The Effect of Atrial and Ventricular Tachycardia on Cardiac Output, Coronary Blood Flow and Mean Arterial Blood Pressure

Abstract

The effect of electrically induced auricular and ventricular tachycardia of various rates was studied in the anesthetized dog. When, the control heart ranging between 140 and 190 per minute, atrial tachycardia of a rate only slightly higher than the control rate was induced, a very temporary initial decrease in arterial blood pressure, cardiac output and coronary blood flow occurred, then all three parameters essentially returned to control level. With atrial tachycardia of a higher rate, blood pressure, cardiac output and coronary flow fell more markedly, then blood pressure and cardiac output rose to or toward control level, remaining below control level with higher rates of tachycardia, whereas the coronary flow rose to or above control level and only exceptionally remained below control level. Ventricular tachycardia had essentially the same effects as atrial tachycardia, but a ventricular tachycardia of a given rate had the same quantitative effect as an atrial tachycardia of a higher rate.A LTHOUGH there has been a great deal of work on the effect of changes in heart rate on the coronary circulation, most of it has been done on artificial preparations such as the isolated heart or the heart-lung preparation. Since under average cardiovascular conditions, more coronary flow occurs during diastole than during systole, it would be expected that, within certain Limits, an increase in heart rate per se would tend to decrease the amount of coronary flow per minute, and a decrease in heart rate would tend to increase it. This was proved to be correct by Anrep and Hiiusler 1 who found that an increase iu heart rate decreased the coronary flow in the heart-lung preparation in which a coronary artery was perfused under constant pressure. However, these authors also found that if the heart rate was so high that each beat became very weak, the decrease in coronary flow, due to the relatively greater shortening of diastole than of systole, might be offset by the decrease in the restriction of flow due to systole, and that the coronary flow might remain unchanged or even increase instead of decreasing as the heart rate increased. On the other hand, in experiments by Anrep and King 2 on the denervated heartlung preparation, and by Anrep and Segall 3 on the innervated heart-lung preparation, changes in heart rate within wide limits were found to have no effect on the coronary flow. Different results were later reported by Hausner, Essex, Herrick and Mann,4 who obseryed that an increase in coronary flow resulted from an increase in heart rate in the denervated heart-lung preparation. Wegria and Keating 5 reported that an increase in heart rate in the anesthetized dog produced a very temporary decrease in coronary flow followed by a rise above control level within wide ranges of tachycardia. More recently, Laurent, Bolene-Williams, Williams and Katz 0 studied the effect of heart rate on the coronary circulation in a preparation in which the output of the right ventricle consisted only 624

Hemodynamic effects after conversion of arrhythmias

“…However, the changes in rate were less in the present study than in those studies which demonstrate a clear relation between coronary flow and heart rate (49,50). The failure to find any significant change in the coronary blood flow after conversion of atrial fibrillation to sinus rhythm is compatible with the results of Wegria who demonstrated in the open-chest dog that electrically induced atrial or ventricular tachycardias usually produced no change or a slight increase in the coronary blood flow (51,52). Corday, Gold, DeVera, Williams, and Fields, however, believed that a decrease in the systemic blood pressure associated with tachycardias resulted in a decrease in coronary blood flow (53).…”

Effects of pacing location on coronary circulation in dogs.

“…Previous reports have consistently demonstrated a marked augmentation of coronary blood flow by rapid heart rates in both atrial and ventricular pacing (Wegria et al 1958;Maxwell et al 1958;Pitt and Gregg 1968;Cobb et al 1969). …”

“…The data suggest that the coronary circulation would be affected by ventricular pacing because of the decreased perfusion pressure. However, there have been few reports as to whether the pacemaking site of the ventricle influence the coronary circulation (Wegria et al 1958;Badeer and Feisal 1965;Bache et al 1970). It has been well known that the coronary circulation normally responds to increased myocardial oxygen demand with an increase of coronary blood flow (Eckenhoff et al 1947).…”

An analysis of the coronary vascular responses to catecholamines, using a modified Langendorff heart preparation

“…Wiggers (1954) would again contradict this view, claiming that tachycardia increases coronary flow by a massaging effect. Furthermore, tachycardia in the intact heart also improves the coronary flow because of an increased cardiac output (W6gria, Frank, Wang & Lammerant, 1958;Lewis, Coffman & Gregg, 1961). Catecholamines therefore appear to cause an initial resistance to coronary perfusion, firstly by a direct vasoconstriction mediated by a-adrenoceptors and secondly due to extravascular compression during the rate and force increases.…”