Review
Cerebral blood flow after cardiac arrest

https://doi.org/10.1016/S0300-2977(00)00059-0Get rights and content

Introduction

Survivors of a cardiac arrest frequently develop severe postanoxic encephalopathy. The severity of the brain damage depends mainly on pre-arrest factors (temperature, blood glucose), the type of insult (ventricular fibrillation, asphyxia or exsanguination) and the insult time. The insult time consists of the arrest time (no flow), the cardio-pulmonary resuscitation time (low flow) and the post-resuscitation syndrome developing in the first 24 h after cardiac arrest [1]. Unfortunately not all physicians taking care of the resuscitated patient are familiar with the pathophysiological changes in the post-resuscitation period. However, knowledge of the changes in cerebral blood flow during the post-resuscitation period is essential to treat patients in a proper way and give them the best opportunities they can get.

The post-resuscitation syndrome was first mentioned by Negovsky et al. [1], and is characterized by (a) cerebral perfusion failure, (b) reoxygenation injury, (c) extracerebral derangements, including intoxication from postanoxic viscera (release of toxins) and (d) blood derangements due to stasis [2] (Table 1). This article will briefly describe the physiology of cerebral blood flow and metabolism and discuss the changes in cerebral blood flow after cardiac.

Section snippets

Physiology of cerebral blood flow and metabolism

The adult brain weighs about 1500 g (2% body weight), but receives 15% of the cardiac output (750 ml/min), supplied via the carotid (2/3) and vertebral arteries (1/3). The gray matter flow is 60–70 ml/100 g per min and the white matter flow is 25 ml/100 g per min. Cerebral blood flow (CBF) is regulated by changes in cerebrovascular resistance.

The brain needs oxygen and glucose to maintain cellular integrity (approximately 40–50% of total CBF) and to perform electrophysiological activities

Cerebral blood flow after cardiac arrest

In animal experiments, cerebral blood flow after cardiac arrest is characterized by four phases [2]. This is graphically presented in Fig. 2. Immediately after resuscitation there is a short period of multifocal no-reflow (phase I). This is followed by transient global hyperemia lasting 15–30 min (phase II). Thereafter cerebral blood flow becomes severely reduced while the cerebral metabolic rate of oxygen gradually recovers. This period is termed the delayed hypoperfusion phase (phase III).

Conclusion

The prognosis of patients resuscitated from cardiac arrest remains very poor, despite improved methods of CPR and training of doctors, nurses and laypersons in CPR. However, it is important to realize that the resuscitation of patients from a cardiac arrest does not end after return of spontaneous circulation. We should realize that ultimate neurological outcome also depends on effective treatment during the post-resuscitation period. Therefore knowledge of the no-reflow phenomenon and delayed

First page preview

First page preview
Click to open first page preview

References (52)

  • N.A Lassen

    Cerebral blood flow and oxygen consumption in man

    Physiol Rev

    (1959)
  • Harper AM, Glass HI. Effects of alterations in the arterial carbon dioxide tension on the blood flow through the...
  • L.C McHenry et al.

    Cerebral autoregulation in man

    Stroke

    (1974)
  • A.M Harper

    Autoregulation of cerebral blood flow: influence of the arterial blood pressure on the blood flow through the cerebral cortex

    J Neurol Neurosurg Psychiatry

    (1966)
  • N.A Lassen

    Autoregulation of cerebral blood flow

    Circ Res

    (1964)
  • S Strandgaard et al.

    Upper limit of autoregularion of cerebral blood flow in the baboon

    Circ Res

    (1974)
  • M Reivich

    Arterial PCO2 and cerebral hemodynamics

    Am J Physiol

    (1964)
  • D.W Marion et al.

    The use of stable xenon-enhanced computed tomographic studies of cerebral blood flow to define changes in cerebral carbon dioxide vasoresponsivity caused by severe head injury

    Neurosurgery

    (1991)
  • B Widder et al.

    Course of cerebrovascular reactivity in patients with carotid artery occlusions

    Stroke

    (1994)
  • A.A Ames III et al.

    Cerebral ischemia. II. The no-reflow phenomenon

    Am J Pathol

    (1968)
  • E Kågström et al.

    Local cerebral blood flow in the recovery period following complete cerebral ischemia in the rat

    J Cereb Blood Flow Metab

    (1983)
  • S.R Lin

    Cerebral circulation after cardiac arrest. Angiographic and carbon black perfusion studies

    Radiology

    (1975)
  • K.-A Hossman

    Ischemia-mediated neuronal injury

    Resuscitation

    (1993)
  • P Safar et al.

    Amelioration of brain damage after 12 min of cardiac arrest in dogs

    Arch Neurol

    (1976)
  • F Sterz et al.

    Hypertension with or without hemodilution after cardiac arrest in dogs

    Stroke

    (1990)
  • Y Leonov et al.

    Hypertension with hemodilution prevents multifocal cerebral hypoperfusion after cardiac arrest in dogs

    Stroke

    (1992)
  • Cited by (56)

    View all citing articles on Scopus
    View full text