Effects of norepinephrine on renal perfusion, filtration and oxygenation in vasodilatory shock and acute kidney injury
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The use of norepinephrine (NE) in patients with volume-resuscitated vasodilatory shock and acute kidney injury (AKI) remains the subject of much debate and controversy. The effects of NE-induced variations in mean arterial blood pressure (MAP) on renal blood flow (RBF), oxygen delivery (RDO2), glomerular filtration rate (GFR) and the renal oxygen supply/demand relationship (renal oxygenation) in vasodilatory shock with AKI have not been previously studied.
Twelve post-cardiac surgery patients with NE-dependent vasodilatory shock and AKI were studied 2–6 days after surgery. NE infusion rate was randomly and sequentially titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, RBF, GFR and renal oxygen extraction were obtained by pulmonary artery catheter, by the renal vein thermodilution technique and by renal extraction of 51Cr-ethylenediamine tetraacetic acid (51Cr-EDTA), respectively.
At target MAP of 75 mmHg, RDO2 (13%), GFR (27%) and urine flow were higher and renal oxygen extraction was lower (−7.4%) compared with at target MAP of 60 mmHg. However, the renal variables did not differ when compared at target MAPs of 75 and 90 mmHg. Cardiac index increased dose-dependently with NE.
Restoration of MAP from 60 to 75 mmHg improves renal oxygen delivery, GFR and the renal oxygen supply/demand relationship in post-cardiac surgery patients with vasodilatory shock and AKI. This pressure-dependent renal perfusion, filtration and oxygenation at levels of MAP below 75 mmHg reflect a more or less exhausted renal autoregulatory reserve.
KeywordsAcute kidney failure Shock Renal circulation Glomerular filtration rate Oxygen consumption Norepinephrine
We appreciate the skillful technical assistance of Mrs. Marita Ahlqvist, and we are grateful for the support from the nursing staff of the Cardiothoracic Intensive Care Unit of the Sahlgrenska University Hospital. This study was supported by grants from the Swedish Medical Research Council (no. 13156), Medical Faculty of Gothenburg (LUA) and Gothenburg Medical Society.
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