Mechanism of post dialysis hyperventilation in  patients with chronic renal insufficiency.
Several hypotheses have been put forward to explain postdialysis hypocapnia. Three were tested in this study: impairment of tissue oxygenation by dialysis (D)-induced alkalosis (Bohr effect), the D disequilibrium syndrome, and the loss of carbon dioxide  (CO2) in D fluid. In 17 patients pre-DPCO2 was significantly correlated with plasma bicarbonate concentration (HCO3) and no disproportionate reduction of PCO2 was discernible. In 10 patients using a bath acetate concentration of 38 mEq/1 PCO2 was unchanged after D (35.4 versus 35.9 mm Hg before D), and was low relative to HCO3 whic increased from 21.2 to 28.0 mEq/1. After a dialysis using an acetate concentration of 25 mEq/1 HCO3 remained constant (20.4 versus 21.1 mEq/1 pre-D), whereas PCO2 fell from 35.3 to 30.8 mm Hg (P less than 0.001). Consequently PCO2 was again low relative to HCO3. Removal of CO2 by D fluid was excluded as a cause for low blood PCO2: addition of gaseous CO2 to the bath had no influence on arterial blood gases. Since post-D hypocapnia was not prevented when HCO3 was kept constant, it was concluded that post-D alkalosis cannot be the main reason for post-D hyperventilation, and that other factors related to the process of D are responsible.
Mechanism of post dialysis hyperventilation in  patients with chronic renal insufficiency. Several hypotheses have been put forward to explain postdialysis hypocapnia. Three were tested in this study: impairment of tissue oxygenation by dialysis (D)-induced alkalosis (Bohr effect), the D disequilibrium syndrome, and the loss of carbon dioxide  (CO2) in D fluid. In 17 patients pre-DPCO2 was significantly correlated with plasma bicarbonate concentration (HCO3) and no disproportionate reduction of PCO2 was discernible. In 10 patients using a bath acetate concentration of 38 mEq/1 PCO2 was unchanged after D (35.4 versus 35.9 mm Hg before D), and was low relative to HCO3 whic increased from 21.2 to 28.0 mEq/1. After a dialysis using an acetate concentration of 25 mEq/1 HCO3 remained constant (20.4 versus 21.1 mEq/1 pre-D), whereas PCO2 fell from 35.3 to 30.8 mm Hg (P less than 0.001). Consequently PCO2 was again low relative to HCO3. Removal of CO2 by D fluid was excluded as a cause for low blood PCO2: addition of gaseous CO2 to the bath had no influence on arterial blood gases. Since post-D hypocapnia was not prevented when HCO3 was kept constant, it was concluded that post-D alkalosis cannot be the main reason for post-D hyperventilation, and that other factors related to the process of D are responsible.