Arthur Ruskin

Interatrial and sinoatrial block, with an illustrative case

Abstract Sinoatrial block of two types has been described; (1) with progressive prolongation of sinoatrial conduction time leading to a dropped beat; and (2) dropped beats without such preceding conduction changes. These are strictly analogous to the Wenckebach and the Mobitz types of atrioventricular block. The literature on this subject has been surveyed, together with available information on the postulated anatomic and functional pathways of inter- and intra-atrial conduction. We have postulated that, in the present case, both varieties of sinoatrial block coexist, thus explaining the variable distance between the two types of P waves. Such a hypothesis also requires the assumption of functional pathways between the S-A node and the two atria, with dissociation of the two atria, and with partial dissimilar block between each atrium and the S-A node. Although interatrial dissociation, both partial and complete, and each variety of sinoatrial block have been previously described, so far as we have been able to learn, their coexistence has not been previously noted.

Momentary atrial electrical axes: III. A-V nodal rhythm

Abstract Using a method of analysis of the P wave, recorded in three planes of the chest as previously described, we have studied the curves of the consecutive momentary atrial axes in A-V nodal rhythm. In three dimensions, the curves pass up, back, and to the left. The curves obtained in so-called “coronary” nodal rhythm resemble those of ordinary sinus rhythm, passing down, variably forward, and to the left. The available evidence is surveyed, and it is concluded that this latter type of nodal rhythm is actually merely an example of sinus rhythm with relatively rapid conduction of the impulse through the A-V junctional tissues.

Momentary atrial electrical axes: II. Atrial flutter, atrial fibrillation, and paroxysmal tachycardia

Abstract Curves representing the consecutive atrial electrical axes for each 0.01 second have been derived for the frontal, horizontal, and sagittal planes from patients with atrial flutter, atrial fibrillation, and paroxysmal tachycardia, and three-dimensional models have been constructed. The clinical experimental results of Lewis, Drury, and Iliescu have been reproduced and extended in flutter and fibrillation. The same procedure has been applied in eight cases of paroxysmal tachycardia. The type of curve in this disturbance of atrial mechanism has been found to resemble that obtained during sinus rhythm; it differs only in direction. The characteristic features of flutter and fibrillation are not present. This fails to support the idea that a circus movement is present in paroxysmal tachycardia, and although the possibility of a circus involving the S-A node is not finally excluded, we believe that the weight of the evidence points to the existence of an ectopic site of impulse generation. The available information on the physiology and pharmacology of the atrial musculature and nodal tissues has been reconsidered insofar as it bears on the behavior of paroxysmal tachycardia, and the view that in it an ectopic pacemaker may be operative.

Isolated dextrocardia, with diodrast studies

Abstract 1. 1. A case of congenital isolated dextrocardia, without “mirror-image” inversion of the chambers, but with signs of congenital heart disease and attacks of paroxysmal tachycardia is presented. 2. 2. The expected noninversion of the heart chambers was supported by diodrast and electrocardiographic studies. The “apex” of the heart was shown to be formed by the right (venous) ventricle. The left-sided aortic arch and superior vena cava were also demonstrated by diodrast visualization. 3. 3. The rarity of the long survival of the patient and of the attacks of paroxysmal tachycardia is noted.

Momentary atrial electrical axes

Abstract Curves derived from patients with normal hearts show, in general, a shift of the consecutive atrial electrical axes down, forward, and to the left. The variations in this typical pathway are illustrated in Fig. 4, as well as one exception to this rule, in which there was a shift toward the right before the curve turned to the left. Patients with myocardial disease may show a similar, smooth curve, or, more often, will yield curves which are complex, with multiple changes in direction and contour. Acute myocardial disease, as well as chronic myocarditis, may cause conduction defects which markedly alter the curve. Patients with enlargement of other chambers of the heart which has pushed the right atrium toward the right, or, presumably, with enlargement of the right atrium itself, show curves which point to the right before turning to the left. Dextroposition caused by disease in the lung or pleural space, or congenital dextrocardia, will produce curves which point entirely down and to the right. Correlation of curves obtained by this method from persons with normal and diseased hearts with roentgenologic and necroscopic data is being undertaken. They are described at this time primarily for the purpose of setting up a standard for comparison with curves obtained from patients with atrial flutter, atrial fibrillation, and paroxysmal tachycardia, which are discussed in the second paper of this series.

Momentary Atrial Electrical Axes in Paroxysmal Tachycardia.

A recent study 1 of our cases of paroxysmal atrial tachycardia has shown the presence of some grade of A-V block with dropped ventricular beats in a large proportion of the group. The block varied in duration as well as degree, and seemed most likely to appear in patients who had either severe myocardial disease or digitalis over-dosage. This led us to the observation 2 , which has also been reported by Barker and his associates 3 , that this group of patients was prone to develop atrial flutter or fibrillation, or both, in close association with the episodes of paroxysmal tachycardia with block. These facts logically raise the question of a possible resemblance between the fundamental disturbances of atrial mechanism in these 3 types of arrhythmia. Barker et al. 4 have suggested, in fact, that a circus movement is probably present in each instance. Others have made similar proposals, which have been reviewed elsewhere. 2 , 5 Lewis, after preliminary animal experiments, reported studies of 3patients, 6 one who had flutter and 2 who had fibrillation. Using simultaneous chest leads placed in 3 planes, he was able to calculate the direction of movement of the atrial electrical axis for each 1/50 second. His results are compatible with the presence of a circus movement in flutter and fibrillation, though they can scarcely be said to supply conclusive proof. One possible approach to the above problem seemed to be the analysis of similar tracings, taken in patients with paroxysmal atrial tachycardia. It is fortunate that the electrocardiograms of the patients most likely to show flutter or fibrillation, i.e., those with A-V block during the paroxysm, are best suited for this type of analysis; while the block is present, at least half of the P waves will avoid superimposition on the preceding T wave.

Cardiodepressive effects of thiomerin; cardioprotective attempts with BAL, ascorbic acid and thiamin.

Summary and Conclusion1. In the isolated rabbit heart thiomerin appeared to slow atrio-ventricular and intraventricular conduction and prolong the “electrical systole” (Q-T interval) in doses, as to mercury content, over 200 times those of meralluride, and 1000 or more times those of other commonly used mercurial diuretics. The rapidly cardiolethal dosages bore even larger ratios. Idio-ventricular slowing and asystole, associated with marked cardiac dilatation and failure of contractility, and not ventricular ectopic rhythms, constituted the lethal manifestations of the thiomerin perfused heart.2. In contrast to the marked increase in cardiac tolerance to other organic mercurial compounds as a result of preliminary administration of BAL, and to a lesser extent, of ascorbic acid and thiamin, BAL approximately doubled the cardiolethal dosage of thiomerin and the two vitamins were not significantly cardioprotective against the monothiol mercurial.3. BAL markedly reversed the deleterious conduction effects of...

Recovery Curves of Intraventricular Conduction; QRS Aberration

Summary Data have been obtained from the isolated rabbit ventricle, from which have been drawn recovery curves of intraventricular conduction. Similar curves have been drawn after the injection of strophanthin and of quinidine.

Electrical Systole (Q-T Interval) of Rabbit Heart

Summary Curves have been drawn relating the QT interval to the cycle length for the isolated perfused rabbit ventricle. The effect of strophanthin and of quinidine on these curves has been studied.

Effect of Certain Drugs on Properties of the Human Atrioventricular Node

In reciprocal rhythm an impulse originating in the atrioventricular junctional tissue passes to the ventricle, and in addition by retrograde conduction stimulates the atrium. If the retrograde conduction has been rapid, the cycle terminates; however, if conduction has been slowed, the impulse may find the junctional tissue responsive, and after traversing part of the auricle again stimulate the A-V node and ventricle, producing a reciprocal beat, or “Umkehr-Extr asystole.” Clinical examples of such a mechanism were first described by White, 1 who based his concept of the physiological processes present on the circus mechanism observed earlier by Mines. 2 Reciprocal rhythm has been reported by others, and has been discussed most recently by Scherf. 3 We have recently studied a patient who manifested this type of disturbance, and have taken the opportunity to study the effect of several drugs on the properties of the junctional tissue, presumably in the neighborhood of the A-V node. The clinical features of the case will be described elsewhere, together with certain electrocardiographic findings that may be of theoretical importance. The possibility suggested by Luten and Jensen 4 that some of the reported cases represent a parasystole rather than a reciprocal rhythm, has in this instance been definitely excluded. By measuring the RP intervals of a large number of complexes, we have determined the retrograde conduction time below which reciprocal stimulation of the ventricle did not occur, but above which reciprocal beats were seen. This value we have taken to represent the refractory period of the junctional tissue.