Abstract
Aim of the studyEstimation of cerebral anaerobic metabolism in survivors and non-survivors after cardiac arrest. MethodsWe 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 (MFVMCA) 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. ResultsAfter cardiac arrest, MFVMCA 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 MFVMCA 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. ConclusionsIn 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.
Highlights
Cardiac arrest is a leading cause of death in western countries, and most patients die from neurological injury [1]
Whether this decrease in metabolic rate is proportional to the decrease in cerebral blood flow (CBF): disproportional adaptation of CBF to metabolism may result in hypoperfusion and ischemia or hyperperfusion and hyperemia
The changes in jugular CO2 content were accompanied by a continuing decrease in O2EF in patients with a poor outcome, whereas a gradual restoration of O2EF towards normal values occurred in surviving patients
Summary
Cardiac arrest is a leading cause of death in western countries, and most patients die from neurological injury [1]. In comatose patients after cardiac arrest, CBF is initially low and gradually restores towards normal values during the first 72 h after return of spontaneous circulation (ROSC) [2,3,4]. Previous studies reported a decrease in the cerebral metabolic rate of oxygen, secondary to the cardiac arrest, providing a teleological mechanism to match this decreased supply of oxygen and nutrients to the brain [2,3,4] It is yet unknown, whether this decrease in metabolic rate is proportional to the decrease in CBF: disproportional adaptation of CBF to metabolism may result in hypoperfusion and ischemia or hyperperfusion and hyperemia
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