Successful cardiopulmonary resuscitation necessitates that both myocardial and central nervous system function be restored with minimal longterm damage. Recent resuscitation research has emphasized minimizing neurologic damage during and after cardiopulmonary resuscitation. However, whether neurologic damage is a major cause of death or morbidity following successful cardiopulmonary resuscitation is unknown. This study examined the role of neurologic injury as a cause for morbidity and mortality following cardiopulmonary resuscitation, and if parameters used successfullly during resuscitation for assessing the potential for myocardial salvage, could also be used to predict neurologic outcome. Eighty-eight mongrel dogs underwent 3 min of untreated ventricular fibrillation and either 15 or 17 min of cardiopulmonary resuscitation. Twenty-four hour survivors were evaluated with a neurologic deficit scoring system. Thirty-one percent of these animals were never resuscitated. Twenty-eight percent were resuscitated, but expired prior to 24 h. Approximately half of those who expired after resuscitation died from apparent neurologic sequellae. Forty-one percent of the 88 animals survived for 24 h. Two-thirds of these survivors were completely neurologically normal, while one-third were neurologically impaired. Hemodynamic parameters useful in assessing cardiovascular prognosis were not helpful in predicting neurologic outcome. Hence, although the majority of resuscitated animals did not suffer neurologic damage, up to one-third did exhibit neurologic impairment following resuscitation. Neurologic injury is also a major contributor to early death following successful resuscitation. Hemodynamic parameters of cardiovascular recovery do not predict neurologic outcome after prolonged cardiopulmonary resuscitation.
ASJC Scopus subject areas
- Emergency Medicine
- Cardiology and Cardiovascular Medicine