Document Detail


Metabolic acidemia with hypoxia attenuates the hemodynamic responses to epinephrine during resuscitation in lambs.
MedLine Citation:
PMID:  8252896     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To examine the effects of metabolic acidemia and hypoxia on the hemodynamic responses to epinephrine in an intact neonatal animal model. DESIGN: Multi-experiment, randomized, controlled trial. SETTING: Animal research laboratory of a university hospital. SUBJECTS: Sixteen lambs, ranging in age from 2 to 14 days. INTERVENTIONS: The lambs were chronically catheterized; the ductus arteriosus was ligated; and a pulmonary arterial flow probe was inserted to measure cardiac output, blood pressure (BP), and heart rate. In the first protocol, hemodynamic responses to epinephrine during pure metabolic acidemia or metabolic alkalosis were studied in eight lambs. Each lamb was studied on four different days at a different arterial pH: 6.9, 7.1, 7.4, and 7.6. Ventilation was controlled to maintain PCO2 at 35 to 45 torr (4.66 to 5.99 kPa). Acidemia was induced by the infusion of lactic acid and alkalosis by the infusion of sodium bicarbonate. When the appropriate arterial pH was achieved, 10 micrograms/kg of epinephrine was administered intravenously. In a second protocol, hemodynamic responses to epinephrine during metabolic acidemia or alkalosis plus hypoxia were studied in eight lambs. When the appropriate arterial pH was achieved, hypoxia was induced until cardiac output decreased to 40% of baseline. Epinephrine bolus was given, and after 90 secs, the lambs were resuscitated with oxygen. MEASUREMENTS AND MAIN RESULTS: Epinephrine administered during uncompromised hemodynamics led to hypertension, bradycardia, and decreased cardiac output that were unaffected by arterial pH values between 6.9 and 7.6. Acidemia with hypoxia compromised hemodynamics with decreases in heart rate and cardiac output. Epinephrine administered during this compromised condition did not improve cardiac output, heart rate, or BP before resuscitation with oxygen at any arterial pH studied. Resuscitation with epinephrine and oxygen during hemodynamically compromised states led to increases in heart rate, BP, and cardiac output with significant attenuation of these hemodynamic responses during metabolic acidemia at pH values of 6.9 and 7.1. CONCLUSIONS: During the physiologic conditions associated with neonatal resuscitation, that is, hypoxia with a compromised hemodynamic state, metabolic acidemia significantly attenuates the hemodynamic responses to resuscitation with epinephrine and oxygen. Correction of metabolic acidosis may be warranted in newborn resuscitation.
Authors:
M P Preziosi; J C Roig; N Hargrove; D J Burchfield
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Critical care medicine     Volume:  21     ISSN:  0090-3493     ISO Abbreviation:  Crit. Care Med.     Publication Date:  1993 Dec 
Date Detail:
Created Date:  1994-01-07     Completed Date:  1994-01-07     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:  1901-7     Citation Subset:  AIM; IM    
Affiliation:
Department of Pediatrics, University of Florida College of Medicine, Gainesville.
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MeSH Terms
Descriptor/Qualifier:
Acidosis / blood,  complications,  drug therapy*,  physiopathology
Alkalosis / blood,  complications,  drug therapy*,  physiopathology
Animals
Animals, Newborn
Anoxia / blood,  complications,  drug therapy*,  physiopathology
Blood Gas Analysis
Cardiopulmonary Resuscitation / methods*
Disease Models, Animal
Epinephrine / pharmacology,  therapeutic use*
Hemodynamics / drug effects*
Hydrogen-Ion Concentration
Oxygen Inhalation Therapy
Random Allocation
Sheep
Chemical
Reg. No./Substance:
51-43-4/Epinephrine
Comments/Corrections
Comment In:
Crit Care Med. 1993 Dec;21(12):1821   [PMID:  8252883 ]

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


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