Burchell, Howard B.

The artificial pacemaker has been compared to a physiologic ventricular parasystolic focus. In hearts being driven by a pacemaker, in the absence of atrioventricular (AV) block, capture (interference) phenomena are constantly seen. While variations in QRS complexes have been observed when the external pacemaker stimulus occurs early in the T-wave period of a sinus conducted beat, no sequence of aberrant beats has been observed. One patient showed occasional sinus beats interpolated between ventricular beats arising from the artificial pacemaker, and these occurred at a very narrow time band suggesting that AV conduction was permitted by phenomenon of a supernormal phase. At a later date this patient showed also retrograde conduction believed related to a supernormal phase during recovery of junctional tissue penetrated by an impulse entering from above, though the impulse itself was blocked. Records of two patients are used to illustrate grossly aberrant QRS complexes produced by the stimulus of the electric pacemaker when this fell in the semirefractory period. Noteworthy was the presence of a latent period before potentials of the propagated impulse were recorded, there being evident stimulus-to-QRS delays. The situation wherein the rhythm is most chaotic is that where AV block is absent, the sinus rate is fast, and the electric pacemaker rate is relatively slow. In two patients, retrograde activation of the atria occurred as a stable mechanism. In one patient, nodal rhythm of the RP type occurred, and sequences of the records suggested that the AV node might have become synchronized with the extrinsic pacemaker cycle. In this last instance three independent centers of effective impulse formation coexisted, the sinus node, AV node, and stimulating electrodes of the electronic pacemaker. A marked increase in the refractory period of the ventricle, as measured by its response to the set stimulus of the electric pacemaker delivered at varying instants with respect to the sinus mechanism, occurred in one case within a few days. The possibility that reserpine therapy contributed to this change is possible but has not been established, for the effective refractory period, as measured, later remained constant over a period of many weeks.

Among 60 necropsy specimens of isolated ventricular septal defects and more than 300 cases of ventricular septal defect observed at operation, 15 cases demonstrating unusual anatomic positions of the defect were found. The ventricular defect differed from the ordinary ventricular septal defect in that it usually occupied the position of the ventricular component of the defect in persistent common atrioventricular canal. For this reason it was named ventricular septal defect of the persistent common atrioventricular canal type. Deformities of one or both atrioventricular valves were common (nine of 15 cases). No atrial septal defects of the ostium primum type were present. Anatomic studies of the conduction tissue revealed that this tissue skirted the posterior and inferior aspects of the ventricular septal defect and that, as in persistent common atrioventricular canal, the course taken by the conduction tissue was unusually long, as a result of the peculiar posteroinferior position of the lower edge of the defect. The electrocardiographic features were striking. In all cases the mean electrical axis of the QRS lay above the isoelectric point; the vector loop obtained in the frontal plane from the scalar electrocardiogram was directed counterclockwise, and its main mass was above the zero line. In addition, in all cases there were signs of right ventricular overload, and in some cases of left ventricular overload as well. Electrocardiographic findings of this pattern have been thought by some authors to be diagnostic of persistent common atrioventricular canal, but we observed that they also occurred in each of the cases of isolated ventricular septal defect of the variety described herein. We recognize that in the usual variety of ventricular septal defect this electrocardiographic pattern occurs, but it does so uncommonly. We have not studied its exact incidence. The anatomy, hemodynamics, and surgical considerations are different in cases with this defect from those with persistent common atrioventricular canal. The surgical risk in these cases has been higher than that in the usual type of ventricular septal defect. In the discussion of the electrophysiologic theories that seek to explain the unusual electrocardiographic patterns in this group of cases, a new theory is offered, based on studies of the conduction system. In our opinion, the different orientation of the advancing fronts of depolarization is the result of congenital displacement of the bundle of His in its relation to the ventricular septal defect.

A definite correlation can be established between the electrocardiogram and the serum potassium level at hypokalemic levels. A study was made at the Mayo Clinic of 130 hypokalemic patients with relatively stable clinical states. Variations in Q-T intervals, P-R intervals, atrial rhythm, P waves, T/R values, and T-wave and U-wave contour in hypokalemia were noted as were the relationships between the T-U complex, electrical repolarization phenomena and potassium metabolism. Since modifying factors such as drugs, certain electrolyte disturbances, variations in cardiac rate, conduction defects, and myocardial ischemia were eliminated by careful selection of patients, only the influence of acid-base imbalance, sodium-potassium ratio, and hypertension on the electrocardiogram was studied. Acid-base imbalance and hypertension often simulated or obscured electrocardiographic evidence of hypokalemia. Electrocardiographic criteria of hypokalemia include various combinations of the following signs: (1) T/U value of 1 or less in lead II or V 3 , (2) U-wave amplitudes of greater than 0.5 mm. in lead II or greater than 1 mm. in V 3 , and (3) S-T depression of 0.5 mm. or more in lead II or leads V 1 , V 2 , and V 3 . It must be remembered that a normal electrocardiogram does not exclude hypokalemia and that an electrocardiogram which fulfills the established criteria does not necessarily indicate hypokalemia unless the factors discussed have been eliminated or minimized.