Early Inotrope Assisted Diuresis in Acute Decompensated Heart Failure: A Case Report

Background

Acute decompensated heart failure (ADHF) complicated by borderline or low systolic blood pressure (SBP) frequently limits titration of loop diuretics, resulting in incomplete decongestion. Intravenous inotropes are used to augment cardiac output and support diuretic delivery in this setting, though evidence for their benefit is heterogeneous and etiology-dependent.

Case Presentation

A 71-year-old man with ischemic cardiomyopathy and HFrEF (LVEF 25–30%), CKD, paroxysmal atrial fibrillation status post MAZE procedure and left atrial appendage ligation, and sick sinus syndrome with pacemaker placement and ascending aortic aneurysm status post hemiarch replacement presented with progressive exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. On admission, blood pressure was 106/77 mmHg, NT-proBNP 7,547 pg/mL, and chest radiography demonstrated pulmonary vascular congestion and edema. Echocardiography showed LVEF of 25–30%, right ventricular dysfunction, and moderate functional mitral and tricuspid regurgitation.

Intravenous furosemide was initiated for decongestion; however, persistent volume overload was accompanied by progressive hypotension, with SBP falling into the 80s and limiting further diuretic escalation and GDMT. Despite hypotension, he remained warm and without clinical or biochemical evidence of hypoperfusion or cardiogenic shock, with normal lactate levels. On hospital day 2, blood pressure declined to 71/50 - 87/54 mmHg, prompting transfer to the cardiac intensive care unit for inotrope-assisted decongestion. Milrinone was initiated at 0.125 μg/kg/min, allowing escalation of furosemide to 40 mg IV twice daily. Over the following two days of milrinone-assisted diuresis, net fluid balances of approximately −1.5 L and −1.1 L were achieved without evidence of hypoperfusion. Spironolactone 12.5 mg daily was added, and milrinone was successfully discontinued on day 3 in the CCU. The patient remained stable off inotropic support and was discharged euvolemic on furosemide 40 mg twice daily and spironolactone 12.5 mg daily. Persistent hypotension precluded initiation of metoprolol and ACEi/ARB/ARNI therapy; further GDMT optimization was deferred to the outpatient setting with Advanced Heart Failure follow-up.

Findings

In a patient with ADHF, persistent congestion and low-output physiology, progressive hypotension limited adequate diuresis despite a warm-and-wet profile without overt cardiogenic shock. Short-term milrinone (0.125 μg/kg/min) provided hemodynamic support, allowing continued IV diuresis and net negative fluid balances up to 1.5 L with successful decongestion. Milrinone was discontinued after two days, and the patient remained stable off inotropic support. This case supports a potential role for individualized, short-term inotrope-assisted decongestion when fluid removal is limited by hypotension and low-output physiology.

Discussion & Conclusion

This case highlights a common inpatient dilemma in advanced HFrEF: the need for aggressive decongestion when low-normal blood pressure limits diuretic escalation and results in stalled fluid removal. Inotrope-assisted diuresis may augment cardiac output and renal perfusion, allowing more consistent diuretic dosing when hypotension limits conventional therapy. This case supports individualized, short-term inotrope-assisted decongestion in HFrEF patients whose fluid removal is objectively limited by hypotension.