Arthur J. Linenthal

Termination of Ventricular Fibrillation in Man by Externally Applied Electric Countershock

VENTRICULAR fibrillation is usually a rapidly fatal arrhythmia that may occur in cardiac patients, in any patient under anesthesia and in drowning and electrocution. In cardiac patients it is a frequent cause of sudden death in the course of coronary-artery disease, a well recognized mechanism of Stokes–Adams attacks, an uncommon toxic reaction to digitalis, quinidine and procaine amide, an occasional terminating event in ventricular tachycardia and a rare, but dreaded, complication of cardiac catheterization. In the operating room ventricular standstill is the usual initial mechanism of cardiac arrest, but ventricular fibrillation occasionally occurs,1 particularly during hypothermia or during anesthesia with .xa0.xa0.

Treatment of unexpected cardiac arrest by external electric stimulation of the heart.

CARDIAC arrest may occur unexpectedly during various diagnostic and therapeutic procedures, particularly under anesthesia. Though infrequent (1 in every 500 to 5000 operations1 , 2), each accident is a catastrophe. Despite the wide, active interest in this problem current therapy is too often unsuccessful. The commonly recognized mechanisms of cardiac arrest are ventricular standstill and ventricular fibrillation; standstill is the usual cause. In a compilation of 1200 cases of cardiac arrest, Stephenson et al.3 placed the occurrence of standstill at 88 per cent. Of 141 cases4 5 6 7 8 in which the mechanisms were specifically diagnosed by electrocardiograms or direct observations of the heart, .xa0.xa0.

Persistent ventricular pacemaker following basal skull fracture: Report of a Case in a 5-year-old girl

Abstract An unusual case of paroxysmal ventricular tachycardia is presented. The unusual features are: (1) its probable connection with the basal skull fracture, (2) its duration to the time of writing in an otherwise perfectly healthy child, (3) the patients age at the onset of the arrhythmia, 512years, (4) the prolonged administration of quinidine without ill effects, (5) the serial studies with electrocardiographic tracings and plasma level determinations leading to the determination of the effective quinidine plasma level in a child, and (6) the ineffectiveness of procaine amide on the arrhythmia. The persistence of the ectopic focus over a year since its onset suggests that a concept of persistent ventricular pacemaker is probably a better one than that of paroxysmal ventricular tachycardia in this particular case.

Ventricular Fusion Beats during Electric Stimulation in Man: Application to Conduction Velocity and Anomalous AV Excitation

Quantitative studies of ventricular fusion beats were made in 40 patients with Stokes-Adams disease after implantation of electric pacemakers in the left ventricle. The two fusing complexes came from an electric pacemaker and either a second electric pacemaker or a conducted sinoatrial beat. The limit of fusion, that is the maximal time between two fusing complexes, gives a measure of the conduction time and velocity between the two points of initial ventricular depolarization.Conduction between two electric pacemakers and in retrograde direction from an electric pacemaker to the point of entry of a conducted beat was by way of ordinary myocardium; its velocity was about 1 meter per second. Conduction in antegrade direction, on the other hand, was by way of specialized Purkinje tissue; and its velocity was 4.5 to 9 times faster.Variations in conduction times with bundle-branch block support this interpretation: retrograde conduction time did not change; antegrade conduction time was prolonged in left but was usually unchanged in right bundle-branch block.The morphologic similarities of fusion beats in our patients to the features of anomalous AV excitation add strong evidence in man to the previous analogous experimental observations that the WPW complex is a fusion beat. Furthermore, quantitative comparison of WPW and our fusion beats supports the theory that the anomalous excitation in the WPW phenomenon, like the peripherally located artificial stimulus, enters the ventricle peripherally, by way of an accessory AV pathway.

Resuscitation from cardiac arrest due to digitalis by external electric stimulation.

Abstract A case of cardiac syncope due to digitalis intoxication is reported in which episodes of cardiac standstill were terminated by external electric stimulation of the heart. Atropine was of value in accelerating atrioventricular nodal rhythmicity and in hastening the return of sinoatrial activity, thereby probably preventing further seizures.

Sinoauricular nodal depression and atrioventricular nodal rhythm due to quinidine

Abstract Conclusive proof is presented that cessation of sinoauricular control of the heartbeat with immediate development of atrioventricular nodal rhythm was due to quinidine, in a 50-year-old man with premature ventricular beats and short paroxysms of ventricular tachycardia following an acute myocardial infarction. This cardiac phenomenon was definitely related to the administration of quinidine on three separate occasions, although the doses were moderate and the plasma concentration was not high. The changes of pacemaker were abrupt and could not be foreseen despite frequent electrocardiograms. Although unassociated with symptoms in this patient, and quickly reversible when the drug was stopped, such an effect of quinidine is potentially serious.

Quantitative Studies in Man of the Cardiovascular Effects of Reflex Vagal Stimulation Produced by Carotid Sinus Pressure

In a two year period the effect of carotid sinus pressure on auriculoventricular conduction in a 70 year old man with angina pectoris increased markedly. At first, right carotid sinus pressure gave only P-R interval prolongation. Two years later, pressure on either side produced dropped beats. The maximum effect on the sinoauricular rate remained the same. No other change could be detected in the patients heart during this period. The site of the cause of the increased vagal effect was either in the intrinsic cardiac nerves to the atrioventricular node or in the node itself.