Jeroen Wink1, Rob B P de Wilde2, Patrick F Wouters2, Eveline L A van Dorp2, Bernadette Th Veering2, Michel I M Versteegh2, Leon P H J Aarts2, Paul Steendijk2. 1. From the Department of Anesthesiology (J.W., E.L.A.v.D., B.T.V., L.P.H.J.A.), Department of Intensive Care (R.B.P.d.W.), Department of Cardiothoracic Surgery (M.I.M.V.), and Department of Cardiology (P.S.), Leiden University Medical Center, The Netherlands; and the Department of Anesthesia, University Hospitals Ghent, Belgium (P.F.W.). j.wink@lumc.nl. 2. From the Department of Anesthesiology (J.W., E.L.A.v.D., B.T.V., L.P.H.J.A.), Department of Intensive Care (R.B.P.d.W.), Department of Cardiothoracic Surgery (M.I.M.V.), and Department of Cardiology (P.S.), Leiden University Medical Center, The Netherlands; and the Department of Anesthesia, University Hospitals Ghent, Belgium (P.F.W.).
Abstract
BACKGROUND: Blockade of cardiac sympathetic fibers by thoracic epidural anesthesia may affect right ventricular function and interfere with the coupling between right ventricular function and right ventricular afterload. Our main objectives were to study the effects of thoracic epidural anesthesia on right ventricular function and ventricular-pulmonary coupling. METHODS: In 10 patients scheduled for lung resection, right ventricular function and its response to increased afterload, induced by temporary, unilateral clamping of the pulmonary artery, was tested before and after induction of thoracic epidural anesthesia using combined pressure-conductance catheters. RESULTS: Thoracic epidural anesthesia resulted in a significant decrease in right ventricular contractility (ΔESV25: +25.5 mL, P=0.0003; ΔEes: -0.025 mm Hg/mL, P=0.04). Stroke work, dP/dtMAX, and ejection fraction showed a similar decrease in systolic function (all P<0.05). A concomitant decrease in effective arterial elastance (ΔEa: -0.094 mm Hg/mL, P=0.004) yielded unchanged ventricular-pulmonary coupling. Cardiac output, systemic vascular resistance, and mean arterial blood pressure were unchanged. Clamping of the pulmonary artery significantly increased afterload (ΔEa: +0.226 mm Hg/mL, P<0.001). In response, right ventricular contractility increased (ΔESV25: -26.6 mL, P=0.0002; ΔEes: +0.034 mm Hg/mL, P=0.008), but ventricular-pulmonary coupling decreased (Δ(Ees/Ea) = -0.153, P<0.0001). None of the measured indices showed significant interactive effects, indicating that the effects of increased afterload were the same before and after thoracic epidural anesthesia. CONCLUSIONS: Thoracic epidural anesthesia impairs right ventricular contractility but does not inhibit the native positive inotropic response of the right ventricle to increased afterload. Right ventricular-pulmonary arterial coupling was decreased with increased afterload but not affected by the induction of thoracic epidural anesthesia. CLINICAL TRIAL REGISTRATION: URL: http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2844. Unique identifier: NTR2844.
BACKGROUND: Blockade of cardiac sympathetic fibers by thoracic epidural anesthesia may affect right ventricular function and interfere with the coupling between right ventricular function and right ventricular afterload. Our main objectives were to study the effects of thoracic epidural anesthesia on right ventricular function and ventricular-pulmonary coupling. METHODS: In 10 patients scheduled for lung resection, right ventricular function and its response to increased afterload, induced by temporary, unilateral clamping of the pulmonary artery, was tested before and after induction of thoracic epidural anesthesia using combined pressure-conductance catheters. RESULTS: Thoracic epidural anesthesia resulted in a significant decrease in right ventricular contractility (ΔESV25: +25.5 mL, P=0.0003; ΔEes: -0.025 mm Hg/mL, P=0.04). Stroke work, dP/dtMAX, and ejection fraction showed a similar decrease in systolic function (all P<0.05). A concomitant decrease in effective arterial elastance (ΔEa: -0.094 mm Hg/mL, P=0.004) yielded unchanged ventricular-pulmonary coupling. Cardiac output, systemic vascular resistance, and mean arterial blood pressure were unchanged. Clamping of the pulmonary artery significantly increased afterload (ΔEa: +0.226 mm Hg/mL, P<0.001). In response, right ventricular contractility increased (ΔESV25: -26.6 mL, P=0.0002; ΔEes: +0.034 mm Hg/mL, P=0.008), but ventricular-pulmonary coupling decreased (Δ(Ees/Ea) = -0.153, P<0.0001). None of the measured indices showed significant interactive effects, indicating that the effects of increased afterload were the same before and after thoracic epidural anesthesia. CONCLUSIONS: Thoracic epidural anesthesia impairs right ventricular contractility but does not inhibit the native positive inotropic response of the right ventricle to increased afterload. Right ventricular-pulmonary arterial coupling was decreased with increased afterload but not affected by the induction of thoracic epidural anesthesia. CLINICAL TRIAL REGISTRATION: URL: http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2844. Unique identifier: NTR2844.
Authors: Jeroen Wink; Paul Steendijk; Roula Tsonaka; Rob B P de Wilde; Hans J Friedericy; Jerry Braun; Bernadette Th Veering; Leon P H J Aarts; Patrick F Wouters Journal: Eur J Appl Physiol Date: 2021-02-22 Impact factor: 3.078