(Circulation. 2000;101:e174.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
British Heart Foundation Cardiothoracic Research Fellow Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, Hammersmith Hospital, London, UK
| Introduction |
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Wenzel et al1 provide additional evidence in favor of a change away from the use of epinephrine during cardiac arrest, which has been universally adopted due to the advanced cardiac life support guidelines. Unfortunately, the epinephrine doses of 45 and 200 µg/kg used in their study, which equate to 3.15 and 14 mg in a 70-kg patient, do not equate to those used clinically.
A side effect of epinephrine that is widely known but has not been discussed is the potent platelet aggregation that epinephrine induces.2 Indeed, epinephrine is so good at producing platelet aggregation that it is widely used during platelet function tests as an aggregator3 (thus the importance of using equivalent doses of epinephrine to that used clinically).
We have demonstrated that an epinephrine dose of 1 mg in a
70-kg patient, which equates to 14.3 µg/kg, causes
10%
platelet aggregation; however, the doses used in the study by
Wenzel et al,1 45 and 200 µg/kg, cause
20% and 75%
platelet aggregation, respectively. Thus, because they have not
measured platelet aggregation, which could easily be done with the
technique of microaggregation, the results of their study are
confounded by a degree of platelet aggregation that is significant
and that does not occur at the doses used clinically.
Cardiac arrest is mainly due to coronary thrombosis; therefore,
administration of an agent that causes platelet aggregation has to
be detrimental. An increased frequency of a polymorphism of the
-receptor on platelets of patients with acute coronary
syndromes
Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria
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