Cardiopulmonary Arrest

Abstract

Cardiopulmonary arrest is a test of the brain's tolerance to global ischemia. New insights into the pathophysiology of global ischemia have led to the potential use of early prophylactic anticonvulsants, hypothermia, barbiturate coma, glucose manipulations, calcium-blocking agents, and hemodilution. A wide spectrum of neurologic sequelae may follow global ischemia, ranging from brain death, vegetative states, and impairment of higher intellectual function to syndromes of amnesia and cortical blindness, post-anoxic myoclonus, delayed leukoencephalopathy, and spinal stroke. The distinctive features of these sequelae and their pathophysiologic aspects are discussed. Special attention is given to brain death and prognostication.

Expressional Changes in Cerebrovascular Receptors after Experimental Transient Forebrain Ischemia

“…Several clinical conditions can give rise to global ischemic stroke but a frequent cause is cardiac arrest, which is a world-wide devastating health problem [1]–[3]. Even if systemic resuscitation and stable cardiac rhythm is achieved after a cardiac arrest, the post-arrest period often implies a period of cerebral no-reflow with multifocal ischemia followed by a short period of global cerebral hyperaemia, then a phase with prolonged cerebral hypoperfusion that may last for several days and give rise to cognitive and motor deficits [1], [2], [4]–[6]. Today, treatment options for normalization of post-arrest cerebral perfusion are still very poor [2], [3], [7]–[9].…”

Amnesia and Pain Relief after Cardiopulmonary Resuscitation in a Cancer Pain Patient: A Case Report

“…Among these various causes, we assume that the causes of amnesia in the present case are hypoxic brain injury and prolonged seizure after respiratory and cardiac arrest. Many cognitive impairments and memory losses occur by hypoxic brain injury after cardiac arrest, but the precise mechanism of this phenomenon is not yet clearly proven (6). Fleiss et al (7) reported that hypoxic brain injury in an animal model of birth asphyxia produced significant functional deficits in the hippocampus, and caused a reduction of long-term potentiation (LTP), paired pulse facilitation (PRF), and post-tetanic potentiation (PTP).…”

Intérêt de l’IRM cérébrale spectroscopique pour évaluer le pronostic à 6 mois des encéphalopathies anoxiques post-arrêt cardiaque. Étude de faisabilité

“…La survie des patients victimes d'ACR reste médiocre, avec des taux rapportés de retour à une activité cardiaque spontanée (reflétant le succès de la réanimation initiale) variant de 10 à 41%. La survie globale sans séquelle à la sortie de l'hôpital est habituellement comprise entre 4 et 8% [3] Ces anomalies de la coagulation sont particulièrement fréquentes chez les patients qui décèdent rapidement d'un choc post-arrêt cardiaque [27] Nous savons que les cellules nerveuses n'ont pas toutes la même sensibilité à l'anoxie, les neurones étant les plus fragiles [28] ; histologiquement, les lésions anoxiques cérébrales sont hétérogènes, et le cortex cérébral est principalement intéressé avec des lésions dites de nécrose laminaire diffuse [29]. Les noyaux gris centraux sont atteints dans 80% à 90% des cas, alors que l'atteinte du cervelet (cellules De Purkinje) et du tronc cérébral est plus rare [28,29].…”