ASPHYXIATION VERSUS VENTRICULAR-FIBRILLATION CARDIAC-ARREST IN DOGS -DIFFERENCES IN CEREBRAL RESUSCITATION EFFECTS - A PRELIMINARY-STUDY

We explored the hypothesis that brain damage after cardiac arrest caus ed by ventricular fibrillation (VF) needs different therapies than tha t after asphyxiation, which has been studied less thoroughly. In 67 he althy mongrel dogs of both sexes cardiac arrest (at normothermia) by v entricular fibrillation (no blood flow lasting 10 min) or asphyxiation (no blood flow lasting 7 min) was reversed by normothermic external c ardiopulmonary resuscitation, followed by intermittent positive-pressu re ventilation for 20 h, and intensive care to 96 h. To ameliorate isc hemic brain damage, the calcium entry blocker lidoflazine or a solutio n of free radical scavengers (mannitol and L-methionine in dextran 40) plus magnesium sulphate, was given intravenously immediately upon res toration of spontaneous circulation. Outcome was evaluated as function al deficit, brain creatine kinase (CK) leakage into the cerebrospinal fluid (CSF) and brain morphologic changes. Lidoflazine seemed to impro ve cerebral outcome after VF but not after asphyxiation. Free radical scavengers plus magnesium sulphate seemed to improve cerebral outcome after asphyxiation, but not after VF. After VF, scattered ischemic neu ronal changes in multiple brain regions dominated, and total brain his topathologic damage scores correlated with final neurologic deficit sc ores at 96 h (r = 0.66) and with peak CK levels in CSF (I = 0.81). Aft er asphyxiation, in addition to the same ischemic neuronal changes, mi croinfarcts occurred, and there was no correlation between total brain histopathologic damage scores and neurologic deficit scores or CK lev els in CSF. Conclusions: Different mechanisms of cardiac arrest, which cause different morphologic patterns of brain damage, may need differ ent cerebral resuscitation treatments. (C) 1997 Elsevier Science Irela nd Ltd.