Increases in hemodynamic variables and catecholamine levels after rapid increase in isoflurane concentration.

Abstract

Ventilation of the lungs with isoflurane in nitrous oxide and oxygen has been shown to increase the plasma concentration of norepinephrine. Whether this increase is related to the tachycardia and increased arterial blood pressures, seen following a sudden increase in the concentration of isoflurane, was tested in humans. Twenty-two healthy patients in whom the trachea was intubated were given 15 min of stable isoflurane-O2-air anesthesia [end-tidal concentration of isoflurane (ETIso) of 1.3%] (baseline). Patients were then randomly allocated to one of two groups. For 13 "IsoHigh" patients, the inspired concentration of isoflurane was increased abruptly. In those patients, the ETIso was kept at 2.6% for 10 min, i.e., until the end of the study, after which the depth of anesthesia was reduced. For nine "IsoLow" control patients, the ETIso level of 1.3% was continued until the end of the study. Heart rate, arterial pressures, catecholamine levels, and end-tidal concentration of CO2 were recorded at baseline and at 1, 1.5, 2, 4, 6, and 10 min after increase in isoflurane. IsoHigh patients showed significant increases in heart rate (40% from 84.6 to 118.1 beats/min), systolic arterial pressure (SAP, 23%, from 96.4 to 118.3 mmHg), and diastolic arterial pressure (DAP, 30%, from 53.9 to 70.0 mmHg); all three variables peaked at 2 min. Significant increases occurred also in norepinephrine levels (80%, from 0.342 to 0.615 ng/ml) and in end-tidal concentration of CO2 (from 4.22% to 4.43%), both of which peaked at 4 min. Epinephrine levels did not increase significantly, although significant differences were seen between IsoHigh and IsoLow patients during the trial. IsoLow patients had no changes in these variables. A sudden increase in isoflurane concentration is associated with a transient but clinically significant increase in heart rate, arterial pressures, and norepinephrine concentration.