Eyraud D, Brabant S, Nathalie D, Fléron M H, Gilles G, Bertrand M, Coriat P
Department of Anesthesiology and Critical Care, Groupe Hospitalier Pitié-Salpêtrière, Paris, France.
Anesth Analg. 1999 May;88(5):980-4. doi: 10.1097/00000539-199905000-00003.
The goal of the present study was to determine whether terlipressin, an agonist of the vasopressin system, could counteract perioperative hypotension refractory to common vasopressor therapy and to analyze its circulatory effects. We enrolled 51 consecutive vascular surgical patients chronically treated with angiotensin-converting enzyme inhibitors or antagonists of the receptor of angiotensin II, who received a standardized opioid-propofol anesthetic. Of these 51 patients, 32 had at least one episode of hypotension, which responded to epinephrine or phenylephrine. In 10 other patients, systolic arterial pressure (SAP) did not remain above 100 mm Hg for 1 min, despite three bolus doses of ephedrine or phenylephrine. In these patients, we injected a bolus of 1 mg of terlipressin, repeated twice if necessary. Hemodynamic and echocardiographic variables were recorded every 30 s over 6 min. In eight patients, arterial pressure was restored with one injection of terlipressin; in two other patients, three injections were necessary. One minute after the last injection of terlipressin, the SAP increased from 88+/-3 to 100+/-4 mm Hg and reached 117+/-5 mm Hg (P = 0.001) 3 min after the injection and remained stable around this value. This increase in SAP was associated with significant changes in left ventricular end-diastolic area (17.9+/-2 vs 20.2+/-2.2 cm2; P = 0.003), end-systolic area (8.1+/-1.3 vs 9.6+/-1.5 cm2; P = 0.004), end-systolic wall stress (45+/-8 vs 66+/-12; P = 0.001), and heart rate (60+/-4 vs 55+/-3 bpm; P = 0.001). Fractional area change and velocity of fiber shortening did not change significantly. No additional injection of vasopressor was required during the perioperative period. No change in ST segment was observed after the injection.
Terlipressin is effective to rapidly correct refractory hypotension in patients chronically treated with antagonists of the renin-angiotensin system without impairing left ventricular function.
本研究的目的是确定血管加压素系统激动剂特利加压素是否能对抗普通血管升压药治疗无效的围手术期低血压，并分析其循环效应。我们纳入了51例连续接受血管手术的患者，这些患者长期接受血管紧张素转换酶抑制剂或血管紧张素II受体拮抗剂治疗，并接受标准化的阿片类药物 - 丙泊酚麻醉。在这51例患者中，32例至少有一次低血压发作，对肾上腺素或去氧肾上腺素有反应。在另外10例患者中，尽管静脉推注了三次麻黄碱或去氧肾上腺素，收缩压（SAP）仍未能在1分钟内维持在100 mmHg以上。在这些患者中，我们静脉推注了1 mg特利加压素，必要时重复两次。在6分钟内每隔30秒记录一次血流动力学和超声心动图变量。在8例患者中，一次注射特利加压素后血压恢复正常；在另外2例患者中，需要三次注射。最后一次注射特利加压素1分钟后，SAP从88±3 mmHg升至100±4 mmHg，注射后3分钟达到117±5 mmHg（P = 0.001），并在此值附近保持稳定。SAP的升高与左心室舒张末期面积（17.9±2 vs 20.2±2.2 cm²；P = 0.003）、收缩末期面积（8.1±1.3 vs 9.6±1.5 cm²；P = 0.004）、收缩末期壁应力（45±8 vs 66±12；P = 0.001）和心率（60±4 vs 55±3次/分钟；P = 0.001）的显著变化相关。面积变化分数和纤维缩短速度没有显著变化。围手术期无需额外注射血管升压药。注射后未观察到ST段变化。
特利加压素可有效快速纠正长期接受肾素 - 血管紧张素系统拮抗剂治疗患者的难治性低血压，且不损害左心室功能。
