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Hemodynamic consequences of sequential atrioventricular pacing
Hemodynamic Sequential
Atrioventricular
Subjects PHILIP SAMET,
Consequences
M.D., F.A.c.c., CESAR CASTILLO, M.D. and WILLIAM H. BERNSTEIN, M.D., F.A.C.C.
curves were recorded on an &channel Electronics for Medicine recorder and were calibrated by three dyein-blood concentration levels. The semilog replot extrapolation method was used to calculate cardiac output. Three varieties of pacing were utilized, atrial, ventricular and sequential atrioventricular pacing, all with a Medtronic paired-pulse pacing unit. Since the patients were in sinus rhythm, all rates employed were faster than the control sinus rate. Measurements of cardiac output were made at one to two minutes after institution of any given rhythm. The justification for measurements at this time interval has been given elsewhere.’ The technics of atria1 and ventricular pacing are readily visualized. The technic of sequential atrioventricular pacing requires some discussion. In this approach, a stimuius is applied to the atrium by way of a bipolar electrode catheter at a rate above the control sinus rate. At a preset interval less than the control P-R interval, a second stimulus is applied to the right ventricle by way of the second right ventricular endocardial catheter, utilizing the paired pulsing setting of the Medtronic unit. The interval between the two stimuli may be decreased to 0.00 sec. or less if desired, i.e., the ventricles may be activated before the atria. In atria1 pacing the normal sequential relation between atria1 and ventricular activity is maintained, and the normal pathway of ventricular
MATERIALS ANDMETHODS Studies were performed in 20 subjects without demonstrable heart disease. Two 3.5 F. bipolar electrode catheters, 125 cm. long, were passed, one into the right atrium and a second into the right vencatheter
was passed
into
Florida
monary artery or into the left atrium with the transseptal left atria1 puncture technic. This catheter permitted injection of 2.5 to 3 mg. indocyanine green for determination of cardiac output by indicator-dilution technic. The dye curves were inscribed by blood aspirated from a systemic artery through a Cournand needle with a Harvard constant infusionwithdrawal unit and Gilford densitometers. The dye
REVIOUS studies from this laboratory have stressed the role of atria1 systole in maintaining ventricular function both in patients with complete heart block and in normal subjects and cardiac patients in sinus rhythm.lW5 Similar data have been obtained in man and the experimental animal by other investigators.6-10 Some of these studies in subjects in sinus rhythm’,; have demonstrated that atria1 pacing results in larger cardiac output than ventricular pacing at the same rate. However, these differential effects of atria1 and ventricular pacing may be due to the role either of atria1 systole or That is, of aberrant ventricular depolarization. in atria1 pacing the normal time sequential relation between atria1 and ventricular systole is maintained, and ventricular depolarization follows the normal pathways. III contrast, in ventricular pacing not only is the sequential relation between atria1 and ventricular activity disturbed, but an aberrant pathway of ventricular depolarization is necessarily utilized. The major purpose of this report is to determine in 20 subjects with normal hearts which of these two factors is primary in the pathogenesis of the abnormal hemodynamics resulting from ventricular as opposed to atria1 pacing.
P
A third
Pacing
with Normal Hearts* Miami Beach,
tricle.
of
the pul-
* From the Section of Cardiology, Department of Medicine, Mount Sinai Hospital, Miami Beach, and the UniThis study was supported by Grants HE-08503-03 and versity of Miami School of Medicine, Coral Gables, Fla. HE-09X2-01 from the National Heart Institute, U. S. Public Health Service. Address for reprints: Philip Samet, M.D., Section of Cardiology, Dept. of Internal Medicine, Mount Sinai Hospital, 4300 Alton Rd., Miami Beach, Fla. 33140. VOLUME
21,
FEBRUARY
1968
207
208
Samet,
Castillo
and Bernstein
N0IlM.L /
,/.’ /
f’
//’ .
1.
/
I ,, /-*^
i
/
’
/
, ,’
,
Cardiac index data during ventricular V.P.) and sequential atrioventricular (S.A.V.P.) pacing in 61 paired studies. The data are clearly skewed to the right. Ten and 20 per cent deviations from the line of identity are shown. FIG.
1.
/’ /I/
,i
FIG. 4. Four atriovrntricular
. .
.j
comparisons of atria1 and pacing at rates of 60 to 89.
sequential
is utilized. In ventricular pacing depolarizaLion neither normal atrioventricular activity nor the normal ventricular depolarization path\vay is availahle. In sequential atrioventricular pacing the advantage of sequential atrioventricular activity is maintained, Ijut the pathway of ventricular depolarization is. of course. abnormal. RESULTS
FIG. 2. Comparison of atria1 / .\.I’.) atrioventricular pacing. The differences
3. Four at&ventricular FIG.
and srqltential al-r minimal.
comparisons of ventricular and sequential pacing at rates of 60 to 89 beats/min.
Sixth--one colnparisons of the effects of atrial, \.cntricrllar and sequential atrioventricular activity were nlade in the 20 normal subjects. Four observations were made at rates of 60 to 89 beats/min., 28 at rates of 90 to 109 and 29 at rates of 110 to 140. t:or the entire group of 61 comparisons, the average cardiac index during atria1 pacing was 3.17 L.,/min./M.‘; the corresponding figures during ventricular and sequential atrioventricular activity were 2.66 and 3.08 L./min.,M.” (Fig. 1, 2). The difference between the mean indexes for atria1 and ventricular pacing was significant (/J < O.OOl), for atria1 and sequential pacing, significant only at the 0.05 level; for ventricular and sequential pacing, significant (p < 0.001). I;or the group with rates of 60 to 89, the mean indexes during atrial, ventricular and sequential pacing were 3.19, 2.49 and 2.99 L./min./M.‘, respectively (Fig. 3, 4). The differences between ventricular pacing and the other two pacing methods were significant only at the 0.05 level. There was no difference, however, between atria1 and sequential atrioventricular pacing. ‘THE: AMERICAN
JOURNAL
OF CARDIOI.OG’I
Hemodynamics
FIB. 5. Twenty-eight comparisons sequential atrioventricular pacing 109.
of Atrioventricular
Pacing
209
of ventricular and at rates of 90 to
For the group with rates of 90 to 109, the mean indexes during atrial, ventricular and sequential pacing were 3.09, 2.61 and 3.03 L./min./M.2, respectively (Fig. 5, 6). The differences between the ventricular and the other two pacing means were significant at the 0.001 level; that between the atria1 and sequential pacing mean was significant only at the 0.05 level. For the group with rates of 170 to 140, the atrial, ventricular and sequential pacing means indexes were 3.26, 2.74 and 3.15, respectively (Fig. 7, 8). The differences between the ventricular and the other two pacing means were significant at the 0.001 level. The difference between the atria1 and sequential pacing means was not significant. The institution of atria1 pacing resulted in little or no change in atria1 or systemic arterial dynamics (Fig. 9). Ventricular pacing resulted in the well known decreases in systemic arterial pressure and elevation of atria1 mean pressure with ventricularization of the curve4v5 (Fig. 10). Sequential atrioventricular pacing, on the other hand, also resulted in no alteration of systemic arterial and atria1 pressure curves (Fig. 11). In 5 other patients with heart disease, multiple measurements of cardiac index were made at repeated intervals after institution of sequential atrioventricular pacing to again verify the belief that valid flow measurements may be made at one to two minutes after institution of pacing.’ The results (Table I) demonstrate that a steady state is indeed achieved within this period.
comparisons of atria1 and FIG. 6. Twenty-eight sequential atrioventricular pacing at rates of 90 to 109.
FIG. 7. Twenty-nine comparisons of ventricular and sequential atrioventricular pacing at rates of 110 to 140.
DISCUSSION The data in the present study clearly demonstrate the hemodynamic superiority of sequential VOLUME
21,
FEBRUARY
1968
FIG. 8. Twenty-nine comparisons of atria1 and sequential atrioventricular pacing at rates 110 to 140.
Samet, Castillo and Bernstein
210 A.P.
FIG.
9.
N.S.R.
N.S.R.
,
I
A.P.
.\trial pacing produces little Patient with rheumatic llcart disease. = normal sinus rhythm: F.A. = femoral artery; LA. = left atrium.
Both atria1 alid scatrioventricular activity. quential atrioventricular pacing, unlike \,cntricular pacing, preserl-e the normal temporal reMost lation between atrium and ventricle. of the hemodynamic difference between atria1 and ventricular pacing is, therefore, due not to
V.P.
Fro. 10.
Same patient.
Ventricular
change.
aberrant pathways of ventricular depolarization but to lack of synchronized atrioventricular activity. Even in the subject with a normal heart, atria1 systole makes a very significant The failure contribution to ventricular systole. of Benchimol et al.‘,” to reach similar conclu-
N.S.R.
pacing results in obwous pressure changes. THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Hemodynamics Seq. A.V. pacing
I
I
FIG. 11.
change.
Same patient.
of Atrioventricular I
Sequential
I
sions is probably due to study of fewer patients and internal inconsistencies in their data.
2.
3.
4.
5
TABLE I Time-Cardiac
Index Relations 6.
Cath. No.
Ventricular Rate Change
1639 1640 1641 1642 1648
90-100 76-100 100-110 77-100 100-110
Cardiac Index (L. /min./M.r) 2-5 5-7 o-2 Min. Min. Min.
Average
2.13 1.73 3.22 3.00 3.02
1.97 1.79 3.01 2.71 2.94
2.18 1.98 3.36 2.76 3.21
2.62
2.48
2.69
Cath. = catheterization. VOLUME 21 FEBRUARY 1968
N.S.R.
pacing (Seq.
I
211 I
A.V.) produceslittle
REFERENCES 1.
,%MMARY
The hemodynamic sequelae of sequential atrioventricular pacing were compared to those of atria1 and ventricular pacing and analyzed. The results clearly demonstrate that aberrant ventricular depolarization per se is of relatively minor hemodynamic import but that sequential atria1 and ventricular activity is essential for optimal ventricular function even in the normal subject.
I
I
atrioventricular
Pacing
7.
8.
9.
P., BERNSTEIN,W. H., LEVINE, S. and LOPEZ, A. Hemodynamic effects of tachycardias produced by atria1 and ventricular pacing. Am. J. Med., 39: 905, 1965. SAMET, P., BERNSTEIN, W. H., NATHAN, D. A. and LOPEZ, A. Atria1 contribution to cardiac Am. J. Cardiol., output in complete heart block. 16: 1, 1965. SAMET, P., BERNSTEIN, W. H. and LEVINE, S. Significance of the atria1 contribution to ventricular filling. Am. J. Cardiol., 15: 195, 1965. SAMET, P. and BERNSTEIN,W. H. Hemodynamic considerations in complete heart block. J. Mt. Sinai Hosp., 32: 153, 1965. SAMET, P., JACOBS, W., BERNSTEIN, W. H. and SHANE, R. Hemodynamic sequelae of idioventricular pacing in complete heart block. Am. J. Cardiol., 11: 594, 1963. BROCKMAN, S. K. Cardiodynamics of complete heart block. Am. J. Cardiol., 16: 72, 1965. BENCHIMOL,A., ELLIS, J. G. and DIMOND, E. G. Hemodynamic consequences of atria1 and ventricular pacing in patients with normal and abnormal hearts. Effect of exercise at a fixed atria1 and ventricular rate. Am. J. Med., 39: 911,1965. MITCHELL, J. H., GILMORE, J. P. and SARNOFF, S. J. The transport function of the atrium. Factors influencing the relation between mean left atria1 pressure and left ventricular end-diastolic pressure. Am. J. Cardiol., 9: 237, 1962. GESELL, R. A. Auricular systole and its relation to ventricular output. Am. J. Physiol., 29: 32, 1911-12.
SAMET,
212
Samet,
Castillo and Bernstein
10. BRAUNWALD, E. and FRAHM, C:. J. Studies on Starling’s law of the heart. IV. Observations on the hemodynamic functions of the left atrium in man. Circulatim. 24: 633. 1961.
11. BENCHIMOL, :\. and DIMOND, E. G. Cardiac function in man during artificial stimulation of the left ventricle, right ventricle, and right atrium. Am. J. Cardiol., 17: 118, 1966.
THE AMERICAN JOURNAL OF CARDIOLOGY
Atrioventricular
Subjects PHILIP SAMET,
Consequences
M.D., F.A.c.c., CESAR CASTILLO, M.D. and WILLIAM H. BERNSTEIN, M.D., F.A.C.C.
curves were recorded on an &channel Electronics for Medicine recorder and were calibrated by three dyein-blood concentration levels. The semilog replot extrapolation method was used to calculate cardiac output. Three varieties of pacing were utilized, atrial, ventricular and sequential atrioventricular pacing, all with a Medtronic paired-pulse pacing unit. Since the patients were in sinus rhythm, all rates employed were faster than the control sinus rate. Measurements of cardiac output were made at one to two minutes after institution of any given rhythm. The justification for measurements at this time interval has been given elsewhere.’ The technics of atria1 and ventricular pacing are readily visualized. The technic of sequential atrioventricular pacing requires some discussion. In this approach, a stimuius is applied to the atrium by way of a bipolar electrode catheter at a rate above the control sinus rate. At a preset interval less than the control P-R interval, a second stimulus is applied to the right ventricle by way of the second right ventricular endocardial catheter, utilizing the paired pulsing setting of the Medtronic unit. The interval between the two stimuli may be decreased to 0.00 sec. or less if desired, i.e., the ventricles may be activated before the atria. In atria1 pacing the normal sequential relation between atria1 and ventricular activity is maintained, and the normal pathway of ventricular
MATERIALS ANDMETHODS Studies were performed in 20 subjects without demonstrable heart disease. Two 3.5 F. bipolar electrode catheters, 125 cm. long, were passed, one into the right atrium and a second into the right vencatheter
was passed
into
Florida
monary artery or into the left atrium with the transseptal left atria1 puncture technic. This catheter permitted injection of 2.5 to 3 mg. indocyanine green for determination of cardiac output by indicator-dilution technic. The dye curves were inscribed by blood aspirated from a systemic artery through a Cournand needle with a Harvard constant infusionwithdrawal unit and Gilford densitometers. The dye
REVIOUS studies from this laboratory have stressed the role of atria1 systole in maintaining ventricular function both in patients with complete heart block and in normal subjects and cardiac patients in sinus rhythm.lW5 Similar data have been obtained in man and the experimental animal by other investigators.6-10 Some of these studies in subjects in sinus rhythm’,; have demonstrated that atria1 pacing results in larger cardiac output than ventricular pacing at the same rate. However, these differential effects of atria1 and ventricular pacing may be due to the role either of atria1 systole or That is, of aberrant ventricular depolarization. in atria1 pacing the normal time sequential relation between atria1 and ventricular systole is maintained, and ventricular depolarization follows the normal pathways. III contrast, in ventricular pacing not only is the sequential relation between atria1 and ventricular activity disturbed, but an aberrant pathway of ventricular depolarization is necessarily utilized. The major purpose of this report is to determine in 20 subjects with normal hearts which of these two factors is primary in the pathogenesis of the abnormal hemodynamics resulting from ventricular as opposed to atria1 pacing.
P
A third
Pacing
with Normal Hearts* Miami Beach,
tricle.
of
the pul-
* From the Section of Cardiology, Department of Medicine, Mount Sinai Hospital, Miami Beach, and the UniThis study was supported by Grants HE-08503-03 and versity of Miami School of Medicine, Coral Gables, Fla. HE-09X2-01 from the National Heart Institute, U. S. Public Health Service. Address for reprints: Philip Samet, M.D., Section of Cardiology, Dept. of Internal Medicine, Mount Sinai Hospital, 4300 Alton Rd., Miami Beach, Fla. 33140. VOLUME
21,
FEBRUARY
1968
207
208
Samet,
Castillo
and Bernstein
N0IlM.L /
,/.’ /
f’
//’ .
1.
/
I ,, /-*^
i
/
’
/
, ,’
,
Cardiac index data during ventricular V.P.) and sequential atrioventricular (S.A.V.P.) pacing in 61 paired studies. The data are clearly skewed to the right. Ten and 20 per cent deviations from the line of identity are shown. FIG.
1.
/’ /I/
,i
FIG. 4. Four atriovrntricular
. .
.j
comparisons of atria1 and pacing at rates of 60 to 89.
sequential
is utilized. In ventricular pacing depolarizaLion neither normal atrioventricular activity nor the normal ventricular depolarization path\vay is availahle. In sequential atrioventricular pacing the advantage of sequential atrioventricular activity is maintained, Ijut the pathway of ventricular depolarization is. of course. abnormal. RESULTS
FIG. 2. Comparison of atria1 / .\.I’.) atrioventricular pacing. The differences
3. Four at&ventricular FIG.
and srqltential al-r minimal.
comparisons of ventricular and sequential pacing at rates of 60 to 89 beats/min.
Sixth--one colnparisons of the effects of atrial, \.cntricrllar and sequential atrioventricular activity were nlade in the 20 normal subjects. Four observations were made at rates of 60 to 89 beats/min., 28 at rates of 90 to 109 and 29 at rates of 110 to 140. t:or the entire group of 61 comparisons, the average cardiac index during atria1 pacing was 3.17 L.,/min./M.‘; the corresponding figures during ventricular and sequential atrioventricular activity were 2.66 and 3.08 L./min.,M.” (Fig. 1, 2). The difference between the mean indexes for atria1 and ventricular pacing was significant (/J < O.OOl), for atria1 and sequential pacing, significant only at the 0.05 level; for ventricular and sequential pacing, significant (p < 0.001). I;or the group with rates of 60 to 89, the mean indexes during atrial, ventricular and sequential pacing were 3.19, 2.49 and 2.99 L./min./M.‘, respectively (Fig. 3, 4). The differences between ventricular pacing and the other two pacing methods were significant only at the 0.05 level. There was no difference, however, between atria1 and sequential atrioventricular pacing. ‘THE: AMERICAN
JOURNAL
OF CARDIOI.OG’I
Hemodynamics
FIB. 5. Twenty-eight comparisons sequential atrioventricular pacing 109.
of Atrioventricular
Pacing
209
of ventricular and at rates of 90 to
For the group with rates of 90 to 109, the mean indexes during atrial, ventricular and sequential pacing were 3.09, 2.61 and 3.03 L./min./M.2, respectively (Fig. 5, 6). The differences between the ventricular and the other two pacing means were significant at the 0.001 level; that between the atria1 and sequential pacing mean was significant only at the 0.05 level. For the group with rates of 170 to 140, the atrial, ventricular and sequential pacing means indexes were 3.26, 2.74 and 3.15, respectively (Fig. 7, 8). The differences between the ventricular and the other two pacing means were significant at the 0.001 level. The difference between the atria1 and sequential pacing means was not significant. The institution of atria1 pacing resulted in little or no change in atria1 or systemic arterial dynamics (Fig. 9). Ventricular pacing resulted in the well known decreases in systemic arterial pressure and elevation of atria1 mean pressure with ventricularization of the curve4v5 (Fig. 10). Sequential atrioventricular pacing, on the other hand, also resulted in no alteration of systemic arterial and atria1 pressure curves (Fig. 11). In 5 other patients with heart disease, multiple measurements of cardiac index were made at repeated intervals after institution of sequential atrioventricular pacing to again verify the belief that valid flow measurements may be made at one to two minutes after institution of pacing.’ The results (Table I) demonstrate that a steady state is indeed achieved within this period.
comparisons of atria1 and FIG. 6. Twenty-eight sequential atrioventricular pacing at rates of 90 to 109.
FIG. 7. Twenty-nine comparisons of ventricular and sequential atrioventricular pacing at rates of 110 to 140.
DISCUSSION The data in the present study clearly demonstrate the hemodynamic superiority of sequential VOLUME
21,
FEBRUARY
1968
FIG. 8. Twenty-nine comparisons of atria1 and sequential atrioventricular pacing at rates 110 to 140.
Samet, Castillo and Bernstein
210 A.P.
FIG.
9.
N.S.R.
N.S.R.
,
I
A.P.
.\trial pacing produces little Patient with rheumatic llcart disease. = normal sinus rhythm: F.A. = femoral artery; LA. = left atrium.
Both atria1 alid scatrioventricular activity. quential atrioventricular pacing, unlike \,cntricular pacing, preserl-e the normal temporal reMost lation between atrium and ventricle. of the hemodynamic difference between atria1 and ventricular pacing is, therefore, due not to
V.P.
Fro. 10.
Same patient.
Ventricular
change.
aberrant pathways of ventricular depolarization but to lack of synchronized atrioventricular activity. Even in the subject with a normal heart, atria1 systole makes a very significant The failure contribution to ventricular systole. of Benchimol et al.‘,” to reach similar conclu-
N.S.R.
pacing results in obwous pressure changes. THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Hemodynamics Seq. A.V. pacing
I
I
FIG. 11.
change.
Same patient.
of Atrioventricular I
Sequential
I
sions is probably due to study of fewer patients and internal inconsistencies in their data.
2.
3.
4.
5
TABLE I Time-Cardiac
Index Relations 6.
Cath. No.
Ventricular Rate Change
1639 1640 1641 1642 1648
90-100 76-100 100-110 77-100 100-110
Cardiac Index (L. /min./M.r) 2-5 5-7 o-2 Min. Min. Min.
Average
2.13 1.73 3.22 3.00 3.02
1.97 1.79 3.01 2.71 2.94
2.18 1.98 3.36 2.76 3.21
2.62
2.48
2.69
Cath. = catheterization. VOLUME 21 FEBRUARY 1968
N.S.R.
pacing (Seq.
I
211 I
A.V.) produceslittle
REFERENCES 1.
,%MMARY
The hemodynamic sequelae of sequential atrioventricular pacing were compared to those of atria1 and ventricular pacing and analyzed. The results clearly demonstrate that aberrant ventricular depolarization per se is of relatively minor hemodynamic import but that sequential atria1 and ventricular activity is essential for optimal ventricular function even in the normal subject.
I
I
atrioventricular
Pacing
7.
8.
9.
P., BERNSTEIN,W. H., LEVINE, S. and LOPEZ, A. Hemodynamic effects of tachycardias produced by atria1 and ventricular pacing. Am. J. Med., 39: 905, 1965. SAMET, P., BERNSTEIN, W. H., NATHAN, D. A. and LOPEZ, A. Atria1 contribution to cardiac Am. J. Cardiol., output in complete heart block. 16: 1, 1965. SAMET, P., BERNSTEIN, W. H. and LEVINE, S. Significance of the atria1 contribution to ventricular filling. Am. J. Cardiol., 15: 195, 1965. SAMET, P. and BERNSTEIN,W. H. Hemodynamic considerations in complete heart block. J. Mt. Sinai Hosp., 32: 153, 1965. SAMET, P., JACOBS, W., BERNSTEIN, W. H. and SHANE, R. Hemodynamic sequelae of idioventricular pacing in complete heart block. Am. J. Cardiol., 11: 594, 1963. BROCKMAN, S. K. Cardiodynamics of complete heart block. Am. J. Cardiol., 16: 72, 1965. BENCHIMOL,A., ELLIS, J. G. and DIMOND, E. G. Hemodynamic consequences of atria1 and ventricular pacing in patients with normal and abnormal hearts. Effect of exercise at a fixed atria1 and ventricular rate. Am. J. Med., 39: 911,1965. MITCHELL, J. H., GILMORE, J. P. and SARNOFF, S. J. The transport function of the atrium. Factors influencing the relation between mean left atria1 pressure and left ventricular end-diastolic pressure. Am. J. Cardiol., 9: 237, 1962. GESELL, R. A. Auricular systole and its relation to ventricular output. Am. J. Physiol., 29: 32, 1911-12.
SAMET,
212
Samet,
Castillo and Bernstein
10. BRAUNWALD, E. and FRAHM, C:. J. Studies on Starling’s law of the heart. IV. Observations on the hemodynamic functions of the left atrium in man. Circulatim. 24: 633. 1961.
11. BENCHIMOL, :\. and DIMOND, E. G. Cardiac function in man during artificial stimulation of the left ventricle, right ventricle, and right atrium. Am. J. Cardiol., 17: 118, 1966.
THE AMERICAN JOURNAL OF CARDIOLOGY