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

85 Citations (Scopus)

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
JournalCritical Care Medicine
Volume24
Issue number2 SUPPL.
StatePublished - Dec 1 1996
Externally publishedYes

Fingerprint

Heart Arrest
Resuscitation
Brain
Free Radicals
Brain Hypoxia
DNA Cleavage
Asphyxia
Cardiopulmonary Resuscitation
Brain Diseases
Brain Ischemia
Basement Membrane
Lipid Peroxidation
Catecholamines
Neurotransmitter Agents
Blood Vessels
Glutamic Acid
Dogs
Neurons
Membranes

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

Cite this

Vaagenes, P., Ginsberg, M., Ebmeyer, U., Ernster, L., Fischer, M., Gisvold, S. E., ... Zhou, Y. (1996). Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms. Critical Care Medicine, 24(2 SUPPL.).

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

In: Critical Care Medicine, Vol. 24, No. 2 SUPPL., 01.12.1996.

Research output: Contribution to journalArticle

Vaagenes, P, Ginsberg, M, Ebmeyer, U, Ernster, L, Fischer, M, Gisvold, SE, Gurvitch, A, Hossmann, KA, Nemoto, EM, Radovsky, A, Severinghaus, JW, Safar, P, Schlichtig, R, Sterz, F, Tonnessen, T, White, RJ, Xiao, F & Zhou, Y 1996, 'Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms', Critical Care Medicine, vol. 24, no. 2 SUPPL..
Vaagenes P, Ginsberg M, Ebmeyer U, Ernster L, Fischer M, Gisvold SE et al. Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms. Critical Care Medicine. 1996 Dec 1;24(2 SUPPL.).
Vaagenes, Per ; Ginsberg, Myron ; Ebmeyer, Uwe ; Ernster, Lars ; Fischer, Matthias ; Gisvold, Sven Erik ; Gurvitch, Alexander ; Hossmann, Konstantin A. ; Nemoto, Edwin M. ; Radovsky, Ann ; Severinghaus, John W. ; Safar, Peter ; Schlichtig, Robert ; Sterz, Fritz ; Tonnessen, Tor ; White, Robert J. ; Xiao, Feng ; Zhou, Yuan. / Cerebral resuscitation from cardiac arrest : Pathophysiologic mechanisms. In: Critical Care Medicine. 1996 ; Vol. 24, No. 2 SUPPL.
@article{1dfbf083d6c3470798d39fad6f1adabd,
title = "Cerebral resuscitation from cardiac arrest: Pathophysiologic mechanisms",
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.",
keywords = "Angiogenesis, Anoxia, Cardiac arrest, Cardiopulmonary resuscitation, Cerebral blood flow, Cerebral excitotoxicity, Cerebral ischemia, Histopathology, Hypothermia, Reoxygenation injury",
author = "Per Vaagenes and Myron Ginsberg and Uwe Ebmeyer and Lars Ernster and Matthias Fischer and Gisvold, {Sven Erik} and Alexander Gurvitch and Hossmann, {Konstantin A.} and Nemoto, {Edwin M.} and Ann Radovsky and Severinghaus, {John W.} and Peter Safar and Robert Schlichtig and Fritz Sterz and Tor Tonnessen and White, {Robert J.} and Feng Xiao and Yuan Zhou",
year = "1996",
month = "12",
day = "1",
language = "English",
volume = "24",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "2 SUPPL.",

}

TY - JOUR

T1 - Cerebral resuscitation from cardiac arrest

T2 - Pathophysiologic mechanisms

AU - Vaagenes, Per

AU - Ginsberg, Myron

AU - Ebmeyer, Uwe

AU - Ernster, Lars

AU - Fischer, Matthias

AU - Gisvold, Sven Erik

AU - Gurvitch, Alexander

AU - Hossmann, Konstantin A.

AU - Nemoto, Edwin M.

AU - Radovsky, Ann

AU - Severinghaus, John W.

AU - Safar, Peter

AU - Schlichtig, Robert

AU - Sterz, Fritz

AU - Tonnessen, Tor

AU - White, Robert J.

AU - Xiao, Feng

AU - Zhou, Yuan

PY - 1996/12/1

Y1 - 1996/12/1

N2 - 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.

AB - 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.

KW - Angiogenesis

KW - Anoxia

KW - Cardiac arrest

KW - Cardiopulmonary resuscitation

KW - Cerebral blood flow

KW - Cerebral excitotoxicity

KW - Cerebral ischemia

KW - Histopathology

KW - Hypothermia

KW - Reoxygenation injury

UR - http://www.scopus.com/inward/record.url?scp=17444435016&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17444435016&partnerID=8YFLogxK

M3 - Article

VL - 24

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 2 SUPPL.

ER -