Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms

Per Vaagenes, Myron Ginsberg, Uwe Ebmeyer, Lars Ernster, Matthias Fischer, Sven Erik Gisvold, Alexander Gurvitch, Konstantin A. Hossmann, Edwin M. Nemoto, Ann Radovsky, John W. Severinghaus, Peter Safar, Robert Schlichtig, Fritz Sterz, Tor Tonnessen, Robert J. White, Feng Xiao, Yuan Zhou

Research output: Contribution to journalArticle

88 Scopus citations

Abstract

Both the period of total circulatory arrest to the brain and postischemic-anoxic encephalopathy (cerebral postresuscitation syndrome or disease), after normothermic cardiac arrests of between 5 and 20 mins (no-flow), contribute to complex physiologic and chemical derangements. The best documented derangements include the delayed protracted inhomogeneous cerebral hypoperfusion (despite controlled normotension), excitotoxicity as an explanation for selectively vulnerable brain regions and neurons, and free radical-triggered chemical cascades to lipid peroxidation of membranes. Protracted hypoxemia without cardiac arrest (e.g., very high altitude) can cause angiogenesis; the trigger of it, which lyses basement membranes, might be a factor in post-cardiac arrest encephalopathy. Questions to be explored include: What are the changes and effects on outcome of neurotransmitters (other than glutamate), of catecholamines, of vascular changes (microinfarcts seen after asphyxia), osmotic gradients, free-radical reactions, DNA cleavage, and transient extracerebral organ malfunction? For future mechanism-oriented studies of the brain after cardiac arrest and innovative cardiopulmonary-cerebral resuscitation, increasingly reproducible outcome models of temporary global brain ischemia in rats and dogs are now available. Disagreements exist between experienced investigative groups on the most informative method for quantitative evaluation of morphologic brain damage. There is agreement on the desirability of using not only functional deficit and chemical changes, but also morphologic damage as end points.

Original languageEnglish (US)
Pages (from-to)S57-S68
JournalCritical care medicine
Volume24
Issue number2 SUPPL.
StatePublished - Dec 1 1996
Externally publishedYes

Keywords

  • Angiogenesis
  • Anoxia
  • Cardiac arrest
  • Cardiopulmonary resuscitation
  • Cerebral blood flow
  • Cerebral excitotoxicity
  • Cerebral ischemia
  • Histopathology
  • Hypothermia
  • Reoxygenation injury

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

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  • Cite this

    Vaagenes, P., Ginsberg, M., Ebmeyer, U., Ernster, L., Fischer, M., Gisvold, S. E., Gurvitch, A., Hossmann, K. A., Nemoto, E. M., Radovsky, A., Severinghaus, J. W., Safar, P., Schlichtig, R., Sterz, F., Tonnessen, T., White, R. J., Xiao, F., & Zhou, Y. (1996). Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms. Critical care medicine, 24(2 SUPPL.), S57-S68.