Reducing Heart Rate of the Dog by Electrical Stimulation

Abstract

1) The frequency of effective ventricular contractions could be reduced by almost 50% in dogs by stimulating the ventricles (or atria) with electrical impulses of long duration (2 volts, 200 to 350 msec). 2) A similar result was obtained when pairs of impulses (2 volts), each 3 msec in duration, were used, with the time interval between the two impulses of the pair similar to that between the make and break of the long impulses (noted above). 3) The dogs were under general anesthesia and positive pressure breathing was maintained. After thoracotomy, platinum electrodes were implanted in the epicardial surface of the right ventricle or atrium. Pressures were measured in all heart chambers and the unipolar electrocardiogram was recorded from the right atrium with a catheter electrode. Several frequencies of stimulation, below the inherent sinus rate, were tested and at each frequency the time interval between pairs of stimuli was progressively increased from 100 to 350 msec. 4) In all dogs reduction of the frequency of the effective ventricular contractions could be obtained with pairs of stimuli 200 and 350 msec apart. Only the make of the long impulse or the first of the pair of short impulses produced an effective ventricular contraction, while the break of the long impulse or the second short impulse stimulated the ventricles so early in the cycle that no effective mechanical contraction followed. However, the refractory period produced by the break prevented the sinus impulse from reaching the ventricles. The several mechanisms involved are discussed. 5) In one dog the reduction of the frequency of the effective ventricular contractions could be maintained during the 24 hours of survival. 6) The method was applied to a patient being treated for Stokes-Adams attacks. Right atrial stimulation produced a noticeable reduction in ventricular frequency. This involved a reduction in the frequency of electrical responses of the ventricles as well, ensuring a reduction of the per minute energy cost and oxygen consumption of the heart. Such a reduction of the frequency of electrical responses of the ventricles could not be accomplished, so far, in the dog by atrial stimulation. 7) Reduction of the frequency of effective ventricular responses was obtained in one dog with induced atrial flutter and in another with a pacemaker induced "parasystolic" ventricular tachycardia by employing an artificial ventricular pacemaker similar to that used with sinus rhythm. 8) The significance of the findings is discussed. This experimental approach suggests a possible method of slowing the heart rate in clinical cases of ventricular or atrial tachycardia refractory to other methods of treatment. 9) Finally, this approach offers a means of studying certain properties of the heart in the dog which may give insight into the mechanisms involved in some of the more complex arrhythmias encountered in man.