Remifentanil induces systemic arterial vasodilation in humans with a total artificial heart
Remifentanil induces systemic arterial vasodilation in humans with a total artificial heart
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DOI：
10.1097/00000542-200403000-00021
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发表时间：
2004-03-01
期刊：
影响因子：
8.8
通讯作者：
Coriat, P
中科院分区：
文献类型：
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作者：
Ouattara, A;Boccara, G;Coriat, P
背景：为了评估瑞芬太尼对血管的内在影响，我们对装有全人工心脏的危重病人输注了浓度较高的瑞芬太尼。方法：选取全人工心脏植入术后早期需要短时间全身麻醉的通气患者9例。静脉注射0.3 mg/kg依托咪酯诱导麻醉后，修改人工心脏设置，使心输出量“独立于负荷前”。在持续输注依咪酯确保麻醉维持的同时，在血流动力学监测下，分5分钟输注瑞芬太尼浓度（从0.1到1马克杯（.）千克（-1）分钟），包括左右心房压、全身和肺动脉压以及左右心脏指数。侵入性手术在患者耐受的最高浓度的瑞芬太尼下开始。有创手术结束时停止输注瑞芬太尼，维持输注依托咪酯。在12分钟恢复期结束时进行新的血流动力学测量。结果：瑞芬太尼浓度为0.25马克杯（.）千克（-1）分钟（-1）时，可产生剂量依赖性且显著降低全身动脉压和血管阻力（n = 9）。肺血管阻力无明显变化（n = 6）。右心房压（n = 9）和左心房压（n = 6）均未受瑞芬太尼输注的影响。血流动力学指标在12分钟恢复期恢复到基线值。结论：在人类全人工心脏中，瑞芬太尼诱导全身动脉血管扩张，对电容血管无明显影响。
Background: To assess intrinsic vascular effects of remifentanil, increased concentrations were infused in critically ill patients with a total artificial heart.Methods: In the early postoperative period after implantation of a total artificial heart, nine ventilated patients requiring short general anesthesia were included in this study. After anesthesia was induced with 0.3 mg/kg intravenous etomidate, the artificial heart settings were modified to render cardiac output "preload-independent." While maintenance of anesthesia was ensured by a continuous infusion of etomidate, increased concentrations of remifentanil (from 0.1 to 1 mug(.)kg(-1.)min(-1)) were infused in steps of 5 min under hemodynamic monitoring, including left and right atrial pressures, systemic and pulmonary arterial pressures, and left and right cardiac indices. The invasive procedure was started under the highest concentration of remifentanil tolerated by the patient. Infusion of remifentanil was stopped at the end of the invasive procedure, while etomidate infusion was maintained. New hemodynamic measurements were performed at the end of the 12-min recovery period.Results: Remifentanil produced a dose-depcndent and significant decrease in systemic arterial pressure and vascular resistances (n = 9) from a concentration of 0.25 mug(.)kg(-1.)min(-1). No significant changes were observed on pulmonary vascular resistances (n = 6). Neither right (n = 9) nor left (n = 6) atrial pressures were affected by remifentanil infusion. Hemodynamic variables returned to baseline value over the 12-min recovery period.Conclusions: In humans with a total artificial heart, remifentanil induces a systemic arterial vasodilation without significant effect on the capacitance vessels.