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QJM Advance Access published online on February 8, 2006
QJM, doi:10.1093/qjmed/hcl009
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© The Author 2006. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: Journals.permissions@oxfordjournals.org

Review

The role of vasopressin in cardiorespiratory arrest and pulmonary hypertension

A.M. Smith 1, C.M. Elliot 2, D.G. Kiely 2, and K.S. Channer 3 *

1 From the Hormone & Vascular Biology Group, Academic Unit of Endocrinology, Division of Genomic Medicine, The University of Sheffield, UK; From the Department of Cardiology, Sheffield, UK
2 From the Sheffield Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, UK
3 From the Department of Cardiology, Sheffield, UK; From the Faculty of Health and Well-being, Sheffield Hallam University, Sheffield, UK

* To whom correspondence should be addressed.
K.S. Channer, E-mail: Kevin.Channer{at}sth.nhs.uk


  Abstract

Vasopressin is a peptide synthesized in the hypothalamus whose primary role is in fluid homeostasis. It has recently gained interest as a potential agent in the treatment of cardiorespiratory arrest. Initial human studies have shown benefits with vasopressin in patients with out of hospital ventricular fibrillation and asystolic cardiac arrest. One subgroup of patients not included in these trials is patients with pulmonary hypertension, who have a five-year mortality rate of 50%. Animal studies have shown vasopressin to be a vasodilator in the pulmonary vascular system of rats, under normoxic and hypoxic conditions, with conflicting results in canines. Human studies have shown conflicting results with increases, decreases and no changes seen in pulmonary artery pressures of patients with a variety of clinical conditions. Research needs to be done in patients with pulmonary hypertension regarding the potential role of vasopressin during cardiac arrest in this subgroup.


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