The effects of CO2 on respiratory mechanics in anesthetized paralyzed humans

Background: There is little information concerning the carbon dioxide-related effects on respiratory mechanics in anesthetized, paralyzed subjects; however, hypocapnia or hypercapnia is often permitted in patients with severe brain injury or acute respiratory distress syndrome. Therefore, the carbon dioxide dependence of respiratory mechanics in healthy anesthetized, paralyzed subjects was investigated. Methods: Interrupter resistance (Rint), additional tissue viscoelastic resistance (DeltaR), and quasi-static elastance (Est) of lung (L) and chest wall were assessed by means of the rapid end-inspiratory occlusion method in two groups of seven healthy paralyzed subjects anesthetized with diazepam or isoflurane. They underwent ventilation with a fixed pattern and hyperoxic gas mixtures with different fractions of inspired carbon dioxide (FICO2) to produce a partial pressures of arterial carbon dioxide (PaCO2) of 24.4 +/- 3.4, 39.6 +/- 3.2, and 62 +/- 4.1 (SD) mmHg. Results: Chest wail mechanics and Est,L were unaffected by PaCO2 changes. With diazepam anesthesia, Rint,L decreased linearly, with increasing PaCO2, from 2.3 to 1.4 cm H2O.s.I-1, whereas DeltaR,L decreased from 2 to 1.7 cm H2O.s.I-1, though not significantly. With isoflurane anesthesia, the decrease of Rint,L (0.2 +/- 05 cm H2O.s.I-1) was not significant, and Delta RL remained unchanged. With diazepam Rint,L was 45 (hypercapnia) to 110% (hypocapnia) greater than with isoflurane. Conclusions: Changes of PaCO2 from 20-65 mmHg cause in creasing bronchodilation in anesthetized paralyzed subjects, this effect being attenuated or abolished by drugs (e.g., halogenated anesthetics) that depress smooth muscle tone substantially. The carbon dioxide bronchodilating effects are probably direct for peripheral structures and are paralleled by a tendency of lung tissue resistance to decrease. Because local PaCO2-related changes in bronchomotor tone promote (V) over dotA/(Q) over dot matching, this mechanism should be impaired by anesthetics that cause bronchodilation.