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In the intact, anesthetized dog, an intravenous infusion of 0.02 U/kg body weight/min of Vasopressin increased the total peripheral, pulmonary, and coronary vascular resistance and decreased coronary blood flow and cardiac output There was a slight increase in systemic arterial blood pressure, A dec

Ten grams of oral potassium salts were administered to 60 patients with functionally inverted (anxiety induced) left ventricular T waves, to 119 patients with organically inverted T waves and 4 patients with inverted T waves of indeterminate etiology. All functionally inverted T waves were reverted to normal 90 minutes after ingestion of K+. The T wave inversion resulting from 10 to 15 seconds of brisk hyperventilation likewise was abolished. Organic T waves of myocardial infarction were generally unaltered following ingestion of K+. Several of the inverted T waves due to infarction showed increased negativity. On the other hand, inverted T waves over the “fringe areas” of lateral wall ischemia in either anterior or posterior wall infarction occasionally showed a tendency to normalization. In a single instance of an acute posterior wall infarction, K+ ingestion improved the T wave contour in lead II only. Of the 40 instances of acute myocardial ischemia, 32 showed no change; 2 showed slightly increasing T wave negativity; 4 showed improvement although not normalization of the ischemie zone; and 2 showed normalization. In 1 of these last 2 patients the control tracing had shown almost complete resolution of the ischemie episode. Ten instances of left bundle branch block, 10 of digitalis effect and 2 of subacute pericarditis showed no alteration of T wave polarity following K+ ingestion. As previously noted in the literature, electrocardiograms of left ventricular preponderance showed the greatest variability of T wave configuration following K+ ingestion. Eight tracings showed no change; 1 showed slight improvement and 3, moderate improvement. None, however, showed complete normalization. The K+ salt was generally well tolerated when administered 1 1 2 hours following the noon meal. It must be regarded as a potentially dangerous drug, particularly in patients with acute ischemie episodes. Adequate renal function is a prerequisite for the test. This procedure appears to be of considerable clinical usefulness in evaluating T wave abnormalities of obscure etiology. It should not, however, usurp clinical judgment since the results to date are purely empirical and lack a sound pathophysiologic basis.

This report summarizes our experience with the oral potassium-loading test in a group of patients who presented with abnormal T wave inversion on routine resting electrocardiograms. The test empirically normalizes most T wave abnormalities that are unassociated with clinically demonstrable heart disease, particularly the T wave changes induced by brief hyperventilation or by anxiety reactions. The response to the test procedure is dosage-dependent and is not related to a nonspecific osmolar load. It is recommended that the oral potassium-loading test not be utilized as a clinical testing procedure. Although the results frequently clarify the significance of T wave abnormalities in asymptomatic patients, false positives and false negatives will occur. At best, awareness of this study will recall to the clinicians mind that anxiety, hyperventilation and standing may result in T wave abnormalities entirely similar to those of an acute myocardial ischemic episode, pericarditis or myocarditis.

The systemic and coronary hemodynamic effects of relatively large doses of propranolol have been studied following its infusion into intact anesthetized dogs at rest and during simulated exercise. At rest, the administration of propranolol was associated with decreased cardiac output and ventricular work and increased peripheral, pulmonary, and coronary vascular resistances. Coronary blood flow and coronary sinus oxygen content decreased while myocardial oxygen consumption and the index of cardiac efficiency were unchanged. The usual hemodynamic response to mild exercise was obtained, with increased cardiac output, cardiac work, body oxygen consumption, and a modest but insignificant increase in coronary blood flow. When propranolol was given and the same exercise continued, body oxygen consumption, cardiac output, and left ventricular work significantly decreased. Insignificant decreases occurred in coronary blood flow, left ventricular oxygen usage, and coronary sinus oxygen content. The present observations are consistent with the thesis that beta-adrenergic blockade induced by propranolol decreases cardiac work at rest and reduces the cardiovascular response to exercise.

The sudden appearance of tall or peaked T waves may be the earliest electrocardiographic expression of acute myocardial ischemia and impending myocardial infarction. They are most apt to be seen in records taken during or within several hours of the onset of the chest pain. The “modus operandi” of this puzzling electromotive phenomenon, abetted by a review of pertinent experimental data, remains unanswered and offers a challenge for continued basic and sophisticated research. Most of the investigators believed that these acutely peaked T waves were due to acute subendocardial ischemia, but this was based more on electromotive hypothesis than fact. The sudden shift of the intracellular potassium seemingly plays a key role.

Systemic and coronary hemodynamic parameters were determined during an arrhythmia and immediately after a direct current transthoracic shock given in an attempt to convert the arrhythmia to a sinus mechanism. No anesthesia or drugs were administered between the two studies. 16 patients with atrial fibrillation converted to sinus rhythm and five did not. In two patients with atrial flutter and one with supraventricular tachycardia, the arrhythmia was corrected. The arrhythmia persisted in a single patient with ventricular tachycardia. Utilizing each patient as his own control, we compared statistically various hemodynamic parameters before and after the shock. In addition, the group of patients whose atrial fibrillation terminated was compared to the group treated in the same manner but in which the atrial fibrillation persisted. Pressures in the right side of the heart decreased in both groups so that the changes appeared to be caused by factors associated with the transthoracic direct current shock or the catheterization procedure. The differences between those with atrial fibrillation who converted to sinus rhythm as compared to those who did not were a decrease in heart rate, an increase in stroke volume, and an increase in cardiac efficiency. There was no immediate effect on the cardiac output or coronary blood flow.