Myocardial dysfunction after successful resuscitation from cardiac arrest

Objective: To investigate the functional and metabolic changes in the myocardium after successful resuscitation from cardiac arrest. Design: Prospective, randomized, sham-cantrolled study. Setting: Animal laboratory at a university center. Subjects: Domestic pigs. Interventions: Electric induction of ventricular fibrillation by alternating current delivered to the right ventricular endocardium through a pacing electrode. Electric defibrillation was attempted after an interval of 12 mins of: ventricular fibrillation, which included 4 mins of untreated ventricular fibrillation and 8 mins of precordial compression in 13 animals, seven of which were successfully resuscitated. Seven additional animals were randomized to serve as ''sham'' controls, in which cardiac arrest was not induced. Measurements and Main Results: Left ventricular pressure-volume relationships utilizing the conductance method were obtained in conjunction with conventional hemodynamic and metabolic measurements at baseline and during a 6-hr interval after successful cardiac resuscitation, Progressive and striking increases in left ventricular volumes were observed after successful cardiac resuscitation. The end-diastolic volume increased from a prearrest level of 89 +/- 21 ml. to a maximum of 1.54 +/- 53 mL (p <.05) at 360 mins after successful resuscitation. The time-coincident end-systolic volume increased from 54 +/- 21 to 126 +/- 54 mL (p < .05), such that the ejection fraction was reduced from 0.41 +/- 0.10 to 0.21 +/- 0.07 (p <.05). Ventricular dilation was associated with marked reductions in stroke volume and ventricular work. However, compensatory increases in heart rate maintained cardiac output at levels that sustained adequate systemic oxygen delivery. The slope of the end-systolic pressure-volume relationships progressively decreased from 5.04 +/- 1.88 to 2.00 +/- 0.57 mm Hg/mL (p < .05) at 360 mins after successful resuscitation. The volume intercept at left ventricular pressure of 100 mm Mg increased from 43 +/- 19 to 94 +/- 51 mL (p = .03). Both the decrease in the slope and the increase ist the volume intercept were characteristic of progressive impairment in contractile function. The rate of Left ventricular pressure decrease was unchanged. Accordingly, no substantial changes in lusitropic properties were identified. Despite large increases in end diastolic volume, the end-diastolic pressure remained unchanged. Conclusion: Postresuscitation myocardial dysfunction in this animal model was characterized by impaired contractile function, decreased work capability, and ventricular dilation.