Effects of hemodialysis on hemoglobin oxygen affinity and cardiac function

Hemoglobin affinity for oxygen is modulated by ambient oxygen tension, acid/base status, 2,3 diphosphoglycerate (2,3DPG) concentrations and other factors, facilitating tissue oxygenation under changing conditions. 2,3DPG is a key regulator of oxygen affinity within red blood cells and its levels are affected by blood phosphate. P50, the partial pressure of oxygen at which 50% of its hemoglobin binding sites are occupied, is a marker of oxygen delivery to tissues. We measured P50 during hemodialysis and explored its relationship with mineral metabolites and left ventricular strain as a marker of cardiac function.

Venous blood gas and other laboratory parameters were measured in 20 prevalent patients pre- and post-hemodialysis. To avoid arterio-venous mixing, we selected patients dialyzing through tunneled dialysis catheters. Associations of P50 with demographics, laboratory parameters and echocardiographic measurements were examined using linear regression models.

P50 levels decreased from 27.1 ± 0.9 mmHg to 26.2 ± 0.7 mmHg during hemodialysis (P < .001). Among 18 predictors evaluated, older age, and greater reductions in phosphate during hemodialysis were the strongest predictors of P50 changes in multivariate models. There was acute worsening in left ventricular global longitudinal strain (LVGLS) during hemodialysis (reduction of 1.4 ± 3.9%; P = .03). Greater reductions in P50 during hemodialysis and older age were significantly associated with greater reductions in LVGLS.

Hemodialysis consistently reduces P50. The magnitude of P50 change was strongly associated with concurrent phosphate changes. P50 reductions correlated with acute lowering of LVGLS. These observations illuminate a potential cause of systemic tissue hypoxia and potential cardiac dysfunction during hemodialysis.