SAT-143 MILD HYPERCAPNIA DURING MAJOR SURGERY, A POSSIBLE STRATEGY TO PREVENT RENAL MEDULLARY HYPOXIA AND THE DEVELOPMENT ACUTE KIDNEY INJURY

Abstract

Acute kidney injury (AKI) is a common complication of major surgery that increases short- and long-term morbidity and mortality. There is emerging evidence that decreased renal medullary perfusion, resulting in hypoxia, contributes to the development of AKI during prolonged surgery. Since hypercapnia can provide a degree of organ protection, possibly due to its vasodilator effects, we investigated whether increases in arterial carbon dioxide level (PaCO2) improve global and regional kidney oxygenation in anesthetised sheep. In addition, positive end expiratory pressure (PEEP) is used to increase oxygenation, but it also decreases cardiac output and may therefore reduce renal perfusion and oxygenation. Thus, we determined the effects of PEEP (0, 5, 10, 15 and 20 cmH2O for 15 min), and PEEP with mild hypercapnia (PaCO2 45-55mmHg), on renal perfusion and oxygenation. In Merino ewes, surgery was performed to implant pulmonary and renal artery flow probes and laser-Doppler and oxygen-sensing probes in the renal medulla and cortex and to cannulate a renal vein. In anaesthetised sheep (isoflurane 2.5%), FiO2 was held at 0.4 and respiratory rate was changed to achieve target PaCO2 (normocapnia 35-45, mild hypercapnia 45-55 and severe hypercapnia 55-65 mmHg) for periods of 20 minutes, in random order. PEEP was held at (0, 5, 10, 15 and 20 cm H2O) for periods of 15 min during normocapnia and mild hypercapnia. Increases in PaCO2 from normocapnia, to mild and severe hypercapnia significantly increased medullary PO2 (39.1±5.5, 48.6±4.2 and 51.9±4.8 mmHg, respectively) and perfusion (336±66, 449±72 and 453±82 blood perfusion units, respectively). There were no changes in cortical perfusion or PO2, renal blood flow or renal oxygen delivery. During normocapnia, PEEP decreased cardiac output, renal blood flow, renal oxygen delivery, medullary perfusion (342±101 to 243±64 blood perfusion units (BPU)) and medullary PO2 (33.5±5.4 to 22.6±8.9 mmHg). Mild hypercapnia, for 30 min before and during PEEP, prevented the PEEP-induced decreases in medullary perfusion (586±165 to 491±93 BPU) and PO2 (54.6±7.8 to 57.4±7.6 mmHg), despite reductions in cardiac output and renal blood flow. Under volatile anaesthesia, increases in PaCO2 caused progressive increases in renal medullary perfusion and oxygenation. PEEP had detrimental effects on cardiac output, renal blood flow and medullary perfusion and PO2. Mild hypercapnia prevented the PEEP-induced decreases in medullary perfusion and PO2. During prolonged major surgery, increasing PaCO2 to prevent decreases in renal medullary PO2 may be a useful strategy to reduce the incidence of post-operative AKI.