CEREBRAL RESUSCITATION FROM CARDIAC-ARREST - PATHOPHYSIOLOGIC MECHANISMS

Both the period of total circulatory arrest to the brain and postische mic-anoxic encephalopathy (cerebral postresuscitation syndrome or dise ase), after normothermic cardiac arrests of between 5 and 20 mins (no flow), contribute to complex physiologic and chemical derangements. Th e best documented derangements include the delayed protracted inhomoge neous cerebral hypoperfusion (despite controlled normotension), excito toxicity as an explanation for selectively vulnerable brain regions an d neurons, and free radical triggered chemical cascades to lipid perox idation of membranes. Protracted hypoxemia without cardiac arrest (e.g ., very high altitude) can cause angiogenesis; the trigger of it, whic h lyses basement membranes, might be a factor in post-cardiac arrest e ncephalopathy. 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 asphyxi a), osmotic gradients, free radical reactions, DNA cleavage, and trans ient extracerebral organ malfunction? For future mechanism oriented st udies of the brain after cardiac arrest and innovative cardiopulmonary cerebral resuscitation, increasingly reproducible outcome models of t emporary global brain ischemia in rats and dogs are now available. Dis agreements exist between experienced investigative groups on the most informative method for quantitative evaluation of morphologic brain da mage. There is agreement on the desirability of using not only functio nal deficit and chemical changes, but also morphologic damage as end p oints.