Hemodynamic effects of ventricular defibrillation.
Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage. Responses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO(2) increased but pO(2) and the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine.THESE RESPONSES WERE RELATED PRIMARILY TO CONVERSION OF VENTRICULAR FIBRILLATION RATHER THAN TO THE ELECTRICAL DISCHARGE OF COUNTERSHOCK BECAUSE COUNTERSHOCK WITHOUT VENTRICULAR FIBRILLATION CAUSED MORE TRANSIENT AND SMALLER RESPONSES THAN THOSE OBSERVED WITH DEFIBRILLATION: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure; D001919:Bradycardia / Q000209:etiology; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D004285:Dogs; D004395:Dye Dilution Technique; D004554:Electric Countershock; D004562:Electrocardiography; D006325:Heart Atria; D006327:Heart Block / Q000209:etiology; D006339:Heart Rate; D006439:Hemodynamics; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000097:blood; D008297:Male; D010100:Oxygen / Q000097:blood; D010275:Parasympathetic Nervous System / Q000502:physiology; D010313:Partial Pressure; D010643:Phenoxybenzamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D014628:Vagotomy; D014655:Vascular Resistance; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*
D007773:Lactates; D010643:Phenoxybenzamine; D002245:Carbon Dioxide; D001285:Atropine; D011433:Propranolol; D010100:Oxygen