Admission serum bicarbonate is associated with early diuretic resistance in acute decompensated heart failure.
Acute decompensated heart failure (ADHF) exhibits a heterogeneous diuretic response. Chloride-bicarbonate imbalances may reduce loop diuretic efficiency. The effect of admission bicarbonate levels on diuretic resistance in unselected ADHF patients remains unclear. We aimed to evaluate whether higher admission bicarbonate identifies patients at risk of early diuretic dose escalation and less effective early decongestion.
Our study was planned as a retrospective, single-centre, consecutive ADHF cohort. This study included 1000 hospitalised patients with ADHF (mean age 69 years, ± 11.2 years, 42.7% female) who underwent arterial blood sampling and pH ranging from 7.35 to 7.45. Patients were divided into three groups according to their admission bicarbonate value (< 22 mmol/L-group 1, 22-28 mmol/L-group 2, > 28 mmol/L-group 3). The primary endpoint was early diuretic escalation within 48 hours (dose doubling and/or thiazide add-on or infusion switch). Secondary endpoints included diuretic efficiency, 24/48-hour net fluid balance, 48-hour weight change, early spot urine sodium, and safety/utilisation metrics. Multivariable models adjusted for prespecified clinical and laboratory covariates and baseline diuretic regimen.
Higher admission bicarbonate (particularly > 28 mmol/L) was independently associated with greater odds of early escalation and with less effective decongestion. Patients with higher bicarbonate demonstrated lower diuretic efficiency, smaller 24-48 hour net fluid losses, attenuated early weight reduction, and lower early urine sodium. Companion markers (lower chloride, higher pH and pCO2) paralleled these findings, consistent with an alkalosis phenotype.
Admission bicarbonate is a simple, physiologically coherent marker of early decongestion dynamics in ADHF. Embedding this chemistry-based flag within urine-sodium-guided protocols may enable earlier, objective intensification of pharmacologic therapy and more efficient decongestion. Prospective trials should test bicarbonate-informed pathways against usual care on clinical outcomes.
Our study was planned as a retrospective, single-centre, consecutive ADHF cohort. This study included 1000 hospitalised patients with ADHF (mean age 69 years, ± 11.2 years, 42.7% female) who underwent arterial blood sampling and pH ranging from 7.35 to 7.45. Patients were divided into three groups according to their admission bicarbonate value (< 22 mmol/L-group 1, 22-28 mmol/L-group 2, > 28 mmol/L-group 3). The primary endpoint was early diuretic escalation within 48 hours (dose doubling and/or thiazide add-on or infusion switch). Secondary endpoints included diuretic efficiency, 24/48-hour net fluid balance, 48-hour weight change, early spot urine sodium, and safety/utilisation metrics. Multivariable models adjusted for prespecified clinical and laboratory covariates and baseline diuretic regimen.
Higher admission bicarbonate (particularly > 28 mmol/L) was independently associated with greater odds of early escalation and with less effective decongestion. Patients with higher bicarbonate demonstrated lower diuretic efficiency, smaller 24-48 hour net fluid losses, attenuated early weight reduction, and lower early urine sodium. Companion markers (lower chloride, higher pH and pCO2) paralleled these findings, consistent with an alkalosis phenotype.
Admission bicarbonate is a simple, physiologically coherent marker of early decongestion dynamics in ADHF. Embedding this chemistry-based flag within urine-sodium-guided protocols may enable earlier, objective intensification of pharmacologic therapy and more efficient decongestion. Prospective trials should test bicarbonate-informed pathways against usual care on clinical outcomes.