Volume 12 Supplement 2
Cerebral blood flow and cerebrovascular reactivity during hypothermia after cardiac arrest
© BioMed Central Ltd 2008
Published: 13 March 2008
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.
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.
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).
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.
This article is published under license to BioMed Central Ltd.