Low cerebral blood flow after cardiac arrest is not associated with anaerobic cerebral metabolism

Aim of the study: Estimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest.

Methods: We performed an observational study in twenty comatose patients after cardiac arrest and 19 healthy control subjects. We measured mean flow velocity in the middle cerebral artery (MFV_MCA) by transcranial Doppler. Arterial and jugular blood samples were used for calculation of the jugular venous-to-arterial CO₂/arterial to-jugular venous O₂ content difference ratio.

Results: After cardiac arrest, MFV_MCA increased from 26.0[18.6-40.4]cm/sec on admission to 63.9[48.3-73.1]cm/sec after 72h (p<0.0001), with no significant differences between survivors and non-survivors (p=0.4853). The MFV_MCA in controls was 59.1[52.8-69.0]cm/sec. The oxygen extraction fraction (O₂EF) was 38.9[24.4-47.7]% on admission and decreased significantly to 17.3[12.1-26.2]% at 72h (p<0.0001). The decrease in O₂EF was more pronounced in non-survivors (p=0.0173). O₂EF in the control group was 35.4[32.4-38.7]%. The jugular bulb-arterial CO₂ to arterial-jugular bulb O₂ content difference ratio was >1 at all time points after cardiac arrest and did not change during admission, with no differences between survivors and non-survivors. Values in cardiac arrest patients were similar to those in normal subjects.

Conclusions: In this study, low CBF after cardiac arrest is not associated with anaerobic metabolism. Hypoperfusion appears to be the consequence of a decrease of neuronal functioning and metabolic needs. Alternatively, hypoperfusion may decrease cerebral metabolism. Subsequently, metabolism increases in survivors, consistent with resumption of neuronal activity, whereas in non-survivors lasting low metabolism reflects irreversible neuronal damage.