Thoracic epidural anesthesia impairs the hemodynamic response to acute pulmonary hypertension by deteriorating right ventricular-pulmonary arterial coupling.

OBJECTIVE

Thoracic epidural anesthesia is increasingly used in critically ill patients. This analgesic technique was shown to decrease left ventricular contractility, but effects on right ventricular function have not been reported. A deterioration of right ventricular performance may be clinically relevant for patients with acute pulmonary hypertension, in which right ventricular function is an important determinant of outcome. In the present study, we tested the hypothesis that thoracic epidural anesthesia decreases right ventricular contractility and limits its capacity to tolerate pulmonary hypertension.

DESIGN

Prospective, placebo-controlled study using an established model of acute pulmonary hypertension.

SETTING

University hospital laboratory.

SUBJECTS

A total of 14 pigs (mean weight, 35 +/- 2 kg).

INTERVENTIONS

After instrumentation with an epidural catheter, biventricular conductance catheters, a pulmonary flow probe, and a high-fidelity pulmonary pressure catheter, seven pigs received thoracic epidural anesthesia and seven pigs served as control. Hemodynamic measurements were performed in baseline conditions and after induction of pulmonary hypertension via hypoxic pulmonary vasoconstriction (Fio2 of 0.15).

MEASUREMENTS AND MAIN RESULTS

Ventricular contractility was assessed using load- and heart rate-independent variables. Right ventricular afterload was characterized with instantaneous pressure-flow measurements. In baseline conditions, thoracic epidural anesthesia decreased left but not right ventricular contractility. In untreated animals, pulmonary hypertension was associated with an increase in right ventricular contractility and cardiac output. Pretreatment with thoracic epidural anesthesia completely abolished the positive inotropic response to acute pulmonary hypertension. As a result, ventriculo-vascular coupling between the right ventricle and pulmonary-arterial system deteriorated, and cardiac output was significantly lower in animals with thoracic epidural anesthesia than in untreated controls during hypoxia-induced pulmonary hypertension.

CONCLUSIONS

Thoracic epidural anesthesia inhibits the native positive inotropic response of the right ventricle to increased afterload and deteriorates the hemodynamic effects of acute pulmonary hypertension.