Hypercapnia augments cardiac output and can initiate a sympathetically mediated release of catecholamines to increase cardiac output. Many studies of hemodynamic changes by hypercapnia under general anesthesia with inhalation anesthetics besides sevoflurane. This study examined the hemodynamic changes by increasing end-tidal carbon dioxide (EtCO₂) under sevoflurane-N₂O anesthesia.

Twenty patients were enrolled in the study. We studied stable, mechanically ventilated patients under general anesthesia maintained with O₂ 2 L/min - N₂O 2 L/min - sevoflurane (1.5-2.5 vol%). Hypercapnia were obtained by reducing tidal volume and respiratory rate. EtCO₂ was adjusted to 30, 40, 50 mmHg with each concentration maintained for 15 min. Global hemodynamic variables were monitored with a pulmonary artery catheter.

There were no changes in mean arterial pressure or heart rate by hypercapnia. Acute moderate hypercapnia increased cardiac output (4.9 ± 1.7, 5.5 ± 1.7, 6.2 ± 2.1 L/min; P < 0.05), cardiac index (3.0 ± 0.9, 3.4 ± 0.9, 3.8 ± 1.1 L/min/m²; P < 0.05), pulmonary artery pressure (16.9 ± 3.7, 19.6 ± 4.2, 23.0 ± 4.7 mmHg), but did not decrease systemic vascular resistance (1,558.3 ± 500.4, 1,423.5 ± 678.6, 1,156.8 ± 374.0 dynes·sec/cm⁵; P > 0.05).

When we changed patient EtCO₂ to 30, 40, and 50 mmHg, there were no changes in mean arterial blood pressure and heart rate, but systemic vascular resistance decreased, and cardiac output, cardiac index and mean pulmonary arterial pressure increased significantly.