The Netherlands Journal of Medicine
ReviewCerebral blood flow after cardiac arrest
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
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