Cerebral blood flow and cerebrovascular reactivity during hypothermia after cardiac arrest

Introduction

Anoxic neurological injury is a major cause of morbidity and mortality in cardiac arrest patients. After restoration of spontaneous circulation, pathophysiological changes in cerebral perfusion appear, known as postresuscitation syndrome. In the delayed hypoperfusion phase, the cerebral blood flow is reduced, resulting in a potential mismatch between cerebral oxygen supply and demand, and secondary neurological damage. The aim of this study was to assess cerebral blood flow and cerebrovascular reactivity to changes in PaCO₂ in patients after cardiac arrest treated with mild hypothermia.

Methods

We performed an observational study in 10 adult comatose patients after out-of-hospital cardiac arrest. All patients were cooled to 32–34°C for 24 hours, followed by passive rewarming. Blood flow velocity in the middle cerebral artery (MCA) was measured by transcranial doppler. Oxygen saturation in the jugular bulb (SjbO₂) was measured by repeated blood sampling. Hypocapnia and hypercapnia were induced by a 20% increase and decrease in minute ventilation during 20 minutes. Data are expressed as the mean ± SEM. Changes over time were analysed by ANOVA. The relation between MCA velocity and SjbO₂ was determined by linear regression analysis.

Results

We present the results of the first five patients. All patients were male, with a mean age of 66 ± 5 years. Ventricular fibrillation was the cause of cardiac arrest in all patients. The mean time from collapse to return of spontaneous circulation was 25 ± 15 minutes. At the start of the experiment, mean flow velocity in the MCA was low (32.2 ± 9.6 cm/s), increasing significantly to 62.5 ± 11.3 cm/s at 48 hours (P < 0.001). The SjbO₂ at the start of the experiment was 68.2 ± 4.0%, increasing significantly to 79.7 ± 3.8% at 48 hours (P < 0.001). Regression analysis showed that the change in SjbO₂ correlated significantly with the change in PaCO₂ (P < 0.001). A 1 kPa decrease in PaCO₂ resulted in a 9.5% decrease in SjbO₂. A decrease in PaCO₂ also resulted in decreased flow velocities in the MCA (P = 0.09).

Conclusion

During mild hypothermia after cardiac arrest, MFV in the MCA is low, suggesting active cerebral vasoconstriction. Cerebrovascular reactivity to changes in PaCO₂ is preserved in comatose cardiac arrest patients during mild hypothermia. Hyperventilation may induce cerebral ischemia in the postresuscitation period.