The effects of hypothermia on cerebral perfusion during CPR after increasing periods of cardiac arrest

Donald H. Shafber, Scon M. Eteff, Raymond C. Koehler, Richard J. Traystman

Research output: Contribution to journalArticle

Abstract

Introduction: We have previously shown in dogs that the cerebral blood flow produced by cardiopulrnonary resuscitation (CPR) decreases as die arrest time prior to CPR increases despite constant cerebral perfusion pressure (CPP). The mechanism for the deterioration in blood flow during CPR after increasing arrest time is unknown. Cardiac arrest induced increases in viscosity, pen-vascular edema, or constriction of blood vessels are possible mechanisms for the deterioration in flow during CPR. Hypothermia would add to viscosity but may prevent edema or vasoconstriction. Hypothermia during CPR after various arrest times was studied in an attempt to better understand die potential mechanisms of poor blood flow during CPR and to determine if hypothermia will protect against the worsening effectiveness of CPR as arrest time increases. Methods: Thirty six mongrel dogs were anesthetized, mechanically ventilated, and instrumented to study vascular pressures and determine microsphere cerebral blood flow. The normothennic groups had brain and rectal temperatures maintained at 38 deg C while the hypothermie groups woe cooled to 28 deg C before ventricular fibrillation. Vest CPR with a CPP of 25 mmHg commenced 1 J, 3, or 6 minutes after arrest Cerebral blood flow determinations were made at 5,15, and 25 minutes of CPR. Results: During nonnothermia supratentonal blood flow fell from 46.1±4 mL/100gm /min pre-arrest to 7.9±1 mL/100gm/mnj during CPR after a 6 min arrest (p<0.0001). Widi hypothermia flow was 26.3±3 mL/100gm/min pre-arrest and 14.7±1 mL/100gnVnun during CPR after a 6 min arrest (p<0.0005). After 6 minutes of arrest me flow during CPR with hypothermia was greater than the flow with normomermia (14.7±1 vs. 7.9±1, p<0.05). The cerebral metabolic rate for O2 (CMRO2) was 2.2±0.2 mL/100gm/min prearrest and 0.9±0.1 mL/100gm/min during CPR after a 6 min arrest (p<0.0005) in the normothermic group. Hypothermia maintained CMRO2 at 0.9±0.1 mL/100gm/min prearrest and 0.9±0.1 mL/100gm/min during CPR after a 6 min arrest. Conclusion: Hypothermia protects against cerebral hypoperfusion during CPR after 6 minutes of cardiac arrest Hypothermia öfters potential protection from neurologic injury caused by the impact of arrest time on blood flow during subsequent CPR.

Original languageEnglish (US)
Pages (from-to)A55
JournalCritical care medicine
Volume26
Issue number1 SUPPL.
StatePublished - Dec 1 1998

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ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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