The hemodynamic response to dexmedetomidine loading dose in children with and without pulmonary hypertension.

The hemodynamic response to dexmedetomidine loading dose in children with and without pulmonary hypertension.
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DOI:
10.1213/ane.0b013e3182a15aa6
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发表时间:
2013-10
影响因子:
5.7
通讯作者:
Ivy DD
Ivy DD
中科院分区:
医学2区
文献类型:
--
作者:
Friesen RH;Nichols CS;Twite MD;Cardwell KA;Pan Z;Pietra B;Miyamoto SD;Auerbach SR;Darst JR;Ivy DD

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右美托咪定是一种α-2受体激动剂,广泛用于儿童心脏病。右美托咪定给药后报告了显著的血流动力学反应,包括全身和肺血管收缩。我们这项前瞻性观察性研究的主要目的是量化右美托咪定初始负荷剂量对伴和不伴肺动脉高压儿童平均肺动脉压(PAP)的影响。受试者是接受心脏导管插入术的儿童,用于心脏移植后的常规监测(n = 21)或肺动脉高压研究(n = 21)。在七氟烷麻醉诱导和气管插管后,停用七氟烷,并通过咪达唑仑0.1 mg/kg IV(或术前口服0.5 mg/kg)和瑞芬太尼0.5 - 0.8 μg/kg/min IV输注维持麻醉。机械控制通气以维持Pco 2 35 - 40 mm Hg。当呼气末七氟烷为0%,吸入氧分数(Fio 2)为0.21时,测量基线心率、平均动脉压、PAP、右心房压、肺动脉闭塞压、右心室舒张末期压、心输出量和动脉血气,并计算指数全身血管阻力、指数肺血管阻力和心脏指数。然后,每例受试者接受10分钟1 μg/kg、0.75 μg/kg或0.5 μg/kg右美托咪定输注。在输注结束时重复测量和计算。有肺动脉高压和无肺动脉高压的儿童大多数血流动力学反应相似。心率显著降低,平均动脉血压和全身血管阻力指数显著增加。心脏指数无变化。在移植患者中观察到PAP的小幅统计学显著性增加,但在肺动脉高压受试者中未观察到。肺血管阻力指数的变化不显著。右美托咪定初始负荷剂量与显著的全身血管收缩和高血压相关,但在肺血管中未观察到类似的反应,即使在肺动脉高压儿童中也是如此。右美托咪定似乎不禁忌用于肺动脉高压儿童。
Dexmedetomidine, an α-2 receptor agonist, is widely used in children with cardiac disease. Significant hemodynamic responses, including systemic and pulmonary vasoconstriction, have been reported after dexmedetomidine administration. Our primary goal of this prospective, observational study was to quantify the effects of dexmedetomidine initial loading doses on mean pulmonary artery pressure (PAP) in children with and without pulmonary hypertension. Subjects were children undergoing cardiac catheterization for either routine surveillance after cardiac transplantation (n = 21) or pulmonary hypertension studies (n = 21). After anesthetic induction with sevoflurane and tracheal intubation, sevoflurane was discontinued and anesthesia was maintained with midazolam 0.1 mg/kg IV (or 0.5 mg/kg orally preoperatively) and remifentanil IV infusion 0.5 to 0.8 μg/kg/min. Ventilation was mechanically controlled to maintain Pco2 35 to 40 mm Hg. When end-tidal sevoflurane was 0% and fraction of inspired oxygen (Fio2) was 0.21, baseline heart rate, mean arterial blood pressure, PAP, right atrial pressure, pulmonary artery occlusion pressure, right ventricular end-diastolic pressure, cardiac output, and arterial blood gases were measured, and indexed systemic vascular resistance, indexed pulmonary vascular resistance, and cardiac index were calculated. Each subject then received a 10-minute infusion of dexmedetomidine of 1 μg/kg, 0.75 μg/kg, or 0.5 μg/kg. Measurements and calculations were repeated at the conclusion of the infusion. Most hemodynamic responses were similar in children with and without pulmonary hypertension. Heart rate decreased significantly, and mean arterial blood pressure and indexed systemic vascular resistance increased significantly. Cardiac index did not change. A small, statistically significant increase in PAP was observed in transplant patients but not in subjects with pulmonary hypertension. Changes in indexed pulmonary vascular resistance were not significant. Dexmedetomidine initial loading doses were associated with significant systemic vasoconstriction and hypertension, but a similar response was not observed in the pulmonary vasculature, even in children with pulmonary hypertension. Dexmedetomidine does not appear to be contraindicated in children with pulmonary hypertension.