Document Detail

The effects of epinephrine/norepinephrine on end-tidal carbon dioxide concentration, coronary perfusion pressure and pulmonary arterial blood flow during cardiopulmonary resuscitation.
MedLine Citation:
PMID:  10694173     Owner:  NLM     Status:  MEDLINE    
End-tidal CO2 concentration correlates with pulmonary blood flow during cardiopulmonary resuscitation and has been claimed to be a useful tool to judge the effectiveness of chest compression. A high concentration of end-tidal CO2 has been related to a better outcome. However, most authors have noticed a decrease in end-tidal CO2 concentration after administration of epinephrine, concomitant with an increase in coronary perfusion pressure and an increased incidence of return of spontaneous circulation. This study was performed to evaluate changes in end-tidal CO2 concentration after injection of vasopressors during cardiopulmonary resuscitation and to investigate the time-course of the response and possible explanations for it. After 1 min of electrically induced cardiac arrest and 5 min of chest compressions, 18 pigs were randomly assigned to receive 0.045 mg kg(-1) epinephrine, 0.045 mg kg(-1) norepinephrine or no drug. After another 4 min of chest compressions the pigs were defibrillated. End-tidal CO2, pulmonary blood flow and coronary perfusion pressure decreased immediately after the induction of cardiac arrest, increased slightly during chest compressions and increased initially to supernormal levels after the return of spontaneous circulation. Injection of epinephrine or norepinephrine during chest compressions decreased end-tidal CO2 51 +/- 2%, (mean +/- S.E.M.), and 43 +/- 1%, respectively, and pulmonary blood flow by 134 +/- 13 and 125 +/- 16%, respectively, within 1 min, simultaneously increasing coronary perfusion pressure from 10 +/- 2 to 45 +/- 5 mm Hg and from 11 +/- 1 to 38 +/- 5 mm Hg, respectively. The coronary perfusion pressure slowly fell, but the effects on end-tidal CO2 and pulmonary blood flow were prolonged. In conclusion, vasopressors increased coronary perfusion pressure and the likelihood of a return of spontaneous circulation, but decreased end-tidal CO2 concentration and induced a critical deterioration in cardiac output and thus oxygen delivery in this model of cardiopulmonary resuscitation.
L Lindberg; Q Liao; S Steen
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Resuscitation     Volume:  43     ISSN:  0300-9572     ISO Abbreviation:  Resuscitation     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-03-08     Completed Date:  2000-03-08     Revised Date:  2009-08-25    
Medline Journal Info:
Nlm Unique ID:  0332173     Medline TA:  Resuscitation     Country:  IRELAND    
Other Details:
Languages:  eng     Pagination:  129-40     Citation Subset:  IM    
Department of Anesthesiology and Intensive Care, University Hospital, Lund, Sweden.
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MeSH Terms
Blood Flow Velocity / drug effects
Blood Pressure / drug effects
Carbon Dioxide / physiology*
Cardiopulmonary Resuscitation*
Coronary Circulation / drug effects*
Epinephrine / pharmacology*
Heart Arrest / physiopathology,  therapy
Norepinephrine / pharmacology*
Pulmonary Artery / physiology*
Pulmonary Gas Exchange / drug effects*
Random Allocation
Vasoconstrictor Agents / pharmacology*
Reg. No./Substance:
0/Vasoconstrictor Agents; 124-38-9/Carbon Dioxide; 51-41-2/Norepinephrine; 51-43-4/Epinephrine

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

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