Br J: first published as 10.1136/hrt.43.2.138 on 1 February 1980. Downloaded from

Br Heart Y 1980; 43: 138-142

Mechanism of influence of PR interval on loudness of first heart sound

GRAHAM LEECH, NICHOLAS BROOKS, ANNE GREEN-WILKINSON, AUBREY LEATHAM From the Cardiac Department, St. George's Hospital, Hyde Park Corner, London

SUMMARY It is well known that the loudness of the first heart sound is influenced by the duration of the PR interval and the position of the atrioventricular valve cusps at the moment of ventricular contraction, but the exact mechanism of this phenomenon has not been explained satisfactorily. In this study, high speed echophonocardiograms were used to correlate the timing of mitral valve closure with the electrocardiogram and in 67 normal subjects. Measurements were made of the PR interval and of the delay between the onset of ventricular depolarisation and mitral valve closure (Q-MC). To permit comparison of sound intensity between individuals, the amplitude of the mitral component ofthe first sound (MI) was compared with that of the aortic component ofthe second sound (A2) in the same subject. When the PR interval was very long, mitral valve closure occurred soon after the onset of the electrocardiogram QRS complex, and there was no accompanying sound. Since the Q-MC interval in these cases was less than the electromechanical interval of 40 ms, the valve was already closed before the onset of ventricular contraction and closure must have been effected by atrial contraction and relaxation. With PR intervals of less than 180 ms mitral closure was audible as a sharp sound coinciding with echocardiographic closure and occurring after the onset of ventricular contraction as judged by a Q-MC of 40 ms or more; the shorter the PR interval the later and louder the mitral closure sound.

Thus a primary determinant of the intensity of Ml is the timing of mitral closure in relation to the http://heart.bmj.com/ left ventricular pressure . A full length PR interval gives time for coaptation of the mitral leaflets and closure occurs early as soon as left ventricular pressure starts to rise and the resulting sound is soft. A shorter PR interval, however, results in a wide open valve at the moment of ventricular contraction and hence delay in reaching its final closing halt which, therefore, occurs on a later and steeper part of the left ventricular pressure pulse and the sound is loud. on October 1, 2021 by guest. Protected copyright. The effect of PR interval on the loudness, of the should cause such great variations in loudness. It first heart sound was first described in atrio- has been suggested that the critical factor is the ventricular blockl 2; its importance as a major timing of valve closure in relation to the ventricular influence on the character of the sound in patients pressure pulse,7 8 but correlation between this with conducted was appreciated some timing and the loudness of the first sound has not time later.3 4 It is widely acknowledged that the previously been demonstrated in man. There are a effect is mediated through the partial atrio- number of possible explanations for the difficulty ventricular valve closure induced by atrial contrac- in establishing such a relation. Because of the tion and relaxation, so that with a short PR interval differing sound transmission properties of the lungs the valve leaflets are widely separated, and with a and chest wall, direct comparison of phonocardio- long PR interval they are nearly apposed, when grams between one person and another is not ventricular contraction begins.5 6 When one con- meaningful. In addition, alterations in the time siders the small mass of the valve leaflets, however, between the onset of ventricular contraction (or it is difficult to understand why distance of travel electrical depolarisation) and valve closure are likely alone, with implied variation in closing velocity, to be small and detectable only by sensitive Received for publication 9 March 1979 techniques. Finally, it is frequently difficult to 138 Br Heart J: first published as 10.1136/hrt.43.2.138 on 1 February 1980. Downloaded from

PR interval and the first sound 139 identify separately the mitral and tricuspid con- Five cardiac cycles were measured and the average tributions to the first sound on conventional value expressed to the nearest millisecond. The phonocardiograms.9 mitral component of the first sound (Ml) was The present study has used high-speed identified on the phonocardiogram from the exact simultaneous recordings of the echo and phono- coincidence of its onset with the earliest point of co- cardiogram to study the effect of atrioventricular aptation of the anterior and posterior cusps of the conduction time on the timing of mitral valve mitral valve on the echogram (Fig. 4). The peak-to- closure and its corresponding component of the first peak amplitude of the maximum trace deflection heart sound (Ml) in normal subjects. An attempt to was measured and from this the width of the base- overcome the problem of calibrating the sound line (2-5 mm) was subtracted. The maximum recording has been made by comparing the amplitude of the aortic component of the second amplitude of Ml with that of the aortic component sound (A2) was determined in the same manner. of the second sound, A2. From these measurements the Ml/A2 amplitude ratio was determined from the mean of five Methods consecutive cycles. Sixty-seven normal subjects were studied. Their Results ages ranged from 19 to 56 (mean 32) years and there were 27 men and 40 women. The mitral valve echogram was suitable for analysis The three standard bipolar limb leads of the in every case. Satisfactory phonocardiograms were electrocardiogram were recorded at 100 mm/s recorded in 58 subjects. paper speed and at four times normal calibration In six subjects, all with PR intervals equal to or (1 mV =40 mm). The lead showing the earliest exceeding 180 ms, no sound occurred at the time QRS deflection was selected for recording with the of mitral valve closure. In all the others valve echocardiogram and phonocardiogram. closure was synchronous with the onset of the Echocardiograms were recorded with a Smith- sound. Kline Ekoline 20 ultrasonoscope (2-25 MHz focused transducer, pulse repetition frequency 1850 s-1) 80 interfaced with a Cambridge six-channel photo- 0 graphic recorder which had been modified to double echo depth magnification and with the 70 maximum recording speed increased to 200 mm/s. *. http://heart.bmj.com/ The mitral valve was identified by the standard 0 . technique, and transducer angulation and position 60 were adjusted to demonstrate the moment of valve closure, defined as the point of complete apposition 50 of its anterior and posterior leaflets. r=-072 A high frequency phonocardiogram was recorded E * 0 simultaneously with the echocardiogram using a -) 40Q 0

Cambridge crystal microphone attached to the on October 1, 2021 by guest. Protected copyright. skin by suction. The microphone was placed 0 accurately over the apex beat and the sensitivity of 30- 0 the amplifier was adjusted so that whenever possible both the first and second heart sounds could be recorded. The recordings were made in 20 shallow held expiration, with maximal magnification of the echo display and at a film speed of 200 mm/s. The PR interval was measured on the simul- 10- taneous standard lead electrocardiogram recording from the earliest P wave onset to the earliest deflection of the QRS complex. The mean value 0 measured was determined from five cardiac cycles 100 120 140 160 180 200 220 to the nearest 0-5mm (5 ms). The time from the PR electrocardiogram Q wave to mitral valve closure interval (ims) (Q-MC) was measured on the echocardiogram to Fig. 1 The influence of PR interval on the timing of the nearest 0 5 mm (2 5 ms) using a hair-line cursor. mitral valve closure. Br Heart J: first published as 10.1136/hrt.43.2.138 on 1 February 1980. Downloaded from

140 Leech, Brooks, Green-Wilkinson, Leatham

a regression analysis. The correlation was highly significant (r-=065; p <0 001), and is shown in 3. Fig. 4. In Fig. 3, the closing velocity of the anterior a mitral valve leaflet is obviously faster in the subject with a short PR interval and a loud first sound than 2 * * in the individual with a long PR interval and a soft first sound, but there was no overall correlation " " between closing velocity and M1/A2 ratio. This is ,. * slightly surprising because such a relation has been observed in individual patients with complete 1- *0 *0 0 ~ @e* *.12 However, since the closing mitral *0 * * valve inscribes a curved line it is quite difficult to * *o determine its velocity immediately before the point

0 * gO 1 * of complete closure, and we suspect that closing 0' 0 @00 -1 , , , , velocity is related to first sound amplitude, even 0 20 40 60 80 though we have not been able to show it. Q-MC ( ms) Fig. 2 The relation between the amplitude ratio Ml/A2 Discussion and the timing of mitral valve closure (Q-MC). By using a high recording speed we have been able to detect small differences in the timing of mitral The influence of PR interval on the timing of mitral valve closure and Ml is described in detail elsewhere.9 When the PR interval was long the valve leaflets were almost apposed at the time of ventricular depolarisation and Q-MC was short. With short PR intervals the valve was still widely open at the onset of the QRS complex and Q-MC was long. This relation between PR interval and Q-MC is shown in Fig. 1, from which it can be seen that for a PR interval of 180 to 190 ms Q-MC is about 40 ms, which is approximately the time http://heart.bmj.com/ between the initiation of depolarisation and the onset of left ventricular contraction."' 11 Thus, with PR intervals of 180 ms or greater, mitral valve closure occurs before the onset of ventricular contraction and is brought about entirely by atrial contraction and relaxation, while with shorter conduction times closure is completed after the

beginning of ventricular contraction. on October 1, 2021 by guest. Protected copyright. The relation between Q-MC and the ratiQ M1/A2 is shown in Fig. 2. Early mitral closure resulting from a long PR interval was associated with a small ratio and late valve closure in the presence of a short PR interval with a large ratio. When Q-MC fell to less than about 35 ms no Ml was recorded (that is mitral closure was silent) and the ratio was Fig. 3 Echophonocardiograms from two subjects aligned zero. Fig. 3 shows the recordings from two subjects on the Q waves of the electrocardiogram (ECG) to aligned on the Q wave of the electrocardiogram to illustrate the influence of PR interval on the timing of illustrate these findings. In the first trace the PR mitral valve closure and the amplitude of Ml relative to A2 (see text). The onset of the P wave is not clearly interval is 110 ims, Q-MC is 77 ms, and a large defined on these recordings; PR interval was measured on amplitude Ml is recorded. In the second recording the separate simultaneous recording of the three standard from a subject with a PR interval of 170 ms, Q-MC leads. is 48 ms and Ml has a very small amplitude. With a, anterior cusp of mitral valve; p, posterior cusp of Ml /A2 expressed as a logarithm the relation of mitral valve. The maximum sound deflections are marked log M1/A2 with Q-MC was examined by linear by short horizontal bars. Br Heart J: first published as 10.1136/hrt.43.2.138 on 1 February 1980. Downloaded from

PR interval and the first sound 141

a apex beat. An immediate criticism is that variations a in the loudness of Ml may be associated with 0 4- d * @ changes in its frequency, an alteration which would, % itself affect transmission through the body tissues.1' Furthermore, the different frequency spectra of Ml and A2 result in different degrees of attenuation r=065 * a b,* during their transmission to the body surface. However, these criticisms do not invalidate our /* * results, since variations in the amplitudes of A2 0 / 9* and Ml unrelated to PR interval would tend to 0 *@/ * scatter the results, rather than improve the correla- 0 * tion we have shown. Clearly, the method cannot be / S * applied if the aortic valve is diseased or if left * ventricular ejection dynamics are altered by -08 * * peripheral, myocardial, or conduction abnormalities. The effect of PR interval on the timing of mitral valve closure has been discussed elsewhere9; our . observations support the conclusions of others, -1-2 namely that when the PR interval is longer than 0 20 40 60 80 180 to 200 ms, valve closure is brought about G-MC (mis) entirely by atrial activity and before the left starts to contract.5 6 12 In the present Fig. 4 The relation between loqg MJ/A2 and the timing investigation with a PR interval of 180 to 190 ms, the mitral valve closure VIC). of (Q-A when presystolic valve closure was complete, the Ml /A2 ratio fell to zero because of the total valve closure and its corres,ponding component of disappearance of Ml. With shorter PR intervals the first heart sound (Ml) as,sociated with variations valve closure occurred later in relation to the onset in the PR interval on the electrocardiogram. Use of of QRS (and, therefore, later in relation to the the echo to identify Ml is eessential because under onset of left ventricular contraction), and was certain circumstances the first sound may be associated with the production of a sound: the produced solely by tricuspiid valve closure, mitral shorter the PR interval, the later valve closure, and closure being silent.6 9 Furthermore, the method the louder the sound. This concept of loudness http://heart.bmj.com/ allows differentiation of Ml ifrom the low-frequency being associated with lateness, widely accepted for vibrations which commonly precede it. mitral stenosis,14 has now been shown to be true The major difficulty in s;tudying any particular also in normal subjects. We have confirmed the influence on the amplitude of heart sounds is the fact that closure of the mitral valve from the wide wide variation in anatomico al factors which affect open position produces a loud sound and from a sound transmission from the site of production to semiclosed position a soft sound.5 6 These differ- the surface of the chest. iWe have attempted to ences are not directly the result of distance of travel overcome the problem by cc mparing the amplitude of the cusps (always difficult to understand), but of on October 1, 2021 by guest. Protected copyright. of M1 with that of the ao:rtic component of the varying delay related to distance of travel. This is second sound (A2) at a fix:ed point on the prae- in agreement with the concept put forward by cordium, since both are affected by the same McKusick15 and supported by Stept et al.8 that influences during their transsmission to the surface. the critical factor determining the loudness of the The validity of the study clearly rests on the sound is the change in momentum as blood being assumption that the sound e.nergy of A2 is constant accelerated towards the left is suddenly in a group of resting normal subjects. The loudness checked by the valve closure. The momentum of of A2 is known to be influencced by arterial pressure, the blood is determined by the force acting on it the rate of pressure fall inl late , and the (ventricular pressure) and the time over which the physical properties of the aortic valve and root13; force acts. Thus the wider the separation of cusps it was thought to be a fair assumption that these the greater the delay in coming to a final halt and factors were 'normal' in ouIr subjects though there the louder the sound. We believe that it is the delay must be some degree of biological variation. On consequent upon the distance of travel which causes this premise the energy of M1 was estimated by the final halt of the valve to be later, at a point measuring the ratio of its an:iplitude compared with where the rate of rise of the ventricular pressure that of A2, with the microphone placed over the pulse is steeper, and it is therefore the delay which is Br Heart J: first published as 10.1136/hrt.43.2.138 on 1 February 1980. Downloaded from

142 Leech, Brooks, Green-Wilkinson, Leatham responsible for the increase in intensity of the first Mechanism of closure of the A-V valves. Circ Res sound associated with a short PR interval. 1954; 2: 48-52. 8Stept ME, Heid CE, Shaver JA, Leon DF, Leonard JJ. GL and NB were supported by British Heart Effect of altering P-R interval on the amplitude of the first sound in the anesthetized dog. Cir Res 1969; 25: Foundation Research Fellowships. 255-63. 9Brooks N, Leech G, Leatham A. Factors responsible The work described is part of a study submitted by for normal splitting of first heart sound. High-speed NB to the University of London for the degree of echophonocardiographic study of valve movement. Doctor of Medicine. Br Heart J 1979; 42: 695-702. "Braunwald E, Fishman AP, Cournand A. Time relationship of dynamic events in the cardiac chambers, and aorta in man. Circ Res 1956; 4: 100-7. References "Luisada AA, Cortis B. The dynamic events of the normal heart in man. Acta Cardiol (Brux) 1970; 25: 'Griffith TW. Remarks on two cases of heart block. 203-12. Heart 1912; 3: 143-60. "Shah PM, Kramer DH, Gramiak R. Influence of the 2Lewis T. Lectures on the heart. New York: PB Hoeber, timing of atrial systole on mitral valve closure and on 1915. the first heart sound in man. Am J Cardiol 1970; 26: 3Wolferth CC, Margolies A. The influence of auricular 231-7. contraction on the first heart sound and the radial "Ravin A. Auscultation of the heart. Chicago: Yearbook pulse. Arch Intern Med 1930; 46: 1048-71. Medical Publishers, 1967. 4Levine SA, Harvey WP. Clinical auscultation of the 4Weiss 0, Joachim G. Registrierung von Herztonen heart. Philadelphia: W B Saunders, 1949. und Herzgerauschen mittels des Phonoskops und ihre 5Zaky A, Steinmetz E, Feigenbaum H. Role of atrium Beziehungen zum Elektrokardiogramm. Z. klin Med in closure of the mitral valve in man. Am J Physiol 1911; 73: 240-56. 1969; 217: 1652-9. "McKusick VA. Cardiovascular sound in health and 6Burggraf GW, Craige E. The first heart sound in disease. Baltimore: Williams & Wilkins, 1958. complete heart block. Phono-echocardiographic cor- relations. Circulation 1974; 50: 17-24. Requests for reprints to Dr Nicholas Brooks, 7Little RC, Hilton JG, Schaefer RD. The first heart Cardiac Department, The London Chest Hospital, sound in normal and ventricular ectopic contractions. Bonner Road, London E2 9JX. http://heart.bmj.com/ on October 1, 2021 by guest. Protected copyright.