hemodynamic consequences of atrial and ventricular arrhythmias in man

Hemodynamic consequences of

atrial and ventricular arrhythmias in man

Albert0 Benchimol, M.D.* Jose$h G. Ellis, M.D. E. Grey Dimond, M.D. Teh-lu Wu, M.D.

La Jolla, Calif.

C ertain cardiac arrhythmias occur com- monly in patients with or without

cardiovascular disease. Because of their fleeting and intermittent nature, very little is known of the effects of these arrhythmias on cardiac function in man since accurate measurements of cardiac output and other parameters are difficult to obtain.

It is the purpose of this report to de- scribe the hemodynamic consequences of certain atria1 and ventricular arrhythmias in man.

Material and methods

Thirty-two patients who exhibited some form of atria1 or ventricular arrhythmia were studied. All but 5 had evidence of heart disease by clinical or laboratory evidence. Among the normal subjects, one had Wolff-Parkinson-White syndrome. Car- diac output was determined by the indicator-dilution technique, using indocya- nine green as an indicator.‘m3 Measurements of cardiac functions were made during the episode of cardiac arrhythmia and after conversion to sinus rhythm,4 the exception being in patients with permanent heart block.

Details of our technique have been described in previous reports.1-3 Approxi- mately half of the subjects underwent cardiac catheterization, and the indicator was injected into the right ventricle for determination of cardiac output. In the remainder of the subjects the indicator was injected into the left antecubital vein. Sampling was from the right brachial artery in all cases. In our earlier studies the Stewart-Hamilton formula was used for calculation of the cardiac output, but more recently we have used a computer5 coupled to a Gilford densitometer for electronic computation of the area encompassed by the dye curves.

Pressures were recorded with a P23Db Statham pressure transducer, and the mean pressure was obtained by electronic filter- ing. Peak derivative of the brachial arterial pressure, i.e., dp/dt, was obtained using an R/C differentiating circuit. Mechanical systole was measured as the interval between the first vibration of the first heart sound and the beginning of the aortic com- ponent of the second sound as shown on a phonocardiogram recorded at the mitral area.6 Ejection time was measured from

From the Institute for CardioPulmonary Diseases, Scripps Clinic and Research Foundation, La Jolla, Calif. Supported in part by National Institutes of Health Research Grant No. HE-07983-02 and Graduate Training Grant

No. HE-5513-03, and by the Timken-Sturgis Foundation. Received for publication Feb. 4. 1965. *ilddress: Scripps Clinic and Research Foundation, 476 Prospect St., La Jolla, Calif.

775

776 Benchimol, Ellis, Dimond, and WZL

the indirect carotid tracing obtained with a Sanborn No. 374 linear crystal micro- phone. Ejection time minus mechanical systole was taken as the period of isometric contraction. Peak q.stolic pressure was used in Sarnoff’s formula7 to calculate the tension-time index. The tracings were recorded on the Electronics for Medicine recorder at a paper speed of 200 mm. per second with 20-msec. time lines. Exercise studies were obtained using a calibrated bicycle ergometer. All the studies were performed with the subjects in a supine position.

Results and comments

I. Atria1 arrhythmias. 1. AKTIFICI.kLLY INDI’CED ATRIAL TACHT-

CARDIA. Six patients with normal sinus rhythm were paced from the right atrium at rapid rates with a bipolar electrode catheter connected to an external pace-

HEART RATE - beotslmtn.

Fig. 1. Cardiac output (C.O.), stroke volume (S.V.), mean systolic ejection rate (M.S.E.R.), mean pressure (23.A .-mean prcs.), and peripheral resistance (I’. Res.) during artificially induced atria1 and ventricular tachycardia in one normal subject. The control heart rate for the atria1 pacing was 70 beats per minute, and for the ventricular pacing 60 beats per minute. The remainder of the hemodynamic data are illustrated in Fig. 5.

tiEART RATE - bwt#/mtn.

Fig. 2. Ejection time (E.T.), tension-time index (I”. T.I.), ventricular power (V.P.), stroke power (S.P.), and the first derivative of brachial arterial pressure (dp/dt) during artificially induced atrial and ventricular tachycardia in one normal subject. See Fig. 4.

Fig. 3. Cardiac output (C.O.), stroke volume (S. V.), central blood volume (C.B.V.), and heart rate (H. Rate) in one patient before, during, and after atria1 tachycardia.

Hemodynamic consequences of atria1 and ventricular arrhythmias 777

maker. Three had a norma heart, and 3 had heart disease, but only one showed evidence of congestive heart failure. The atria1 rate was increased from a base-line control figure of 50 to 75 beats per minute to a maximum of 120 beats per minute. As the rate rose, the cardiac output, mean systemic pressure, tension-time index, ventricular power, and stroke power rose, reaching their maximum values at 100 beats per minute. At the same time, stroke volume, right ventricular systolic pressure, and the first derivative of brachial arterial

pressure remained unchanged, whereas the peripheral resistance and ejection time decreased (Figs. 1 and 2). At faster rates, cardiac output decreased slightly and there was a greater decrease in stroke volume, peripheral resistance, ejection time, and stroke power. However, systemic pressure, tension-time index, and ventricular power continued to rise. The changes observed for the group are illustrated in one case in Figs. 4 and 5.

It was interesting to observe that the response of the cardiac output and other

Fig. 4. Left ventricular pressure curves in a patient with sinus rhythm and during an episode of atrial tachycardia. The hemodynamic hndings in this patient are illustrated in Fig. 1.

Fig. 5. Right atria1 pressure curve in a patient with sinus rhythm and during an episode of atrial tachycardia The hemodynamic findings in this patient are illustrated in Fig. 1.

778 Benchimol, Ellis, Dimond, and Wu

Al --^‘-I PI Al

501 ’ I I I

R. Ex. Al,. I?. El. A,,. ATRIAL FIBRILLATION SINUS RHYTHM

Fig. 6. Average cardiac index (C.I.), stroke index (S.I.), stroke power (ST.), and heart rate (H. Rate) at rest, and during and after exercise during atria1 fibrillation and after conversion to sinus rhythm.

R. El. AI,. ATRIAL FISRILLATION

1 -ia I?. Er A‘,. SINUS RHYTHM

Fig. 7. Average brachial arterial mean pressure (B.d .-wean pres.), peripheral resistance (P. Res.), ventricular power (V.P.), and tension-time index (T.T.I.) at rest, and during and after exercise during atria1 fibrillation and after conversion to sinus rhythm. See Fig. 6.

parameters to artificial pacing was quali- tatively identical to that observed for ventricular pacing (Figs. 1 and 2).

2. PAROXYSMAL ATRIAL TACHYCARDIA.

Hemodynamic studies were made in a 22- year-old man with Wolff-Parkinson-White syndrome who developed during cardiac catheterization an episode of paroxysmal atria1 tachycardia which reverted spon- taneously to sinus rhythm. Base-line data had been obtained prior to the development of this arrhythmia. During the episode of tachycardia the heart rate rose to 180 beats per minute, the cardiac output decreased from 7.42 to 6.90 L. per minute (a decrease of 8 per cent), and the stroke volume fell from 95 to 38 ml. per beat (a decrease of 60 per cent). The central blood volume decreased slightly (Fig. 3). The left ventricular systolic and end- diastolic pressures did not change significantly during the episode of tachycardia (Fig. 4). The average ventricular power decreased by 7 per cent, and the right atria1 pressure increased from 5 to 10 mm. Hg (Fig. 5).

3. ATRIAL FIBRILLATION. Eight patients who had atria1 fibrillation which was sue. cessfully converted to sinus rhythm with a,> external direct-current shock8 were studied. Four of them had rheumatic heart disease with mitral involvement, and there lvere single instances of arteriosclerotic heart disease, hyperthyroidism, J’aget’s disease, and idiopathic atria1 fibrillation. The patients were studied at rest and during exercise before and after conversion to sinus rhythm. Postconversion studies were obtained 30 minutes after conversion to sinus rhythm, and repeated again in 4 patients 5 to 30 days after the initial procedure.

The cardiac index for the group at rest was at the lower limits of normal prior to conversion, with an average. for the group of 2.86 L. per minute per square meter. After conversion to sinus rhythm this parameter did not change significantly and averaged 3.05 L./min./RJ.2 (an increase of 6 per cent). During exercise the cardiac index increased in both pre:onversion and postconversion studies, and again the difference was not significant (Figs. 6 and 7).

Other parameters showed significant changes. After conversion, the stroke index increased 22 per cent at rest and 30 per

Hemodynamic consequences of’ atria1 and ventricular arrhythmias 779

cent during exercise; heart rate slowed by 16 per cent at rest and was 24 per cent slower during exercise; mean arteriai pres- slu-e \vas 10 per cent lower at rest and rose less with exercise; peripheral resistance at rest dropped 12 per cent, and 17 per cent during exercise; ventricular power at rest decreased 18 per cent; stroke power decreased by 13 per cent; and the tension- time index decreased 58 per cent. The figures obtained several days after conversion to sinus rhythm were essentially identical \\-ith those obtained immediately after conversion (Figs. 8 and 9).

t’OMdlEN1‘S: Experimentally induced atria1 tachycardiaY-‘3 in dogs results in a significant fall in the mean systemic arterial pressure, atria1 pressures, cardiac output, and stroke volume. Corday and Irving I1 have also shown that, in experimental atria1 tachlrcardia, lvhen the ventricular rate exceeded 190 per minute, the systemic pressure, cardiac output, cerebral, renal, and mesenteric blood flow decreased significantly. In addition, this arrhythmia resulted in a 25 to 3.5 per cent decrease in the coronary blood flow.” However, Wegria and associates’” and ,1Iaxwell and associates’j have sho\vc variable changes in the coronary flow during this arrhythmia.

Cotton16 demonstrated elevated levels of catecholamines in the blood of dogs \vith experimentall). induced atria1 tachycardia. 1lclntosh and associates’7 postulated that this increase in catecholamines might have resulted from a decrease in the mean arterial pressure and pulse pressure, which, in turn, stimulates the baroreceptors and results in sympathetic stimulation and the secretion of catecholamines.

*\n elevation of the atria1 pressure is a part of the hemodynamic findings in experimental supraventricular arrhythmias (Fig. 3). This probably results from a shortening of ventricular diastole, as well as from the occurrence of atria1 systole partially or completely while the atrioventricular valves are still closed. The contour of the atria1 pressure curve in atria1 tachycardia is often characterized bJr a single \yave form, as demonstrated in Fig. 3. Kakano” has shown that the above- described hemodynamic effects are almost indistinguishable from those of ventricular tachycardia, except that the effects ob-

c I 2 3 Min. DURING EXERCISE AFTER EXER

Fig. 8. Cardiac indes (C.I.), stroke index (S.I.), stroke power (ST.), and heart rate (H. Kafei at rest, and during and after exercise in one patient during atrial fibrillation, 1 hour and 21 da).s after ionversion to sinus rhythm. See Fig. 0.

Min. DURING EXERCISE I AFTER EXER.

Fig. Y. Mean brachial arterial pressure (13.~1:nze~~n pres.), peripheral resistance (P. Res.), tension-titnc index (T.T.I.), and ventricular power (V.P.), at rest, and during and after exercise in one patient, dllrily atria1 fibrillation, 1 hour and 2 1 days after convcr- sion to sintls rhythm See Fig. 8.

780 Benchimol, Ellis, Dimond, and Wu Am. Heart I. December, 1965

served with ventricular tachycardia are always greater than those which follow atria1 tachycardia of an equivalent rate.

Only a fe\?; studies have been made of the hemodynamic consequences of supraven- tricufar tachycardia in man. Saunders and Ord18 demonstrated in 3 patients lvith Wolff-Parkinson-White syndrome that during the episode of tachycardia there was a significant decrease in the systemic pressure, with little change in the peripheral resistance and in the cardiac output. The stroke volume fell markedly during tachycardia, and there was also a prompt rise in pulmonary arterial and “wedge” pressures. These observations had been made previously by Ferrer and co-\vorkerslYb’O in 2 patients with Wolff-Parkinson-White syndrome who developed nodal tachycardia during cardiac catheterization.

Our studies in one patient with spontaneous atria1 tachycardia confirm the above-mentioned findings (Fig. 1). In addition, in the group with artificially induced atria1 tachycardia, both in patients with normal hearts and in those with heart disease, the changes observed were some- what similar to the ones described with spontaneous tachycardia. In this group of patients a stepwise increase in heart rate resulted in a stepwise rise in the cardiac output, tension-time index, and ventricular power, with a decrease in the ejection time, peripheral resistance, stroke polver, mean systolic ejection rate, and systemic pulse pressure (Figs. 4 and 3). There were no significant changes in the first derivative of the brachial arterial pressure, stroke volume, right ventricular pressure, and isometric contraction time.

Studies describing the hemodynamic consequences of converting atria1 fibrillation to sinus rhythm with direct-current shock in man are just now becoming avail- able. Oram and associates21 studied 10 patients who showed no significant changes in cardiac output shortly after conversion to sinus rhythm. However, there was a 70 per cent increase in cardiac output in the repeated studies performed several days after conversion to sinus rhythm. Our findings in 8 cases also did not show any changes in the cardiac output in the resting figures after conversion to sinus rhythm. During exercise, the cardiac output rose in

both groups, but patients with sinus rhythm had a greater increase in the stroke volume and a lesser degree of rise in the heart rate (Figs. 6 and 7). Studies repeated several days (Figs. 8 and 9) after conversion to sinus rhythm failed to reveai any significant improvernent in the cardiac output as described by Oram. Our observations are, therefore, in agreement with

Fig. 10. Cardiac output (C.O.), stroke volume (S. V.), and mean brachial arterial pressure (R.d .-nzean pras.) in one patient with complete heart block and an artificial pacemaker rhythm. Reg. Pacem. Rlzyt.: Regular pacemaker rhythm. V.P.C.: Multiple ventricular premature contractions.

Fig. 11. Peripheral resistance (I’. lies.), ventricular power (VP.), tension-time index (T.T.I.), and stroke power (5’2.) in the same patient as in Fig. IO.

Volume 70 Number 6 Hemodynamic consequences of atria1 and ventriular arrhythmias 781

those of Boer and associates22 and Graet- tinger and associates,23 whose studies also failed to demonstrate improvement in the cardiac output after conversion to sinus rhythm.

The explanation for the lack of a significant increase in cardiac functions after conversion of atria1 fibrillation to sinus rhythm is not clear. Bramwell and Jonesz4 in 1944, developed the concept of “atria1 failure,” and they indicated that a diseased atrium may not be able to perform its function adequately. Therefore, it is con- ceivable that the restoration of coordinated atria1 contraction in these patients may indeed be of no great benefit to cardiac function. This concept of “atria1 failure” has been recently revised by Mitchell, Gilmore and SarnoffF5 Braunwaldz6 has also shown that the atria1 contraction waves are so diminutive in many patients with long-standing heart disease and atria1 fibrillation that it is unlikely that these weak atria1 contractions may significantly influence ventricular filling when restoration of sinus rhythm is accomplished.

II. Ventricular arrhythmias. 1. MULTIFOCAL VENTRICULAR PREMATURE

CONTRACTIONS. Three cases were studied which demonstrated the presence of several ventricular premature contractions, during the determination of the cardiac output with spontaneous reversion to a regular rhythm. These 3 patients had complete heart block and the ventricular rate was being controlled by means of an electrode catheter placed in the right ventricle and connected to the output of an external pacemaker. The findings illustrated in Figs. 10 and 11 were typical for the group.

With a regular and fixed ventricular rate the cardiac output was 4.5 L. per minute. When the patient developed multiple premature beats, the cardiac output fell to 3.71 L. per minute (a decline of 21 per cent). At the same time, stroke volume decreased by 18 per cent. Mean systemic arterial pressure, peripheral resistance, and tension-time index increased, whereas ventricular power and stroke power remained the same (Figs. 10 and 11). Since a number of “regular” beats failed to appear, heart rate stayed about the same.

2. BIGEMINAL RHYTHM. Two patients with

complete heart block and permanently im- planted pacemakers developed temporary bigeminal rhythm during the course of a study, with spontaneous reversion to a regular rhythm.

Base-line data had been obtained prior

Fig. 12. Cardiac output (C.O.), stroke volume (S.V.), central blood volume (C.B.V.), and mean brachial arterial pressure (B.A.-mean fires.) in one patient with complete heart block during regular pacemaker rhythm and during gibeminal rhythm. See Fig. 13.

Fig. 13. Peripheral resistance (P. Bes.), ventricular power (VT.), tension-time index (T.T.I.), and stroke power (ST.) in the same patient as in Fig. 12.

Fig. 14. Dye-dilution cur\m obtained iu the same patient as in Fig. 12, recorded during bigeminal rhythm and during the regulnr pacemaker rh\-thnl.

VEWIR. l&CHY

Fig. 15. T)ye-dilution curves obtained in a patient during spontaneous \wltricul;w hwhycnrdia anti alter con- vcrsiou to sirlus rhythm. Set Figs. 16 :u~cl 17.

to development of the bigeminal rhythm. I>uring the period of this arrhythmia the cardiac output fell from 5.39 to 3.17 L. per minute (42 per cent), and the stroke volume decreased from 73 to 47 1~11. per beat (a decrease of 36 per cent). The central blood volume, mean systemic pressure, ventricular power, and stroke power fell 24, 10, 39, and 35 per cent, respectively. The mean circulation time increased by 24 per- cent, and the peripheral resistance increased bq, 54 per cent (Figs. 12, 13, and

14). There was also a significant variation in the pulse pressure. The “regular” pacemaker beat had an average peak systolic pressure of 110 II~J. Hg, with Little variation from one beat to another, I\-hereas the spontaneous ectopic beats had significant beat-to-beat variation, with the peak systolic figures in the range of 73 to 9.5 mn~.

Hg. The ectopic beats produced a peripheral pulse of sufficient magnitude to result in palpable pulse and measurable pressure. Nevertheless, this abnormal rhxthm \vas

Hemodynamic coruequencex of atria1 and ventricular arrhythmias 783

associated with a significant disturbance in cardiac function, as demonstrated by the above-mentioned figures.

3. SPONTANEOCTS VENTRICULAR TACHY-

CARDIA. A 61-year-old patient with arteriosclerotic heart disease who developed a ventricular tachycardia which was converted to regular sinus rhythm \\:ith the use of a U.C. defibrillator was studied. The studies were repeated 4 days later \vhen ventricular tachycardia recurred. The cardiac output was below the limits of normal during the ventricular tachycardia (3.92 L. per minute), with a marked reduction in stroke volume to 27 ml. per beat. The heart rate was 144 beats per minute (Fig. 15). Conversion to regular sinus rhythm resulted in no significant change in cardiac output, peripheral resistance, and ventricular power. The stroke volume, ejection time, and stroke power increased by 70, 24, and 40 per cent, respectively. Heart rate, mean arterial pressure, and tension- time index decreased by 56, 4, and 35 per cent, respectivelv (Figs. 16 and 17). Variations in the peripheral pulse pressure were present, with changes in the systolic pressure of greater magnitude than those observed in the diastolic pressure. This same type of response was reproduced in the second study.

4. COMPLETE HEART BLOCK ANI) ARTIFICIAL

PACING. Cardiac functions were determined in 18 patients with complete heart block in whom an ectopic right ventricular focus at various fixed frequencies was induced by means of an electrode catheter placed in the right ventricle and connected to an external pacemaker. At a fast ventricular rate this type of rhythm is some- what identical to ventricular tachycardia. These patients were studied at slow ventricular rates and during progressive increases in heart rate to a maximum of 12.5 beats per minute.

At a slow ventricular rate the cardiac output \vas abnormally Ioa-. The right atria1 pressure, right ventricular systolic pressure, pulmonary and systemic resistances, stroke volume, and ejection time were significantly increased above the normal figures. With an increase in the rate of ventricular stimulation a bell- shaped type of curve was obtained, with a peak response occurring at a rate of

Fig. 16. Cardiac output (C.O.), stroke volume (S. V.), stroke power (S.P.), and heart rate (H. Rate) during ventricular tachycardia and after conversion to sinus rhythm. See Fig. 17.

Fig. 17. Ejection time (E.T.), mean brachial arterial pressure (BA .-wean), peripheral resistance (I’. Res.). ventricular power (V.P.), and tension-time index (T.T.I.) during ventricular tachycardia and after conversion to sinus rhythm. See Fig. 16.

stimulation in the range of 62 to 93 beats per minute (average of 76 beats per minute-Figs. 18 and 19). At this range of rate the cardiac index and the mean systemic arterial pressure increased by 67 and 15 per cent, respectively. The stroke index de-

784 Bench&d, Ellis, Dimond, and Wu Am. Heart J. December, 1965

Fig. 18. Average cardiac index (C.I.), stroke index (XI.), central blood volume index (C.B. V.I.), and ejection time (E.T.) in a group of 18 patients with complete heart block. MUX. Resp.: Maximal response. Max. Rate: Maximal rate of pacing. Pacem. Of: Pacemaker off. See Fig. 19.

Fig. 19. Average brachial arterial mean pressure (B.A.-mean pres.), peripheral resistance (P. I&s.), ventricular power (V.P.), and mean systolic ejection rate (M.S.E.R.) in a group of 18 patients with complete heart block. (The legend is the same as that in Fig. 18.)

creased by 20 per cent. There was also a decrease in the peripheral resistance and an increase in the ventricular power, in relation to the control figures obtained at slow rates. A further increase in the rate of artificial ventricular stimulation (maximum rate of 125 beats per minute) beyond the peak response resulted in a 27, 50, 70, and 22 per cent decrease, respectively, in the cardiac index, stroke index, average ventricular power, and ejection time, as compared with the figures obtained at the point of maximal response (average rate of 76 beats per minute). At the same time, the peripheral resistance and mean circulation time increased by 50 and 19 per cent, respectively.

The contribution of atria1 systole to the cardiac functions could be studied in these patients because atria1 systole occurred at various intervals during the cardiac cycle. It was shown that, when atria1 systole occurred 1 to 300 msec. away from ventricular systole, the ejection time, first derivative of the brachial arterial pressure, tension-time index, and brachial arterial

I80 t

8

IOOl- ” . -

1000-

9 . 400 I

ms.c. 100 200 X10 400 IS. TIME INTERVAL P-ORS

Fig. 20. Ejection time (E.T.), brachial arterial systolic pressure (B.P. Syst.), and first derivative of the brachial arterial pressure (Q/O?) as a function of the P-R interval.

Hemodynamic consequences of atria1 and ventricular arrhythmias 785

systolic pressure increased by 13, 14, 33, and 12 per cent, respectively, as compared to when atria1 systole occurred during ventricular systole (Fig. 20).

5. VENTRICULAR TACHYCARDIA IN NORMAL

HEARTS. Four normal subjects were studied and the ventricular rate was controlled by means of an electrode catheter placed in the right ventricle and connected to an external pacemaker. The heart rate was increased from the base-line rate of 60 to 90 beats per minute to a maximum of 125 beats per minute. At the base-line rate the cardiac output, stroke volume, systemic pressure, peripheral resistance, tension-time index, ventricular power, and dp/dt of the brachial arterial pressure were within normal limits. A stepwise increase in heart rate resulted in a stepwise increase in cardiac output and peripheral resistance. The stroke volume, systemic systolic arterial pressure, ejection time, stroke power, average ventricular power, mean systolic ejection rate, and first derivative of the brachial arterial pressure fell significantly. The brachial arterial diastolic pressure and mean pressure, right ventricular systolic and diastolic pressures, tension-time index, and isometric contraction time did not change significantly (Fig. 5).

COMMENTS: Multiple ectopic beats decrease cardiac output because they occur at times in the cardiac cycle when ventricular filling is inadequate to yield a good stroke volume. Variations in atria1 pressure result from regurgitant beats and might account for the sensation of pulsa- tions, fullness, or throbbing in the neck felt by these patients. A vigorous ventricular contraction with a large stroke volume which follows a premature contraction most likely is responsible for the palpitation referred to by these patients. The reduction in stroke volume, pulse pressure, and cardiac output which accompanies ventricular ectopic beats may precipitate congestive heart failure in a borderline compensated heart, such as might occur after acute myocardial infarction. It is unlikely that this would ever happen in a normal heart, however.

It has been shown previously by Wig- gers27 that, in normal hearts, ventricular filling takes place most effectively and rapidly during the early part of diastole.

This period of rapid ventricular filling begins immediately after the opening of the atrioventricular valve and lasts ap- proximately 80 to 140 msec., as demonstrated in the apexcardiogram.18 As the heart rate increases and diastole becomes shorter, rapid ventricular filling, and, thus, stroke volume and cardiac output, will be progressively impaired. In fact, Rushmer and associates2g demonstrated that an increase in heart rate results in a significant decrease in the systolic and diastolic volume of the ventricles.

Experimental studies in dogs by Nakanog and others have shown that a stepwise increase in heart rate in ventricular tachycardia is associated with a stepwise decrease in mean arterial pressure, stroke volume, and cardiac output, and a stepwise increase in pulmonary arterial pressure, left and right atria1 pressures, and pulmonary and peripheral resistances. The decrease in the ventricular function curves seen under these circumstances is also in- directly related to the impairment of myocardial contraction that results from tachycardia-induced hypoxia of the heart.30s3’

Duff and associates32 and Starzl and as- sociates33 demonstrated that, in dogs with complete heart block in which the heart rate was controlled by means of electrical stimulation of the ventricles, the cardiac work increased with the heart rate, reaching a maximum between 120 and 180 beats per minute, and then decreased at higher rates. At rates above 200 beats per minute the cardiac output and systolic, diastolic, and mean systemic pressures decreased. The atria1 pressures also rose at this level of rate. Our observations in patients with complete heart block indicate that the peak response of cardiac output to electrical stimulation of the ventricle occurs at rates in the range of 62 to 93 beats per minute (average of 76 beats per minute). This early peak response is most likely related to the fact that these patients with complete heart block are operating at the peak of their cardiac re- serve and, therefore, do not tolerate \vell great decreases in the diastolic filling time. Thus, any further rise in the rate beyond the critical period of filling time results in a prompt elevation of the atria1 and ventricular pressures, with a decline in stroke volume and cardiac output. In fact, this

786 Benchimol, Ellis, Dimond, und Wu

observation is confirmed by our studies performed in normal subjects in whom artificial and temporary acceleration of the heart rate was accomplished b,- means of an electrode catheter placed in the right ventricle. Their peak response in cardiac output occurred at a faster ventricular rate than that in the group with diseased hearts. Thus, ventricular tachycardia is an arrhythmia of serious hemodynamic con-

-i BP +: si

CONSECUTIVE BEATS.

Fig. 21. Consecutive beat-to-beat variation in the brachial arterial systolic (B.-l. pues.), ejection time (ET.), mean systolic ejection rate (M.S.E.R.), and tensiowtime index (T.T.I.) in one patient with ventricular tachycardia. See Figs. 15 and 16.

sequence in patients with heart disease, because it usually precipitates congestive heart failure. This arrhythmia in otherlvise “normal hearts” does not appear to be of great hemodynamic consequence.

Evolutional changes in experimental ventricular tachycardia have been shown to occur in dogs by Wegria and associates.lKJ6 They demonstrated that, shortly after the onset of tachycardia, compensator>. changes rapidly take place in an attempt to normalize circulatory dynamics. The compensatory mechanism implicated37 is related to stimulation of the sympatho- adrenal system through the activation of the baroreceptors, which promptly respond to a decrease in pulse pressure. As a result of the release of catecholamines, myocardial contractility- is increased, with an increase in the peripheral resistance, venous return, and, eventually, cardiac output.

Of interest is the fact that, for the same range of heart rate, ventricular tachycardia results in a qualitative change m the measured cardiac functions similar to that \vith atria1 tachJ,cardia. The basic difference between the two rhythms appears to be related to the magnitude of the observed changes. The basic physiologic difference bet\veen the t\\-o rhJ-thms resides in the fact that in ventricular tachycardia the atria1 contraction is dissociated from the ventricles, so that this rhythm is basicall). a form of complete heart block. In addition, the sequence of ventricular activation in

Fig. 22. Brachial arterial pressure curve with the heart sounds recorded at the mitral area (Al.1 ) in ;I patient with ventricular tachycardin. See Fig. 20.

Hemodynamic consequences of atria1 and venfricdar arrhythmias 787

ventricular tachycardia follows an abnormal pathway, whereas in atria1 tachycardia the sequence of atria1 and ventricular contraction occurs in a normal fashion. As a result of the asynchronous atria1 and ventricular contractions, patients with ventricular tachycardia have a variable degree of mitral and/or tricuspid regurgitation, which certainly must contribute to the decrease in cardiac functions seen in this condition. The presence of atrial-ventricular dissociation in ventricular tachycardia also explains the beat-to-beat variations in systolic arterial pressure, ejection time, tension-time index, and mean systolic ejection rate (Figs. 21 and 22). The variations in systolic pressures and the changes in the amplitude and character of the heart sounds are useful adjunct signs for the diagnosis of this condition.

The hemodynamic changes described during artificially induced ventricular tachycardia in normal hearts may not be of the same nature and magnitude as the changes observed during spontaneous ventricular tachycardia in diseased hearts. This is primarily related to the fact that homeo- static mechanisms are operating fairly well during the initial phase of ventricular tachycardia, and that they worsen after the paroxvsm has lasted for a prolonged period of time.

Summary and conclusions

1. Cardiovascular hemodynamics were described in 32 patients with various forms of atria1 and ventricular arrhythmias.

2. It was shown that paroxysmal atria1 tachycardia resulted in no significant changes in the cardiac output. Artificially induced atria1 tachycardia caused a significant rise in the cardiac output, mean systemic pressure, tension-time index, and stroke power up to a range of rate from 90 to 110 beats per minute. Further increase in the rate resulted in a slight fall in the cardiac output, with a significant decrease in the stroke volume, peripheral resistance, ejection time, and stroke power.

3. Conversion of atria1 fibrillation to sinus rhythm resulted in no significant changes in the cardiac output at rest. During exercise, the cardiac output rose under both circumstances. Stroke volume, heart rate, mean systemic arterial pressure, peripheral

resistance, ventricular power, and tension- time index showed greater changes during exercise in the group with sinus rhythm than in the group with atria1 fibrillation.

4. Multifocal ventricular pretnature contractions and ventricular bigeminal rhythm resulted in a significant fall in the cardiac output, stroke volume, central blood volume, mean systemic pressure, ventricular power, and stroke power.

5. Spontaneous ventricular tachycardia caused no significant changes in the cardiac output, but a marked decrease in the stroke volume, ejection time, and stroke power.

6. Patients with complete heart block and slow ventricular rates showed a markedly diminished cardiac output, with an increase in the right atrial, ventricular, and pulmonary arterial pressures and the stroke volume. With an increase in the ventricular rate a bell-shaped curve for the cardiac output was observed, with a peak response occurring at a rate of stimulation of 62 to 93 beats per minute.

7. In patients lvith complete heart block, properly timed atria1 contractions (P-R interval of 1 to 300 tnsec.) resulted in a significant rise in the ejection time, mean systolic ejection rate, tension-time index, and brachial arterial pressures.

8. Thus, it is concluded t,hat, in general, atria1 arrhythmias are of less consequence to the cardiac functions than are ventricular arrhythmias. Atria1 systole is important to the cardiac functions in man as long as the atria retain the ability to contract appropriately.

\t:e wish to thank Miss Marilyn Hanna, Mrs. Mary Vensel, Miss Shirley Cardwell, and Miss Ann \Vall for their technical assistance.

REFERENCES

Benchimol, ii., Li, Y. B., Dimond, E. G., Voth, R. B., and Roland, A. S.: Effect of heart rate. exercise and nitroglycerin on the cardiac dynamics in complete heart block, Circulation 28510, 1963. Benchimol, A., Li, Y. B., and Dimond, E. G.: Cardiovascular dynamics in complete heart block at various heart rates. Effect of exercise at a fixed heart rate, Circulation 30543, 1964. Benchimol, .I., Palmero, H. *A., Liggett, M. S., and Dimond. E. G.: Influence of digitalization on the contribution of atria1 q&e to the cardiac dynamics at a fixed ventricular rate, Circulation 32:84, 1965. Benchimol, A., Lowe, H. M., and Akre, P. R.:

788 Benchimal, Ellis, Dimond, and Wu Am. Heart I. December, 1965

Cardiovascular response to exercise during atria1 fibrillation and after conversion to sinus rhythm, Am. J. Cardiol. 16:31, 1965.

5. Benchimol, A., Akre, P. R., and Dimond, E. G.: Clinical experience with the use of computers for calculation of the cardiac output, Am. J. Cardiol. 15:213, 1965.

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13. Wegria, R. C., Frank, C. W., Wang, H. H., and Lammerant, J.: The effect of atria1 and v.entricular tachycardia on the cardiac output, coronary blood ilow and arterial blood pressure, Circulation Res. 6:624, 1958.

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man. A clinico-physiologic correlation, ,qM. HEART J. 68:153,1964.

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36. U’egria, R., Frank, C. W.. Wang, H. H., and Kantcr, D. M.: Effect of auricular and ventricular tachycardias on cardiac output, coronary ilow and arterial blood pressure, Fed. hoc. 12:1.51, 1953.

37. Nakano, J., Zekert, H., Griege, C. W., Wang, K. M., Schaefer, H. S., and Wegria, R.: Effect of ventricular tachycardia and arteriovenous listula on cathecholamines blood level, .4n1. J. Physiol. 200:413, 1961.

hemodynamic consequences of atrial and ventricular arrhythmias in man

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