What is the optimal management of persistent volume overload in an 81‑year‑old woman with diastolic heart failure (heart failure with preserved ejection fraction) and pulmonary hypertension who is already on standard oral furosemide?

Optimal Management of Persistent Volume Overload in Diastolic Heart Failure

This 81-year-old woman with HFpEF and persistent fluid overload despite oral furosemide requires immediate escalation to intravenous loop diuretics, with the initial IV dose at least matching her total daily oral dose, followed by aggressive uptitration until euvolemia is achieved. 1

Immediate Diuretic Escalation Strategy

Transition to Intravenous Therapy

• Hold oral furosemide and initiate IV furosemide at a dose equal to or exceeding the total daily oral dose (e.g., if taking 40 mg PO twice daily, start with ≥80 mg IV). 1, 2
• Administer the initial IV bolus slowly over 1–2 minutes to minimize rapid hemodynamic shifts. 2
• Insert a urinary catheter to measure hourly urine output during the acute phase, targeting >0.5 mL/kg/h. 1, 2

Dose Escalation Protocol

• If adequate diuresis is not achieved within 2 hours, increase the dose by 20 mg increments every 2 hours until desired urine output is obtained. 1, 2
• Do not exceed 100 mg total furosemide in the first 6 hours or 240 mg in the first 24 hours to limit toxicity while achieving effective decongestion. 1, 2
• Continue aggressive diuresis until all clinical evidence of fluid retention is eliminated (no jugular venous distension, no peripheral edema, clear lung fields). 1

Sequential Nephron Blockade for Diuretic Resistance

When to Add a Second Diuretic

• If adequate diuresis is not achieved after 24–48 hours despite IV furosemide doses of 160 mg/day or higher, add a second diuretic class rather than further increasing the loop diuretic dose. 1, 3

Combination Diuretic Options

• Add metolazone 2.5–5 mg PO once daily for potent sequential nephron blockade, particularly effective in diuretic-resistant states. 1, 3
• Alternatively, add hydrochlorothiazide 25 mg PO once daily as a thiazide-type diuretic. 1, 2
• Consider spironolactone 25–50 mg PO once daily if serum potassium is <5.0 mmol/L and creatinine is <2.5 mg/dL. 1, 2
• Low-dose combination therapy is more effective with fewer adverse effects than high-dose monotherapy. 1, 2

Critical Monitoring with Combination Therapy

• Intensify electrolyte monitoring to every 1–2 days initially when using dual diuretic regimens due to increased risk of severe hypokalemia and renal deterioration. 2

Management of Concurrent Medications

Beta-Blocker Management

• Continue the beta-blocker at the pre-admission dose unless the patient develops marked hypoperfusion (SBP <90 mmHg with end-organ dysfunction) or requires intravenous inotropic support. 2
• Abrupt beta-blocker withdrawal is associated with clinical deterioration; maintain therapy while escalating diuretics. 2

ACE-Inhibitor/ARB Management

• Do not discontinue ACE inhibitors or ARBs during acute decompensation unless true hypoperfusion is present (SBP <90 mmHg with altered mental status, cool extremities, oliguria, or elevated lactate). 2
• Modest blood pressure reductions or creatinine rises ≤0.3 mg/dL are insufficient reasons to stop these disease-modifying agents. 2

Avoiding NSAIDs

• Avoid all non-steroidal anti-inflammatory drugs during IV diuretic therapy because they blunt diuretic response and worsen renal function. 2

Critical Monitoring Requirements

Hourly Monitoring During Acute Phase

• Urine output (target >0.5 mL/kg/h using bladder catheter for accuracy). 1, 2
• Blood pressure and signs of hypoperfusion (cool extremities, altered mental status, oliguria). 1, 2
• Respiratory status and oxygen saturation; provide supplemental oxygen if SpO₂ <90%. 1, 2

Daily Monitoring During Active Diuresis

• Body weight at the same time each morning (after waking, before dressing, after voiding, before eating), targeting 0.5–1.0 kg loss per day. 1, 2
• Serum electrolytes (especially potassium), BUN, and creatinine to detect dyselectrolytemia and renal changes. 1, 2
• Hold furosemide if potassium falls below 3.0 mEq/L until corrected, as severe hypokalemia increases arrhythmia risk. 2

Managing Hypotension During Diuresis

Decision Thresholds

• Do not withhold furosemide unless SBP is <90 mmHg AND there are clear signs of hypoperfusion (cool extremities, altered mental status, oliguria, elevated lactate). 2
• If SBP ≥90 mmHg, continue IV furosemide at full doses; mild-to-moderate hypotension without end-organ hypoperfusion is not a contraindication to diuresis. 2
• Continue diuresis until congestion is resolved, even if blood pressure falls modestly, provided the patient remains asymptomatic. 1, 2

Pathophysiologic Rationale

• Acute decompensated HFpEF often presents with simultaneous volume overload and low blood pressure because the failing heart operates on the flat portion of the Frank-Starling curve, where additional preload does not increase stroke volume. 2
• Persistent congestion raises ventricular wall stress and activates neurohormonal pathways (RAAS, sympathetic nervous system), worsening both hypotension and edema. 2
• Diuresis lowers filling pressures and wall stress, potentially improving cardiac output by shifting the heart toward a more favorable segment of the Frank-Starling curve. 2

Managing Worsening Renal Function

Acceptable Creatinine Changes

• Mild or moderate increases in blood urea nitrogen and serum creatinine should not lead to efforts to minimize diuretic intensity, provided renal function stabilizes. 1
• Continue diuresis even with mild azotemia during active decongestion; persistent volume overload itself worsens renal perfusion and diminishes diuretic responsiveness. 1, 2

When to Hold or Reduce Diuretics

• Hold or reduce furosemide if creatinine rises >0.3 mg/dL during hospitalization, as this increases in-hospital mortality nearly three-fold. 2
• Hold furosemide if eGFR falls below 30 mL/min/1.73 m² or creatinine exceeds 2.5 mg/dL. 2
• Halve the loop diuretic dose when serum creatinine rises markedly, and continue close laboratory monitoring. 2

Adjunctive Therapies

Respiratory Support

• Apply non-invasive ventilation (CPAP or BiPAP) with PEEP of 5–7.5 cm H₂O for respiratory distress or pulmonary edema. 2
• Consider low-dose IV morphine (2.5–5 mg) for severe dyspnea, anxiety, or restlessness. 2

Vasodilator Therapy

• Add IV nitroglycerin or nitroprusside when SBP >110 mmHg to reduce afterload, improve cardiac output, and facilitate diuresis. 1, 2
• IV nitroglycerin acts primarily through venodilation, lowers preload, and may help rapidly reduce pulmonary congestion, particularly in patients with hypertension, coronary ischemia, or significant mitral regurgitation. 1

Inotropic Support (Reserved for Hypoperfusion)

• Initiate short-term IV inotropic therapy (dobutamine or milrinone) only when patients exhibit hypoperfusion (SBP <90 mmHg with end-organ hypoperfusion) despite adequate volume status. 2
• Prefer milrinone over dobutamine when the patient is on beta-blockers, as milrinone acts independently of β-adrenergic receptors. 2

Ultrafiltration for Refractory Congestion

• Ultrafiltration may be considered for patients with obvious volume overload to alleviate congestive symptoms and fluid weight. 1
• Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy, though consultation with a nephrologist is appropriate before initiating. 1
• If all diuretic strategies are unsuccessful, hospitalization is generally required for further adjustment of therapy, possibly including ultrafiltration or hemofiltration. 1

Dietary and Lifestyle Measures

• Restrict dietary sodium to 2–3 grams daily as the cornerstone of volume management; this greatly assists in maintenance of volume balance. 1, 3
• Consider fluid restriction to 2 liters daily if persistent volume overload despite sodium restriction and high-dose diuretic use. 1, 3

Discharge Planning

• Patients should not be discharged from the hospital until a stable and effective diuretic regimen is established, and ideally not until euvolemia is achieved. 1
• Patients sent home before these goals are reached are at high risk of recurrence of fluid retention and early readmission, because unresolved edema may itself attenuate the response to diuretics. 1
• Once euvolemia is achieved, define the patient's dry weight and use it as a continuing target for adjustment of diuretic doses. 1
• Many patients can modify their own diuretic regimen in response to weight changes that exceed a predefined range. 1

Special Considerations for HFpEF with Pulmonary Hypertension

• The mainstay of therapy for pulmonary hypertension in HFpEF remains treatment of the underlying HFpEF condition, primarily through aggressive volume management. 4
• There is limited evidence to support the use of pulmonary vasculature-targeting therapies (PDE inhibitors, prostacyclin analogs, endothelin receptor antagonists) in PH-HFpEF, as these have not consistently improved hemodynamics or functional outcomes. 4
• Current practice guidelines focus on remedying volume overload, aggressively controlling hypertension, and treating comorbid conditions that contribute to decompensation. 5

Common Pitfalls to Avoid

• Excessive concern about hypotension and azotemia can lead to underutilization of diuretics and a state of refractory edema. 1
• Persistent volume overload not only contributes to persistence of symptoms but may also limit the efficacy and compromise the safety of other drugs used for treatment of HF. 1
• Do not hold diuretics solely for isolated low blood pressure without first confirming true hypoperfusion. 2
• Avoid initiating diuretic doses lower than the patient's home oral regimen in those already on chronic diuretics. 2
• Do not discontinue ACE-I/ARB or beta-blockers unnecessarily during acute decompensation unless severe hypoperfusion is present. 2