Response of the Cerebral Circulation to Profound Hypocarbia in Neonatal Lambs

Hyperventilation to extremely low arterial carbon dioxide tension (Paco2) has been used in the management of persistent pulmonary hypertension in newborn infants. With progressive hypocarbia, cerebral vasoconstriction occurs, raising the concern that extreme hypocarbia may result in cerebral oxygen deprivation. Therefore, I evaluated regulation of the cerebral circulation during acute hypocarbia in 10 newborn lambs. Whole-brain and regional blood flows measured using radioactive microspheres, arterial and venous (sagittal sinus) blood gases, and oxygen contents were measured in each lamb at four arterial carbon dioxide tensions. Whole-brain oxygen delivery, oxygen consumption, and fractional oxygen extraction were calculated. Finally, arterial and venous lactate concentrations were measured to assess cerebral lactate production. Whole-brain blood flow (CBF) decreased in a nonlinear fashion as Paco2 ranged from 46 to 12 mm Hg [ln(CBF) = 0.025(Paco2) + 3.38; r=0.70, p<0.001]. Similar responses were demonstrated for all regional blood flows examined. Cerebral fractional oxygen extraction (E) increased in a nonlinear fashion [ ln ( l-E) = 0.023(Paco2)-1.37; r=0.80, /»<0.001], and cerebral metabolic rate for oxygen was unchanged with hypocarbia. Cerebral venous lactate concentration increased significantly (3.49 ±0.23 vs. 2.01 ±0.22 mM, p<0.001