The renal medulla is susceptible to hypoxia during cardiopulmonary bypass (CPB), which may contribute to the development of acute kidney injury. But the speed of onset of renal medullary hypoxia remains unknown.

We continuously measured renal medullary oxygen tension (MPO₂) in 24 sheep, and urinary PO₂ (UPO₂) as an index of MPO₂ in 92 patients, before and after induction of CPB.

In laterally recumbent sheep with a right thoracotomy (n = 20), even before CPB commenced MPO₂ fell from (mean ± SEM) 52 ± 4 to 41 ±5 mmHg simultaneously with reduced arterial pressure (from 108 ± 5 to 88 ± 5 mmHg). In dorsally recumbent sheep with a medial sternotomy (n = 4), MPO₂ was even more severely reduced (to 12 ± 12 mmHg) before CPB. In laterally recumbent sheep in which a crystalloid prime was used (n = 7), after commencing CPB, MPO₂ fell abruptly to 24 ±6 mmHg within 20–30 minutes. MPO₂ during CPB was not improved by adding donor blood to the prime (n = 13). In patients undergoing cardiac surgery, UPO₂ fell by 4 ± 1 mmHg and mean arterial pressure fell by 7 ± 1 mmHg during the 30 minutes before CPB. UPO₂ then fell by a further 12 ± 2 mmHg during the first 30 minutes of CPB but remained relatively stable for the remaining 24 minutes of observation.

Renal medullary hypoxia is an early event during CPB. It starts to develop even before CPB, presumably due to a pressure-dependent decrease in renal blood flow. Medullary hypoxia during CPB appears to be promoted by hypotension and is not ameliorated by increasing blood hemoglobin concentration.