Cerebrovascular Reactivity to CO2 in Patients with Metabolic Encephalopathy

The effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) and cerebral metabolic rate for oxgen (CMRO2) were evaluted in 7 patients with hepatic or septec encephalopathy. A positive linear relationship between CBF and PaCO2 was observed in hepatic patients (CBF=3.12PaCO2-81.4,r=0.739) and in septic patients (CBF=1.96PaCO2-36.1, r=0.535). Although these regression equations were not statistically different from that of awake patients (CBF=0.87PaCO2+12.0,r=0.866),　a tendency to augment the cerebrovas cular reactivity to CO2 was observed in patients with hepatic or septec encephalopathy. Therefore, hypocapnic- hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 7 patients. As an index of cerebral ischemia, the ratio of CBF to CMRO2 was examined in the same patients during alteration of PaCO2. A good limer correlation was observed between CBF/CMRO2 and juglar venous PO2 (JPvO2) (CBF/CMRO2=0.97JPvO2-15,4, r=0.917). It is concluded that cerebrovascular reactivity to CO2 was preserved in patients with hepatic and septic encephalopathy, therefore, intentional or inadvertent hyperventilation may produce cerebral ischemia in these patients. The JPvO2 may be useful as a monitor for cerebral oxgenation in patients with metabolic encephalopathy.

Metabolic encephalopathy

CBF

CO2 response

Hyperventilation

Brain hypoxemia