- Email: [email protected]
Complete heart block and the role of atrial activity
Complete and the
heart block role of atrial
Hugo A, Pahero, La Jolla, Cal$.
activity
M.D.*
T
he atrium has been studied by different methods, including auscultation, phonocardiography, electrocardiography, vectorcardiography, venous pulse tracings, apex cardiography, ballistocardiography, and electrokymography. The information obtained by these methods is primarily concerned with hypertrophy and time relationships between atria1 and ventricular contractions. The booster effect of atria1 systole on the filling of the ventricles has long been recognized, 1s3,4-8but more recent experimental work done in animals with surgically induced complete atrioventricular heart block has corroborated and extended the previous studies.3Js7 The human subject with acquired complete heart block offers a means of analyzing (a) the contribution of the atria1 contraction to the performance of the following ventricular contraction, and (b) the changes that will occur when a sympathomimetic amine is administered. Material
and
methods
Ten patients with complete atrioventricular block due to arteriosclerotic heart disease were studied ; 4 were women and 6 were men. The mean age was 70.6 years. Four of the cases were Grade I, 4 were Grade TI, and 2 were Grade TTI according From the Institute for Cardiopulmonary Diseases, Received for publication Nov. 16. 1964. *National Institutes of Health Trainee. Cardiovascular Privado, Ciudad de Cordoba, Argentina.
449
to the New York Heart Association classification. Four of the patients had had an infarction; the most recent one had occurred 2 years prior to the study. An electrical pacemaker had been inserted into the wall of the left ventricle in all of the patients, and at the time of the study all of the patients were being regularly paced by the pacemaker at a rate of 62 to 75 beats per minute. Two patients, because of signs of heart failure, were on digitalis at the time of the study. All studies were performed with the patient in the horizontal position. Ejection times were taken from the carotid tracing during halted expiration at a high paper speed (200 mm. per second) and a time line of 20 msec. Punctures of the brachial artery were performed and arterial pressure curves were recorded with a P23Db Statham strain gauge. The transducer was placed at the level of the right atrium. The length and internal diameter of the tubing from the needle to the transducer was 50 cm. and 0.08 inches, respectively. Precordial electrocardiograph electrodes were placed in the positions best for recording the P waves. Cardiac outputs were determined by the dyedilution technique. The first derivative of the arterial pressure curves was either calculated matheScripps
Clinic
Graduate
and Training
Research Grant
Foundation, HE-5513.
La Jolla, Present
Calif.
address:
Hospital
4.50
Palmer0
matically or, more recently, obtained by means of an R-C differentiating circuit. In 4 patients, isoproterenol was given intravenously for 10 to 15 minutes at a constant rate of 2 micrograms per minute. Cardiac outputs, intra-arterial blood pressures, and ejection times were determined at 2, 4, 8, 10, and 15 minutes during the administration of this drug. The figures shown in Table II were obtained before the administration of the drug and at the time of maximum increase in the cardiac output. Results Ejection time. The average ejection time achieved was 286 f 17 msec. when the P-R interval was 100 to 250 msec. (optimum zone’) (see Table I). When the P wave of the electrocardiogram fell during the QRS complexes (basal zone), the average ejection time for the group was 250 f 19 msec. The absolute difference was 36 msec., which represents 12.5 per cent of the maximum ejection time. The statistical
Table I. Contribution of the atria1 derivative oj the arterial pressure
contraction
difference between these two groups is highly significant (p < 0.001). Fig. 1 represents the changes in ejection time in one typical case. It is interesting to observe that when the atria1 systole occurred during the T wave, it was still partially effective in prolonging the ejection time. Arterial blood pressure. The average systolic and diastolic pressures during the “optimum zone” were 133 f 19 and 64 =t 9 mm. Hg, respectively. During the “basal zone” the average systolic pressure was 119 f 20 mm. Hg, and the average diastolic pressure was 62 zt 16 mm. Hg. The absolute differences between the blood pressures for “optimum zone” and for “basal zone” were 14 and 2 mm. Hg for systolic and diastolic, respectively. The increments (in per cent) for the systolic and diastolic pressures given by the atria1 activity were 10.5 and 3.1 per cent in each case (Table 1). The statistical difference for systolic blood pressures was highly significant
to ejection
time,
blood
pressure,
and
peak $rsf
Patient
290 290 290 300 272 286
255 290
320 267 286 -tl7
263 260 257 259 242 249 206 266 269 2.11
134 144 145 160 12s 90 135
62 70 68 71 58 47 75
'SO +19
133 + 10
64
.zo I’.$
-t_ (1
121 131 135 147
60 68 65 69 58 a7 66
110 81 108
119
61
*20 1-C 10
813 815 85.5 811 870 778 880
Slh 2 5
3 8
650 597 652 592 690 524 539
8.12
006
Ik 3-k
ir48 ‘25 27. I
Complete hew-t block und role 01 utriul uctivity
451
Fig. 1. Ejection time, systolic and diastolic arterial pressures, and peak positive dp/dt of the arterial pressure curve in one typical case. The T wave in this case occurred between 400 and 490 msec.
Fig. 2. Ejection time, systolic and diastolic blood pressure, and peak positive dp/dt during the two zones (100-250 msec. and during QRS) of the P-R interval before and during the administration of isoproterenol.
(p < O.OOl), whereas the difference for diastolic pressures was not significant (p < 0.1). It can be observed that atria1 systole properly timed will contribute primarily to the increase in the systolic pressure. This measurement followed approximately the same pattern of ejection time when plotted against P-R intervals (Fig. 1).
tration of isoproterenol (Table II and Fig. 2). The ejection times of the “basal zone” did not change significantly, but actually rose from a control of 254 msec. to 258 msec. during administration of the drug. It can be observed that the decrease in ejection time is due entirelv to diminution of the atria1 filling capadity. In fact, the atria1 contribution dropped from 11 to 4 per cent of the corresponding maximum ejection times. The statistical analysis of the differences in ejection times between the two zones (optimum and basal) before and during the administration of isoproterenol gives a value of p < 0.02. ARTERIAL RLOOD PRESS-RE. Roth the systolic and diastolic pressures fell with the infusion of the isoproterenol from a control value of 124/59 mm. Hg to 109/38 mm. Hg when ;ltrial contraction occurred during the “optiiiiuln zone,” and from a control of 112/57 mm. Hg to 96/37 mm. Hg when the atria1 activity was at the “basal zone” (Table II and Fig. 2).
Peak positive jirst derivative
of
the arterial
czLrve. The peak positive dp/dt was 832 f 34 mm. Hg per second during the “optimum zone” and 606 f 48 mm. Hg per second during the “basal zone.” The absolute difference was 225 mm. Hg per second, which represents 27.1 per cent of the maximum peak dp/dt. The statistical difference is highly significant (p < 0.001). pressure
IlJECTIoN TIME. The ejection time of the “optimum zone” fell from an average of 286 msec. during the control period to an average of 269 msec. during the adminis-
452
Palmer0
Table
II. Changes
Am. Heart J. October, 1965
in ejection
time, blood pressure,
and peak jirst
derivative
Ejection time (msec.)
msec.
Average Difference Per cent change
During
QRS
;
100-250 msec.
i
! lhlriny QRS
100250 msec.
I
I 1
During QRS
292 286 295 272
255 249 270 242
280 260 280 255
270 252 270 240
134/62 90/47 145/68 125/s
121/60 81/46 135/65 110/58
286
254 32 11
269
‘58 11 4
121/59
Il2/57 12/2 9.7/3.4
The percentage of atria1 contribution to arterial pressures did not change before or during the administration of the drug. It was 12 and 2 per cent for systolic and diastolic pressures, respectively, during the control, and 11 and 1 per cent during the administration of isoproterenol. The p value resulting from a comparison of the differences in systolic pressures before and after isoproterenol is greater than 0.20 and also not significant for the diastolic pressure. PEAK ARTERIAL
Before
,
, 100-250
B.B. T.K. ST. B.A.
I------
nuring
__-
POSITIVE FIRST DERIVATIVE PRESSURE CURVE. The
OF
THE
peakdp/dt increased in both zones of the P-R interval (Table II and Fig. 2). During the control, peak dp/dt was 829 mm. Hg per second at the “optimum zone,” and 629 mm. Hg per second at the “basal zone,” representing an increase of 24.1 per cent. When isoproterenol was given, peak dp/dt values were 1,107 and 971 mm. Hg per second in these two zones. The percentage of atria1 contribution was only 12.2 per cent (Table II and Fig. 2). Although there was a tendency of the gradient to decrease between the two zones before and during the administration of isoproterenol, it was not statistically significant (p > 0.20). As can be seen in Table II, the stroke volume increased by an average of 53 of this per cent with administration drug.
pres
Blood pressure (mm. Hg) -
Before
Patient
of the arterial
Discussion
The role of the atria, as has been previously demonstrated, is primarily that of increasing the filling of the ventricles2~3~5~7 and of “setting” the A-V valves in a semiclosed position at the beginning of ventricular contraction.3 It is believed that venous return is a result of three main forces: a passive “vis a tergo,” a possible active “vis a fronte” that occurs during systole and an early diastolegJU--“sucking action” of the ventricles, and, finally, active atria1 contraction. There is no reason to believe that the first two factors just mentioned did change significantly. Consequently, it is inferred that the changes in the different parameters are due to different timings of the atria1 contractions. As can be seen in Fig. 1, the correct timing of atria1 systole results in clear prolongation of the ejection time and increase in systolic pressure and peak dp/dt. When the atria1 contraction fell during the T wave (Fig. l), it was still partially effective in increasing the above-mentioned parameters. This could sound illogical since the A-V valves are closed during the T wave, and the atria1 action would be expected to 1~ ineffective. However, it is known that the interval from the beginning of the P wave
Complete
453
heart block and role of atria1 activity
sure, before and during the administration of isoproterenol Peak dp/dt (mm. Hg/sec.)
Blood pressure (mm. Hg)
Stroke volume (ml.)
During _-~_ 100-250 msec.
DtWing QRS
i
MI;tIBe~D;$~~
IWZ;ODu~D;;;g
126/40 89/38 105/35 115/40
122/38 80/38 98/34 85/38
813 778 855 870
6.50 524 652 690
1240 781 1102 1305
109/38
96/37 11/l 10/2.6
829
629 200 24.1
1107
of the electrocardiogram to the end of the “a” wave in an atria1 pressure tracing varies from 170 to 240 msec.,3 and this may explain this late and partial contribution. A P wave falling during the QRS complex does not add anything to the following ventricular contraction. In fact, it is conceivable that it will produce a slight regurgitation through the A-V valve.7 Ejection time, pressure, and peak dp/dt are higher during the optimum “P-R interval,” probably because the semiclosed position of the mitral valve at the time of ventricular contraction gives a steeper rise in ventricular pressure. In other words, it would take less time for the ventricles at the beginning of the systole to close an already semiclosed mitral valve. This has been observed previously by Siecke and Essex3 in dogs with surgically induced complete A-V block. As a matter of fact, the A-V pressure difference is negative at the onset of ventricular systole for “P-R intervals” of 100 to 300 msec., favoring a partial closure of the A-V valves. Animal studies on the booster action of the atrium have demonstrated that the aortic flow is significantly increased by the proper timing of the atria1 contraction.7 It is possible, then, that the increase in stroke volume occurs as a result of
Before
1145 630 1029 1082 971 135 12.2
During
55 74 56 57
99 91 97 80
60
92
synchronous atria1 activity. This would explain the present findings of increased ejection time, systolic and diastolic pressures, and peak dp/dt on the basis of increased distention of the fiber length. The rise in blood pressure should then be considered to be a result of increased output against an unprepared peripheral resistance. The hemodynamic response to the administration of isoproterenol that is supposed to act in the beta receptorslgJO has been extensively studied. It has been proved to increase contractility and cardiac output and decrease systolic ejection time and peripheral resistance.ii-r4J6 Peak dp/dt from the ventricular pressure curve has been observed to increase significantly with the administration of isoproterenol .I7 These data show that atria1 systole during the administration of isoproterenol is proportionately less effective in prolonging ejection time. However, its effect in elevating the systolic pressure is tnaintained. Peak dp/dt gradient between the two zones showed a tendency to decrease after the administration of the drug. This is most likely due to a significant diminution of myocardial compliance and, therefore, makes the filling function of the atrium more difficult. This is probably not due to increased venous pressure, since isoproterenol, on the contrary, de-
454
Am. Heart /. October. 1965
Palmer0
creases venous pressure.‘~~L~’ The fact that the relationship of mean left atria1 pressure to left ventricular end-diastolic pressure is independent of changes in stroke volume and aortic pressuren also rules out these factors as determinants of this relative insufficiency of the atrium during infusion of isoproterenol. Indirect evidence of the increased work of the atrium during the administration of isoproterenol comes from the electrocardiographic changes observed with this drug. There is an increase in the amplitude of the I’ wave and augmentation of the auricular gradient by, increasing T3.r8 Summary Ten patients with complete atrioventricular block were studied in order to evaluate the contribution bf the atria1 contraction to the following ventricular contraction. Ejection times, intra-arterial blood pressures, and peak dp/dt were measured. These data indicate that proper atria1 timing produces a considerable increase in ejection time, systolic arterial pressure, and peak positive dp/dt. Administration of isoproterenol resulted in a substantial decrease in ejection time when atria1 systole occurred at only the proper time, but no change was observed before and during the administration of isoproterenol when the atria1 systole was not synchronous. Systolic and diastolic pressures decreased during administration of the drug, and the contribution of the atrium was maintained. Peak positive dp/dt rose in both zones of the “P-R and the atria1 contribution interval,” slightly decreased. The conclusion is that isoproterenol decreases myocardial compliance, and the action of the atrium is diminished proportionately--. REFERENCES 1. Harvey, W. : Movement of the heart and blood in animals. An anatomical essay, translated by 1;. F. Franklin, Oxford, 1957, Blackwell Scientific Publications, p. 34. 2. Gesell, R. A.: Cardiodynamics in heart block as affected by auricular systole, auricular fibrillation and stimulation of the vagus nerve, Am. J. Physiol. 40:267, 1916. 3. Siecke, H., and Essex, H. E.: Relation of the difference in pressure across the mitral valve
4.
5.
6.
7.
8. 9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19. 20.
to the amplitude of the lirst heart zouncl in dogs with atrioventricular block, .2n1. J. l’hysiol. 192:135, 1958. Jochim, K.: The contribution of the auricles to ventricular filling in complete heart block, .Am. J. Physiol. 122:639, 1938. Braunwald, E., and Frahm, C. J.: Studies on Starling’s law of the heart. IV. Observations on hemodynamic functions of left atrium in man, Circulation 24:633, 1961. Mitchell, J. H., Gilmore, J. I’., and Sarnoff, S. J,: The transport function of the atrium, Am. J. Cardiol. 9:237, 1962. Skinner, S. N., Jr., Mitchell, J. II., Wallace, ~1. G., ancl Sarnoff, S. J.: Hemodynamic. effects of altering the timing of atria1 systole, ;\m. J. I’hysiol. 205:499, 1963. Henderson, Y., and Johnson, F. E.: Two modes of closure of the heart val\:es. Heart 4:69, 1912. 13rccher, G. A.: Critical review of recent work on ventricular suction, Circulation Res. 6:554, 1958. Brecher, G. A., and Kissen, A. ‘I‘.: Ventricular diastolic suction at normal arterial pressures. Circulation Kes. 6:100, 1958. Winterscheid, L. C., Bruce, 1~. -A., Blumberg, J. B., and Merendino, K. -1.: Effects of isoproterenol on carbohydrate metabolism of isolated canine heart, Circulation Res. 12:76, 1963. Lands, A. M., and Howard, J. W’.: =\ comparative study of the effects of 1-arterenol, epinephrinc and isopropylarterenol on the heart, J. Pharmacol. & &per. Therap. 106:65, 1952. Garb, S.: Inotropic action of epinephrine, norepinephrine, and AN-isopropylnorepinephrine on heart muscle, Pror. Sot-. Exper. Biol. & Med. 73:134, 1950. Ilodge, H. T., Lord, J. I)., and Sandler, H.: Cardiovascular effects of isoproterenol in normal subjects and subjects with congestive heart failure, AIM. HEART J. 60:94, 1960. Wallace, A. G., Mitchell, J. H., Skinner, N. S.. and Sarnoff, S. J, : Hemodynamic variables affecting the relation between mean left atrial and left ventricular end-diastolic pressures, Circulation Res. 13:261, 1963. Benchimol, A., Lucena, E. G., and Dimond, E. G.: Stroke volume and peripheral resistance during infusion of isoproterenol at a constant lixed heart rate, Circulation 31:417, 1965. Gleason, W. L., and Braunwald, E.: Studies of the lirst derivative of the ventricular pressure pulse in man, J. Clin. Invest. 41:80, 1962. Littman, A., Grossman, M. I., Gunar, Ii. M.. Isaacs, J. H., Hirschmann, J. H., and Foley, E. F. : Electrocardiographic effects of arterenol and isopropylarterenol in man, with a note on the auricular T-wave, J. Appl. Physiol. 3:235, 1950-1951. Ahlquist, K. P.: A study of the adrenotropic receptors, Am. J. Physiol. 153:.586, 1948. Green, H. D., and Kepchar, J. H.: Control of peripheral resistance in major systemic vascular beds, Physiol. Rev. 39:617, 1959.
heart block role of atrial
Hugo A, Pahero, La Jolla, Cal$.
activity
M.D.*
T
he atrium has been studied by different methods, including auscultation, phonocardiography, electrocardiography, vectorcardiography, venous pulse tracings, apex cardiography, ballistocardiography, and electrokymography. The information obtained by these methods is primarily concerned with hypertrophy and time relationships between atria1 and ventricular contractions. The booster effect of atria1 systole on the filling of the ventricles has long been recognized, 1s3,4-8but more recent experimental work done in animals with surgically induced complete atrioventricular heart block has corroborated and extended the previous studies.3Js7 The human subject with acquired complete heart block offers a means of analyzing (a) the contribution of the atria1 contraction to the performance of the following ventricular contraction, and (b) the changes that will occur when a sympathomimetic amine is administered. Material
and
methods
Ten patients with complete atrioventricular block due to arteriosclerotic heart disease were studied ; 4 were women and 6 were men. The mean age was 70.6 years. Four of the cases were Grade I, 4 were Grade TI, and 2 were Grade TTI according From the Institute for Cardiopulmonary Diseases, Received for publication Nov. 16. 1964. *National Institutes of Health Trainee. Cardiovascular Privado, Ciudad de Cordoba, Argentina.
449
to the New York Heart Association classification. Four of the patients had had an infarction; the most recent one had occurred 2 years prior to the study. An electrical pacemaker had been inserted into the wall of the left ventricle in all of the patients, and at the time of the study all of the patients were being regularly paced by the pacemaker at a rate of 62 to 75 beats per minute. Two patients, because of signs of heart failure, were on digitalis at the time of the study. All studies were performed with the patient in the horizontal position. Ejection times were taken from the carotid tracing during halted expiration at a high paper speed (200 mm. per second) and a time line of 20 msec. Punctures of the brachial artery were performed and arterial pressure curves were recorded with a P23Db Statham strain gauge. The transducer was placed at the level of the right atrium. The length and internal diameter of the tubing from the needle to the transducer was 50 cm. and 0.08 inches, respectively. Precordial electrocardiograph electrodes were placed in the positions best for recording the P waves. Cardiac outputs were determined by the dyedilution technique. The first derivative of the arterial pressure curves was either calculated matheScripps
Clinic
Graduate
and Training
Research Grant
Foundation, HE-5513.
La Jolla, Present
Calif.
address:
Hospital
4.50
Palmer0
matically or, more recently, obtained by means of an R-C differentiating circuit. In 4 patients, isoproterenol was given intravenously for 10 to 15 minutes at a constant rate of 2 micrograms per minute. Cardiac outputs, intra-arterial blood pressures, and ejection times were determined at 2, 4, 8, 10, and 15 minutes during the administration of this drug. The figures shown in Table II were obtained before the administration of the drug and at the time of maximum increase in the cardiac output. Results Ejection time. The average ejection time achieved was 286 f 17 msec. when the P-R interval was 100 to 250 msec. (optimum zone’) (see Table I). When the P wave of the electrocardiogram fell during the QRS complexes (basal zone), the average ejection time for the group was 250 f 19 msec. The absolute difference was 36 msec., which represents 12.5 per cent of the maximum ejection time. The statistical
Table I. Contribution of the atria1 derivative oj the arterial pressure
contraction
difference between these two groups is highly significant (p < 0.001). Fig. 1 represents the changes in ejection time in one typical case. It is interesting to observe that when the atria1 systole occurred during the T wave, it was still partially effective in prolonging the ejection time. Arterial blood pressure. The average systolic and diastolic pressures during the “optimum zone” were 133 f 19 and 64 =t 9 mm. Hg, respectively. During the “basal zone” the average systolic pressure was 119 f 20 mm. Hg, and the average diastolic pressure was 62 zt 16 mm. Hg. The absolute differences between the blood pressures for “optimum zone” and for “basal zone” were 14 and 2 mm. Hg for systolic and diastolic, respectively. The increments (in per cent) for the systolic and diastolic pressures given by the atria1 activity were 10.5 and 3.1 per cent in each case (Table 1). The statistical difference for systolic blood pressures was highly significant
to ejection
time,
blood
pressure,
and
peak $rsf
Patient
290 290 290 300 272 286
255 290
320 267 286 -tl7
263 260 257 259 242 249 206 266 269 2.11
134 144 145 160 12s 90 135
62 70 68 71 58 47 75
'SO +19
133 + 10
64
.zo I’.$
-t_ (1
121 131 135 147
60 68 65 69 58 a7 66
110 81 108
119
61
*20 1-C 10
813 815 85.5 811 870 778 880
Slh 2 5
3 8
650 597 652 592 690 524 539
8.12
006
Ik 3-k
ir48 ‘25 27. I
Complete hew-t block und role 01 utriul uctivity
451
Fig. 1. Ejection time, systolic and diastolic arterial pressures, and peak positive dp/dt of the arterial pressure curve in one typical case. The T wave in this case occurred between 400 and 490 msec.
Fig. 2. Ejection time, systolic and diastolic blood pressure, and peak positive dp/dt during the two zones (100-250 msec. and during QRS) of the P-R interval before and during the administration of isoproterenol.
(p < O.OOl), whereas the difference for diastolic pressures was not significant (p < 0.1). It can be observed that atria1 systole properly timed will contribute primarily to the increase in the systolic pressure. This measurement followed approximately the same pattern of ejection time when plotted against P-R intervals (Fig. 1).
tration of isoproterenol (Table II and Fig. 2). The ejection times of the “basal zone” did not change significantly, but actually rose from a control of 254 msec. to 258 msec. during administration of the drug. It can be observed that the decrease in ejection time is due entirelv to diminution of the atria1 filling capadity. In fact, the atria1 contribution dropped from 11 to 4 per cent of the corresponding maximum ejection times. The statistical analysis of the differences in ejection times between the two zones (optimum and basal) before and during the administration of isoproterenol gives a value of p < 0.02. ARTERIAL RLOOD PRESS-RE. Roth the systolic and diastolic pressures fell with the infusion of the isoproterenol from a control value of 124/59 mm. Hg to 109/38 mm. Hg when ;ltrial contraction occurred during the “optiiiiuln zone,” and from a control of 112/57 mm. Hg to 96/37 mm. Hg when the atria1 activity was at the “basal zone” (Table II and Fig. 2).
Peak positive jirst derivative
of
the arterial
czLrve. The peak positive dp/dt was 832 f 34 mm. Hg per second during the “optimum zone” and 606 f 48 mm. Hg per second during the “basal zone.” The absolute difference was 225 mm. Hg per second, which represents 27.1 per cent of the maximum peak dp/dt. The statistical difference is highly significant (p < 0.001). pressure
IlJECTIoN TIME. The ejection time of the “optimum zone” fell from an average of 286 msec. during the control period to an average of 269 msec. during the adminis-
452
Palmer0
Table
II. Changes
Am. Heart J. October, 1965
in ejection
time, blood pressure,
and peak jirst
derivative
Ejection time (msec.)
msec.
Average Difference Per cent change
During
QRS
;
100-250 msec.
i
! lhlriny QRS
100250 msec.
I
I 1
During QRS
292 286 295 272
255 249 270 242
280 260 280 255
270 252 270 240
134/62 90/47 145/68 125/s
121/60 81/46 135/65 110/58
286
254 32 11
269
‘58 11 4
121/59
Il2/57 12/2 9.7/3.4
The percentage of atria1 contribution to arterial pressures did not change before or during the administration of the drug. It was 12 and 2 per cent for systolic and diastolic pressures, respectively, during the control, and 11 and 1 per cent during the administration of isoproterenol. The p value resulting from a comparison of the differences in systolic pressures before and after isoproterenol is greater than 0.20 and also not significant for the diastolic pressure. PEAK ARTERIAL
Before
,
, 100-250
B.B. T.K. ST. B.A.
I------
nuring
__-
POSITIVE FIRST DERIVATIVE PRESSURE CURVE. The
OF
THE
peakdp/dt increased in both zones of the P-R interval (Table II and Fig. 2). During the control, peak dp/dt was 829 mm. Hg per second at the “optimum zone,” and 629 mm. Hg per second at the “basal zone,” representing an increase of 24.1 per cent. When isoproterenol was given, peak dp/dt values were 1,107 and 971 mm. Hg per second in these two zones. The percentage of atria1 contribution was only 12.2 per cent (Table II and Fig. 2). Although there was a tendency of the gradient to decrease between the two zones before and during the administration of isoproterenol, it was not statistically significant (p > 0.20). As can be seen in Table II, the stroke volume increased by an average of 53 of this per cent with administration drug.
pres
Blood pressure (mm. Hg) -
Before
Patient
of the arterial
Discussion
The role of the atria, as has been previously demonstrated, is primarily that of increasing the filling of the ventricles2~3~5~7 and of “setting” the A-V valves in a semiclosed position at the beginning of ventricular contraction.3 It is believed that venous return is a result of three main forces: a passive “vis a tergo,” a possible active “vis a fronte” that occurs during systole and an early diastolegJU--“sucking action” of the ventricles, and, finally, active atria1 contraction. There is no reason to believe that the first two factors just mentioned did change significantly. Consequently, it is inferred that the changes in the different parameters are due to different timings of the atria1 contractions. As can be seen in Fig. 1, the correct timing of atria1 systole results in clear prolongation of the ejection time and increase in systolic pressure and peak dp/dt. When the atria1 contraction fell during the T wave (Fig. l), it was still partially effective in increasing the above-mentioned parameters. This could sound illogical since the A-V valves are closed during the T wave, and the atria1 action would be expected to 1~ ineffective. However, it is known that the interval from the beginning of the P wave
Complete
453
heart block and role of atria1 activity
sure, before and during the administration of isoproterenol Peak dp/dt (mm. Hg/sec.)
Blood pressure (mm. Hg)
Stroke volume (ml.)
During _-~_ 100-250 msec.
DtWing QRS
i
MI;tIBe~D;$~~
IWZ;ODu~D;;;g
126/40 89/38 105/35 115/40
122/38 80/38 98/34 85/38
813 778 855 870
6.50 524 652 690
1240 781 1102 1305
109/38
96/37 11/l 10/2.6
829
629 200 24.1
1107
of the electrocardiogram to the end of the “a” wave in an atria1 pressure tracing varies from 170 to 240 msec.,3 and this may explain this late and partial contribution. A P wave falling during the QRS complex does not add anything to the following ventricular contraction. In fact, it is conceivable that it will produce a slight regurgitation through the A-V valve.7 Ejection time, pressure, and peak dp/dt are higher during the optimum “P-R interval,” probably because the semiclosed position of the mitral valve at the time of ventricular contraction gives a steeper rise in ventricular pressure. In other words, it would take less time for the ventricles at the beginning of the systole to close an already semiclosed mitral valve. This has been observed previously by Siecke and Essex3 in dogs with surgically induced complete A-V block. As a matter of fact, the A-V pressure difference is negative at the onset of ventricular systole for “P-R intervals” of 100 to 300 msec., favoring a partial closure of the A-V valves. Animal studies on the booster action of the atrium have demonstrated that the aortic flow is significantly increased by the proper timing of the atria1 contraction.7 It is possible, then, that the increase in stroke volume occurs as a result of
Before
1145 630 1029 1082 971 135 12.2
During
55 74 56 57
99 91 97 80
60
92
synchronous atria1 activity. This would explain the present findings of increased ejection time, systolic and diastolic pressures, and peak dp/dt on the basis of increased distention of the fiber length. The rise in blood pressure should then be considered to be a result of increased output against an unprepared peripheral resistance. The hemodynamic response to the administration of isoproterenol that is supposed to act in the beta receptorslgJO has been extensively studied. It has been proved to increase contractility and cardiac output and decrease systolic ejection time and peripheral resistance.ii-r4J6 Peak dp/dt from the ventricular pressure curve has been observed to increase significantly with the administration of isoproterenol .I7 These data show that atria1 systole during the administration of isoproterenol is proportionately less effective in prolonging ejection time. However, its effect in elevating the systolic pressure is tnaintained. Peak dp/dt gradient between the two zones showed a tendency to decrease after the administration of the drug. This is most likely due to a significant diminution of myocardial compliance and, therefore, makes the filling function of the atrium more difficult. This is probably not due to increased venous pressure, since isoproterenol, on the contrary, de-
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creases venous pressure.‘~~L~’ The fact that the relationship of mean left atria1 pressure to left ventricular end-diastolic pressure is independent of changes in stroke volume and aortic pressuren also rules out these factors as determinants of this relative insufficiency of the atrium during infusion of isoproterenol. Indirect evidence of the increased work of the atrium during the administration of isoproterenol comes from the electrocardiographic changes observed with this drug. There is an increase in the amplitude of the I’ wave and augmentation of the auricular gradient by, increasing T3.r8 Summary Ten patients with complete atrioventricular block were studied in order to evaluate the contribution bf the atria1 contraction to the following ventricular contraction. Ejection times, intra-arterial blood pressures, and peak dp/dt were measured. These data indicate that proper atria1 timing produces a considerable increase in ejection time, systolic arterial pressure, and peak positive dp/dt. Administration of isoproterenol resulted in a substantial decrease in ejection time when atria1 systole occurred at only the proper time, but no change was observed before and during the administration of isoproterenol when the atria1 systole was not synchronous. Systolic and diastolic pressures decreased during administration of the drug, and the contribution of the atrium was maintained. Peak positive dp/dt rose in both zones of the “P-R and the atria1 contribution interval,” slightly decreased. The conclusion is that isoproterenol decreases myocardial compliance, and the action of the atrium is diminished proportionately--. REFERENCES 1. Harvey, W. : Movement of the heart and blood in animals. An anatomical essay, translated by 1;. F. Franklin, Oxford, 1957, Blackwell Scientific Publications, p. 34. 2. Gesell, R. A.: Cardiodynamics in heart block as affected by auricular systole, auricular fibrillation and stimulation of the vagus nerve, Am. J. Physiol. 40:267, 1916. 3. Siecke, H., and Essex, H. E.: Relation of the difference in pressure across the mitral valve
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