Hemodialysis changes the QRS amplitude in the electrocardiogram.

We studied eight patients to determine whether changes occur in the QRS amplitude when these patients are submitted to hemodialysis. The following variables were assessed before and after each (N = 28) hemodialysis session: (1) plasma sodium and potassium concentrations, (2) QRS amplitude, (3) the heart rate and its variability, (4) ventricular volumes, ventricular mass, ejection fraction and circumferential fiber shortening, (5) arterial pressure and end systolic stress, and (6) body weight. QRS amplitude was computed as the algebraic sum of the positive and negative waves of each QRS complex of the electrocardiogram. QRS amplitude changes were compared to body weight, ventricular volumes, ventricular mass, ejection fraction, circumferential fiber shortening, plasma potassium and sodium concentrations, arterial pressure, end systolic stress, heart rate, and R-R variability. After the hemodialysis sessions we found a significant increase (P = 0.0006) in QRS amplitude and a significant decrease in body weight (P = 0.0001), end diastolic volume (P = 0.043), plasma potassium concentration (P = 0.000001), end systolic stress (P = 0.025) and systolic arterial pressure (P = 0.023). Hemodialysis did not produce significant changes in the other variables. The statistical analyses performed did not show any significant influence of any of the measured variables on the QRS amplitude change. The QRS amplitude increases after hemodialysis but the cause of this increase is still unclear.

Cardiovascular responses to Valsalva maneuver in physically trained and untrained normal subjects.

To elucidate whether the Valsalva maneuver (VM) can distinguish different degrees of normal ventricular function and parasympathetic tone, we studied 10 physically untrained and 18 trained normal individuals who regularly performed isotonic exercises. Both groups were submitted to an exercise stress test. An electrocardiogram and an M-mode echocardiogram were recorded before and during VM. The arterial pressure, heart rate and ventricular function responses to the maneuver were evaluated. The end diastolic volume, ejection fraction, circumferential fiber shortening and left ventricular posterior wall thickness were greater at rest in the trained group than in the untrained one. In both groups, during the straining phase of the VM the volumes and end systolic stress decreased and the systolic function indexes increased, but the changes were more pronounced in the trained subjects. In spite of these differences, the arterial pressure and heart rate responses were similar in both groups. It can thus be concluded that only changes in ventricular function distinguish physically trained vs untrained subjects during VM.

Vitamin E and ventricular fibrillation threshold in myocardial ischemia.

The effect of vitamin E on the ventricular fibrillation threshold was studied in an experimental model of acute myocardial ischemia. An anterior thoracotomy was performed on 23 anesthetized Wistar rats. The ventricular fibrillation threshold was measured. Vitamin E was then administered intravenously to an experimental group (n = 11) and a placebo to a control group (n = 12). The ventricular fibrillation threshold was measured again. Finally, the left anterior descending coronary artery was occluded, producing anteroapical myocardial ischemia. The ventricular fibrillation threshold was measured again. This threshold did not vary significantly when vitamin E or the placebo was administered before occluding the coronary artery but after the occlusion a threshold decrease in the placebo group was observed, whereas no such decrease was manifested in the vitamin E-treated group. The results suggest that vitamin E prevents ventricular fibrillation in acute myocardial ischemia in rats.