How should I manage a patient with acute decompensated heart failure, including initial oxygen therapy, continuous cardiac monitoring, intravenous loop diuretic, vasodilator for hypertension, inotrope for hypotension, and subsequent guideline‑directed medical therapy?

Management of Acute Decompensated Heart Failure

Start intravenous loop diuretics immediately upon presentation—within 60 minutes—at a dose equal to or exceeding the patient's total daily oral dose (or 20–40 mg IV furosemide if diuretic-naïve), and simultaneously initiate IV vasodilators (nitroglycerin preferred) if systolic blood pressure is ≥110 mm Hg. 1, 2, 3

Immediate Assessment and Triage (First 15 Minutes)

Assess three critical parameters simultaneously to guide therapy:

• Blood pressure phenotype: Hypertensive (SBP >140 mm Hg), normotensive (SBP 90–140 mm Hg), or hypotensive (SBP <90 mm Hg) 4, 1
• Perfusion status: Look for cool extremities, altered mental status, decreased urine output, and signs of end-organ hypoperfusion 2, 3
• Congestion severity: Assess jugular venous pressure (≥15 cm H₂O indicates severe overload), bilateral basal crackles, peripheral edema, ascites, and respiratory distress with accessory muscle use 4, 1

Immediate ICU/CCU admission is required if any of the following are present: respiratory rate >25/min, SpO₂ <90%, use of accessory muscles, SBP <90 mm Hg, heart rate <40 or >130 bpm, or signs of hypoperfusion. 4, 3

Oxygen and Monitoring

• Administer supplemental oxygen only if SpO₂ <90%; routine oxygen in non-hypoxemic patients is not indicated. 4
• Institute continuous monitoring within minutes: pulse oximetry, blood pressure, respiratory rate, continuous ECG, and urine output. 4

Pharmacologic Management by Blood Pressure Phenotype

Hypertensive Acute Heart Failure (SBP >140 mm Hg)

This is the most common presentation—patients are typically older, female, with preserved ejection fraction and acute pulmonary edema. 4

• IV vasodilators (nitroglycerin or nitroprusside) are first-line therapy and must be started immediately—this is a Class I ESC recommendation. 1
• Early IV vasodilator use is associated with lower in-hospital mortality, whereas delays increase mortality. 1
• Combine vasodilators with IV loop diuretics: give furosemide 40 mg IV bolus if diuretic-naïve, or a dose equal to or exceeding the total daily oral dose if already on diuretics. 1, 2
• Target an initial BP reduction of 30 mm Hg within minutes, then gradual reduction over several hours to pre-crisis baseline. 1

Normotensive Acute Heart Failure (SBP 90–140 mm Hg)

• IV loop diuretics are the cornerstone: start furosemide at 2–2.5 times the total daily oral dose (or 20–40 mg if diuretic-naïve). 3, 5
• Add IV vasodilators (nitroglycerin preferred) when SBP ≥110 mm Hg for rapid relief of dyspnea and pulmonary congestion. 3
• Vasodilators are contraindicated when SBP falls below 110 mm Hg. 3
• Continue ACE-inhibitors/ARBs and beta-blockers unless true hemodynamic instability is present—modest BP reductions do not impair decongestion. 3

Hypotensive Acute Heart Failure (SBP <90 mm Hg with Hypoperfusion)

• Inotropes (dobutamine or milrinone) are reserved exclusively for patients with documented severe systolic dysfunction, SBP <90 mm Hg, AND evidence of low cardiac output with hypoperfusion. 3, 6, 7
• Milrinone is FDA-approved for short-term IV treatment of acute decompensated heart failure and may be preferable when significant pulmonary venous hypertension is present. 6, 7
• Do NOT use inotropes in normotensive patients without hypoperfusion—they increase mortality and arrhythmias. 1, 3
• Patients receiving milrinone must have continuous ECG monitoring and immediate access to treatment for life-threatening ventricular arrhythmias. 6

Diuretic Dosing and Monitoring

• Initial IV furosemide dose: 2–2.5 times the total daily oral dose for patients already on diuretics; 20–40 mg for diuretic-naïve patients. 3, 5
• Assess diuretic response at 2 hours: spot urine sodium >50–70 mmol/L, urine output >100–150 mL/h in first 6 hours, or weight loss of 0.5–1.5 kg in 24 hours. 5
• If congestion persists after 24–48 hours of maximized loop diuretic therapy, add a thiazide (metolazone) or acetazolamide as adjunctive therapy. 3, 5
• Consider continuous furosemide infusion if decongestion targets are not met with bolus dosing. 5
• Monitor daily: fluid intake/output, daily weight, vital signs (including supine and standing BP), renal function (creatinine, eGFR), and electrolytes (potassium, magnesium). 1, 2, 3

Therapies to AVOID

• Morphine is discouraged—registry data (ADHERE) show higher rates of mechanical ventilation, ICU admission, and death. 1, 3
• Do NOT use inotropes in normotensive patients—they increase mortality without evidence of benefit. 1, 3
• Digoxin has no role in acute management of decompensated HF with pulmonary edema and hypertension; it is reserved only for rate control in atrial fibrillation. 1
• Do NOT discontinue or reduce ACE-inhibitors/ARBs or beta-blockers unless SBP falls below 85 mm Hg or true hemodynamic instability develops. 1, 3
• Adenosine is inappropriate—tachycardia in hypertensive AHF is compensatory, not a primary arrhythmia. 1

Guideline-Directed Medical Therapy (GDMT) During Hospitalization

The key principle is to continue existing GDMT and initiate new GDMT as soon as clinical stability allows—often beginning on day 1. 2

Sequencing Algorithm for GDMT Initiation

Day 1 (once adequate perfusion confirmed and responding to diuretics):

• Start SGLT2 inhibitors and mineralocorticoid receptor antagonists (MRAs) first—they have minimal BP effects but rapid beneficial effects. 2
• Continue existing beta-blockers and ACE-inhibitors/ARBs unless hemodynamically unstable. 2, 3

Day 2–3 (after volume optimization):

• Initiate or up-titrate ACE-inhibitors/ARBs/ARNIs once volume status is optimized, no marked azotemia or hyperkalemia risk, and SBP >90–100 mm Hg. 2

Day 3–5 (after IV therapies discontinued):

• Start or restart beta-blockers at low dose only after volume optimization is achieved, IV vasodilators and inotropes are discontinued, and clinical stability is confirmed. 2
• Do NOT start beta-blockers on day 1 if the patient required oxygen and is acutely decompensated. 2

Common GDMT Pitfalls

• Only 73% of eligible patients receive ACE-inhibitors/ARBs/ARNIs, 66% receive beta-blockers, and 33% receive MRAs within 30 days post-hospitalization—initiate during hospitalization to avoid this gap. 2
• Do NOT discontinue GDMT for mild renal function decrease or asymptomatic BP reduction unless contraindicated. 2

Diagnostic Workup

• ECG immediately to exclude ST-elevation MI and identify arrhythmias. 4, 2
• Cardiac troponin to identify acute coronary syndrome as a precipitating factor. 2
• BNP or NT-proBNP when the contribution of heart failure to dyspnea is uncertain. 2
• Chest X-ray to assess pulmonary congestion (though normal in 20% of cases). 4, 2
• Echocardiography to assess ejection fraction, chamber size, wall thickness, and valve function—not needed immediately in most cases unless hemodynamic instability is present. 4, 2
• Bedside thoracic ultrasound for interstitial edema and abdominal ultrasound for IVC diameter if expertise is available. 4

Special Situations

• Atrial fibrillation with rapid ventricular response: beta-blockers are first-line for rate control; IV digoxin may be considered when rapid control is needed. 3
• Persistent congestion despite maximal medical therapy: consider ultrafiltration after 24–48 hours. 3, 7
• Pulmonary artery catheterization is indicated only in selected patients with persistent symptoms despite therapy, worsening renal function, or need for vasoactive agents—not routine. 3

Discharge Criteria

Patients are medically fit for discharge when:

• Hemodynamically stable and euvolemic 3
• Established on evidence-based GDMT 3
• Patient education completed 3

Venous Thromboembolism Prophylaxis

• Prophylaxis for VTE is recommended in all hospitalized HF patients unless already anticoagulated or contraindicated. 3