• G Buunk, J G van der Hoeven, and A E Meinders.
• Department of General Internal Medicine (Medical Intensive Care Unit), University Hospital Leiden, The Netherlands. snoeken@worldonline.nl
• Stroke. 1997 Aug 1;28(8):1569-73.

Background And PurposeCerebral blood flow after cardiac arrest is reduced during the delayed hypoperfusion phase, while cerebral metabolic rate of oxygen returns to baseline values. Hypocapnia can induce cerebral ischemia in neurosurgical patients who already have reduced cerebral blood flow. The purpose of the present study was to determine whether comatose patients resuscitated from a cardiac arrest have a normal cerebrovascular reactivity to changes in PaCO2 and whether hypocapnia causes cerebral ischemia.MethodsWe measured mean flow velocity (MFV) and pulsatility index (PI) in the middle cerebral artery, jugular bulb oxygen saturation (SjbO2), and arterial-jugular lactate difference (AJLD) during normo-, hypo-, and hyperventilation in 10 comatose patients resuscitated from a cardiac arrest. The first measurements were made within 6 hours after cardiac arrest and repeated 6, 12, and 24 hours later.ResultsDuring hypoventilation we observed a significant decrease in PI and an increase in MFV and SjbO2. During hyperventilation PI and MFV did not change, but SjbO2 showed a significant decrease. This was accompanied by an increase in AJLD, suggesting cerebral ischemia. In four patients the SjbO2 decreased below the ischemic threshold of 55%.ConclusionsThe cerebrovascular reactivity to changes in arterial carbon dioxide tension is preserved in comatose patients resuscitated from a cardiac arrest. Hyperventilation may induce cerebral ischemia in the postresuscitation period.

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