IMPAIRED NEUROENDOCRINE RESPONSE MEDIATES REFRACTORINESS TO CARDIOPULMONARY-RESUSCITATION IN SPINAL-ANESTHESIA

Objective: To determine the extent of neurogenic control on adrenal se cretion in a canine model of high spinal anesthesia and cardiac arrest , Design: Randomized, controlled, acute intensive study, Setting: Univ ersity intensive care laboratory, Subjects: Nineteen healthy, anesthet ized, mongrel dogs, Interventions: Cardiac arrest was induced in 11 sp inally anesthetized dogs and 8 sham control animals; cardiopulmonary r esuscitation (CPR) was started 60 secs later, Epinephrine was injected at 4 mins and every 2 mins thereafter, Arterial blood samples were ob tained before anesthesia, before arrest, and after 1, 3, 5, 7, 9, and 11 mins of CPR. Measurements and Main Results: At 1 and 3 mins after c ardiac arrest, the control group exhibited significant increases of ep inephrine and norepinephrine concentrations (p < .05) that were absent in the spinal anesthesia group, Plasma renin increased in both groups whereas aldosterone and cortisol remained unchanged, Conclusions: Spi nal anesthesia abolishes the catecholamine release that follows cardia c arrest, while a previously postulated direct adrenal effect of hypox ia stimulating catecholamine release was not confirmed in these experi ments, Since epinephrine treatment restores coronary perfusion pressur e (CPP) during CPR, we conclude that catecholamine deficiency is the m ost likely mechanism for inadequate CPP during CPR conducted in the pr esence of spinal anesthesia.