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BioMed Research International
Volume 2017, Article ID 5383574, 7 pages
Research Article

Postoperative Compensatory Ammonium Excretion Subsequent to Systemic Acidosis in Cardiac Patients

1Institute of Physiological Chemistry, University Hospital Essen, University of Duisburg-Essen, Hufelandstrasse 55, Essen, 45147 North Rhine-Westphalia, Germany
2Department of Thoracic and Cardiovascular Surgery, West German Heart Center, University Hospital Essen, Hufelandstrasse 55, Essen, 45147 North Rhine-Westphalia, Germany

Correspondence should be addressed to Johanna K. Teloh; ed.nesse-ku@holet.annahoj

Received 19 January 2017; Revised 1 March 2017; Accepted 26 April 2017; Published 22 May 2017

Academic Editor: Francesco Onorati

Copyright © 2017 Friederike Roehrborn et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background. Postoperative acid-base imbalances, usually acidosis, frequently occur after cardiac surgery. In most cases, the human body, not suffering from any severe preexisting illnesses regarding lung, liver, and kidney, is capable of transient compensation and final correction. The aim of this study was to correlate the appearance of postoperatively occurring acidosis with renal ammonium excretion. Materials and Methods. Between 07/2014 and 10/2014, a total of 25 consecutive patients scheduled for elective isolated coronary artery bypass grafting with cardiopulmonary bypass were enrolled in this prospective observational study. During the operative procedure and the first two postoperative days, blood gas analyses were carried out and urine samples collected. Urine samples were analyzed for the absolute amount of ammonium. Results. Of all patients, thirteen patients developed acidosis as an initial disturbance in the postoperative period: five of respiratory and eight of metabolic origin. Four patients with respiratory acidosis but none of those with metabolic acidosis subsequently developed a base excess > +2 mEq/L. Conclusion. Ammonium excretion correlated with the increase in base excess. The acidosis origin seems to have a large influence on renal compensation in terms of ammonium excretion and the possibility of an overcorrection.