Preservation of ventricular function by treatment of ventricular fibrillation with phenylephrine

Epinephrine promotes resuscitation from ventricular fibrillation because of its peripheral vasoconstrictive effects. However, the beta-adrenergic effects of epinephrine may be detrimental because of the stimulation of myocardial oxygen demand. To test whether functional recovery from fibrillation in hearts treated with a selective alphaadrenergic agent is greater than in hearts treated with epinephrine, ventricular fibrillation was induced in eight isolated dog hearts white coronary perfusion pressure was maintained at 30 mm Hg. In random order, epinephrine (5 μg/min), phenylephrine (50 μg/min) or no drug was infused for 5 min. The heart was then defibrillated, the drug infusion stopped and coronary perfusion pressure increased to 100 mm Hg. Coronary blood flow (ml/min per 100 g), arteriovenous oxygen difference (ml O2/dl) and myocardial oxygen consumption (ml O2/min per 100 g) measured after 4 min of ventricular fibrillation were greater with epinephrine (mean ± SD 30.9 ± 11.7, 17.5 ± 1.6 and 5.4 ± 1.9, respectively) than with phenylephrine (24.4 ± 6.0, 15.7 ± 2.6 and 3.8± 1.1, respectively) or no drug (19.8± 5.2, 12.8 ± 1.8 and 2.6 ± 9.7, respectively) (p < 9.05, p < 0.05 and p < 0.05, respectively). The slope of the end-systolic pressure-volume relation 19 min after defibrillation and restoration of normal coronary perfusion pressure was depressed (percent of prefibrillation value) most by epinephrine infusion (72 ± 17%, n = 6), less by no drug infusion (82 ± 12%, n = 4) and was increased after phenykphrine infusion (143 ± 17%, n = 6) (p < 0.002). Volume axis intercepts (Vo) were not different (p = NS). It is concluded that at a coronary perfusion pressure of 30 mm Hg, left ventricular function declines as a consequence of epinephrine administration during ventricular fibrillation and is preserved by the use of pheaylephrne. This epinephrwe-associated impairment likely results from increased oxygen demand and intensification of ischemia, whereas the benefit of phenylephrine seem to be the result of a weak and prolonged positive motropic effect.