O2 delivery and CO2 production during cardiopulmonary bypass as determinants of acute kidney injury: time for a goal-directed perfusion management?

Filip de Somer, John W Mulholland, Megan R Bryan, Tommaso Aloisio, Guido J Van Nooten, Marco Ranucci, Filip de Somer, John W Mulholland, Megan R Bryan, Tommaso Aloisio, Guido J Van Nooten, Marco Ranucci

Abstract

Introduction: Acute kidney injury (AKI) is common after cardiac operations. There are different risk factors or determinants of AKI, and some are related to cardiopulmonary bypass (CPB). In this study, we explored the association between metabolic parameters (oxygen delivery (DO2) and carbon dioxide production (VCO2)) during CPB with postoperative AKI.

Methods: We conducted a retrospective analysis of prospectively collected data at two different institutions. The study population included 359 adult patients. The DO2 and VCO2 levels of each patient were monitored during CPB. Outcome variables were related to kidney function (peak postoperative serum creatinine increase and AKI stage 1 or 2). The experimental hypothesis was that nadir DO2 values and nadir DO2/VCO2 ratios during CPB would be independent predictors of AKI. Multivariable logistic regression models were built to detect the independent predictors of AKI and any kind of kidney function damage.

Results: A nadir DO2 level < 262 mL/minute/m2 and a nadir DO2/VCO2 ratio < 5.3 were independently associated with AKI within a model including EuroSCORE and CPB duration. Patients with nadir DO2 levels and nadir DO2/VCO2 ratios below the identified cutoff values during CPB had a significantly higher rate of AKI stage 2 (odds ratios 3.1 and 2.9, respectively). The negative predictive power of both variables exceeded 90%. The most accurate predictor of AKI stage 2 postoperative status was the nadir DO2 level.

Conclusions: The nadir DO2 level during CPB is independently associated with postoperative AKI. The measurement of VCO2-related variables does not add accuracy to the AKI prediction. Since DO2 during CPB is a modifiable factor (through pump flow adjustments), this study generates the hypothesis that goal-directed perfusion management aimed at maintaining the DO2 level above the identified critical value might limit the incidence of postoperative AKI.

Figures

Figure 1
Figure 1
Graph showing acute kidney injury rate according to decile distribution of nadir oxygen delivery (DO2) level during cardiopulmonary bypass (CPB).
Figure 2
Figure 2
Acute kidney injury rate according to decile distribution of nadir DO2/VCO2 ratio during CPB.
Figure 3
Figure 3
Receiver operating characteristic curves for acute kidney injury stage 2 rate prediction based on nadir DO2 level, nadir DO2/VCO2 ratio and nadir hematocrit (HCT) level.
Figure 4
Figure 4
Acute kidney injury rates in patient groups according to the critical values of DO2, DO2/VCO2 ratio and hematocrit, with sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV).

References

    1. Dasta JF, Kane-Gill SL, Durtschi AJ, Pathak DS, Kellum JA. Costs and outcomes of acute kidney injury (AKI) following cardiac surgery. Nephrol Dial Transplant. 2008;23:1970–1974. doi: 10.1093/ndt/gfm908.
    1. Mangano CM, Diamondstone LS, Ramsay JG, Aggarwal A, Herskowitz A, Mangano DT. Renal dysfunction after myocardial revascularization: risk factors, adverse outcomes, and hospital resources utilization. Ann Intern Med. 1998;128:194–203.
    1. Provenchère S, Plantefève G, Hufnagel G, Vicaut E, De Vaumas C, Lecharny JB, Depoix JP, Vrtovsnik F, Desmonts JM, Philip I. Renal dysfunction after cardiac surgery with normothermic cardiopulmonary bypass: incidence, risk factors, and effect on clinical outcome. Anesth Analg. 2003;96:1258–1264.
    1. Chertow GM, Lazarus JM, Christiansen CL, Cook EF, Hammermeister KE, Grover F, Daley J. Preoperative renal risk stratification. Circulation. 1997;95:878–884.
    1. Llopart T, Lombardi R, Forselledo M, Andrade R. Acute renal failure in open heart surgery. Ren Fail. 1997;19:319–323. doi: 10.3109/08860229709026296.
    1. Wijeysundera DN, Karkouti K, Dupuis JY, Rao V, Chan CT, Granton JT, Beattie WS. Derivation and validation of a simplified predictive index for renal replacement therapy after cardiac surgery. JAMA. 2007;297:1801–1809. doi: 10.1001/jama.297.16.1801.
    1. Fischer UM, Weissenberger WK, Warters RD, Geissler HJ, Allen SJ, Mehlhorn U. Impact of cardiopulmonary bypass management on postcardiac surgery renal function. Perfusion. 2002;17:401–406. doi: 10.1191/0267659102pf610oa.
    1. Ranucci M, Romitti F, Isgrò G, Cotza M, Brozzi S, Boncilli A, Ditta A. Oxygen delivery during cardiopulmonary bypass and acute renal failure after coronary operations. Ann Thorac Surg. 2005;80:2213–2220. doi: 10.1016/j.athoracsur.2005.05.069.
    1. Fang WC, Helm RE, Krieger KH, Rosengart TK, DuBois WJ, Sason C, Lesser ML, Isom OW, Gold JP. Impact of minimum hematocrit during cardiopulmonary bypass on mortality in patients undergoing coronary artery surgery. Circulation. 1997;96(9 suppl):II-194–II-199.
    1. Habib RH, Zacharias A, Schwann TA, Riordan CJ, Durham SJ, Shah A. Adverse effects of low hematocrit during cardiopulmonary bypass in the adult: should current practice be changed? J Thorac Cardiovasc Surg. 2003;125:1438–1450. doi: 10.1016/S0022-5223(02)73291-1.
    1. Swaminathan M, Phillips-Bute BG, Conlon PJ, Smith PK, Newman MF, Stafford-Smith M. The association of lowest hematocrit during cardiopulmonary bypass with acute renal injury after coronary artery bypass surgery. Ann Thorac Surg. 2003;76:784–792. doi: 10.1016/S0003-4975(03)00558-7.
    1. Ranucci M, De Toffol B, Isgrò G, Romitti F, Conti D, Vicentini M. Hyperlactatemia during cardiopulmonary bypass: determinants and impact on postoperative outcome. Crit Care. 2006;10:R167. doi: 10.1186/cc5113.
    1. Ranucci M, Isgrò G, Romitti F, Mele S, Biagioli B, Giomarelli P. Anaerobic metabolism during cardiopulmonary bypass: predictive value of carbon dioxide derived parameters. Ann Thorac Surg. 2006;81:2189–2195. doi: 10.1016/j.athoracsur.2006.01.025.
    1. Baker RA, Newland RF. Continuous quality improvement of perfusion practice: the role of electronic data collection and statistical control charts. Perfusion. 2008;23:7–16. doi: 10.1177/0267659108093853.
    1. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A. Acute Kidney Injury Network. Acute Kidney Injury Network: a report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11:R31. doi: 10.1186/cc5713.
    1. Mehta RH, Grab JD, O'Brien SM, Bridges CR, Gammie JS, Haan CK, Ferguson TB, Peterson ED. Bedside tool for predicting the risk of postoperative dialysis in patients undergoing cardiac surgery. Circulation. 2006;114:2208–2216. doi: 10.1161/CIRCULATIONAHA.106.635573.
    1. Ratcliffe PJ, Endre ZH, Tange JD, Ledingham JG. Ischaemic acute renal failure: why does it occur? Nephron. 1989;52:1–5. doi: 10.1159/000185573.
    1. Pinsky MR. Beyond global oxygen supply-demand relations: in search of measures of dysoxia. Intensive Care Med. 1994;20:1–3. doi: 10.1007/BF02425045.
    1. Steltzer H, Hiesmayr M, Mayer N, Krafft P, Hammerle AF. The relationship between oxygen delivery and uptake in the critically ill: is there a critical optimal therapeutic value? A meta-analysis. Anaesthesia. 1994;49:229–236.
    1. Randall HM Jr, Cohen JJ. Anaerobic CO2 production by dog kidney in vitro. Am J Physiol. 1966;211:493–505.
    1. Lieberman JA, Weiskopf RB, Kelley SD, Feiner J, Noorani M, Leung J, Toy P, Viele M. Critical oxygen delivery in conscious humans is less than 7.3 -1.min-1. Anesthesiology. 2000;92:407–413. doi: 10.1097/00000542-200002000-00022.
    1. Zhang H, Vincent JL. Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion. Am Rev Respir Dis. 1993;148:867–871. doi: 10.1164/ajrccm/148.4_Pt_1.867.
    1. Mekontso-Dessap A, Castelain V, Anguel N, Bahloul M, Schauvliege F, Richard C, Teboul JL. Combination of venoarterial PCO2 difference with arteriovenous O2 content difference to detect anaerobic metabolism in patients. Intensive Care Med. 2002;28:272–277. doi: 10.1007/s00134-002-1215-8.
    1. Heyman SN, Khamaisi M, Rosen S, Rosenberger C. Renal parenchimal hypoxia, hypoxia response and the progression of chronic kidney disease. Am J Nephrol. 2008;28:998–1006. doi: 10.1159/000146075.
    1. Rosenberger C, Rosen S, Heyman SN. Renal parenchymal oxygenation and hypoxia adaptation in acute kidney injury. Clin Exp Pharmacol Physiol. 2006;33:980–988. doi: 10.1111/j.1440-1681.2006.04472.x.
    1. Welch WJ, Baumgartl H, Lubbers D, Wilcox CS. Nephron PO2 adrenal oxygen usage in the hypertensive rat kidney. Kidney Int. 1991;40:632–642. doi: 10.1038/ki.1991.255.

Source: PubMed

3
Prenumerera