Cerebrovascular effects of prolonged hypocarbia and hypercarbia after experimental global ischemia in cats.
Hyperventilation therapy is often recommended after an episode of global cerebral ischemia (cardiac arrest), even though several workers have shown that under such circumstances the cerebral vasculature is unresponsive to changing PaCO2. However, no study has examined the effects of prolonged PaCO2 changes. We therefore studied the cerebrovascular effects of a 3-h period of continuous hypercarbia (40 to 45 torr) or hypocarbia (15 to 20 torr) in cats resuscitated from 12 min of electrically induced ventricular fibrillation. There were no differences in postresuscitation cerebral blood flow (CBF) or EEG, but intracranial pressure was lower in the hypocapnic animals. Furthermore, hypocapnic cats retained some CBF responsiveness to varying PaCO2 levels, while no such response was noted in previously hypercapnic animals. These findings suggest that some measurable changes in postarrest cerebrovascular behavior can result from prolonged hypocapnia (possibly related to tissue pH alterations). Whether such changes will have clinical utility is unclear.
D000818:Animals; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood / Q000627:therapeutic use*; D002415:Cats; D004569:Electroencephalography; D005260:Female; D006339:Heart Rate; D006863:Hydrogen-Ion Concentration; D007427:Intracranial Pressure; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D010100:Oxygen / Q000097:blood; D012151:Resuscitation
D002245:Carbon Dioxide; D010100:Oxygen