胸段硬膜外麻醉降低右心室收缩功能而不影响心室-肺耦联。
Thoracic Epidural Anesthesia Reduces Right Ventricular Systolic Function With Maintained Ventricular-Pulmonary Coupling.
机构信息
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.).
出版信息
Circulation. 2016 Oct 18;134(16):1163-1175. doi: 10.1161/CIRCULATIONAHA.116.022415. Epub 2016 Sep 14.
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 (ΔESV: +25.5 mL, P=0.0003; ΔEes: -0.025 mm Hg/mL, P=0.04). Stroke work, dP/dt, 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 (ΔESV: -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.
背景
胸段硬膜外麻醉阻滞心脏交感神经纤维可能会影响右心室功能，并干扰右心室功能与右心室后负荷之间的耦联。我们的主要目的是研究胸段硬膜外麻醉对右心室功能和心室-肺耦联的影响。
方法
在 10 例行肺切除术的患者中，使用组合压力-导纳导管在诱导胸段硬膜外麻醉前后测试右心室功能及其对肺动脉临时单侧夹闭引起的后负荷增加的反应。
结果
胸段硬膜外麻醉导致右心室收缩性显著降低（ΔESV：+25.5mL，P=0.0003；ΔEes：-0.025mmHg/mL，P=0.04）。收缩功能的每搏功、dp/dt 和射血分数也显示出类似的下降（均 P<0.05）。有效动脉弹性（ΔEa：-0.094mmHg/mL，P=0.004）的同时下降导致心室-肺耦联不变。心输出量、全身血管阻力和平均动脉血压保持不变。肺动脉夹闭显著增加了后负荷（ΔEa：+0.226mmHg/mL，P<0.001）。作为回应，右心室收缩性增加（ΔESV：-26.6mL，P=0.0002；ΔEes：+0.034mmHg/mL，P=0.008），但心室-肺耦联降低（Δ（Ees/Ea）=-0.153，P<0.0001）。测量的指标均未显示出显著的交互作用，这表明在胸段硬膜外麻醉前后，增加后负荷的影响是相同的。
结论
胸段硬膜外麻醉会损害右心室收缩性，但不会抑制右心室对增加后负荷的固有正性肌力反应。右心室-肺动脉耦联在增加后负荷时降低，但不受胸段硬膜外麻醉的影响。
临床试验注册
网址：http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=2844. 独特标识符：NTR2844。
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