Miller J A, Dacey R G, Diringer M N
Department of Neurology, Washington University School of Medicine, St Louis, Mo., 63110-1093, USA.
Stroke. 1995 Dec;26(12):2260-6. doi: 10.1161/01.str.26.12.2260.
Hypertensive hypervolemic therapy has been shown to reverse delayed ischemic deficits after aneurysmal subarachnoid hemorrhage. Concern has been raised about systemic complications of therapy, including pulmonary edema and myocardial ischemia, especially when high doses of vasopressors are used. Patients in whom delayed ischemic deficits were treated with hypervolemia and phenylephrine were prospectively evaluated for signs of systemic toxicity.
Twenty-four consecutive patients treated with hypertensive hypervolemic therapy after aneurysmal subarachnoid hemorrhage were studied. Sixty-seven percent had underlying cardiac disease, vascular disease, or hypertension. No patient was excluded because of age or preexisting cardiac disease. Patients were closely monitored for signs of congestive heart failure (physical examination, chest x-ray films, arterial blood gases, cardiac index, pulmonary artery wedge pressure, and oxygen requirement). Indicators of cardiac ischemia and other extracerebral toxicity that were monitored included cardiac enzymes, electrocardiograms, serum creatinine, electrolyte and lactic acid levels, gastrointestinal motility, and urine output.
Volume expansion and phenylephrine infusion produced an increase in several hemodynamic parameters including pulmonary artery wedge pressure, which rose 28% (13 +/- 3.6 to 16 +/- 1.9 mm Hg), mean arterial blood pressure, which rose 25% (99 +/- 12.5 to 123 +/- 11.4 mm Hg), and systemic vascular resistance, which rose 46% (1234 +/- 294 to 1739 +/- 315 dyne.s-1.cm-5); however, there was no change in cardiac index (3.9 +/- 0.9 to 4.0 +/- 0.6 L.min-1.m-2). There were no clinically significant episodes of pulmonary edema requiring a change in vasopressor therapy and no myocardial infarctions. Phenylephrine was stopped in only one patient (incidence, 4%; 95% confidence interval, 0% to 12%), who developed an exacerbation of his preexisting bradycardia. There was no evidence of noncardiac organ system toxicity. Eighty-eight percent of the patients exhibited neurological improvement.
Hypertensive hypervolemic therapy with the use of high-dose phenylephrine can be administered with acceptable systemic toxicity, even in patients with previous cardiac disease, provided that close monitoring is performed. To minimize risk, aggressive treatment should probably be reserved for patients with signs of delayed ischemia rather than administered prophylactically.
高血压高血容量疗法已被证明可逆转动脉瘤性蛛网膜下腔出血后的迟发性缺血性神经功能缺损。人们对该疗法的全身并发症表示担忧,包括肺水肿和心肌缺血,尤其是在使用高剂量血管升压药时。对接受高血容量疗法和去氧肾上腺素治疗迟发性缺血性神经功能缺损的患者进行前瞻性评估,以观察全身毒性迹象。
对24例动脉瘤性蛛网膜下腔出血后接受高血压高血容量疗法的连续患者进行研究。67%的患者患有潜在的心脏病、血管疾病或高血压。没有患者因年龄或原有心脏病而被排除。密切监测患者是否出现充血性心力衰竭迹象(体格检查、胸部X线片、动脉血气、心脏指数、肺动脉楔压和氧需求)。监测的心脏缺血和其他脑外毒性指标包括心肌酶、心电图、血清肌酐、电解质和乳酸水平、胃肠蠕动和尿量。
扩容和输注去氧肾上腺素使包括肺动脉楔压在内的多个血流动力学参数增加,肺动脉楔压升高28%(从13±3.6mmHg升至16±1.9mmHg),平均动脉血压升高25%(从99±12.5mmHg升至123±11.4mmHg),全身血管阻力升高46%(从1234±294dyn·s-1·cm-5升至1739±315dyn·s-1·cm-5);然而,心脏指数没有变化(从3.9±0.9L·min-1·m-2升至4.0±0.6L·min-1·m-2)。没有出现需要改变血管升压药治疗的具有临床意义的肺水肿发作,也没有心肌梗死发生。只有1例患者(发生率4%;95%置信区间,0%至12%)停用了去氧肾上腺素,该患者原有心动过缓加重。没有非心脏器官系统毒性的证据。88%的患者神经功能得到改善。
即使是患有心脏病的患者,在密切监测的情况下,使用高剂量去氧肾上腺素进行高血压高血容量疗法时,全身毒性也是可以接受的。为了将风险降至最低,积极治疗可能应仅用于有迟发性缺血迹象的患者,而不是预防性使用。