Influence of high thoracic epidural anesthesia on left ventricular contractility assessed using the end‐systolic pressure‐length relationship

Abstract

The effect of high thoracic epidural anesthesia (TEA on left ventricular contractility was studied in a prospective clinical trial. Forty-eight patients with ASA physical status 1 and 2 and without cardiovascular disease were included in the study. Thirty-six patients scheduled for elective upper abdominal surgery were randomly assigned to Group 1 (TEA, bupivacaine 0.25%, n = 12), Group 2 (TEA, bupivacaine 0.5%, n = 12) or to Group 3 (control without TEA, n = 12). TEA induced a sensory block which extended over all cardiac segments. In order to assess the effect of systemically absorbed bupivacaine, we studied a separate group of patients who received lumbar epidural anesthesia without involvement of the cardiac segments: Group 4 (LEA, bupivacaine 0.5%, n = 10). Left ventricular contractility was assessed using the end-systolic pressure-length relationship. Left ventricular dimensions were measured by transesophageal echocardiography. All hemodynamic measurements were performed under general anesthesia. There was no significant difference in systolic or diastolic arterial pressure, heart rate, left ventricular end-systolic and end-diastolic cross-sectional areas and left ventricular wall stress between the four groups. Left ventricular maximum elastance as a measure of left ventricular contractility was significantly (P < 0.001) reduced in Groups 1 and 2 [8.1 (+/- 3.5) and 9.6 (+/- 4.4) kPa.cm-1, respectively] as compared to Groups 3 and 4 [18.4 (+/- 8.8) and 17.7 (+/- 7.7) kPa.cm-1, respectively]. No significant difference could be demonstrated between Groups 1 and 2 or between Groups 3 and 4. It is concluded that high TEA severely alters left ventricular contractility even in subjects without pre-existing cardiac disease.

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits

“…Goertz et al reported that high thoracic EA decreases Ees in humans by 50%. 30 The decrease in Ees in humans is similar to that observed during thoracolumbar EA in the present study. Thoracolumbar EA causes the blockade of afferences and efferences between the heart and the central nervous system (cardiac denervation).…”

“…In spite of several previous clinical and experimental studies, questions remain about the effect of EA on left ventricular contractility, which has variously been reported to be unchanged, 27,28 decreased, 29,30 or even increased. 31,32 This variability is attributable to differences in study design, the subjects studied, and the measures used to assess left ventricular contractility.…”

Thoracic epidural blockade preserves left ventricular early diastolic filling assessed by transesophageal echocardiography

“…Goertz et al [9] administered about 20ml of mepivacaine (0.25% and 0.5%) in the thoracic epidural space and found that TEA produced no significant change in any of the systolic, diastolic, MAP, HR, LV endsystolic and end-diastolic areas, and ESWS, although the LV maximal elastance (Emax) was reduced significantly by TEA. E .... is known to be a most powerful indicator of LV contractility independently of loading conditions, derived from the pressure-volume relationship [15].…”

“…High TEA has been reported to impair LV systolic function with a blockade of cardiac sympathetic segments [8][9][10][11][12]. However, this observation remains controversial.…”

Acute Postoperative Pain Control Following Thoracic Surgery

“…The extent of sympatholysis may be variable, and only loosely related to the sensory level. TEA sympathetic blockade extending to the "cardiac accelerators" (T1-T4) likely exerts a negative inotropic eff ect, ( 8 ) in addition to eff ects on loading conditions. Vascular tone: TEA sympatholysis results in vasodilation and increased venous and arterial capacitance.…”