexler et al,3
is that sound occurs only when the ventricular walls and
the septum have reached a certain degree of tension as
a result of ventricular contraction.
The cardiac valves, with their closure and opening,
time the onset of the heart sounds, but they also time
the onset and the subsequent changes of acceleration
and deceleration that occur during the phases of ventricular contraction and relaxation. To establish a
cause-effect relation, time coincidence is not enough and
a more accurate analysis of the dynamic system is necessary. Such analysis was done by Mac&non et al, who
tried to establish a relation between the energy of the
first heart sound (vibrations >30 Hz recorded at the
epicardial surface of anesthetized dogs), motion of the
mitral valve and mass of the vibrating valve structures.
Their conclusion was that not more than one tenth of

The Vibrations of the Heart

The cardiac vibrations are the result of energy applied
to a system; therefore, they should be considered and
studied as a single phenomenon regardless of their frequency and amplitude. Instead, because our hearing
apparatus has upper and lower limits of frequency and
amplitude, beyond which it would not yield the sensation of sound, we instinctively regard the heart sounds
as a distinct entity, different from the pulse waves,
which cannot be heard, although they can be palpated.
Therefore, when we record cardiac vibrations, the impression is that the phonocardiograms
as well as the
pulse or pressure tracings are giving us information that
is unrelated and may represent the expression of separate manifestations of cardiac energy. However, we are
using the same transducer for recording the 2 sets of
phenomena simply by introducing 2 types of filtration.
This means that we electronically separate the lower
frequencies (pressure and pulse waves) from the higher
frequencies (heart sounds)* even though they are part
of the same basic vibratory phenomenon.
There is also a technical reason for this separation: the energy
Of low-frequency
vibrations of the heart is much greater than
that of high-frequency vibrations. In an unfiltered recording of heart
vibrations, it would be extremely difficult to clearly record high
freWenCieS
because of the predominance of the low-frequency vibrations.
l

Content

From the Departments of Physiology and Medicine, The Chicago

Medical School/University of Health Sciences, and the Department of
Cardiology, Oak Forest Hospital, Chicago, Illinois. Manuscript received
May 27, 1963; revised manuscript received July 5, 1983, accepted July
8, 1983.
Address for reprints: Aldo A. Luisada, MD, 5000 S. Cornell Avenue,
Chicago, llinois 60615.
1133

EDITORIALS

1134

the energy could be due to the mitral valve. This excludes the atrioventricular
(AV) valves from being the
major cause of the first heart sound, both in regard to
their closure and in regard to their subsequent tension.
The pressure gradients between the heart chambers
and vessels cause the opening and closure of the valves.

r/\
\

(2) Mitral valve closure preceding LVsystole (cases

with long PR interval, complete AV block, or atria1
fibrillation) causes no sound. If sound is found in co-

ECG+&
I

PRESS
III-D

\
,=bC

PRESS -m.--J

E--vi-

The lack of coincidence between pressure crossover and

final closure of a valve (e.g., the mitral valve) should not
be interpreted as contradicting this statement. In fact,
pressure crossovers may not coincide with valve closures, due to the inertia of the blood column and of the
valves themselves. Based on new, authoritative studies,
the relation between ventricular dynamics, mitral closure and the first heart sound can be established as
follows:
(1) The first heart sound always follows the onset
of left ventricular (LV) systole. This is proved by recording either a LV pressure tracing or an apex cardiogram together with a phonocardiogram (Fig. 1). The
rapid increase in LV pressure generated by ventricular
systole is responsible for the final closure of the mitral
valve. This coincides with the onset of the first heart
sound.s,5-1a

incidence with a diastolic closure of the mitral valve, this

is a low-amplitude sound, different from the normal,
high-amplitude first heart sound.ls
(3) The timing and the amplitude of the first heart
sound is related to the position of the mitral leaflets
at the onset of LVsystole. That position is determined

by the left AV pressure gradient, so that we can state

that the timing and the amplitude of the first heart
sound are a function of the left AV gradient at the onset
of ventricular systole. Assuming a constant LV enddiastolic pressure, a relatively high atrial pressure causes
a large and delayed first sound; a relatively low atria1
pressure, in contrast, causes a faint and early first
sound.11m20The louder sound is not related to a more
forceful closure of the valve, as it was considered in some
reports; rather, a LV contraction against increased atrial
pressure generates, at the time of the first heart sound,
a more rapid deceleration, and thus more intense vibrations of the cardiohemic system. Occasionally, the
position of the mitral leaflets is totally unrelated to the
intensity of the first heart sound (Fig. 2).
(4) The amplitude of the first heart sound is also a
function
traction

of the rapidity of development of LV con(expressed by LV dPldt). Sakamoto et all6

demonstrated this relation by the use of sympathomimetic drugs, myocardial stimulants and depressants,
and constriction of the aortic root, as well as other maneuvers.

ID

FIGURE 1. Top, left ventricular pressure (PRESS) of an anesthetized

dog, recorded with a catheter-tip manometer; third derivative of pressure
(PRESS III-D); and external phonocardiogram (PCG) at the apex (nominal
frequency of 100 Hz; 24 dbloctave slope). There is a close similarity
between the third derivative of pressure (rate of acceleration) and the
external PCG. Both tracings show 3 components within the first sound
and 2 components within the second. Bottom, tracings recorded in a
normal 24-year-old man. The external PCG is recorded at the apex
(nominal frequency of 100 Hz; 24 dbloctave slope); the apex cardiogram (ACG) is recorded together with the first, second and third derivatives (ID, IID, IIID). Note the identical appearance of the first and second
sounds in the PCG and the third derivative (rate of acceleration) of the
ACG.

November 1, 1983

THE AMERICAN JOURNAL OF CARDIOLOGY Volume 52

1135

FIGURE 2. Recording from a 91-year-old woman with complete atrioventricular block. The lowest tracing (EMV) is an echocardiogram of the anterior
leaflet of the mitral valve (A mode). The first complex has a PR interval of 0.26 and a large a wave of the echo; despite large valve motion, the first
sound is of minimal amplitude. The second complex has a PR interval of 0.16. A large a wave in the EMV is followed by closure of the valve; amplitude
and rate of closure are similar to those of the previous cycle, but the phonocardiogram shows a cannon sound. The third complex has a PR of only
0.08. Again, a cannon sound is seen but the previously closed valve shows only minimal reopening. Thus, 3 cycles show different dynamic events
with no correlation with valve motion. ECG = electrocardiogram.

(5) Ventricular
hypertrophy
and ventricular
damage (ischemia, infarct, aneurysm)
cause a decreased amplitude of the first heart sound. This has

been demonstrated
in trained
clinical conditions.21-24

athletes

as well as in

The Mechanism of the Heart Sounds

Based on the above evidence, the major component
of the first heart sound is generated by the active force
of LV contraction. Atria1 contraction alone does not
produce a first sound, but atria1 pressure at the beginning of ventricular systole affects the timing and the
quality of the first sound. The existence and the function of the AV floor (including the mitral valve leaflets),
which becomes one of the LV walls when the valve is
closed, modify the acceleration and deceleration of the
whole ventricle and its contents. The higher the pressure of the left atrium, the more resistance will be given
to the rise of LV pressure, and thus the higher will be the
rate of deceleration, revealed by the first heart sound.25
This occurs in certain cycles of AV block (Fig. 2) and in
certain ectopic beats as an occasional phenomenon, as
well as in mitral stenosis as a lasting phenomenon. A
similar importance should also be attributed to the
ventricular septum. This structure is an essential contributor to the LV contraction and to the rise of LV
pressure. However, whenever the modality of its contraction is altered (especially in left bundle branch block
and LV ectopic beats), the septum behaves like a passive
wall absorbing energy instead of contributing energy;
then the LV isovolumic period becomes prolonged and
the first sound becomes smaller.26-2g A similar phenomenon occurs when part of the LV wall is involved in
a scar and behaves like a passive instead of an active
structure.
The closures of the mitral and the aortic valves
coincide with (and often slightly precede) the onset of
the vibrations of the first and second sounds, respectively, but the vibrations occur in the entire cardiohemic
system.c In a most recent study, Kupari31 demon-

strated vibrations of the ventricular septum (and also

the LV wall and the ascending aorta) in coincidence
with the vibrations of the first and second heart sounds.
Accordingly, the alterations of the myocardium that
decrease the intensity of the first heart sound (hypertrophy, ischemia, infarction and ventricular aneurysm)
act by decreasing either the intrinsic LV vibratory
ability, the effective contractile force, or both.21
A final point in establishing a cause-effect relation
between heart dynamics and heart sounds is supplied
by mathematical analysis. Through it, different investigators have proved the existence of a linear relation
between the phonocardiogram
recorded at the chest
surface and the left intraventricular
pressure tracing,
the proportionality
coefficient being a function of
myocardial stiffness. 8,32-34 The phonocardiographic
signal was proved to be proportional to the acceleration
of the outer wall of the heart muscle, and the latter was
proved to be proportional to the changes of intraventricular pressure. As a result, it was possible to convert
the LV pressure into a theoretical thoracic acceleration
tracing (theoretical phonocardiogram) that was almost
identical to the actual phonocardiogram recorded on the
chest surface both in normal and in some clinical conditions.sSJ4
RushmerY5 first proposed the theory that accelerations and decelerations of the cardiohemic system were
the cause of heart sounds. This theory is confirmed by
the fact that the third derivative (rate of acceleration)
of either the LV pressure or of the apex cardiogram is
similar to the tracing of heart sounds25 (Fig. 1).
Conclusions
New studies have demonstrated:
(1) a great complexity in the closure of the valves so that different parts
of each leaflet and different cusps may not close at the
same moment; (2) a good correlation between ventricular wall tension and first heart sound; (3) that the mitral valve plus chordae can only contribute a small
fraction of the energy of the first sound; (4) that the first

1136

EDITORIALS

sound always follows the onset of LV systole and only

occurs after the LV pressure has reached a certain level;
(5) that the AV floor, on the one hand, and the ventricular septum, on the other, contribute to the changes
of the first sound in AV block, left bundle branch block
and mitral stenosis; (6) that both mathematical analysis
and direct recording of acceleration tracings reveal that
the heart sounds are similar to the deflections of the rate
of acceleration of LV pressure.
The above factors are strong evidence that the cardiac
vibrations are the result of the accelerations and decelerations caused in the entire cardiohemic system by
the process of LV contraction and relaxation.
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