Cerebrovascular reactivity in comatose patients resuscitated from a cardiac arrest.

Abstract:

BACKGROUND AND PURPOSE:Cerebral 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. METHODS:We 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. RESULTS:During 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%. CONCLUSIONS:The 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.

journal_name

Stroke

journal_title

Stroke

authors

Buunk G,van der Hoeven JG,Meinders AE

doi

10.1161/01.str.28.8.1569

subject

Has Abstract

pub_date

1997-08-01 00:00:00

pages

1569-73

issue

8

eissn

0039-2499

issn

1524-4628

journal_volume

28

pub_type

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