General anesthesia and exhaled breath hydrogen peroxide

Abstract

To study the role of free radical formation on the impairment of pulmonary function seen with general anesthesia, we measured the hydrogen peroxide (H2O2) concentration in the exhaled breath condensate of 27 patients. Patients were divided into three study groups: a healthy patient group (group 1, n = 15) consisting of ASA physical status 1 and 2 patients undergoing elective noncardiothoracic surgery; a specific anesthetic event group (group 2, n = 6) composed of patients undergoing cardiopulmonary bypass (CPB); and a positive control group (group 3, n = 6) consisting of patients with the adult respiratory distress syndrome (ARDS). The exhaled breath condensate was collected by diverting exhaled breath through a glass condensation coil submerged in an ice/salt water bath. The exhaled breath condensate samples were then assayed using a spectrophotometric method. In group 1, samples were collected before and after the induction of general anesthesia with intravenous drugs, and before and after the administration of the inhalational anesthetics isoflurane (1.5%) (n = 7) or N2O (70%) (n = 8). In group 2, samples were collected pre- and post-CPB, and in group 3, when specific diagnostic criteria for ARDS were met. There was no significantly detectable H2O2 (not significantly different from zero) in any of the samples from the group 1 patients. Similarly, group 2 patients had exhaled breath H2O2 concentrations near zero except for one patient who was positive for the lupus anticoagulant. Group 3 patients had a mean (± SE) exhaled breath H2O2 concentration of 0.55 (± 0.08) μM, which was significantly greater than zero (P < 0.001). We conclude that neither the intravenous induction of general anesthesia nor the maintenance of anesthesia with clinically relevant concentrations of N2O or isoflurane increases the H2O2 production in the exhaled breath of healthy patients undergoing elective noncardiothoracic surgery. Similarly, patients without active pulmonary disease undergoing CPB did not demonstrate any significant exhaled breath H2O2, whereas patients with ARDS elaborated increased amounts. Mechanisms other than increased H2O2 production are probably responsible for the decrement in pulmonary function usually seen with general anesthesia.