Document Detail


Vasopressor agents for cardiopulmonary resuscitation.
MedLine Citation:
PMID:  12808484     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents produce systemic vasoconstriction. This increases aortic diastolic pressure, and consequently, coronary and cerebral perfusion pressures. The pharmacologic responses to the adrenergic agents are mediated by a group of receptors that are classified as alpha (alpha), including alpha1 and alpha2, and beta (beta), including beta1 and beta2. Epinephrine, which has each of these adrenergic actions, has been the preferred adrenergic agent for the management of cardiac arrest for almost 40 years. Its primary efficacy is due to its alpha-adrenergic vasopressor effects. This contrasts with its beta-adrenergic actions, which are inotropic, chronotropic, and vasodilator. Accordingly, beta-adrenergic actions prompt increases in myocardial oxygen consumption, ectopic ventricular arrhythmias, and transient hypoxemia due to pulmonary arteriovenous shunting. This may account for the failure to demonstrate that epinephrine improves ultimate outcomes in human victims of cardiac arrest. Major interest has more recently been focused on selective alpha-adrenergic agonists. Both alpha1-agonists and alpha2-agonists are peripheral vasopressors. However, rapid desensitization of alpha1-adrenergic receptors occurs during cardiopulmonary resuscitation. Moreover, alpha1-adrenergic receptors are present in the myocardium, and beta1-agonists, like beta-adrenergic agonists, increase myocardial oxygen consumption. If they cross the blood-brain barrier, alpha2-adrenoceptor agonists also have centrally acting vasodilator effects. In the absence of central nervous system access, alpha2-adrenergic agonists have selective peripheral vasoconstrictor effects. Under experimental conditions of cardiopulmonary resuscitation, selective alpha2-agonists, which do not gain entrance into the brain, produce only systemic vasoconstriction. Experimentally, these selective alpha2-agonists are as effective as epinephrine for initial cardiac resuscitation and have the additional advantage of minimizing myocardial oxygen consumption during the global myocardial ischemia of cardiac arrest. Accordingly, myocardial ischemic injury during cardiopulmonary resuscitation is minimized, and postresuscitation myocardial function is preserved with improved survival.
Authors:
Lan Cao; Max Harry Weil; Shijie Sun; Wanchun Tang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology and therapeutics     Volume:  8     ISSN:  1074-2484     ISO Abbreviation:  J. Cardiovasc. Pharmacol. Ther.     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-06-16     Completed Date:  2003-08-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9602617     Medline TA:  J Cardiovasc Pharmacol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  115-21     Citation Subset:  IM    
Affiliation:
The Institute of Critical Care Medicine, Palm Springs, California 92262, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / therapeutic use
Adrenergic beta-Agonists / therapeutic use
Animals
Brain Ischemia / complications,  drug therapy,  therapy
Cardiopulmonary Resuscitation*
Epinephrine / therapeutic use
Heart Arrest / complications,  drug therapy,  therapy*
Humans
Vasoconstrictor Agents / therapeutic use*
Vasopressins / therapeutic use
Grant Support
ID/Acronym/Agency:
HL-54322/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Adrenergic beta-Agonists; 0/Vasoconstrictor Agents; 11000-17-2/Vasopressins; 51-43-4/Epinephrine

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


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