SAFETY OF HYPERTENSIVE HYPERVOLEMIC THERAPY WITH PHENYLEPHRINE IN THETREATMENT OF DELAYED ISCHEMIC DEFICITS AFTER SUBARACHNOID HEMORRHAGE

Citation
Ja. Miller et al., SAFETY OF HYPERTENSIVE HYPERVOLEMIC THERAPY WITH PHENYLEPHRINE IN THETREATMENT OF DELAYED ISCHEMIC DEFICITS AFTER SUBARACHNOID HEMORRHAGE, Stroke, 26(12), 1995, pp. 2260-2266
Citations number
30
Categorie Soggetti
Neurosciences,"Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
26
Issue
12
Year of publication
1995
Pages
2260 - 2266
Database
ISI
SICI code
0039-2499(1995)26:12<2260:SOHHTW>2.0.ZU;2-4
Abstract
Background and Purpose Hypertensive hypervolemic therapy has been show n to reverse delayed ischemic deficits after aneurysmal subarachnoid h emorrhage. Concern has been raised about systemic complications of the rapy, including pulmonary edema and myocardial ischemia, especially wh en high doses of vasopressors are used. Patients in whom delayed ische mic deficits were treated with hypervolemia and phenylephrine were pro spectively evaluated for signs of systemic toxicity. Methods Twenty-fo ur consecutive patients treated with hypertensive hypervolemic therapy after aneurysmal subarachnoid hemorrhage were studied. Sixty-seven pe rcent had underlying cardiac disease, vascular disease, or hypertensio n. No patient was excluded because of age or preexisting cardiac disea se. Patients were closely monitored for signs of congestive heart fail ure (physical examination, chest x-ray films, arterial blood gases, ca rdiac index, pulmonary artery wedge pressure, and oxygen requirement). Indicators of cardiac ischemia and other extracerebral toxicity that were monitored included cardiac enzymes, electrocardiograms, serum cre atinine, electrolyte and lactic acid levels, gastrointestinal motility , and urine output. Results Volume expansion and phenylephrine infusio n produced an increase in several hemodynamic parameters including pul monary artery wedge pressure, which rose 25% (13+/-3.6 16+/-1.9 mm Hg) , mean arterial blood pressure, which rose 25% (99+/-125 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 c ardiac index (3.9+/-0.9 to 4.0+/-0.6 L . min(-1). m(-2)). There were n o clinically significant episodes of pulmonary edema requiring a chang e in vasopressor therapy and no myocardial infarctions. Phenylephrine was stopped in only one patient (incidence, 4%; 95% confidence interva l, 0% to 12%), who developed an exacerbation of his preexisting bradyc ardia. There was no evidence of noncardiac organ system toxicity. Eigh ty-eight percent of the patients exhibited neurological improvement. C onclusions 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 mo nitoring is performed. To minimize risk, aggressive treatment should p robably be reserved for patients with signs of delayed ischemia rather than administered prophylactically.