Abdo Bisteni

Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block (right and left), ventricular premature beats and wolff-parkinson-white syndrome

Summary The diagnostic difficulties in the recognition of myocardial infarction in the presence of bundle branch block and the Wolff-Parkinson-White syndrome are discussed. However, through a “deductive” approach in the analysis of the electrocardiogram, such difficulties may be eliminated to a great extent. The knowledge of the sequence of cardiac activation in normal and abnormal circumstances as in bundle branch block, “pre-excitation syndrome”, and extrasystolia, is fundamental. To sum up, the “deductive” approach to clinical electrocardiography not only facilitates the general diagnosis but also indicates the limitations in arriving at a precise diagnosis of infarction.

VENTRICULAR PREMATURE BEATS IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION.

The importance of ventricular premature beats (VPB) in the clinical diagnosis of myocardial infarctions has been pointed out by several authors. Dressler (1943) reported a case in which the electrocardiographic signs of infarction were present in such beats (deep and slurred Q waves in lead III) and absent in the sinus beats. Simonson et al. (1945), Bellet (1953), Scherf and Schott (1953), Katz et al. (1958), Silverman and Salomon (1959), and Anttonen et al. (1959) recognized that myocardial infarctions can be diagnosed from VPB and, at times, even earlier from these cycles than from the sinus beats. The similarity of ventricular activation in VPB and in right bundle-branch block (RBBB) and left bundle-branch block (LBBB) has long been accepted. Consequently, VPB with unipolar patterns of LBBB are right VPB, and VPB with patterns of RBBB are left VPB. The same considerations apply also for supraventricular premature beats (SVPB) with aberrant conduction, since the aberration is due to some degree of either RBBB or LBBB (Bisteni et al., 1960). Thus, right VPB and SVPB with aberration similar to that in LBBB are analysed in the same manner as sinus beats with LBBB. In fact, in these three situations the process of ventricular activation follows a similar sequence: the right ventricle is activated before the left. This type of reasoning applies also for left VPB, RBBB, and SVPB with RBBB: in these three instances the left ventricle is activated before the right. A better knowledge of the ventricular activation process in normal conditions and in bundlebranch block has served for a new approach to the diagnosis and localization of myocardial infarctions. Sodi-Pallares et al. (1957, 1960) have shown that tracings with electrical signs of infarction are better understood when analysed in the light of recent studies concerning the ventricular activation process (Sodi-Pallares et al., 1955; Medrano et al., 1956, 1957, and 1958). It has been demonstrated also that septal infarctions may be more easily recognized in the presence of bundle-branch blocks (Sodi-Pallares, 1956), in contrast with the view generally held. On the basis of these considerations the significance of experimental and clinical VPB in the diagnosis of myocardial infarction is studied in this paper.

Effectiveness of Nupercaine Hydrochloride and Phenobarbital Sodium in the Suppression of Ventricular Tachycardia Associated with Acute Myocardial Infarction

In 22 dogs with ventricular tachycardia accompanying myocardial infarction, Nupercaine hydrochloride was found to be a potent suppressor of ectopic impulses. When used alone Nupercaine also produced vomiting and convulsive movements. When combined with morphine, vomiting was eliminated, but convulsions still occurred. When combined with phenobarbital sodium or pentobarbital sodium, the ectopic impulse suppressor action of Nupercaine was enhanced and both vomiting and convulsive movements were prevented. The duration of ectopic impulse suppressor action was significantly greater in the phenobarbital-Nupercaine experiments than in any other group. No deaths occurred.

Dibucaine hydrochloride in the control of K-strophanthoside-induced ventricular tachycardia and other toxic manifestations.

Dibucaine hydrochloride in relatively small doses terminated high frequency ventricular tachycardia induced by toxic doses of K-strophanthoside in 9 of 10 dogs. Dibucaine was antidotal to glycoside-induced vagotonia and improved the alertness and apparent general condition of the animals that received it. One death occurred in the 10 strophanthoside tachycardia animals treated with dibucaine, a mortality rate of 10 per cent. Four deaths occurred in seven dogs that received similar doses of strophanthoside but no dibucaine, a mortality rate of 57 per cent.

The Electrical Activity of the Heart and Brain Under Acute Experimental Anoxia: The Protective Effect of Polarizing Solutions

Acute anoxia was produced in 80 dogs under anesthesia with sodium pentobarbital. Respiration was maintained with a Palmers pump through an endotracheal tube. The anoxia was produced by stopping the pump and occluding the endotracheal tube. Polarizing solution (glucose-potassium-insulin) was perfused in 40 of the animals, starting three hours prior to the anoxia. The remaining 40 dogs comprised the control group. Peripheral electrocardiograms, as well as electroencephalograms, were simultaneously recorded before and during the period of anoxia. Recordings were continuously obtained until no more than one ventricular complex in a ten-second period was observed, even though the electrical brain activity had disappeared by this time. Our present experimental work suggests the beneficial effect of polarizing solutions by delaying the anoxic degradation of the electrical phenomenon of the heart and the brain.