New concept on the mechanism of the first heart sound

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

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LfIechallisrn

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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,.

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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

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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

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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. 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 I_..\. rt al. Comportement du premier bruit du coeur dam la stCnose aortique cliniqucet c~xperimentalc. .4rch. ClViU. 56 : 40. mul. 1963. 16. v.4~ HOGAERT, .I., v:w GENAHW,K, A., .\~zor.o~, bl. and \VAI!TERS, .I. La composante prCsystoliqur et systolique du premier bruit dam la st+nosc mitl-ale. Arc/l. mni. co~ur. 57: 1062, 1964.

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