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Electrocardiogram of the Month: The Genesis of the First Heart Sound with Varying P-R Intervals
ELECTROCARDIOGRAM OF THE MONTH
The Genesis of the First Heart Sound with Varying P-R Intervals* LAWRENCE GOULD, M .D.,** DINO BELLETTI, M.D.t AND ALAN
F.
LYON, M.D.:!:
Bronx, New York
I
T HAS BEEN OBSERVED THAT THE INTEN-
sity of the first heart sound varies with the P-R interval when the rate is constant. One explanation offered in the past for this phenomenon was that in cases with a P-R interval of .04 to .12 seconds the A-V valve leaflets are quite low and relaxed and snap back through a wide arc resulting in a loud sound. It was further hypothesized that if the ventricles contract at a time later than normal after the atria (PR=.22 - .34), the leaflets would have already floated up to a higher position, almost closing the orifices, and the sound produced by ventricular systole at that moment would be much fainter.' This theory is no longer plausible since it now seems certain that the valves are closed prior to the production of the first heart sound .' It has further been noted that there is a linear correlation between the first sound and the speed of left ventricular contraction (dpydt );' .s thus relating the intensity of the sound to acceleration of blood rather than to valve position. In the present study, the phenomenon of variation of the first sound with the P-R interval was again evaluated. An alternative explanation is offered to fit the current concept of heart sound production.
insure high fidelity tracings, the needle was directly connected to a pressure transducer. The first derivative of the brachial artery pressure was continuously computed by an R-C differentiating circuit. A phonocardiogram was recorded at the second left intercostal space and left sternal border in the patient with complete heart block. A standard Cambridge microphone was used to record a medium range (40 to 200 cycles per second) phonocardiogram. The microphone was held rigidly to the chest wall by strips of adhesive tape and by a rubber strap, placed around the chest. I
I
I
I
I 1
METHODS
Two patients, one with complete heart block and the other with second degree AV block of the Wenckebach type, were studied in the supine position and at rest. The brachial artery was cannulated with an 18-gauge Cournand needle. In order to
"......... 1 n-
v
*From the Medical Service, Veterans Administration Hospital, Bronx. ** Assistant Chief, Cardiology Section . t Attending Physician, Cardiology Section. tChief, Cardiology Section.
v I
FIGURE I: Brachial artery first derivative falls as the P-R interval lengthens.
817
818
Disea ses of the Chest
GOULD, BELLETTI AND LYON
Simultaneous records of the electrocardiogram, rate of rise of the brachial artery pressure (dpjdt) and a phonocardiogram, were obtained. Two additional normal patients were studied in the supine position. The patients were then told to stand by the side of the table, and the arterial pressure and its first derivative were measured in the erect position using the mid-cardiac level as the zero reference point. A phonocardiogram was simultaneously recorded from the rigidly attached microphone. In order to exclude the possibility that the observed changes in heart sound intensity on standing were not due to postural differences in the relation of the heart to the chest wall, in one additional patient, simultaneous intracardiac sound , left ventricular pressure and left ventricular dpjdt were recorded by means of an AllardLaurens micromanometer mounted at the tip of a No.8 French cardiac catheter. The intracardiac micromanometer, manufactured by Telco of Paris, permits recording of pressure and sound, without catheter delay and yields pressure tracings of uniform high quality so that precise timing of sound and pressure events is possible. The catheter was introduced through a right brachial arteriotomy and advanced to the
t.. !
PR
dp /dl
.42 1
16 67
left ventricle under visualization with an image intensifier. An external electrocardiogram was recorded simultaneously. These various parameters were recorded in the supine, sitting and erect position. RESULTS
The first derivative of the brachial artery pressure fell as the P-R interval lengthened with little change in rate in the patient with the Wen ckebach phenomenon. The maximal rise of the brachial artery pressure was 1433 mm Hgj sec when the P-R interval was .22 seconds, 1367 mm Hg jsec when the P-R interval was .30 seconds and 1300 mm Hgjsec when the P-R interval was .40 seconds (Fig. 1) . In the patient with complete heart block and a constant ventricular rate, the first derivative of the brachial artery pressure showed beat to beat variations. When the P-R interval lengthened, the first derivative fell and the first sound diminished in intensity. The opposite was observed when the P-R interval shortened. However, when the P wave fell just before, in, or after the QRS complex, the first derivative diminished and the first heart sound was of low intensity ( Fig. 2) . '''hen he assumed the erect position, the first normal patient's P-R interval fell from .19 to .18 seconds, and his brachial artery
IH -' .....,.., l
•
~I
•
PR '
.14
I
:
151
101
~
•
J
dp/dl
1733
FIG URE 2 : Brachial artery first derivative (lower) and ph onocardiogram during complete heart block . The arrows point to the P wave in the electrocardiogram. Note t hat the first heart sound and the first derivative decrease when th e P·R interval is .42 seconds and 0 seconds. The opposite occurs when the p. R interval is .14 seconds.
Volume 52, No .6 December, 1967
81 9
GENESIS OF FIRST HEART SOUND
.
- ., .... • r
PR
PR
.19
.1 8 SUP INE
ERECT
3 : Brachial artery first derivative (lower), phonocardiogram and electrocardiogram in the supine and erect position. Note that the first heart sound decreases in intensity when the first derivative falls in spite of a decrease in the P-R interval. FIGURE
pressure derivative changed from 700 to 533 mm Hg /sec. His first heart sound decreased markedly in intensity in the erect position (Fig. 3). The second normal patient showed a similar decrease in the first I
-"'rI,-"",,_..J""-ioJ~
heart sound on standing. In the change from the supine to the erect position, the P-R interval fell from .18 to .15 seconds, and his dpjdt changed from 733 to 500 (Fig. 4).
I
i st
,
~\-PR .15 SUPINE
,
J~
dp/dt 500 ERECT
FIGURE 4 : Brachial artery first derivative (lower), phonocardiogram and electrocardiogram in the supine and erect position . Again note that the first heart sound decreases in intensity when the first derivative falls in spite of a decrease in the P-R interval.
820
Diseases of the Chest
GOULD, BELLETTI AND LYON
Thus, when the first sound varies in conjunction with the P-R interval, there is a change in the brachial artery dpjdt and in the same direction as the sound intensity. When another variable, in this case posture, changes dpjdt in the opposite direction from that expected from the effect of changing P-R intervals, the intensity of the first sound follows the dpjdt rather than the P-R interval. In the patient with the intracardiac phono catheter, the P-R interval remained . 18 seconds and the left ventricular dpjdt increased from 1700 to 2190 mm Hgjsec in the change from the supine to the sitting position. His first heart sound increased markedly in the sitting position. On the assumption of the erect position, the P-R interval decreased to .16 seconds, while the left ventricular dp jdt and first heart sound showed no change from the previous determination in the sitting position (Fig. 5) . These findings confirm the observation made with the microphone on the chest wall, that the intensity of the first heart sound is proportional to the speed of ventricular contraction rather than the P-R interval when these measurements change independently.
COMMENTS
The mechanism of production of the first heart sound has been in dispute . Earlier workers were of the opinion that closure of the atrioventricular valves was the sole or most important factor" However, recent studies have convincingly demonstrated that the heart sounds are produced by the acceleration and deceleration of blood..·• Luisada' concluded that the normal first sound contains three components. The first component results from the rapid rise of pressure in the left ventricle, which causes sudden tension of the ventricular wall, the septum, the chordae and closed mitral valve. A second rapid component (25 to 40 msec. later) coincides with a change in rate of the rise of pressure as revealed by the left ventricular first derivative. A third component occurs 50 to 70 msec. after the first and coincides with the rise of pressure within the ascending aorta. Van Bogaert" has independently developed these same concept s. Luisada and Van Bogaert have also correlated the height of the left ventricular dp jdt with the amplitude of the first sound. Piemme and his co-workers' believe that the normal first sound consists of two com1st
---_I',. ·_. . .
•.•\00\00
f'Yi·~
...._
~~ .t" ./Wi ~~
.....
I , . ,-
'
1
__ .............,'''''1 ,.,.,'):,' '''-;1.~
,
PR
l' F
.18
- - -"..-----dp/dt
10050-
LV.
LV. o- -= : : : :
=- --
-~=
SUPI NE
=
-- - - -- -- ;....--- - - - SITTING
ERECT
F1C l!RF. 5 : Left ventricular pressure (lower) , left ventricular dp/dt, electrocardiogram and phonocardiogram in the supine, sitting and erect position. Note that in the change from the supine to sitting position, the first sound increases in intensity when the first derivative rises in spite of no change in th e P-R interval.
Volume 52. No.6 December. 1967
821
GENESIS OF FIRST HEART SOUND
ponents. The first component occurs during early isometric ventricular contraction. The second component occurs during ventricular ejection, and appears to be a function of acceleration of aortic blood flow. All of these workers stress that left ventricular contractility is the major factor producing the first heart sound. ..Atrial contraction closes the A-V valves before the onset of isometric ventricular contraction.I" Thus, the changing intensity of the first sound with varying P-R intervals cannot be explained by mitral valve position at the time of ventricular contraction since the valve is already closed. The changing intensity of the first sound with changing P-R intervals can be adequately explained by the newer concept that acceleration of blood produces the first sound. We have demonstrated that a properly timed atrial contraction can result in an increase in the speed of the left ventricular contraction, and a resultant increase in the magnitude of the first heart sound. Benchimol" has shown that in patients with complete heart block a P-R interval of 1 to 300 msec. results in a 14 per cent increase in the dpjdt of arterial pressure as compared to the derivative obtained when atrial systole occurred during ventricular systole. He also noted that the contribution of a properly timed atrial contraction appears to be of greater significance in patients with compensated heart disease and heart failure than in normal hearts." Our data further shows that when the dpjdt falls and the P-R interval decreases in subjects in the erect position, the intensity of the first sound varies with dpjdt and not the P-R interval. This finding supports the contention that valve position does not c au se changing intensity of the first sound with varying P-R intervals. On the other hand, it is well established that atrial systole contributes to ventricular filling to a significant degree. Wiggers and Katz" found t hat the ventricular filling effect of atrial systole averaged about 35 per cent. Jochim 12 calculated that the atrial contribution to ventricular filling was 21
per cent when the atrial systolic-ventricular systolic interval was 0.1 second. Recently Snyder" determined that the stroke volume increased 8 per cent when atrial systole occurred 0.1 second prior to closure of the atrioventricular valves, and decreased in a similar magnitude when a trial emptying into the ventricles was prevented by closed A-V valves. These findings enable us to present a unifying concept for the production of the first heart sound with varying P-R intervals, that is, a properly timed atrial contraction can indirectly lead to an enchancement of the first heart sound by increasing ventricular filling and causing an increase in left ventricular dpjdt or left ventricular contractility, while an excessively long or short P-R interval leads to a decrease in the intensity of the first sound by reducing ventricular filling and contractility. An apparent exception to this rule is mitral stenosis in which the first sound is commonly accentuated, since we observed a normal or low brachial artery first derivative in patients with this entity. It must therefore be concluded that the power and rapidity of left ventricular contraction cannot solely explain the increased amplitude of the first sound in mitral stenosis. Van Bogaert" has recently reported that, when the valvular apparatus is more rigid, its displacement toward the atrium is reduced. This increases the incompressibility of the blood mass and contributes to an increase in the frequency of the first component of the first sound, rather than the second component, which is the portion of the first sound affected by changes in contractility, and which is the important determinant of first sound intensity in all other entities. 1
REFERENCES
S. A. AND HARVEY, W. P.: Clinical auscultation of the heart, W. B. Saunders, Philadelphia. 2 LUISADA, A.: From auscultation to phonocardiography, C. V. Mosby, St. Louis, 1965. 3 VAN BOGAERT, A.: "New concept on the mechanism of the first heart sound," Am. ]. Cardiol., 18:253, 1966. 4 DOCK, W.: "Mode of production of the first heart sound," Arch. Internal M ed., 51: 737,. 1933. LEVINE,
822
GOULD, BELLETTI AND LYON
5 PIEMME, T. E., BARRETT, G. O. AND DEXTER, L.: "Relationship of heart sounds to acceleration of blood flow," Circulation Res., 18: 303, 1966. 6 RUSHMER, R. F.: Cardiac diagnosis, W. B. Saunders Comp., Philadelphia, 1955. 7 LITTLE, R. C.: "Effect of atrial systole on ventricular pressure and closure of the A-V valve," Am. /. Physiol., 166: 289, 1951. 8 BROCKMAN, S. K.: "Mechanism of the movements of the atrioventricular valves," Amer. /. Cardiol., 17: 682, 1966. 9 BROCKMAN, A., DUENAS, A., LIGGETT, M. S. AND DIMONEL, E. G.: "Contribution of atrial systole to the cardiac function at a fixed and at a variable ventricular rate," Amer. ]. Cardiol., 16: 11, 1965.
Diseases of the Chest
10 BENCHIMOL, A. AND LIGGETT, M. S.: "Cardiac hemodynamics during stimulation of the right ventricle and left ventricle in normal and abnormal hearts," Circulation, 33: 933, 1966. 11 WIGGERS, C. J. AND KATZ, L. N.: "The contour of the ventricular volume curves under different conditions," m. ]. Physiol., 58: 439, 1922. 12 JOCHIM, K.: "The contribution of the auricles to ventricular filling in complete heart block," Am. I. Physiol., 122: 639, 1938. 13 SNYDER, J. H., BENDER, F., KITCHIN, A. H., ZITNIK, R. S., DONALD, D. E. AND WOOD, E. H.: "Atrial contribution to stroke volume in dogs with chronic heart block," Circulation Res., 19: 33, 1966.
Readers are invited to submit articles for the Electrocardiogram of the Month. Please submit material to Stephen R. Elek, M.D.. 46~ North Roxbury Drive. Beverly Hills. California.
AMERICAN COLLEGE OF CHEST PHYSICIANS' 1968 ESSAY CONTEST Medical students wishing to enter the 1968 Alfred A. Richman Essay Contest of the American College of Chest Physicians must observe the following rules: 1. Complete application form in duplicate, have original copy signed by the dean of the medical school, and return original copy at once to the offices of the American College of Chest Physicians, 112 East Chestnut Street, Chicago, Illinois 60611. 2. Five copies of the manuscript, typewritten in English (double spaced) must be submi tted to the American College of Chest Physicians offices in Chicago not later than March 15, 1968. 3. The length for manuscripts- is optional; 2500-4500 words suggested. 4. The only means of identification of the au thor shall be a motto or other device on the title page. A sealed envelope bear-
ing the same motto on the outside and enclosing the n am e and address of the author must accompany the essay. (Motto may be a word or brief phrase which has a significant meaning to the author).
The First Prize will be $500; Second Prize will be $300; Third Prize will be $200. Each winner will also receive a certificate of merit. A trophy, inscribed with the name of the First Prize winner and the name of his school will be awarded to the winner's school. The winning contributions will be selected by a committee of chest specialists and will be announced at the 34th Annual Meeting of the American College of Chest Physicians to be held in San Francisco, California, June 13-17, 1968. All manuscripts become the property of the American College of Chest Physicians and may be considered for publication in the College journal.
The Genesis of the First Heart Sound with Varying P-R Intervals* LAWRENCE GOULD, M .D.,** DINO BELLETTI, M.D.t AND ALAN
F.
LYON, M.D.:!:
Bronx, New York
I
T HAS BEEN OBSERVED THAT THE INTEN-
sity of the first heart sound varies with the P-R interval when the rate is constant. One explanation offered in the past for this phenomenon was that in cases with a P-R interval of .04 to .12 seconds the A-V valve leaflets are quite low and relaxed and snap back through a wide arc resulting in a loud sound. It was further hypothesized that if the ventricles contract at a time later than normal after the atria (PR=.22 - .34), the leaflets would have already floated up to a higher position, almost closing the orifices, and the sound produced by ventricular systole at that moment would be much fainter.' This theory is no longer plausible since it now seems certain that the valves are closed prior to the production of the first heart sound .' It has further been noted that there is a linear correlation between the first sound and the speed of left ventricular contraction (dpydt );' .s thus relating the intensity of the sound to acceleration of blood rather than to valve position. In the present study, the phenomenon of variation of the first sound with the P-R interval was again evaluated. An alternative explanation is offered to fit the current concept of heart sound production.
insure high fidelity tracings, the needle was directly connected to a pressure transducer. The first derivative of the brachial artery pressure was continuously computed by an R-C differentiating circuit. A phonocardiogram was recorded at the second left intercostal space and left sternal border in the patient with complete heart block. A standard Cambridge microphone was used to record a medium range (40 to 200 cycles per second) phonocardiogram. The microphone was held rigidly to the chest wall by strips of adhesive tape and by a rubber strap, placed around the chest. I
I
I
I
I 1
METHODS
Two patients, one with complete heart block and the other with second degree AV block of the Wenckebach type, were studied in the supine position and at rest. The brachial artery was cannulated with an 18-gauge Cournand needle. In order to
"......... 1 n-
v
*From the Medical Service, Veterans Administration Hospital, Bronx. ** Assistant Chief, Cardiology Section . t Attending Physician, Cardiology Section. tChief, Cardiology Section.
v I
FIGURE I: Brachial artery first derivative falls as the P-R interval lengthens.
817
818
Disea ses of the Chest
GOULD, BELLETTI AND LYON
Simultaneous records of the electrocardiogram, rate of rise of the brachial artery pressure (dpjdt) and a phonocardiogram, were obtained. Two additional normal patients were studied in the supine position. The patients were then told to stand by the side of the table, and the arterial pressure and its first derivative were measured in the erect position using the mid-cardiac level as the zero reference point. A phonocardiogram was simultaneously recorded from the rigidly attached microphone. In order to exclude the possibility that the observed changes in heart sound intensity on standing were not due to postural differences in the relation of the heart to the chest wall, in one additional patient, simultaneous intracardiac sound , left ventricular pressure and left ventricular dpjdt were recorded by means of an AllardLaurens micromanometer mounted at the tip of a No.8 French cardiac catheter. The intracardiac micromanometer, manufactured by Telco of Paris, permits recording of pressure and sound, without catheter delay and yields pressure tracings of uniform high quality so that precise timing of sound and pressure events is possible. The catheter was introduced through a right brachial arteriotomy and advanced to the
t.. !
PR
dp /dl
.42 1
16 67
left ventricle under visualization with an image intensifier. An external electrocardiogram was recorded simultaneously. These various parameters were recorded in the supine, sitting and erect position. RESULTS
The first derivative of the brachial artery pressure fell as the P-R interval lengthened with little change in rate in the patient with the Wen ckebach phenomenon. The maximal rise of the brachial artery pressure was 1433 mm Hgj sec when the P-R interval was .22 seconds, 1367 mm Hg jsec when the P-R interval was .30 seconds and 1300 mm Hgjsec when the P-R interval was .40 seconds (Fig. 1) . In the patient with complete heart block and a constant ventricular rate, the first derivative of the brachial artery pressure showed beat to beat variations. When the P-R interval lengthened, the first derivative fell and the first sound diminished in intensity. The opposite was observed when the P-R interval shortened. However, when the P wave fell just before, in, or after the QRS complex, the first derivative diminished and the first heart sound was of low intensity ( Fig. 2) . '''hen he assumed the erect position, the first normal patient's P-R interval fell from .19 to .18 seconds, and his brachial artery
IH -' .....,.., l
•
~I
•
PR '
.14
I
:
151
101
~
•
J
dp/dl
1733
FIG URE 2 : Brachial artery first derivative (lower) and ph onocardiogram during complete heart block . The arrows point to the P wave in the electrocardiogram. Note t hat the first heart sound and the first derivative decrease when th e P·R interval is .42 seconds and 0 seconds. The opposite occurs when the p. R interval is .14 seconds.
Volume 52, No .6 December, 1967
81 9
GENESIS OF FIRST HEART SOUND
.
- ., .... • r
PR
PR
.19
.1 8 SUP INE
ERECT
3 : Brachial artery first derivative (lower), phonocardiogram and electrocardiogram in the supine and erect position. Note that the first heart sound decreases in intensity when the first derivative falls in spite of a decrease in the P-R interval. FIGURE
pressure derivative changed from 700 to 533 mm Hg /sec. His first heart sound decreased markedly in intensity in the erect position (Fig. 3). The second normal patient showed a similar decrease in the first I
-"'rI,-"",,_..J""-ioJ~
heart sound on standing. In the change from the supine to the erect position, the P-R interval fell from .18 to .15 seconds, and his dpjdt changed from 733 to 500 (Fig. 4).
I
i st
,
~\-PR .15 SUPINE
,
J~
dp/dt 500 ERECT
FIGURE 4 : Brachial artery first derivative (lower), phonocardiogram and electrocardiogram in the supine and erect position . Again note that the first heart sound decreases in intensity when the first derivative falls in spite of a decrease in the P-R interval.
820
Diseases of the Chest
GOULD, BELLETTI AND LYON
Thus, when the first sound varies in conjunction with the P-R interval, there is a change in the brachial artery dpjdt and in the same direction as the sound intensity. When another variable, in this case posture, changes dpjdt in the opposite direction from that expected from the effect of changing P-R intervals, the intensity of the first sound follows the dpjdt rather than the P-R interval. In the patient with the intracardiac phono catheter, the P-R interval remained . 18 seconds and the left ventricular dpjdt increased from 1700 to 2190 mm Hgjsec in the change from the supine to the sitting position. His first heart sound increased markedly in the sitting position. On the assumption of the erect position, the P-R interval decreased to .16 seconds, while the left ventricular dp jdt and first heart sound showed no change from the previous determination in the sitting position (Fig. 5) . These findings confirm the observation made with the microphone on the chest wall, that the intensity of the first heart sound is proportional to the speed of ventricular contraction rather than the P-R interval when these measurements change independently.
COMMENTS
The mechanism of production of the first heart sound has been in dispute . Earlier workers were of the opinion that closure of the atrioventricular valves was the sole or most important factor" However, recent studies have convincingly demonstrated that the heart sounds are produced by the acceleration and deceleration of blood..·• Luisada' concluded that the normal first sound contains three components. The first component results from the rapid rise of pressure in the left ventricle, which causes sudden tension of the ventricular wall, the septum, the chordae and closed mitral valve. A second rapid component (25 to 40 msec. later) coincides with a change in rate of the rise of pressure as revealed by the left ventricular first derivative. A third component occurs 50 to 70 msec. after the first and coincides with the rise of pressure within the ascending aorta. Van Bogaert" has independently developed these same concept s. Luisada and Van Bogaert have also correlated the height of the left ventricular dp jdt with the amplitude of the first sound. Piemme and his co-workers' believe that the normal first sound consists of two com1st
---_I',. ·_. . .
•.•\00\00
f'Yi·~
...._
~~ .t" ./Wi ~~
.....
I , . ,-
'
1
__ .............,'''''1 ,.,.,'):,' '''-;1.~
,
PR
l' F
.18
- - -"..-----dp/dt
10050-
LV.
LV. o- -= : : : :
=- --
-~=
SUPI NE
=
-- - - -- -- ;....--- - - - SITTING
ERECT
F1C l!RF. 5 : Left ventricular pressure (lower) , left ventricular dp/dt, electrocardiogram and phonocardiogram in the supine, sitting and erect position. Note that in the change from the supine to sitting position, the first sound increases in intensity when the first derivative rises in spite of no change in th e P-R interval.
Volume 52. No.6 December. 1967
821
GENESIS OF FIRST HEART SOUND
ponents. The first component occurs during early isometric ventricular contraction. The second component occurs during ventricular ejection, and appears to be a function of acceleration of aortic blood flow. All of these workers stress that left ventricular contractility is the major factor producing the first heart sound. ..Atrial contraction closes the A-V valves before the onset of isometric ventricular contraction.I" Thus, the changing intensity of the first sound with varying P-R intervals cannot be explained by mitral valve position at the time of ventricular contraction since the valve is already closed. The changing intensity of the first sound with changing P-R intervals can be adequately explained by the newer concept that acceleration of blood produces the first sound. We have demonstrated that a properly timed atrial contraction can result in an increase in the speed of the left ventricular contraction, and a resultant increase in the magnitude of the first heart sound. Benchimol" has shown that in patients with complete heart block a P-R interval of 1 to 300 msec. results in a 14 per cent increase in the dpjdt of arterial pressure as compared to the derivative obtained when atrial systole occurred during ventricular systole. He also noted that the contribution of a properly timed atrial contraction appears to be of greater significance in patients with compensated heart disease and heart failure than in normal hearts." Our data further shows that when the dpjdt falls and the P-R interval decreases in subjects in the erect position, the intensity of the first sound varies with dpjdt and not the P-R interval. This finding supports the contention that valve position does not c au se changing intensity of the first sound with varying P-R intervals. On the other hand, it is well established that atrial systole contributes to ventricular filling to a significant degree. Wiggers and Katz" found t hat the ventricular filling effect of atrial systole averaged about 35 per cent. Jochim 12 calculated that the atrial contribution to ventricular filling was 21
per cent when the atrial systolic-ventricular systolic interval was 0.1 second. Recently Snyder" determined that the stroke volume increased 8 per cent when atrial systole occurred 0.1 second prior to closure of the atrioventricular valves, and decreased in a similar magnitude when a trial emptying into the ventricles was prevented by closed A-V valves. These findings enable us to present a unifying concept for the production of the first heart sound with varying P-R intervals, that is, a properly timed atrial contraction can indirectly lead to an enchancement of the first heart sound by increasing ventricular filling and causing an increase in left ventricular dpjdt or left ventricular contractility, while an excessively long or short P-R interval leads to a decrease in the intensity of the first sound by reducing ventricular filling and contractility. An apparent exception to this rule is mitral stenosis in which the first sound is commonly accentuated, since we observed a normal or low brachial artery first derivative in patients with this entity. It must therefore be concluded that the power and rapidity of left ventricular contraction cannot solely explain the increased amplitude of the first sound in mitral stenosis. Van Bogaert" has recently reported that, when the valvular apparatus is more rigid, its displacement toward the atrium is reduced. This increases the incompressibility of the blood mass and contributes to an increase in the frequency of the first component of the first sound, rather than the second component, which is the portion of the first sound affected by changes in contractility, and which is the important determinant of first sound intensity in all other entities. 1
REFERENCES
S. A. AND HARVEY, W. P.: Clinical auscultation of the heart, W. B. Saunders, Philadelphia. 2 LUISADA, A.: From auscultation to phonocardiography, C. V. Mosby, St. Louis, 1965. 3 VAN BOGAERT, A.: "New concept on the mechanism of the first heart sound," Am. ]. Cardiol., 18:253, 1966. 4 DOCK, W.: "Mode of production of the first heart sound," Arch. Internal M ed., 51: 737,. 1933. LEVINE,
822
GOULD, BELLETTI AND LYON
5 PIEMME, T. E., BARRETT, G. O. AND DEXTER, L.: "Relationship of heart sounds to acceleration of blood flow," Circulation Res., 18: 303, 1966. 6 RUSHMER, R. F.: Cardiac diagnosis, W. B. Saunders Comp., Philadelphia, 1955. 7 LITTLE, R. C.: "Effect of atrial systole on ventricular pressure and closure of the A-V valve," Am. /. Physiol., 166: 289, 1951. 8 BROCKMAN, S. K.: "Mechanism of the movements of the atrioventricular valves," Amer. /. Cardiol., 17: 682, 1966. 9 BROCKMAN, A., DUENAS, A., LIGGETT, M. S. AND DIMONEL, E. G.: "Contribution of atrial systole to the cardiac function at a fixed and at a variable ventricular rate," Amer. ]. Cardiol., 16: 11, 1965.
Diseases of the Chest
10 BENCHIMOL, A. AND LIGGETT, M. S.: "Cardiac hemodynamics during stimulation of the right ventricle and left ventricle in normal and abnormal hearts," Circulation, 33: 933, 1966. 11 WIGGERS, C. J. AND KATZ, L. N.: "The contour of the ventricular volume curves under different conditions," m. ]. Physiol., 58: 439, 1922. 12 JOCHIM, K.: "The contribution of the auricles to ventricular filling in complete heart block," Am. I. Physiol., 122: 639, 1938. 13 SNYDER, J. H., BENDER, F., KITCHIN, A. H., ZITNIK, R. S., DONALD, D. E. AND WOOD, E. H.: "Atrial contribution to stroke volume in dogs with chronic heart block," Circulation Res., 19: 33, 1966.
Readers are invited to submit articles for the Electrocardiogram of the Month. Please submit material to Stephen R. Elek, M.D.. 46~ North Roxbury Drive. Beverly Hills. California.
AMERICAN COLLEGE OF CHEST PHYSICIANS' 1968 ESSAY CONTEST Medical students wishing to enter the 1968 Alfred A. Richman Essay Contest of the American College of Chest Physicians must observe the following rules: 1. Complete application form in duplicate, have original copy signed by the dean of the medical school, and return original copy at once to the offices of the American College of Chest Physicians, 112 East Chestnut Street, Chicago, Illinois 60611. 2. Five copies of the manuscript, typewritten in English (double spaced) must be submi tted to the American College of Chest Physicians offices in Chicago not later than March 15, 1968. 3. The length for manuscripts- is optional; 2500-4500 words suggested. 4. The only means of identification of the au thor shall be a motto or other device on the title page. A sealed envelope bear-
ing the same motto on the outside and enclosing the n am e and address of the author must accompany the essay. (Motto may be a word or brief phrase which has a significant meaning to the author).
The First Prize will be $500; Second Prize will be $300; Third Prize will be $200. Each winner will also receive a certificate of merit. A trophy, inscribed with the name of the First Prize winner and the name of his school will be awarded to the winner's school. The winning contributions will be selected by a committee of chest specialists and will be announced at the 34th Annual Meeting of the American College of Chest Physicians to be held in San Francisco, California, June 13-17, 1968. All manuscripts become the property of the American College of Chest Physicians and may be considered for publication in the College journal.