Epidural anesthesia modifies the cardiovascular response to marked hypercapnia in dogs

There is little information on the cardiovascular response to marked hypercapnia during epidural anesthesia (EA). Our objective was to assess the potential modifying effects of various levels of EA on this response.

We randomly assigned 48 mongrel dogs anesthetized with halothane (0.5%) to one of four groups: control (n = 12), receiving general anesthesia alone; lumbar (n = 12), also receiving lumbar EA; thoracic (n = 12), also receiving thoracic EA; and thoracolumbar (n = 12), also receiving thoracolumbar EA. During marked hypercapnia (mean arterial CO2 tension > 90 mmHg for 15 min), we measured hemodynamic parameters and plasma catecholamine concentrations in each group.

In the control condition, marked hypercapnia increased cardiac output, reduced systemic vascular resistance, modestly increased mean arterial blood pressure. Lumbar EA abolished the increase in cardiac output, and thoracic and thoracolumbar EA caused CO2 to depress the cardiac output and the mean arterial blood pressure during marked hypercapnia. The physiologic increase in circulating catecholamines during marked hypercapnia was abolished only in the thoracolumbar EA group.

We conclude that sympathetic blockade by EA modifies the cardiovascular response to marked hypercapnia in dogs. Although modest hypoventilation is often effective in treating hypotension during general anesthesia, the current results suggest that hypoventilation may be detrimental during the combination of EA and general anesthesia.