Document Detail

Cardiopulmonary actions of intravenously administered enalaprilat in trauma patients.
MedLine Citation:
PMID:  8205828     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: To determine the cardiopulmonary actions of the intravenous administration of the angiotensin-converting enzyme inhibitor enalaprilat in hypertensive trauma patients. DESIGN: Prospective, before/after trial. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: Twenty critically injured and hypertensive ICU patients. All patients were receiving continuous sedation (fentanyl and midazolam) for at least 2 days before the injection of enalaprilat and had a mean arterial pressure (MAP) of > 95 mm Hg. "Responders" were defined as having a decrease in MAP of > 15% within 30 mins after enalaprilat injection. INTERVENTIONS: Intravenous administration of 0.06 mg/kg of the angiotensin-converting enzyme inhibitor enalaprilat. Repeated doses were given when no sufficient response (decrease of MAP of > 15% within 30 mins after injection) was seen ("nonresponders"). MEASUREMENTS: In addition to standard hemodynamic monitoring, right ventricular hemodynamics and oximetric variables were also documented. Measurements were carried out before enalaprilat injection (during hemodynamic steady state [baseline values]) and at 1, 5, 10, 20, 30, 60, and 120 mins after enalaprilat administration. MAIN RESULTS: MAP was successfully controlled in 17 of 20 patients (maximum decrease -27 mm Hg [-26%]). In the three other patients, even reinjection of enalaprilat (0.06 mg/kg) did not sufficiently reduce MAP. In the 17 responders, heart rate did not increase, whereas central venous pressure, pulmonary arterial pressure, and pulmonary artery occlusion pressure decreased significantly after intravenous administration of enalaprilat. Cardiac index changed only slightly (mean maximum +0.70 L/min/m2 [+18%]). Right ventricular ejection fraction increased from 36% to 45% (p < .05); right ventricular end-diastolic and end-systolic volume index decreased significantly. Both systemic and pulmonary vascular resistance indices decreased within the investigation period (-31% and -16%, respectively). Pao2/FIO2, intrapulmonary right-to-left shunting, and oxygen extraction ratio were not altered. Oxygen delivery index (+17%) and oxygen consumption index (+20%) increased during the investigation period (p < .04). CONCLUSIONS: The intravenous administration of enalaprilat successfully decreased blood pressure in most of our patients. Mechanisms other than the renin-angiotensin system also appear to be involved in hypertensive, critically ill patients. Pulmonary function was not altered; right ventricular function, and both oxygen consumption and oxygen delivery improved in the enalaprilat responder group. Thus, the availability of intravenous enalaprilat seems to enlarge our armamentarium for treating hypertension in the critically ill patient.
J Boldt; T Menges; M Wollbrück; H Hammermann; G Hempelmann
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article    
Journal Detail:
Title:  Critical care medicine     Volume:  22     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  1994 Jun 
Date Detail:
Created Date:  1994-07-08     Completed Date:  1994-07-08     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0355501     Medline TA:  Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  960-4     Citation Subset:  AIM; IM    
Department of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University, Giessen, FRG.
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MeSH Terms
Acute Disease
Analysis of Variance
Enalaprilat / administration & dosage*
Heart / drug effects*,  physiopathology
Hemodynamics / drug effects
Hypertension / drug therapy,  etiology,  physiopathology
Injections, Intravenous
Lung / drug effects*,  physiopathology
Middle Aged
Prospective Studies
Time Factors
Wounds and Injuries / complications,  drug therapy*,  physiopathology
Reg. No./Substance:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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