Myocardial effects of ventricular fibrillation in the isolated rat heart

Objective: Ventricular fibrillation (VF) is known to increase myocardial ox ygen requirements and to alter coronary vascular physiology, However, the s ignificance of these effects during cardiac arrest and resuscitation is not well understood. A model was developed in the isolated rat heart to invest igate the myocardial effects of VF during a simulated episode of cardiac ar rest and resuscitation, We hypothesized that VF would intensify the severit y of myocardial ischemia and consequently accentuate postischemic myocardia l dysfunction. Design: Prospective and randomized. Setting: Research laboratory. Subjects: Twenty Sprague-Dawley rats. Interventions: Hearts were harvested and perfused at a constant flow rate o f 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. In five hearts, VF was induced by a 0.05-mA current del ivered to the right ventricular endocardium. The perfusate flow was then st opped for a 10-min interval and resumed at 20% of baseline flow for another 10 mins, After 20 mins of VF, the perfusate flow was returned to baseline and a sinus rhythm reestablished by epicardial electrical shocks. The studi es were randomized and included three additional groups to control for the effects of ischemia without VF (n = 5), the effects of VF without ischemia (n = 5), and the stability of the preparation (n = 5). Measurements and Main Results: Isovolumic indices of left ventricular funct ion were obtained using a latex balloon advanced through the mitral valve a nd distended to an end-diastolic pressure of 10 mm Hg. The coronary effluen t was collected from the right ventricular cavity. YF during myocardial isc hemia was associated with a higher coronary effluent PCO2, increased corona ry vascular resistance, and development of ischemic contracture as indicate d by Increases in left ventricular pressure from 9 +/- 3 to 33 +/- 6 mm Hg (p < .05). After defibrillation, contractility and relaxation rapidly retur ned to baseline values, whereas the isovolumic end-diastolic pressure remai ned elevated for 20 mins, These changes were much less prominent when ische mia was not accompanied by YF. Conclusions: These findings indicate that VF may adversely affect myocardia l ischemia by hastening the development of ischemic contracture, increasing coronary vascular resistance, and favoring the development of diastolic pu mp failure early after resuscitation from cardiac arrest.