Background and Purpose—Under normal circumstances, autoregulation maintains cerebral blood flow (CBF) constant within a wide range of mean arterial pressure (MAP). It remains unknown whether patients resuscitated from cardiac arrest have preserved CBF autoregulation. In this study, CBF autoregulation was investigated within the first 24 hours after resuscitation from cardiac arrest. Methods—Eighteen patients and 6 healthy volunteers had relative changes in CBF determined by transcranial Doppler mean flow velocity (V mean) in the middle cerebral artery during a stepwise rise in MAP by use of norepinephrine infusion. V mean was plotted against MAP, and a lower limit of autoregulation was identified by double regression analysis based on the least-squares method. Results—In patients, V mean increased from a median of 33 (range 19 to 73) to 37 (22 to 100) cm/s (PϽ0.001) during a norepinephrine-induced rise in MAP from 78 (46 to 118) to 106 (60 to 149) mm Hg. Eight of 18 patients had impaired CBF autoregulation, and in 5 of the 10 patients with preserved CBF autoregulation, the lower limit of autoregulation could be identified. The lower limit of CBF autoregulation was 76 mm Hg (41 to 105 mm Hg) in the volunteers and 114 mm Hg (80 to 120 mm Hg) in the 5 patients with preserved autoregulation (PϽ0.01). Conclusions—We conclude that in a majority of patients in the acute phase after cardiac arrest, cerebral autoregulation is either absent or right-shifted. These results indicate that MAP should be kept at a higher level than commonly accepted to secure cerebral perfusion. We recommend, however, that further randomized clinical trials are performed to determine whether sympathomimetic drugs improve neurological outcome. (Stroke. 2001;32:128-132.) Key Words: arrest Ⅲ arterial pressure Ⅲ brain Ⅲ cerebral blood flow Ⅲ norepinephrine Ⅲ perfusion Ⅲ resuscitation Ⅲ transcranial Doppler I n patients resuscitated from cardiac arrest, neurological outcome depends on prompt restoration of systemic circu-lation and oxygenation to meet the cerebral oxygen demand. Experimental studies of cerebral blood flow (CBF) after resuscitation indicate that a brief episode of transient and multifocal absence of perfusion is followed by a short period of global cerebral hyperemia 1 associated with a high meta-bolic rate of oxygen (CMRO 2) and glucose. Subsequently, cerebral hypoperfusion with a parallel reduction of CMRO 2 develops. 1–3 Little is known about the regulation of CBF during these phases. Normally, changes in arterial pressure have only a minor influence on CBF because of reactive dilatation and constric-tion of cerebral resistance vessels in response to arterial hypotension and hypertension, ie, CBF autoregulation. 4 In experimental studies of global cerebral ischemia, a preserved CBF autoregulation in the delayed hypoperfusion period has been reported. 5–7 In patients studied 3 days after resuscitation from cardiac arrest, it has been found that the internal jugular vein oxygen saturation increases when mean arterial pressure (MAP) increases during norepinephrine infusion. 8 Whether this reflects impairment of autoregulation, a decrease in the cerebral metabolic rate of oxygen (CMRO 2), or an increase in the perfusion of the extracerebral tissue drained into the internal jugular vein remains to be settled. In this study, we tested the hypothesis that patients resus-citated from cardiac arrest have impaired CBF autoregulation in the secondary delayed hypoperfusion period. Thus, the purpose of this study was to determine whether CBF auto-regulation is compromised within the first 24 hours after resuscitation from cardiac arrest.
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