Eyraud D, Mouren S, Teugels K, Bertrand M, Coriat P
Department of Anesthesiology and Intensive Care, Hôpital de la Pitié-Salpétrière, Paris, France.
Anesth Analg. 1998 Feb;86(2):259-63. doi: 10.1097/00000539-199802000-00007.
Although angiotensin II bolus administration may be used to increase blood pressure in patients chronically treated with angiotensin-converting enzyme inhibitors (ACEI) who have severe hypotension on anesthetic induction, no data are available describing its time course and its effects on the left ventricular function. Fourteen patients chronically treated with ACEI for hypertension and scheduled for vascular surgery were prospectively studied. Patients with cardiac insufficiency were excluded. A transesophageal echocardiography probe was inserted to assess systolic left ventricular function. When hypotension was observed (systolic arterial pressure [SAP] <85 mm Hg), an I.V. bolus of 2.5 microg of angiotensin II (AII) was given, and hemodynamic variables were recorded each 30 s over 5.5 min. Results are expressed as mean +/- SEM. Sixty seconds after the AII bolus injection, the SAP increased from 78 +/- 3 to 152 +/- 6 mm Hg. SAP remained higher than control until the 5th min. This was associated with significant increases in end-diastolic area (from 15.1 +/- 0.6 to 19.3 +/- 1.0 cm2, P < or = 0.001), end-systolic area (from 6.6 +/- 0.4 to 10.7 +/- 0.7 cm2, P < or = 0.001), end-systolic wall stress (from 32 +/- 0.05 to 82 +/- 7 kdynes/cm2, P < or = 0.001). In addition, a decrease in fiber-shortening velocity (from 1.1 +/- 0.05 to 0.76 +/- 0.04 circ/s, P < or = 0.05) and in fractional area change (from 0.57 +/- 0.02 to 0.44 +/- 0.02, P < or = 0.05) was observed. Heart rate did not significantly change during the study. Increases in preload and afterload were observed. However, the administration of AII causes a transient impairment in left ventricular function. We conclude that AII, given as an I.V. bolus of 2.5 microg, is effective in restoring arterial blood pressure within 60 s in patients chronically treated with ACEI.
Severe hypotension on anesthetic induction in patients chronically treated with angiotensin-converting enzyme inhibitors for hypertension could be treated with an I.V. bolus of 2.5 microg of angiotensin II.
尽管在麻醉诱导时严重低血压的长期接受血管紧张素转换酶抑制剂（ACEI）治疗的患者中，可使用静脉推注血管紧张素II来升高血压，但尚无关于其时间进程及其对左心室功能影响的数据。对14例因高血压长期接受ACEI治疗并计划进行血管手术的患者进行了前瞻性研究。排除了心脏功能不全的患者。插入经食管超声心动图探头以评估左心室收缩功能。当观察到低血压时（收缩动脉压[SAP]<85 mmHg），静脉推注2.5微克血管紧张素II（AII），并在5.5分钟内每隔30秒记录一次血流动力学变量。结果以平均值±标准误表示。在推注AII后60秒，SAP从78±3 mmHg升高至152±6 mmHg。直到第5分钟，SAP一直高于对照值。这与舒张末期面积（从15.1±0.6 cm²增加至19.3±1.0 cm²，P≤0.001）、收缩末期面积（从6.6±0.4 cm²增加至10.7±0.7 cm²，P≤0.001）、收缩末期壁应力（从32±0.05 kdynes/cm²增加至82±7 kdynes/cm²，P≤0.001）的显著增加相关。此外，观察到纤维缩短速度（从1.1±0.05周/秒降至0.76±0.04周/秒，P≤0.05）和面积变化分数（从0.57±0.02降至0.44±0.02，P≤0.05）降低。在研究过程中，心率没有显著变化。观察到前负荷和后负荷增加。然而，推注AII会导致左心室功能短暂受损。我们得出结论：对于长期接受ACEI治疗的患者，静脉推注2.5微克AII可在60秒内有效恢复动脉血压。
对于因高血压长期接受血管紧张素转换酶抑制剂治疗的患者，麻醉诱导时的严重低血压可用静脉推注2.5微克血管紧张素II进行治疗。
