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Anesth Analg 2001;92:1391-1395
© 2001 International Anesthesia Research Society


CARDIOVASCULAR ANESTHESIA

The Clinical Onset of Heparin Is Rapid

Edward K. Heres, MD*, Kevin Speight, MD{dagger}, Daniel Benckart, MD{ddagger}, Jose Marquez, MD*, and Glenn P. Gravlee, MD§

Departments of *Anesthesiology and {ddagger}Cardiothoracic Surgery, Allegheny General Hospital, MCP Hahnemann School of Medicine, Pittsburgh, Pennsylvania; and {dagger}Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina, and §Department of Anesthesiology, Ohio State University, Columbus, Ohio

Address correspondence and reprint requests to Edward K. Heres, MD, Department of Anesthesiology, Allegheny General Hospital, 320 E. North Ave., Pittsburgh, PA 15212. Address e-mail to EKH56{at}home.com

This study used the activated clotting time (ACT) to determine the clinical onset of four different doses of heparin after bolus injection into the central circulation. Ten consenting adults (Group A) undergoing coronary artery bypass grafting were given 350 U/kg of bovine lung heparin and had simultaneous duplicate arterial and venous ACT determinations at baseline and at 30, 60, 90, 120, 180, and 600 s after heparin injection. Twenty additional coronary artery bypass grafting patients were alternately assigned to one of two 10-patient groups (B and C), which were given 200 and 300 U/kg of bovine lung heparin, respectively. Group D consisted of 10 abdominal aortic aneurysmectomy patients who received 70 U/kg of bovine lung heparin. In Groups B, C, and D, duplicate ACT measurements were taken from an indwelling arterial catheter at baseline and at 30, 60, 90, 120, 180, and 300 s after completion of a bolus injection of heparin into the central circulation. After a 70 U/kg heparin dose, all patients had significant ACT prolongation within 30 s, and 8 of 10 had effectively achieved their peak anticoagulation response by that time. In all patients receiving 200, 300, and 350 U/kg of heparin, arterial anticoagulation (ACT > 300 s) occurred and in most patients peaked within 30 s after heparin administration (P < 0.05). Arterial and venous ACTs did not differ significantly from each other at any measurement period, but venous ACTs peaked slightly later than arterial ACTs (within 60 s in 9 of 10 patients). When 200 U/kg or more of heparin is administered into the central venous circulation in hemodynamically stable anesthetized patients, peak arterial ACT prolongation occurs within 30 s and peak venous ACT prolongation within 60 s.

Implications: When 200 U/kg or more of heparin is administered into the central venous circulation in hemodynamically stable anesthetized patients, peak arterial activated clotting time (ACT) prolongation occurs within 30 s and peak venous ACT prolongation within 60 s. This information may assist physicians in making decisions about vascular interventions such as aortic cannulation or cross-clamping and strongly suggests that blood sampling to determine the adequacy of heparin-induced anticoagulation can occur as soon as 30–60 s after heparin administration. The drug heparin is given to patients during blood vessel surgery to temporarily inhibit blood clotting when blood vessels are clamped. The activated clotting test was used to determine just how fast heparin works after it is administered.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2001 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2001 by the International Anesthesia Research Society.