Van Bogaert 1966

Review
New Concept
on the Mechanism
First Heart
.\DALBERT
U.D.
Belgiunl
rise of left ventricular
pressure, is essential for
an understanding
of the nlechanisni of the first
The study of Laurens” again confirnled
sound.
this concept.
However, the rapidity of rise of
left \.entricular pressure is not the only- factor
because, as we have denlonstrated,
the po\vel
of nlyocardial
contraction
and the diastolic
tonus of the left ventriclilar
\vall arc’ also of
importance.
The following discussion will briefI>. present
the main points demonstrated in our studies.
lncchanisnl of the first sound has been
repeatedly
investigated
in the author’s
This study will discuss the experi1aboratory.t
uiental and clinical data obtained, which conclusively show that older theories are no longer
tenable.
,4nlong previoils \corkcrs, Hess as well as
Frey and also Schiitz’
should be nlentioned
because their theories are different
and less
anatomic than that of Kouanet, which was srtbA concept sinlilar
sequently re\,ived by Dock.”
to ours published
in 19623 had been independently developed in Luisada’s laboratory,4
even though that stud)- was unknown to us at
the tirne.
It seenled obvious that, since the first sorind
occurred sonle time afl.er the closure of the A-\*
valves, this sound was due to tension of the
valves, the blood and the niuscle during rapid
0~11
isometric contraction of the left ventricle.
first study already showed that the left ventricle
was of parall!olult importance in the production
of the first solu~l, a fact also denlonstrated
b>
Lriisada and his group.
Our first study also
revealed a strict connection between anlplitude
of the first solnid and rapidity of rise of presstIre
within the left ventricle.
This fact \vas confirrued by Shah et al.,” who proved the existence
of a lnathelnatical
relation between alllplittide
of the first sound and atnplitudc of the systolic
rise of the first derivative
of left ventricular
pressure.
This paraunetrr, i.e., the rapidity of
T
Sound*
VAS BOGAERT,
Bercheln-Anvers,
HE
THE
FIRST
SOLTND ORIGINATES
AL-GUST
1966
C:LOSC-RE
Experinients
nlade in open-chest
dogs \vith
siruultaneous
intracardiac
phonocardiograins
and left ventricular
and left atria1 pressure
tracings have denlonstrated the fo11oGng:
1. One or two low frequency \vaves, larger
than those due to the previous phase of diastolic
filling, are observed after the P wave of the
clectrocardiogranl.
These
\vavcs start from
10.04 to 0.06 second after the beginning of P
and coincide with the ascending lintb of the
atria1 wave recorded in the left atriunl.
2. Larger waves occur a few hundredths of a
second later.
These precede ventricular
contraction and end suddenly, 0.02 to 0.04 second
later, slightly before or at the peak of the \vavc of
atria1 contraction
(Fig. 1).
These waves disappear bvith atria1 fibrillation and occur earlier
if there is a long P-R interval;
therefore? th?y
are caused by atria1 contraction.
At this tilile,
no secondary rise of ventricular pressure occlirs,
indicating that the niitral valve is already closed.
We have reached the conclusion that the niitral
* From the Cardiological Laboratory of the Institute Bung-e (Berchrm-Anvers,
Belgium).
by grants of the Fund Group Comte de Launoit and the National Fund for Medical Research.
18,
AFTER
OF THE 24-L: VALVES
i’ Thew studies were made between 1960 and 1965
in collaboration
with Dr?. van Genabeek,
.Imoldy,
\Vauters, and van dcr 17[enst, and with the trchnical aid
of I2 \vouters.
\‘o1 IJME
of the
253
This study was aidrd
254
van
closes earl\-, at the time of the llrasilrial rise 01
left atria1 prcss~~rc, and this closlue is anticipated
if there is a high pressure ill the left atri(llrl
[compare Fig. l(2) and 1 I,.?)1. This valvl&u.
C~OSIW callses s011le low frccl~~c~~c~M-a\-cs (50~~90
c.p.s.) of low amplitnde
and brief duration
(0.01 0.02. sec.) ; both factors arc not favorable
Thcsc \caves are poorl!,
to altdibilit!. of solund.
recorded!
or not at all: in the cuternal
or
These facts conepicardial phollocarcliogl.all?.
fir111 the concllGons
of Henderson
and Johnson7 and Yoshida et al.? It-e have 11ever accepted that the first sound \vas cartsed by actual
closure and tension of the A-\. valve alone, as
nlentioned
by Dock.Y
THE FIRST SOUND COMPLEX Is WE
EXEJRESSIOK(11:PROGRESSOK 012 Isovo~.u~~c~
CONTRACTION0F THE \‘ENTRICLES
(3~ concept is that the first sound results
from the sudden vibration of the complex mass
which includes the blood, the ventricular
walls
Bogaert
and the val\~ due to the fact that ejection of
blood nrass is blocked on all sides. Should there
be any- colllprcssibility
of this IIIXS (as in the
sltbseqlLel]t phase of qjcction), there would be
no so~md bccallsc the mass \vorlld then bc
rmablc to \ril)rate.
The elasticit), of the Inass
increases fro111 the beginning
of colitraction
to
the molllcllt
iI1 \vhich the total ventricular
ninscle is contracting.
The corllpressive cooltraction of the left \-erltricle dcvclops front the
inflow to the olltflow chalnber”
alid involves a
litnited displacement
of thr contaillcd
blood,
due to l)ulging of the \.alves towards the atria
and the \-esscls and to bulging of the septutn
towards the right ventricle,
as well as to a
limited distention
of those vcntricrllar
sections
This graduwhich arc not as yet contracting.
ally de\,rlopillg
contraction
catlscs, on the one
hand, a rise of pressure and on the other, a
series of arldible vibrations.
This development
of energy occtlrs in two phases.
The first takes
place \vhen the outflow chamber
is still de‘rtfl’ AMERICAN
JO”RNA1
OF
CARDIOI.OCY
LfIechallisrn
of’ Fir.st Hca1.t
and
is sublnitted
to a slohz- risr of
pressure (the vibrations are of low frequent)
and small
aulplitude).
The
second
phase
occurs when the total ventricular
mass is contracting and is accompanied
by a rapid rise of
pressure and a high frequency
of the sound
vibrations.
LVe have called the first phase the
“initial
phase,”
and the second the “preejectional phase” because both of the111 can be
well recognized in pressrrre tracings and phonocardiograms recorded at a rapid speed of film.
The opening of the semilunar valves ends the
stage of incompressibility
of the blood mass.
Since the peripheral resistance still opposes the
blood flow, the vibrations may continue for a
short time.
This will be particularl)
observed
in systemic hypertension
or valvular or supravalvular aortic stenosis.
forinable
Tile sequences of sound vibrations is as follows:
The series of initzal waves starts from 0.04
to 0.07 second after the Q wave, and is made of
low frequency waves bet\veen 40 and 150 c.p.s.
1.
SOUI~C~
1 .i 5
These coincide with the desccndillg li~nb of K
and nlay extend to the end of S. They start
slightly before the initial rise of left \.cntriculat
pressure and continlle as lony as the pressIll-c
rises slowl>- in its initial period.
This phase
corresponds
to the distention
of the olltflow
chan:ber, the bulging of the \.entricular septlllll,
and the bulging of the h-1. \-al\.es. It ma) be
preceded b>- a few oscillations of extremelv low
freqllency
caused b>- residual activity of the
atria,
initial
contraction
of the
papillar!,
muscles, or initial chaiigc
in shape of the
ventricular mass.
2. =1 second serifs of waves of hi’hcr ,frtyuenr~
(150.-250
c.p.s.) starts front 0.06 to 0.10 second
after the peak of the Q wave.
It corresponds
to the rapid rise of left ventricular
pressllre,
precedes
ejection
and represents
the nlain
section of the first sound; it corresponds to the
contraction
of the outflow chamber and of the
total left ventricular
mass as revealed b>r cinrmatography ; it starts with the masinlal
ac-
FIG.
3.
Exj~~~tmn/al
lpff hmdlc~ l/~an~li.
celer-ation of the ciirve of pressrm
and ends mith
It cormponds
to
the beginning
of ejection.
the actrml “tonsegment”
of Holldack et al.”
3. A third suies oj. lore! frequency
oscillations
OCCIII~S after
the second
(“llachsegnient”
of
These oscillations
are of
Holldack
et al.“).
louver frequency, rtiay continlie slightly after the
begiilning of ejection and arc probably due to
either turbulence of blood or vibrations arising
iit the left ventricle and the roots of the aorta and
pttlntonary
artery, caused by. 1)raking of the
blood flo\v.
THE
%X-ND AND MODIFI(:A.TIONS OF
\7~~~~~~~~~~ CONTRACTIONS
FIRST
If there is a close relation between frcqttency
of vibrations of the first sound and rapidity of
rise of left ventricular
pressrue,
in itself a
function of the contraction of the inuscle oz’er its
incompressible
content,
the first sorrnd will vary
when this mechanism of contraction is modified.
The various components
of the sound will be
independently
modified when we change the
rapidity of either the first or the second part of
this rise of pressiire.
The part played by the
A-V vale-es is otll>- onr of the elements forrning
the vibratory left \eiitr.iciilar IIMSS diiring the
isovoluinic phase.
INCREASE 01
~:O\ll’RESSIBII.IT~’
01.
TIIE
\‘ENTRI(:IJ-
A left \cntricular sy-stolic leak or an alteration
of intravcntricular
condriction should decrease
the coinpressibilit);
of the intraventriciilar
content or iilodify the chronology
of contraction
and result in a inodification of the first sound.
A lrft rrrrtricular leak
was experimentally
obtained by- our group
throitgh a special device
which respected
the integrity of the va1xTe.i”
Applicatioli of this caused a slower rise of left
ventricular
pressure and was followed by a
smaller amplitude of the first sortnd; the high
frequency waves were especially affected.
LYe
found a sitiiilar modification
in 44 per cent of
our clinical
cases of mitral
irisrtfticiency.‘z
This phenomenon does not occur in all clinical
cases becalise of the increase of left atria1 and
THI,.
AMERICAN
7OURNAI.
OF
CARDIOI.OC:,
7.57
hlec~hanism of First Heart Sound
left \.entrlcular
initial presslnxz that cause a
secondary- increase of the power of contraction
of the left vc.ntricle.
‘-1 distztrhmce of I!eJt intrauentrzcular conduction
(left hundlr branch block) causes almost a disappearance
of the sc,cond group of high frequency vibrations (colnpare Fig. 2a and 2b) of
the first solmd while an increase in the initial
low frequency vibrations takes place13 (Fig. 3b).
In brmclle branch
block, a decrease in the
rapidity of rise of left ventricular
pressure is
constantly
observed. * Epinephrine
reinforces
the sound by increasing
the rapidity of contraction
(Fig.
2~).
These
facts are chiefly
observed iI1 left bundle branch block but less
frequelltly
in right bundle branch block.
In
transient
b[mdle branch
block,
the modifications of the first sound occur only in correspondence
with the abnormal
electrocardiographic
conlplexes
(Fig.
3).
However,
in
* Both the initial group and the second group of vibrations am drlayrd,
excluding
the possibility
that
either
of them lniKht he rrlatrd
to the contraction
of the right
ventrick.
VOLUME
18. AUGUST
1966
neithc,r left nor right bnndle branch block can
one observe a splitting of the first sound, as one
would expect if the first sound were caused b>valvular vibrations dissociated by the ventricular as)nchronism.
INCREASE
IN
THE
ELASTICITY
OF
THE
CONT.I\IXER
If the rapid vibrations of the first sound are
caused by the conditions of the structures surrounding the blood, an increase of the elastic
rigidity of these structures should bring about
an increase in the amplitude of the first sound.
Sl~ch an increase in rigidity can be obtained by
either increasing the z’entricular tonus during diastole
(with increase of power and rapidity of contraction
during the isovolumic
phase) or if
there is a greater rigidity (anatomical or functionul)
of the aalrwlar areas.
Role of the End-Diastolic Left Ventricular Ihlume:
Heart-lung
preparations
allow us to study the
effect of changes in left ventricular volume on
the first sound.
An empty left ventricle does
not cause an\’ first sound a fact which excludes
258
12iri
Bogaert
lrltcred at 150 c.p.s.; phonocardiogram
at 70
FIG. 4. Thr hem/ 1.1
fmrd ml X0/m/n. F~orrcabow: Phollocardiogram
c.p.s,;
tracing of aortic pressure (.\o) just above the valve;
tracing of left intrawntricular
pressure (V.G.);
electric
II. corziroi: C:ardiac output 900 cc./min.
h, L~LldlU~out,tuf r&cd
lo 600
impulse.
Tracings
recorded
at 200 m~n./srr.
cc./min. Remarkable
decrease has occurred
in amplitude
and frequency
of the prr-ejectional
components;
the aortir
Both
C, snrn~ cnrdm out,but
as ~7,(h) ufl/~m@tmn
oj mprotmnol.
pulse delay is greater than the left ventricular
delay.
‘The delay of the left ventricular
and aortic pulses is decreased.
components
of the first heart sound become larger.
There is a greater rapidity of rise of the left ventricular
pulw which, however, is not qreatrr than in the control.
(Keprinted through courtesy of Arch. mal. coew. I')
the possibility of muscular vibrations as such in
the mechanism of this sound.3
An increase in the end-diastolic
volume (obtained by injecting a known amount of fluid
in diastole into the left ventricle while the heart
is artificially
paced14) increases the amplitude
of the first solund because such change of volume
is followed by an increase in the power and
rapidity
of contraction
of the left ventricle
according
to Starling’s
law (Fig.
4a).
A
moderate decrease of the end-diastolic
volume
(not more than a fourth of normal) causes a
delay in the high frequency
vibrations of 0.01
In some cases, there
to 0.02 second (Fig. 4b).
was an increase of the sound amplitude without
increased rapidity of rise of the left ventricular
presslu-e, a result which might be explained by
an increased
tonus of the wall adapting the
volume of the container to that of the content
because we can also observe an increased frequency of the initial conlponent of the sound,
that preceding the rise of left ventricular prcssure.
Rapidity
qf lentricular
Contraction:
Experiments in dogs during hypothermia3 showed that
the cold temperature,
even though it is still accompanied
by powerful left ventricular
contractions, abolishes the rapid oscillations of the
first sound and causes a marked decrease in the
rapidity of the contraction (Fig. 5).
Subsequent
heating
and application
of epinephrine
(Fig. 6)
increase the rapidity of contraction
and are
followed by a marked increase in the amplitude
of the first heart sound.
Epinephrine
increases
THE
AMERICAN
JOURNAL
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C.ARD101.Of:\r
h4echanisrn
of First
Heart
-0
-3 I)
Souncl
FIG. 5. Hypottirrmic heart with n rate
o/ 2.3/n%
The first sound has
nearly disappeared.
There is a
slower rise of pressure with a greater
delay over the electric
impulse.
However, the power of contraction
is preserved.
(Reprinted
through
courtesy of Arch. mal. coeur.3)
the freqllency of the \ibratiom to sr~h an extent that it may even simulate the occurrence
Isopoterenoi
[a stilnuof a presystolic murmur.
lant of the beta-adrcnergic
endings)
has a
silnilar effect without an increase in peripheral
resistance b>pincreasing the rapidity of vcntricular contractions
(Fig. 4~).
On the contrary,
Znderal” (an inhibitor of the beta adrcnergic cndings), which in moderate dosr does not increase
s\-stenlic pressure, causes a marked decrease in
It is interesting to note
atnplitude of the first sound.
that, while the rapidit
of rontraction
is decreased
(colxl-
pare Fig. 721, 7b, and 7c), this is notfxobortionol
to
the decrease of thefirst sound, a fact \vhich will ha\,e
to be discussed.
Power
q/
Isometric
Contraction:
It is cas)experinlentally
to increase the power of isolnetric contraction
by causing a sul,ravalvular
The latter is followed by an immediate
stenosrs.
increase in the amplitude and frequency of both
components of the first sound.15 The rapidity
of rise of the left ventricular pressure changes in
proportion
to the nlodifications
of the first
Occasional
decrease
in amplitude
is
sound.
observed but only if there is a secondary weakening of contraction,
a fact which can explain
VOLUME18.
AUGUST
1966
clinical
solmd.
cases
xvith
Trme-Concordancr,
a
decrease
of Rapid+
of
and Power
the
tirst
41 Con-
These
t\yo factors can be dissociated
onl!- through
apphcatlon
of cold temperature
or inhibitors
\Ve have the
of the beta adrcnergic endings.
impression that the interesting clccrcxasc in the
first sound obtained through depression of the
beta-adrenergic
cmdings \\-a~ drle to the fact
that svlnpathol).tic
agents, I\-hilt acting both
on ra&iit).
alld po\ver of colltractioll,
causctl a
dissociation
in tinlc of these t\vo elements.
The effect of cold first modifies the rapidity:
the inhibition of the beta adreneryic receptors
depresses the power of contraction
earlier thau
the rapidit)-: the discordance
in the tinriug of
both effects lnodifics remarkably
the intensit!.
of the first sor11~1.
tractlon
in the Production
Anatomic
Rigidity
of the First
Sound:
qf the 17alvular
Floor:
12’hcn
the valvular apparatus is more rigid, its disThis
placement toward the atrium is reduced.
increases
the incompressibility
of the blood
mass and contributes
to an increase in freof the
first sound.16 A functional
quenc)
rigid/(,
tna!. occur in complete A-\. block due to
result of \,ibrations lilnitcd to the l11voc;rrtliutlI.
Even tension of the valvt~lar
lcxaflck
clock riot
seen1 sufficient
I.
for causing
The fuct
that thefirst
the
,outid
first
s0~11Itl.
is formrd
by two or
can olil~ bc ?xplaincd
by the
intervention
of complex
forces occurring
at
different times.
Even if the A-V valves bulge
into the atria1 cavities (a fact denied h\, SOII~C
researchersj,
this does not occur iI1 c&es of
mitral stenosis with calcification
of the leaflets
and certainly occurs only in a very early stage of
the isovolumic contraction.
2. The two components oj- the jrst sound can bu
independently
mod$ed.
\Ve have demonstrated
that in bundle branch block the high frequency
components
occurring
prior to the ejection
decrease in frequency and amplitude while the
initial components
become larger.
Conditions
decreasing
the volume of blood in the ellddiastolic phase tend to increase the initial component ; the high frequency component occurring later may be unchanged unless there is a
simultaneous stimulation of the beta adrenerqic
endings.
3. Splitting
of the jirst
sound in bundle
branch
FIG.
6. Combined uctm~ of heat and epinephrme on the first
sound and cm the rapidity of rise of left ventricular pressure. Same heart as in Figure 5. (Reprinted
through
courtesy of Arch. mal. coe~r.~)
simultaneous
atria1 and ventricular
contractions, and these lead to the occurrence
of the
“cannon
sound.”
In mitral stenosis, the elevated left atria1 pressure has the same effect
and plays a role in the intensity of the first
sound.
DISCUSSION
These experimental
data warrant taking a
“nonconformist”
position regarding the mechanism of production
of the first sound.
We
have never attributed the first sound to valvular
closure, and we never tried to explain it as the
three
component5
block
is not an exi(,ression
of c’entricular
asynchronism.
This “splitting”
has always been one of the
strong points of authors advocating the “valvular mechanism”
of the first sound.
We have
demonstrated
that in left bundle branch block
this splitting, when existent, was due to either
a presystolic atria1 sound (fourth sound) or to a
loud ejection sound.
In right bundle branch
block, if there is splitting of the first sound, it is
always due to an ejection sound.
4. Measurements
based on the relation between the
first sound
and the carotid
tracin,g
or the rlectrocardio-
If one considers the
variability
in the frequency and alnplitude of
the basic components
of the first sound under
the influence of various functional and structural
it becomes apparent
that it is not
changes,
possible to base our measurements
on the dis-
gram
are
open
to question.
tance
of a certain
group
of vibrations
froIn
the Q
from the
This is particuearly rise of the carotid pulse.
larly important in cases of mitral stenosis.
The
experiments
on the role of the end-diastolic
volume and of drugs stimulating the adrenergic
endings have revealed how often the initial
vibrations can increase in frequency and amplitude and can even start earlier in comparison
with those of the normal heart.
The least that
wave
of
the
electrocardiograni
THI<
AMERICAN ,JOURNAL
or
OF
CARDlOLOOY
one could do is to rc\Gse all thcsr chronologic
relations
h!. basing theln on the most contant
colllponcnt.
i.e., the one which barely precedes
ejection.
Even this lvould be subject
to carol
aud would not he reliable.
TUIIIS used in the past, like mitral or trius$d
sound, or mrtral-tricusl,2dsplitting, cannot
be Llsed
an)- more because components
originating
in the
right ventricle
are usually extremeI\,
\veak and of
low frcquc~lc~~~ and no proof was ever gi\:en that
the!. could contribute
significantly
to the vibrations which consistently
appear
in the phonocardiogralll.
The theory
of a valvular
mechanism
of the
first sound is re-examined
on the basis of esperimental studies.
Animal
experiments
demonstrate
that
the
first sound is related
to the power and rapidity
of left ventricular
contraction,
as well as to the
diastolic
tonus
of this chamber,
and that it
arises in the complex
of structures
of the left
ventricle
(including
the blood) during
the isovoirrlnic phase.
VOLUME
18,
AUGUST
1966
(Iinical
CusscY~.
applicatiolis
Clrt‘ dis-
NuAez-DEY.
I).. M~.II:s.~N. G..
M. and LuIs.<D.~. .\. .\.
f lcrnodynamic
corrrlates
of thr lirst heart wuud.
.Irn.
.J. PJzy’s~oZ.,201 : 888, 1961.
5. Srr.m.
P.
M.,
,~‘IoRI,
M., M?(:C:woh.
1). ,\t. and
I,LXAD.A, .I. .\.
Hemodynamir
corrrlatrs
of the
various
components
of the lirst heart
w~wd.
C~rr-u/a/ion Rpr.. 12: 386, 1963.
O. LAUR~NS. P. CIonsidcrations
SUL I‘ori~gitr cles bruit>
du cocur.
Sctii cndiol., 19: 327. 1964.
7, I~FNDEKSON.
E’. and
.IOHNSON.
F. E.
‘l‘wo mocks
ot
Huar/. 4: 09. 1912.
closure
of thr hrart I-alves.
8. YOSHIDA, -II‘. et al.
.\nalysis
of hrart motion with
ultl-asonic Doppler method and its clinical appliration.
.4m. Hrarl J., 61: 61, 1361.
9. I)OCK, I\:.
Hrart sounds from Starr-Edxvnrds
val\rs.
Circulnflon. 31 : 801, 1965.
4. 111 BARTOI a
.hfA&.ANON.
G.,
of thi:: conwpt
I).
262
\-an Bogaert
tionsablauf
in
der
linkrr
I;)P/J/N~%~o~Jc~..
49 : 500,
11.
1Ior.1
DACK,
K..
I Irrzkamnwr.
%/\I-//,
1960.
.\.,
KUHN,
E. and
Die relative
Systolcndauer
in
bei t Icrzfehlern.
%/.X/U.Kr f~.\-
\vVEVG.AND.
I~;HRENPKtls. \I’.
bczug zur QT-Zeit
h[Jor~c/~,
42 : 415, 1953.
12. “AN RDCAERT. .\. et al.
Influence
d’une
fuitr
systolique
wntriculaire
SW I’intensitb
du premiw
bruit
du cocur.
Application
g l’insuffisance
mitralc.
.4rch. mal. COPUI, 55 : 961, 1962.
13. VAN kGAERT.
11. et al.
Modifications
du premier
bruit du coeur dans le bloc de branrhe.
Arch. mrr(.
COP,,,. 56: 1253, 1963.
14. VAN BOG\IXI.,
\.. VAN GI’NAHEEK, I\., .\KNOI I)Y, XI.
and \V.AUTERS. .I.
KBlr de la frequence
ct du
volume de I’onder systoliquc
ventriculairr
Kauchca
SW l‘intensite
et la chronolog-ie
du prcmicr
bruit.
Arc/l. rniil. COPUT,58: 922, 1965.
15. VANBOG\ER
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.4rch.
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16. v.4~ HOGAERT, .I., v:w GENAHW,K,
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.\~zor.o~,
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.I.
La composante
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Arc/l. mni. co~ur. 57: 1062, 1964.
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