Key result
Acetazolamide improves respiratory function, lowering PaCO2 and reducing BNP ~55% in a heart failure patient.
Why the study?
Cardio-renal-pulmonary interactions driven by renal acid-base balance affecting respiratory function are predicted in heart failure pathophysiology but have not yet been confirmed.
Does oral acetazolamide improve hypercapnia and metabolic alkalosis in a heart failure patient with cardio-renal pulmonary syndrome?
Does oral acetazolamide improve hypercapnia and metabolic alkalosis in a heart failure patient with cardio-renal pulmonary syndrome?
Acetazolamide may reduce cardiac burden and enhance pulmonary ventilation in heart failure patients with hypercapnia and metabolic alkalosis, highlighting a potential cardio-renal pulmonary syndrome.
May not yet change practice in hypercapnic HF; hypothesis-generating for acetazolamide in 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.
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Hajime Kataoka (2026) studied this question. Acetazolamide improved respiratory function in a heart failure patient, decreasing BNP from 348 to 158 pg/mL and PaCO2 from 59.7 to 37.8 mmHg.
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