Effects of Thoracic Epidural Anesthesia on Hemodynamic Changes Induced by Hypercapnia during Sevoflurane Anesthesia

Objective: Many studies have demonstrated that carbon dioxide has direct depressive effects on the myocardium and dilates the vascular bed. However, it leads to an increase in arterial blood pressure and cardiac output because of sympathetic stimulating effect. Extensive epidural block may impair the sympathetic innervation to the heart as well as to the adrenal gland. The present study was set up in order to investigate how an extensive epidural block would affect the hemodynamic response to sympathetic stimulation induced by hypercapnia. Methods: Twenty patients were mechanically ventilated under general anesthesia after epidural catheter insertion on T6–T7 intervertebral space. Hypercapnia was obtained by CO2 breathing. PaCO2 (partial pressure of CO2, arterial) was adjusted to 30, 45, and 60 mm Hg with each concentration being maintained for 10 minutes. In each period, hemodynamic variables were monitored by pulmonary artery catheter. After returning to normocarbia for 15 minutes, 20 mL of 0.375% ropivacaine was injected epidurally and PaCO2 was adjusted in the same manner, and then, the hemodynamic variables of each period were checked. Results: There were no changes in mean arterial pressure and heart rate by hypercapnia after combined epidural anesthesia compared with general anesthesia only. Hypercapnia increased cardiac output and cardiac index. Systemic vascular resistance was decreased significantly. Pulmonary artery pressure was increased but not significantly. The degrees of hemodynamic changes were similar between in general anesthesia alone and in combined epidural anesthesia. Conclusion: In spite of an extensive epidural block, hemodynamic changes induced by hypercarbnia were not changed. There are some ‘escaped’ sympathetic nerve fibers.