Anesthesiology
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End-tidal CO2 (PETCO2), arterial CO2 (PaCO2), mixed expired CO2 (PECO2), arterial and mixed venous oxygen contents were measured and the PaCO2 to PETCO2 difference (delta PCO2), physiologic dead space to tidal volume ratios (VD/VT) and venous admixture (Qs/Qt) were calculated in 41 anesthetized infants and children undergoing repair of congenital cardiac lesions. Eighteen children were acyanotic; 9 with normal pulmonary blood flow (PBF) and normal intracardiac anatomy (normal group); and 9 with increased PBF (acyanotic group). Twenty-three children were cyanotic; 14 with right to left intracardiac shunts and decreased PBF (cyanotic (D) group); and 9 with mixing lesions with normal or increased PBF (cyanotic (I) group). ⋯ Mean +/- SD VD/VT for the normal and acyanotic groups were 0.35 +/- 0.17 and 0.39 +/- 0.19, respectively (NS). Corresponding values for the cyanotic (D) group and cyanotic (I) group were 0.38 +/- 0.16 and 0.55 +/- 0.16, respectively (NS), and were significantly greater than those from the normal and acyanotic groups (P less than 0.05). The relationship of delta PCO2 to VD/VT and Qs/Qt demonstrated that VD/VT was the most important determinant of delta PCO2, but in instances where Qs/Qt were large (e.g., cyanotic congenital heart disease) the percentage contribution of Qs/Qt to the delta PCO2 can be considerable.(ABSTRACT TRUNCATED AT 250 WORDS)
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The effect of hypocapnia on autoregulation of cerebral blood flow (CBF) and the lower limit of autoregulation (LLA) was determined in dogs anesthetized with nitrous oxide (66%) and halothane (0.2%, end-expired concentration). CBF and cerebral vascular resistance (CVR) were determined during both normocapnia and hypocapnia (PaCO2 21-22 mmHg) at control cerebral perfusion pressure (CPP) and after reducing CPP (by hemorrhage) to 80%, 60%, 50%, and 40% of control. At control CPP hypocapnia decreased CBF from 75 +/- 5 to 48 +/- 3 ml.100 g-1.min-1 (mean +/- SEM, P less than 0.05). ⋯ Below the LLA the CBF-CPP slopes differed from zero but did not differ between hypocapnia and normocapnia. Hypocapnia does not produce a substantial shift of the LLA, and over the range of CPP values studied here, autoregulatory cerebral vasodilation only partially abolishes hypocapnia-induced cerebral vasoconstriction. The results suggest that when cerebral autoregulation is intact and in the absence of cerebrovascular disease, hypocapnia does not reduce global CBF to a level that is likely to produce ischemia and remains a useful therapeutic treatment so long as CPP remains above the LLA.