Impaired neuroendocrine response mediates refractoriness to cardiopulmonary resuscitation in spinal anesthesia.

Abstract

To determine the extent of neurogenic control on adrenal secretion in a canine model of high spinal anesthesia and cardiac arrest. Randomized, controlled, acute intensive study. University intensive care laboratory. Nineteen healthy, anesthetized, mongrel dogs. Cardiac arrest was induced in 11 spinally anesthetized dogs and 8 sham-control animals; cardiopulmonary resuscitation (CPR) was started 60 secs later. Epinephrine was injected at 4 mins and every 2 mins thereafter. Arterial blood samples were obtained before anesthesia, before arrest, and after 1, 3, 5, 7, 9, and 11 mins of CPR. At 1 and 3 mins after cardiac arrest, the control group exhibited significant increases of epinephrine 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. Spinal anesthesia abolishes the catecholamine release that follows cardiac arrest, while a previously postulated direct adrenal effect of hypoxia stimulating catecholamine release was not confirmed in these experiments. Since epinephrine treatment restores coronary perfusion pressure (CPP) during CPR, we conclude that catecholamine deficiency is the most likely mechanism for inadequate CPP during CPR conducted in the presence of spinal anesthesia.