Rex Steffen, Missant Carlo, Segers Patrick, Wouters Patrick F
Laboratory for Experimental Anesthesiology, Department of Acute Medical Sciences, Katholieke Universiteit Leuven, Leuven, Belgium.
Crit Care Med. 2007 Jan;35(1):222-9. doi: 10.1097/01.CCM.0000250357.35250.A2.
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.
Prospective, placebo-controlled study using an established model of acute pulmonary hypertension.
University hospital laboratory.
A total of 14 pigs (mean weight, 35 +/- 2 kg).
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).
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.
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.
胸段硬膜外麻醉在危重症患者中的应用日益广泛。该镇痛技术已被证明会降低左心室收缩力，但对右心室功能的影响尚未见报道。右心室功能恶化对于急性肺动脉高压患者可能具有临床意义，因为右心室功能是其预后的重要决定因素。在本研究中，我们检验了以下假设：胸段硬膜外麻醉会降低右心室收缩力并限制其耐受肺动脉高压的能力。
采用已建立的急性肺动脉高压模型进行前瞻性、安慰剂对照研究。
大学医院实验室。
共14头猪（平均体重35±2千克）。
在置入硬膜外导管、双心室电导导管、肺血流探头和高保真肺动脉导管后，7头猪接受胸段硬膜外麻醉，7头猪作为对照。在基线条件下以及通过低氧性肺血管收缩诱导肺动脉高压后（吸入氧分数为0.15）进行血流动力学测量。
使用与负荷和心率无关的变量评估心室收缩力。通过瞬时压力-流量测量来表征右心室后负荷。在基线条件下，胸段硬膜外麻醉降低了左心室而非右心室的收缩力。在未治疗的动物中，肺动脉高压与右心室收缩力和心输出量增加有关。胸段硬膜外麻醉预处理完全消除了对急性肺动脉高压的正性肌力反应。结果，在低氧诱导的肺动脉高压期间，右心室与肺动脉系统之间的心室-血管耦联恶化，接受胸段硬膜外麻醉的动物的心输出量显著低于未治疗的对照组。
胸段硬膜外麻醉抑制了右心室对后负荷增加的固有正性肌力反应，并使急性肺动脉高压的血流动力学效应恶化。
