Significance of the contribution of atrial systole to cardiac function in man

Significance

of the Contribution

Systole

to Cardiac ALBERTO

Function

BENCHIMOL, Phoenix,

T

HE VALUE

of atria1

performance

ous reported Studies marily

studies

dealing

contraction

with

atria1

with

atria1

and

using

either

or with

single

sure

and

also

demonstrated

and

pressure,

D.C. at

and

tients

(2)

at various

or synchronous

rates

OF ATRIAL

was

one

FIBRILLATION

of the first

the onset of atria1 fibrillation in the aortic

pressure,

-

of venous

IMPLANTED

SINUS

that

unpredictable

after

conversion

5

PROSE

recent

ment

of arterial

of

studies flow

telemetry

(Fig.

When

MIN.

atria1

response

fall in flow

AFTER

underwent

SINUS

in

a small

cardiac

output

rate

to

during

sinus atria1

110 to 130 beats/min.‘j

with

continuous

in man using system

atria1

a

in pa-

the use of drugs

fibrillation

the heart

flowmeter

ATRIAL

RHYTHM

filling. shown

output who

with

increase

was not above

Our

cipitous

pres-

have

cardiac

fibrillation

providing

1).

as 50 per

ventricular

shock.1-8 Our data6 showed

and

ventricular

results in a decline

elevation

BA FLOW NORMAL

to indicate

atria1

venous

ventricular

by as much others

in the

Geselllg~zo

given

augments

to sinus rhythm

fibrillation

TO SINUS RHYTHM LewisIs

with

rhythm

atrio-

pacing.13-I7

CONVERSION

increase

by

output. any

of passive

reports

or with D.C.

during

for

output

the level

conversion

intervals

that

and cardiac

variable

with

in cardiac

atria1 contraction

Subsequent

in whom (3)

decrease

cent over

pri-

shock*8; block

various

pacing

filling

of atria1

sinus rhythm

cycle9-12; pacing

man.

(1) conversion

heart

occurs

cardiac

Arizona

in numer-

performed

situations:

ventricular

ventricular

been

in Man*

M.D., F.A.C.C.

to cardiac

contribution

complete

contraction the

animals

to regular

the use of drugs1-K

during

the have

in the following

of atria1 fibrillation

analyzed

in both

in man

in patients

contraction

has been

of Atria1

confirm

fibrillation

is present

measure-

the Doppler this finding with

there

and pressures,

with

a fast

is a premarked

MECHANISM

FIBRILLATION

Electrocardiogram (lead II) and Figure 1. Sinus rhythm us. atria1 fibrillation. brachial artery flow (BA) measured with the Doppler ultrasonic flowmeter in a 62 year old woman with sinus rhythm who experienced atria1 fibrillation during cardiac catheterization. Peak arterial flow velocity during atria1 fibrillation is essentially identical to the velocity recorded during sinus rhythm. The ventricular rate is only slightly higher during atria1 fibrillation than during sinus rhythm. * From the Institute for Cardiovascular Diseases, Good Samaritan Hospital, Phoenix, Ariz. This study was supported in part by Grant HE 11131 from the National Institutes of Health and by the Arizona Heart Association and Southwest Foundation for Medical Research and Education. Diseases, Good Samaritan Hospital, Address for reprints: Albert0 Benchimol, M.D., Institute for Cardiovascular 1033 E. McDowell Rd., Phoenix, Ariz. 85002.

568

THE AMERICAN JOURNAL OF CARDIOLOGY

Contribution

560

of Atria1 Systole

Heart block with implantrTd asynchronous pacrmaker. Electrocardiogram Figure 2. (lead II) and transcutaneous measurements of brachial artery flow (BA) in a 74 year old man with complete heart block and implanted asynchronous pacemaker. Arrows indicate the pacemaker artifact. Peak arterial flow velocity is higher when the pacemaker beat is preceded by an atria1 contraction (P) than when atria1 systole does not contribute to the beat.

(lead II) Figure 3. Complete heart block. Electrocardiogram flow velocity obtained with crystals mounted at the tip of a (Doppler ultrasonic flowmeter) in a 54 year old woman with block. Peak aortic flow velocitv is higher in those beats which atria1 systole (P). I

”

decline in ventricular

function curves. In patients with atria1 fibrillation, exercise results in a disproportionate rise in heart rate, and in this situation cardiac output either remains unchanged or falls. However, in some patients with atria1 fibrillation but adequate control of heart rate (between 60 to 100 beats/min.), cardiac output may rise during exercise if major atria1 or ventricular myocardial disease is not present. STUDIES IX PATIENTS WITH COMPLETE HEART BLOCK

Patients with complete heart block offer a unique opportunity to study the contribution of atria1 contraction to the various measures of ventricular function. In earlier investigationsi0*12 in patients with acquired heart block we studied ejection time, mechanical systole, aortic pressure, ventricular systolic and end-diastolic presVOLUME23, APRIL 1969

and peak aortic cardiac catheter complete heart are preceded by

sures, isovolumic contraction time and dp/dt of arterial pressure. In beats in which the atria1 contraction occurred at a P-R interval of 1 to 200 msec. these values were significantly higher than in those beats in which atria1 systole occurred during ventricular systole or too early in diastole (P-R interval greater than 300 msec.). The contribution of atria1 contraction to these variables occurred at a wide range of rates, although its significance appeared to be greater at rates of 60 to 110 beats/min. These observations have also been documented by others. With the development of the Doppler ultrasonic flowmeter by Franklin et a1.21-23 it became possible to obtain continuous measurement of beat to beat arterial flow velocity in man. This development has provided an opportunity to study the contribution of atria1 systole to peripheral flow on a continuous basis. Our initial observations with this technic24-26 have shown

Benchimol

Figure 4. Sinus us. nodal rhythm. Electrocardiogram (lead II), femoral artery flow obtained with a Doppler ultrasonic flowmeter and right atria1 pressure (RA) in a 51 year old woman with patent ductus arteriosus (PDA) and pulmonary hypertension. The tracings were recorded during sinus rhythm and shortly after a nodal rhythm developed during cardiac catheterization. During nodal rhythm, peak arterial flow falls slightly and right atria1 pressures show “cannon” waves (arrow).

that a properly coordinated atrial contraction (P-R interval 1 to 200 msec.) in patients with complete heart block results in higher peak arterial flow velocity (Fig. 2). Subsequent developments by Stegall et a1.,27 who mounted the transducer crystals at the tip of a standard cardiac catheter, offered an opportunity to obtain direct and continuous measurements of aortic blood flow velocity in man. Our initial measurements in man with this technic demonstrated that aortic peak flow velocity is approximately 15 per cent higher in those beats which are preceded by atria1 contraction than in those beats which do not have the contribution of atria1 systole (Fig. 3). In addition, we have observed that if nodal rhythm developed in patients with sinus rhythm, peak arterial flow velocity decreased. (Fig. 4).

Figure 5. Right atria1 us. rzghf ucntricular paczng. Electrocardiogram (lead II), transcutaneous brachial artery flow obtained with the Doppler ultrasonic flowmeter and left (LV) and right ventricular (RV) pressures in a 15 year old boy with coarctation of the aorta. Measurements of arterial flow were made during single right atria1 (A) and right ventricular (B) pacing at progressive increases in rate. Peak arterial flow is more uniform during atria1 pacing than during ventricular pacing, and at rates of lbO/min. becomes quite irregular during ventricular pacing. rates.12-1a This increase in flow occurs at rates of 80 to 140 beats/min., beyond which cardiac output and pressures will fall. However, in patients with heart disease the contribution of atria1 systole at various rates of pacing appears to be of greater significance. In these cases atria1 pacing may result in as much as 20 to 30 per cent higher levels of cardiac output and aortic and ventricular systolic pressures than those that are obtained at equivalent pacing

ATRIAL AND VENTRICULAR PACING IN PATIENTS WITH SINUS RHYTHM Studies in normal subjects whose right atrium and right ventricle were paced by means of a bipolar catheter have shown that levels of cardiac output, aortic and ventricular pressures, stroke power and dp/dt of arterial pressure are 5 to 15 per cent higher during atria1 pacing than during ventricular pacing at identical

THE

AMERICANJOURNAL

OF

CARDIOLOGY

Contribution rates of ventricular pacing. Furthermore, in thcsc patients the significance of atria1 contribution is greater at higher rates of pacing (above 120 heats/min.) (Fig. 5).

of .\trial 11.

1 2.

SUMMARY

Under certain conditions atria1 contraction may contribute to an increase in cardiac output and may enhance over-all cardiac performance in man. The increase in flow and pressures resulting from atria1 contraction is variable, depending on the functional capacity of the atria and ventricles and also on the basic pathologic condition. Atria1 contribution in man appears to be more significant during exercise, during fast heart rates and particularly in patients with hrart disease.

13.

1 4.

1 5.

16.

REFERENCES 1. ~IECHT, H. H., OSHER, W. J. and SAMUELS,A. .J. Cardiovascular adjustments in subjects with organic heart disease before and after conversion of atria1 fibrillation to normal sinus rhythm (Abstr.). J. Clin. Invest., 30: 647, 1951. 2. BROCH, 0. J. and MULLER, 0. Hemodynamic studies during auricular fibrillation and after restoration of sinus rhythm. &it. Heart J., 19: 222, 1957. 3. HECHT, H. H. and LANGE, R. L. The hemodynamic consequences of atria1 fibrillation. Mod. Concepts Card&was. Zk., 25: 351, 1956. 4. SMITH, W. C., WALKER, G. L. and ALT, H. L. The cardiac output in heart disease. 1. Complete heart block, auricular fibrillation before and after the restoration to normal rhythm, subacute rheumatic fever and chronic rheumatic valvular disease. Arch. ht. Med., 45: 706, 1930. 5. HANSEN,W. R., MCCLENDON, R. 0. and KINSMAN, .J. M. Auricular fibrillation. Hemodynamic studies before and after conversion with quinidine. Am. ZZeart J., 44: 499, 1952. 6. BENCHIMOL,A., LOWE, 1-I. M. and AKRE, P. R. Cardiovascular response to exercise during atria1 fibrillation and after conversion to sinus rhythm. Am. J. Cardiol., 16: 31, 1965. 7. RESNEKOV, I,. IHaemodynamic study before and after electrical conversion of atria1 fibrillation and flutter to sinus rhythm. Bit. Heart J., 29: 700, 1968. 8. MORRIS, J. .J., EN~MAN,M., NORTH, W. C., KONG, V. and MCINTOSH, I-1. Changes in cardiac output with reversion of atria1 fibrillation to sinus rhythm. Circulation, 31: 670, 1965. 9. LEONARD, J., KRIJETZ, F., SHAVER, J., TAGUCHI, J. and LANEVE, S. The timing of atria1 systole as a determinant of left ventricular stroke volume. Clin. RPS., 12: 55, 1964. 10. BENCHIMOL,A. Cardiac functions during electrical stimulation of the heart. Effect of exercise and drugs on patients with permanent pacemakers. Am. J. Cardiol., 17: 27, 1966. VOLUME 23, APRIL 1969

17.

18. 19.

20.

21.

22.

23.

24.

Systole

.i- 1

SAMET, P.. BERNSTEIN,W. H., NATIIAX, 1). A. a~ltl LOPEZ, A. Atria1 contribution to cardiac output

in complete heart block. Am. .I. Cardiol.. 16: 1. 1965. BENCHIMOL.A., ELLIS, J. G. and DIMONU. E. G. Hemodynamic consequences of atrial and vcntricular pacing in patients with normal and ahnormal hearts. Am. J. Mpd., 39: 911. 1965. SAMET, I’., BERNSTEIN,W. H., MEDOW. A. and NATHAN, D. A. Effect of alterations in ventricular rate upon cardiac output in complete heart block. Am. J. Cardiol., 14: 477, 1964. NATHAN, D. A.. SAMET, P., CENTER, S. and \vu. C. Y. Long term correction of complete heart block. Clinical and physiological studies of a nrw type of implantable synchronous pacer. Pro,er. Cardiooas. Dis., 6: 538, 1964. .JUDGE, R. D., WILSON, W. S. and SIEGAL, J. l-1. Hemodynamic studies in patients with implanted cardiac pacemakers. NP~) Z+&and J. Med.. 2?(J: 1391, 1964. BENCHIMOL, A., PALMERO,H. A., LICGETT, M. S. and DIMOND, E. G. Influence of digitalization on the contribution of atria1 systole to the cardiac dynamics at a fixed ventricular rate. Circulation. 32: 84, 1965. BENCHIMOL,A., LIGGETT, M. S., DZJENAS,A. and DIMOND, E. G. Effect of nitroglycerin on cardiovascular functions at fixed and at variable heart rate. &it. Hart J., 27: 902, 1965. l.EWIS, T. Fibrillation of the auricles; its effects upon the circulation. J. Exper. >V?d., 16: 395, 1912. GESELL, R. A. Cardiodynamics in heart block as affected by auricular systole, auricular fibrillation and stimulation of the vagus nerve. Am. J. Phy.riol., 40: 267, 1916. GESELL, R. A. Auricular systole and its relation to ventricular output. Am. J. Physiol., 29: 32, 1911.12. FRANKLIN,1). L., SCHLEGEL,W. and RUSHMER,R. F. Blood flow measured by Doppler frequency shift of backscattered ultrasound. Science, 134: 564, 1961. FRANKLIN,D. L., SCHLEGEL,W. and WATSON, N. M’. Ultrasonic Doppler shift blood flowmeter: Circuitry and practical application. Pror. Z.S..-l. Biomed. Sci~nccs Instrum. Symp., 1: 309, 1963. VAN CITTERS, R. L. and FRANKLIN, D. L. The Doppler ultrasonic telemetry Wowmeter. Application in animal experiments. t’roc. 20th .4nn. Conj. Eng. Med. Biol., 27: 7, 1967. BENCHIMOI.,A., MAROKO, P. R., GARTI.AN, J. I... and FRANKLIN, D. L. Continuous measurements of arterial flow in man during atria1 and ventricular arrhythmias. Am. J. MPd., 46: 52, 1969.

25. BENCHIMOL,A., MAIA, I. G., GARTLAN, J. I,. and FRANKLIN, D. L. Telemetry of arterial flow in man with Doppler ultrasonic flowmeter. ,407. J. Card~ol., 22: 75, 1968. 26. BENCHIMOL,.4. Arterial flow in health and diseased states. Proc. ZO!h Ann. Conf. Erq. Med. Biol., 27: 6, 1967. 27. STEGALL, H. F., STONE, H. L., BISHOP, V. S. and LAENGER, C. A catheter tip pressure and velocity sensor. PTOC.20th Ann. Con/. Eng. Med. Hiol., 27: 4,

1967.