The objective of this study was to document the biochemical changes during ventricular fibrillation (VF) with cardiopulmonary resuscitation (CPR), and to identify factors associated with postdefibrillation pulseless electrical activity (PD-PEA).

It has been reliably estimated that as much as 60% of out-of-hospital sudden cardiac death can be attributed to the onset of PD-PEA (Niemann JT, Cruz B, Garner D et al. Immediate countershock versus CPR before countershock in a 5-minute swine model of ventricular fibrillation arrest. Ann Emerg Med 2000;36:543-6). Previous attempts to treat reversible causes of pulseless electrical activity have not been successful clinically (Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity. Crit Care Med 2001;29:2366-70).

This investigation used 22 studies on 14 anesthetized pigs breathing 100% oxygen. Ventricular fibrillation was induced with a right ventricular catheter electrode, and the chest was compressed with a pneumatically driven Chest Thumper (Michigan Instruments) (80-100 lb at 60/min). The electrocardiogram and aortic pressure were recorded continuously. Arterial pH, Po₂, Pco₂, Na⁺, K⁺, Ca²⁺, Cl⁻, SaO₂, glucose, hematocrit, and hemoglobin level were measured at selected times. Ventricular defibrillation was achieved with transchest electrodes.

Typically, during VF with CPR, mean aortic pressure was 20 to 25 mm Hg. In all cases aortic Po₂ decreased to about 20% of the initial value in 10 minutes, and aortic blood K⁺ increased by 50% in 6 minutes. By 5 to 8 minutes, the incidence of PD-PEA was 50%.

Ventricular fibrillation duration, arterial K⁺, and arterial Pco₂ were statistically correlated with the onset of PD-PEA in this study. In addition, trends suggest an association of mean arterial blood pressure and arterial Po₂ with the onset of PD-PEA.