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 labor atory 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 electr ode. Electric defibrillation was attempted after an interval of 12 min s of: ventricular fibrillation, which included 4 mins of untreated ven tricular fibrillation and 8 mins of precordial compression in 13 anima ls, seven of which were successfully resuscitated. Seven additional an imals were randomized to serve as ''sham'' controls, in which cardiac arrest was not induced. Measurements and Main Results: Left ventricula r pressure-volume relationships utilizing the conductance method were obtained in conjunction with conventional hemodynamic and metabolic me asurements at baseline and during a 6-hr interval after successful car diac resuscitation, Progressive and striking increases in left ventric ular 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 v entricular work. However, compensatory increases in heart rate maintai ned cardiac output at levels that sustained adequate systemic oxygen d elivery. The slope of the end-systolic pressure-volume relationships p rogressively decreased from 5.04 +/- 1.88 to 2.00 +/- 0.57 mm Hg/mL (p < .05) at 360 mins after successful resuscitation. The volume interce pt 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 incr ease ist the volume intercept were characteristic of progressive impai rment in contractile function. The rate of Left ventricular pressure d ecrease was unchanged. Accordingly, no substantial changes in lusitrop ic properties were identified. Despite large increases in end diastoli c volume, the end-diastolic pressure remained unchanged. Conclusion: P ostresuscitation myocardial dysfunction in this animal model was chara cterized by impaired contractile function, decreased work capability, and ventricular dilation.