Williams Glyn D, Philip Bridget M, Chu Larry F, Boltz M Gail, Kamra Komal, Terwey Heidi, Hammer Gregory B, Perry Stanton B, Feinstein Jeffrey A, Ramamoorthy Chandra
Department of Anesthesia, Stanford University School of Medicine, Stanford, California 94305-5640, USA.
Anesth Analg. 2007 Dec;105(6):1578-84, table of contents. doi: 10.1213/01.ane.0000287656.29064.89.
The use of ketamine in children with increased pulmonary vascular resistance is controversial. In this prospective, open label study, we evaluated the hemodynamic responses to ketamine in children with pulmonary hypertension (mean pulmonary artery pressure >25 mm Hg).
Children aged 3 mo to 18 yr with pulmonary hypertension, who were scheduled for cardiac catheterization with general anesthesia, were studied. Patients were anesthetized with sevoflurane (1 minimum alveolar anesthetic concentration [MAC]) in air while breathing spontaneously via a facemask. After baseline catheterization measurements, sevoflurane was reduced (0.5 MAC) and ketamine (2 mg/kg IV over 5 min) was administered, followed by a ketamine infusion (10 microg x kg(-1) x min(-1)). Catheterization measurements were repeated at 5, 10, and 15 min after completion of ketamine load. Data at various time points were compared (ANOVA, P < 0.05).
Fifteen patients (age 147, 108 mo; median, interquartile range) were studied. Diagnoses included idiopathic pulmonary arterial hypertension (5), congenital heart disease (9), and diaphragmatic hernia (1). At baseline, median (interquartile range) baseline pulmonary vascular resistance index was 11.3 (8.2) Wood units; 33% of patients had suprasystemic mean pulmonary artery pressures. Heart rate (99, 94 bpm; P = 0.016) and Pao2 (95, 104 mm Hg; P = 007) changed after ketamine administration (baseline, 15 min after ketamine; P value). There were no significant differences in mean systemic arterial blood pressure, mean pulmonary artery pressure, systemic or pulmonary vascular resistance index, cardiac index, arterial pH, or Paco2.
In the presence of sevoflurane, ketamine did not increase pulmonary vascular resistance in spontaneously breathing children with severe pulmonary hypertension.
氯胺酮在肺血管阻力增加的儿童中的应用存在争议。在这项前瞻性、开放标签研究中，我们评估了肺动脉高压（平均肺动脉压>25mmHg）儿童对氯胺酮的血流动力学反应。
研究对象为年龄在3个月至18岁、计划在全身麻醉下进行心导管检查的肺动脉高压患儿。患者通过面罩自主呼吸时，在空气中用七氟醚（1个最低肺泡有效浓度[MAC]）麻醉。在进行基线导管测量后，降低七氟醚浓度（0.5MAC）并静脉注射氯胺酮（5分钟内2mg/kg），随后进行氯胺酮输注（10μg·kg⁻¹·min⁻¹）。在氯胺酮负荷完成后5、10和15分钟重复进行导管测量。比较不同时间点的数据（方差分析，P<0.05）。
研究了15例患者（年龄147、108个月；中位数，四分位间距）。诊断包括特发性肺动脉高压（5例）、先天性心脏病（9例）和膈疝（1例）。基线时，肺动脉血管阻力指数中位数（四分位间距）为11.3（8.2）伍德单位；33%的患者平均肺动脉压高于体循环压力。氯胺酮给药后心率（99、94次/分钟；P=0.016）和动脉血氧分压（95、104mmHg；P=0.07）发生变化（基线，氯胺酮给药后15分钟；P值）。平均体循环动脉血压、平均肺动脉压、体循环或肺血管阻力指数、心脏指数、动脉pH值或动脉血二氧化碳分压无显著差异。
在七氟醚存在的情况下，氯胺酮不会增加重度肺动脉高压自主呼吸儿童的肺血管阻力。
