Prolonged hypoperfusion in the cerebral cortex following cardiac arrest and resuscitation in dogs

✍ Scribed by Blaine C. White; Carl P. Winegar; Orzie Henderson; Raymond E. Jackson; Gary Krause; Thomas O'Hara; Thomas Goodin; David N. Vigor

• Publisher: Elsevier Science
• Year: 1983
• Tongue: English
• Weight: 407 KB
• Volume: 12
• Category: Article
• ISSN: 1097-6760
• DOI: 10.1016/s0196-0644(83)80334-5

✦ Synopsis

Increasing cerebral vascular resistance and brain perfusion failure occur within 90 minutes following cardiac arrest and resuscitation. This study followed cortical perfusion for 18 hours after a 15-minute cardiac arrest. Six dogs were anesthetized with ketamine and gallamine and then mechanically ventilated. They were instrumented for arterial pressure, central venous pressure, and regional cerebral cortical blood flow (rCCBF) determined by thermodilution. A left thoracotomy and pericardiotomy were done. 7~vvo dogs served as non-arrest controls. Cardiac arrest was produced in four dogs with an intravenous bolus of KC1 at I mEq/kg. After 15 minutes of cardiac arrest, the animals were resuscitated with internal massage, NaHC03, epinephrine, and internal defibrillation. Cortical blood flow was followed for 18 hours. Arterial core temperature was never less than 35 C. Pre-arrest cortical blood flows were 0.86 cc/min/g (+_ 0.11). The two control animals had stable rCCBF (0.74 +-0.17) for all determinations during the 18-hour follow-up period. Determinations of rCCBF from 6 to 18 hours in post-arrest animals were 7% to 14% of pre-arrest values. We conclude that the postresuscitation perfusion failure in the cortex is prolonged. Any potential for neuronal recovery, unless perfusion is protected, would not be realized given this phenomenon.