Changes of ventricular impulse formation during carotid pressure in man.

THERE appears to be general agreement that in the mammalian heart vagal stimulation has no effect on ventricular contractility. This was demonstrated by Drury2 who used the myocardiograph of Cushny and was confirmed by optical determination of the intraventricular pressure of the artificially driven heart; when a cardiac alternans existed and weak faradic stimulation of the cardiac sympathetic nerves for a few seconds abolished the alternans and strengthened the contractions of the ventricle, stimulation of the vagus nerves with the strongest possible currents was devoid of effect.'0 Maximal stimulation of either vagus or of both simultaneously had no effect on ventricular excitability or conduction velocity of the dog heart.6 However, some instances are mentioned in the literature where vagal stimulation apparently has had an effect on ventricular ectopic impulse formation. Thus, a ventricular paroxysmal tachycardia was repeatedly abolished by carotid pressure.19 In this case it may be argued that it was not the increase of vagus tonus during the carotid pressure, but the simultaneous decrease of sympathetic tonus' which caused the action. In a patient with complete A-V heart block, ventricular tachycardia and ventricular fibrillation were registered during attacks of the Stokes-Adams type.'7 These attacks appeared during straining at stool and could always be induced by gentle digital stimulation of the rectum. The action of an autonomic reflex can hardly be excluded and the vagus nerves may have played a part. The ap-