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The effects of electrical stimulation of the vagus nerves and the administration of atropine on ventricular fibrillation threshold (VFT) were studied in open-chest hearts of 15 dogs anesthetized by alpha-chloralose. These studies were made in both normal and ischemic ventricles, i.e., before and during acute coronary occlusion. The ventricles were paces at a constant rate to eliminate rate-dependent changes and the minimal current required to induce ventricular fibrillation (or VFT) was determined by delivering a train of rapid rectanglular pulses (100 per second) to the venticle actoss the vulnerable period. In normal ventricles, VFT's were significantly increased by vagal stimulation (P less than 0.01) and decreased by atropine (P less than 0.05). Coronary occlusion markedly decreased VFT's (P less than 0.01), and vagal stimulation or atropine failed to alter VFT's significantly in these ischemic ventricles (P greater than 0.8). In additional 14 dogs, the effects of vagal stimulation and atropine were studied after the administration of propranolol. Propranolol alone increased VFT's significantly in boetreatment with propranolol, vagal stimulation and atropine failed to change VFT's significantly in both normal and ischemic ventricles (P greater than 0.8). These results indicate that the vagus nerves exert their effect on VFT by modifying the sympathetic nerve activity in normal ventricles, but such an effect is not significant enough to alter VFT in ischemic ventricles.

A multifactorial analysis was used in anesthesized dogs in order to characterize the effects of the duration of overdrive, the atrial pacing interval, and the frequencies of vagal and sympathetic stimulation on overdrive suppression of the sinus node. The sinus node recovery time (SNRT) and the summated effect (SE) over the first 20 cardiac cycles were measured with various combinations of the independent variables. We conclude that (1) both the rate and the duration of overdrive have significant effects on SNRT and SE; (2) vagal stimulation has greater effects on SNRT and SE than does the rate or duration of overdrive; (3) sympathetic stimulation had only a small effect on overdrive suppression; and (4) there were significant interactions between vagal stimulation and the duration of overdrive and between the duration and rate of overdrive, but not between sympathetic and vagal stimulation.

The electrocardiographic tracings taken from a sixty-six-year-old man who had no cardiac symptoms showed a typical bundle-branch block which abruptly disappeared with the spontaneous occurrence of 2:1 A-V block, and which disappeared after cardiac slowing, the result of indirect vagal stimulation. This is the fourth instance of proved type 2 bundle-branch block to be reported. It is believed that the conduction disturbance in this instance was primarily the result of fatigue of the bundle and that the depressed tissue was small in extent.

A reduction and an acceleration of the cardiac rate were, within certain limits, associated with a decrease and an increase in the rate of the coronary circulation. The most striking changes in the rate of the coronary flow were observed in those instances in which relatively great changes in cardiac rate were induced. It is suggested, however, that a heart cannot be progressively accelerated to extreme degrees with an accompanying increase in the coronary circulation. In the very slow cardiac rates induced by vagal stimulation, the rate of flow from the coronary sinus was reduced from 20 to 30 per cent below that observed during the control period. The production of auricular or ventricular premature contractions did not have any significant effect on the rate of flow from the coronary sinus. In auricular fibrillation, the rate of the coronary circulation either remained fairly constant or was moderately accelerated. The results seemed to depend on the rate and the force of the ventricular contractions associated with the absolute irregularity.

1. 1. Two cases of complete heart-block are described. Both showed defective bundle-branch conduction, with gradual transitions in the form of the ventricular complex. 2. 2. The curves have a remarkable similarity to those described by Wilson and Herrmann after the experimental production of bilateral bundle-branch block. 3. 3. By the algebraic summation of levocardiogram and dextrocardiogram in varying time relations one to the other, it was found possible to reproduce the transitional complexes for each patient. In this manner the relative amount of delay in the development of levocardiogram or dextrocardiogram was calculated for each strikingly aberrant complex. 4. 4. The phenomenon is briefly discussed and it is concluded that the most likely explanation consists in a change in leadership of the predominant pacemaker from one side of the heart to the other. 5. 5. Various procedures, such as vagal stimulation and paralysis and the administration of adrenalin and digitalis, failed to reproduce the phenomenon in one case which was observed to occur spontaneously. 6. 6. The postmortem findings are described in one case. Examination of the heart showed that the conducting tract was in a sclerosed state without definite interruption of its continuity.

1. 1. Atrial fibrillation has been produced in dogs subjected to various degrees of hypothermia by (a) vagus stimulation; (b) intravenous epinephrine injections; and (c) vagus stimulation following epinephrine injections. 2. 2. Epinephrine injections produced fibrillation only when functional vagi were present and vagal stimulation following epinephrine injections was more effective than either procedure alone. 3. 3. Epinephrine is believed to cause fibrillation (a) by causing reflex vagus excitation; and (b) by exciting ectopic atrial extrasystoles. 4. 4. There is no evidence that hypothermia affected the production of atrial fibrillation by these means.

The relationship of anoxemia of the auricles and vagal stimulation (mecholyl effect) was investigated in the hearts of dogs. In the normally beating heart it was found that: (1) anoxemia apparently renders the heart more sensitive to the action of mecholyl; (2) auricular fibrillation frequently occurs spontaneously, or is easily induced by minute, mechanical, auricular stimuli after small doses of mecholyl during anoxemia; (3) reoxygenation of the blood results in the restoration of normal cardiac mechanism. In another series of experiments, the factor of auricular distension was eliminated by perfusing the coronary vessels of the heart while the heart was beating empty; the administration of mecholyl during perfusion with anoxic blood produced auricular fibrillation. Mecholyl also produced auricular fibrillation in hearts with acute, experimental “mitral stenosis.” The possible mechanisms by which auricular anoxemia, together with the action of mecholyl, may precipitate atrial fibrillation are discussed, and the clinical aspects considered.

In ten dogs the effects of acetylcholine, graded vagal stimulation, and heart rate on both antegrade and retrograde His-Purkinje conduction were evaluated. His bundle pacing was used to obtain the antegrade His-Purkinje conduction time and pacing the ventricle and recording the retrograde His bundle electrogram gave the retrograde His-Purkinje conduction time. Acetylcholine and vagal stimulation sufficient to produce cardiac arrest had no effect on antegrade and retrograde His-Purkinje conduction. Similarly, pacing at cycle lenghts varying from 400 to 200 msec. had no effect on antegrade or retrograde conduction time. However, when the cycle length of ventricular pacing was decreased to less than 200 msec. various degrees of retrograde His-Purkinje conduction delay and block developed.

The electrical activity of the A-V node, the N potential, was recorded in 30 openchested intact dog hearts using close bipolar recording wires. The N potential was recorded as a slow biphasic wave which was contiguous with the atrial and His-bundle electrograms. The most characteristic feature of the N potential was the notching. The earliest activity of the N potential was recorded during the upstroke of the P wave of the surface ECG. During A-V conduction delay, induced by vagal stimulation, atrial pacing, and a combination of these two maneuvers, there occurred an increase in the N potential duration and a loss of N potential amplitude. A-V nodal activity was also recorded during retrograde conduction. Evidence is presented which suggests that the bundle of His and not the A-V node is the pacemaker site in A-V junctional rhythms.

The question whether or not the main branches of the His-Tawara bundle are subject to the influence of the vagus nerves is as yet unsettled. Drury and Mackenzie 1 were unable to demonstrate any effect on branch conduction, either by the use of acetylcholine or by stimulation of the vagi in the neck, in normal dogs. If, however, either the right or the left branch was injured mechanically, bundle branch block complexes appeared in the electrocardiogram for a short period of time, after which what appeared to be full recovery occurred. At a critical period following this recovery, bundle branch block complexes could be made to reappear by stimulation of the vagi in the neck. The authors attributed this effect to action of the vagus on the junctional tissues, rather than on the bundle branches. They thought that vagal stimulation increased the "decrement" through the A-V node and the main bundle, and consequently the impulse arrived at the still partially damaged branch too weak to pass, whereas it passed the undamaged branch readily. This report deals with a patient, one of whose bundle branches was damaged but was still capable of fluctuation in conductivity.

1. 1. In normal adults the administration of strophanthin, of acetylcholine, and vagal stimulation cause the same electrocardiographic changes in the same subject, viz., bradycardia, relative shortening of electrical systole, and, when the bradycardia is pronounced, changes in the P-waves in Leads II and III. 2. 2. The fact that the changes in the electrocardiograms following vagal stimulation and the administration of acetylcholine are identical indicates that acetylcholine is the vagus substance. 3. 3. The changes in the electrocardiogram following the administration of strophanthin may be harmonized with the hypothesis that strophanthin sensitizes the heart muscle to acetylcholine.

1. 1. A case of reversed reciprocating paroxysmal tachycardia is described. 2. 2. This arrhythmia was very sensitive to vagal stimulation, which caused interesting patterns of group beating. 3. 3. The mechanism of reversed reciprocal rhythm is explained on the basis of an anomalous pathway and a degree of anterograde block through the A-V node. 4. 4. A hypothesis is advanced linking reversed reciprocal rhythm with the WPW syndrome.

The occurrence of a ventricular fibrillation upon carotid sinus pressure with spontaneous cardiac recovery is reported in a patient with auricular fibrillation, who had signs and symptoms of severe myocardial degeneration. The newer physiology of the carotid sinus pressure test and its relationship to clinical medicine are briefly mentioned. The pathological physiology of ventricular-rate changes by vagal stimulation in auricular fibrillation is described and the effect of vagal stimulation upon lower automatic centers in ventricular musculature is discussed. It is suggested that the occurrence of ventricular fibrillation in this patient is additional evidence in support of the concept that vagal stimulation, from whatever cause, will produce idioventricular arrhythmias in diseased ventricular musculature.

There are clinical criteria that enable one to make a bedside diagnosis of paroxysmal ventricular tachycardia. These are slight irregularities in the rapid heart rhythm which otherwise appears quite regular, a changing quality and intensity of the first heart sound as heard at the apex, and the failure to slow the heart by vagal stimulation. This condition previously has been considered unrecognizable except by the use of electrocardiograms. There are instances where the differentiation between this condition and paroxysmal auricular tachycardia is of great importance.

The electrocardiographic alterations occurring in normal males during norepinephrine-induced hypertension, before and after the administration of atropine sulfate, are reported. The possible mechanisms of the observed changes are discussed, but no specific conclusions can be reached. Further studies are indicated which may help to elucidate the mechanism of formation of the electrocardiographic “acute strain” pattern. It will be necessary to dissociate the direct myocardial effects of norepinephrine from its hypertensive action and from the marked reflex vagal stimulation which it produces. Since norepinephrine probably plays a significant role under conditions of stress, our results indicate that fluctuations in the contour of the electrocardiogram may at times be explained by norepinephrine secretion.

An overdose of digitalis “can cause practically any form of arrhythmia.” 1 Auricular ectopic rhythms, however, have not been shown to occur with any frequency or to manifest any specific form as a consequence of digitalis intoxication. In our experience in patients with advanced congestive heart failure, one form of auricular arrhythmia is a relatively common manifestation of serious digitalis intoxication. 2 On the basis of the electrocardiographic pattern, the abnormal rhythm has been named paroxysmal auricular tachycardia with block . The following features have been used to distinguish it from other types of rapid heart action: (1) an auricular rate of 150 to 250 per minute, (2) varying degrees of atrioventricular block, (3) an isoelectric baseline between the P waves, (4) diminution of the atrioventricular delay by exercise, (5) augmentation of the delay by vagal stimulation, and finally (6) a tendency for the tachycardia to persist for days or even months. Thus this arrhythmia exhibits some of the features ascribed to both auricular tachycardia and flutter. 3,4 It has been shown that changes in body potassium alter the threshold of the heart to the toxic action of digitalis. 5 Ventricular premature beats caused by an excess of digitalis can be stopped by potassium administration. 6,7 Conversely potassium loss, irrespective of how this is achieved, may precipitate digitalis intoxication in patients on maintenance digitalis therapy. 8 If auricular tachycardia with block is caused by digitalis overdosage, a relationship between this arrhythmia and the potassium balance of the body should be demonstrable. It should be possible to abolish the tachycardia by the administration of potassium and to induce it by depleting body potassium. It is the purpose of this communication to outline such experience gained in the wards of the Peter Bent Brigham Hospital during the past year.

Ventricular extrasystolic tachycardias were provoked by focal application of a hypertonic solution of sodium chloride on the exposed heart of the dog. After these extrasystoles subsided, faradic stimulation of the right vagus nerve made them reappear. This effect was reproducible. The extrasystoles which were observed during vagal stimulation were identical with those which appeared after the application of sodium chloride. A characteristic feature of these extrasystoles was their unusually high rate.

A case of wandering auricular pacemaker is presented. The evaluation of esophageal leads and of auricular vectorcardiograms further elucidates the path of the stimuli. Whereas one rhythm seems to originate in the caudal part of the auricles, the other one has its origin in the sinus node. At least the first beat after the ectopic auricular rhythm seems to have still a caudally situated point of origin. A few beats are necessary to re-establish a regular pattern of sinus rhythm. The etiologic factors, which may be responsible for this, are discussed. Adrenalin caused an almost complete suppression of the (slower) sinus rhythm. Vagal stimulation (by carotid sinus pressure) in all instances suppressed the ectopic auricular rhythm. It came back immediately after release of pressure.

1. 1. Intermittent second degree auriculoventricular block with the Wenckebach phenomenon has been demonstrated in a patient who does not have organic heart disease. The duration of this phenomenon has been at least 6 years. 2. 2. The effects of atropine and vagal stimulation have been discussed.