Renal oxygenation in clinical acute kidney injury
Department of Anesthesiology and Intensive Care Medicine, Sahlgrenska Academy, University of Gothenburg, Sahlgrenska University Hospital, 413 45 Gothenburg, Sweden
Critical Care 2013, 17:221 doi:10.1186/cc12530
This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2013 and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum.com/series/annualupdate2013. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.Published: 19 March 2013
First paragraph (this article has no abstract)
Renal oxygenation is defined as the relationship between renal oxygen delivery (DO2) and renal oxygen consumption (VO2) and it can easily be shown that the inverse of this relationship is equivalent to renal extraction of O2 (O2Ex). An increase in renal O2Ex means that renal DO2 has decreased in relation to renal VO2, i. e., renal oxygenation is impaired, and vice versa. When compared to other major organs, renal VO2 is relatively high, second only to the heart. In sedated, mechanically ventilated patients, renal VO2 is two-thirds (10 ml/min) that of myocardial oxygen consumption (15 ml/min) (Table 1) [1,2]. Renal blood flow, which accounts for approximately 20% of cardiac output, is three times higher than myocardial blood flow in this group of patients. Renal O2Ex in the non-failing kidney is therefore low, 10%, compared with, e.g., the heart, in which O2EX is 55% (Table 1).