Improvement of respiratory function with acetazolamide in heart failure: a case of cardio-renal pulmonary syndrome

As renal handling of chloride (Cl) and bicarbonate (HCO3) under different cardiac states would affect the acid-base balance and subsequently influence respiratory function, cardio-renal-pulmonary interactions can be predicted in heart failure (HF) pathophysiology, but have not yet been confirmed. We report a 93-year-old male HF patient taking diuretics who presented with mild body fluid retention, elevated b-type natriuretic peptide (BNP), and hypercapnia during a hospital stay. To improve the hypercapnia and correct metabolic alkalosis, he was given oral acetazolamide (250 mg/day). Peripheral venous blood tests before and after 1 month on acetazolamide showed that his body weight (39.8 to 36.8 kg) and BNP level (348 to 158 pg/mL) decreased. Arterial blood gas analysis showed that his blood pH (7.41 to 7.37) and PaO2 (91 to 95 mmHg) increased, and PaCO2 (59.7 to 37.8 mmHg), HCO3 (36.7 to 21.3 mmol/L) and base excess (11.5 to -3.1 mmol/L) decreased. These observations indicated that acetazolamide treatment reduced the cardiac burden and enhanced pulmonary ventilation possibly by stimulating the brain's respiratory center. This case highlights a new clinical HF entity of pathophysiologic cardio-renal pulmonary syndrome as a pathologic spectrum defined by cardio-pulmonary interactions linked to kidney function through renal modulation of the acid-base balance.