Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs

• Published in: The American journal of emergency medicine Vol. 1; no. 2; pp. 128 - 138
• Main Authors: White, Blaine C, Winegar, Carl D, Jackson, Raymond E, Joyce, Kathleen M, Vigor, David N, Hoehner, Thomas J, Krause, Gary S, Wilson, Robert F
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.09.1983
• Subjects: Adenosine Triphosphate - metabolism; Animals; Brain - blood supply; Calcium - metabolism; calcium antagonists; Cardiac arrest; Cell Membrane - metabolism; Cerebral Cortex - blood supply; Cerebral Cortex - physiopathology; Cerebrovascular Circulation - drug effects; Cinnarizine - analogs & derivatives; Cinnarizine - pharmacology; CPR brain perfusion; Dogs; Fatty Acids, Nonesterified - metabolism; Flunarizine; Heart Arrest - drug therapy; Heart Arrest - physiopathology; Heart Arrest - therapy; Heart Massage; Hypoxia, Brain - metabolism; Ischemia - metabolism; Lidoflazine - pharmacology; Nervous System Diseases - drug therapy; platelets; Resuscitation; CPR brain perfusion; calcium antagonists; platelets; Cardiac arrest
• ISSN: 0735-6757; 1532-8171
• DOI: 10.1016/0735-6757(83)90080-3

Perfusion of the cerebral cortex during closed chest CPR in dogs, generating systolic pressures of 60 to 70 mmHg, is only 10% of pre-arrest blood flow. In contrast, internal cardiac massage produces normal cortical perfusion rates. Following a 20-min perfusion arrest, during pressure controlled reperfusion, cortical flow rates decay to less than 20% normal after 90 min of reperfusion. This appears to be due to increasing cerebral vascular resistance, and is not due to rising intracranial pressure. The post-arrest cortical hypoperfusion syndrome is prolonged with cortical flow remaining below 20% normal up to 18 hr post arrest. The use of a variety of calcium antagonists, including flunarizine, lidoflazine, verapamil, and Mg 2+, immediately post-resuscitation maintains cerebral vascular resistance and cortical perfusion at normal levels. A prospective blind trial of the calcium antagonist lidoflazine following a 15-min cardiac arrest in dogs and resuscitation by internal massage, demonstrates amelioration of neurologic deficit in the early post-resuscitation period.