What is the optimal acute management to relieve shortness of breath in a patient with acute decompensated heart failure (left ventricular ejection fraction ≤40%)?

Acute Management of Shortness of Breath in Decompensated Heart Failure (LVEF ≤40%)

Immediately initiate non-invasive positive pressure ventilation (CPAP or BiPAP) in patients with respiratory distress (respiratory rate >25 breaths/min, SpO₂ <90%) to rapidly reduce work of breathing, decrease intubation rates, and potentially lower mortality. 1

Immediate Respiratory Support (First Priority)

Oxygen and Ventilatory Management

• Administer supplemental oxygen only if SpO₂ <90% or PaO₂ <60 mmHg (8.0 kPa); avoid routine oxygen in non-hypoxemic patients because it causes vasoconstriction and reduces cardiac output. 1

• Start non-invasive positive pressure ventilation (CPAP or BiPAP) as soon as possible when patients show respiratory distress with SpO₂ <90% and respiratory rate >25 breaths/min; this intervention decreases respiratory distress and reduces mechanical intubation rates. 1

• Use CPAP in the pre-hospital or initial emergency setting because it requires minimal training and equipment compared to pressure-support positive end-expiratory pressure (PS-PEEP). 1

• Switch to BiPAP (PS-PEEP) on hospital arrival if the patient continues to show respiratory distress, acidosis (pH <7.35), or hypercapnia (PaCO₂ >50 mmHg), particularly in those with prior COPD or signs of respiratory muscle fatigue. 1

• Monitor blood pressure continuously during non-invasive ventilation because positive pressure can reduce preload and precipitate hypotension; use with caution in hypotensive patients. 1

• Proceed to endotracheal intubation if respiratory failure persists despite non-invasive support, defined by PaO₂ <60 mmHg, PaCO₂ >50 mmHg, and pH <7.35. 1

Pharmacologic Management (Second Priority)

Intravenous Diuretics

• Administer intravenous loop diuretics immediately to relieve congestion and improve symptoms; furosemide is the most commonly used agent. 1

• For new-onset heart failure or patients not on chronic diuretics, give furosemide 20–40 mg IV bolus; for patients already on oral diuretics, give an IV dose at least equivalent to their oral dose. 1

• Administer diuretics as intermittent boluses or continuous infusion; both strategies are acceptable, though continuous infusion may provide more predictable diuresis. 1

• Monitor urine output, renal function, and electrolytes regularly during IV diuretic therapy to detect azotemia and electrolyte depletion. 1

Intravenous Vasodilators (for Normotensive or Hypertensive Patients)

• Use intravenous vasodilators in patients with systolic blood pressure ≥110 mmHg who present with acute pulmonary edema and normal-to-high blood pressure; vasodilators reduce preload and afterload more effectively than diuretics alone. 1

• Nitroglycerin is the preferred vasodilator for acute pulmonary edema because it provides rapid venous and arterial dilation, reduces pulmonary wedge pressure, and relieves dyspnea. 1, 2

• Do not use vasodilators in patients with systolic blood pressure <110 mmHg due to risk of precipitating hypoperfusion. 1

• Delay in vasodilator administration is associated with higher mortality; initiate therapy as soon as hemodynamic stability permits. 1

Agents to Avoid or Use Cautiously

• Do not routinely administer morphine in acute decompensated heart failure; although it reduces preload and relieves dyspnea, registry data show morphine use is associated with higher rates of mechanical ventilation, ICU admission, and death. 1

• Reserve inotropic agents (dobutamine) and vasopressors for patients with persistent hypoperfusion or cardiogenic shock despite adequate filling pressures; do not use them routinely in patients with systolic blood pressure >110 mmHg or when signs of low cardiac output are absent. 1, 2

• Avoid sympathomimetics in patients with acute pulmonary edema and normal or high systolic blood pressure because they increase myocardial oxygen demand without addressing the primary hemodynamic problem. 1

Rate Control in Atrial Fibrillation

• Administer intravenous digoxin for rapid ventricular rate control in patients with heart failure and atrial fibrillation; beta-blockers are preferred first-line agents but may be poorly tolerated in acute decompensation. 1

• Beta-blockers and/or digoxin are recommended to control heart rate in AF patients with LVEF <40%. 1

Hemodynamic Monitoring and Targets

• The primary therapeutic target is reduction of left ventricular filling pressure (pulmonary capillary wedge pressure); persistently elevated filling pressures predict increased risk of fatal decompensation and sudden death. 3

• Measures of systemic perfusion, arterial pressure, and vascular resistance are less predictive of outcomes than filling pressures, providing stronger rationale for vasodilators over inotropes. 3

• Monitor for signs of adequate decongestion: resolution of orthopnea, decreased respiratory rate, improved oxygen saturation, and adequate urine output (typically >0.5 mL/kg/hr). 1

Common Pitfalls and Caveats

• Hyperoxia should be avoided even after initial stabilization; target SpO₂ 92–96% to prevent vasoconstriction and worsening cardiac output. 1

• In patients with COPD, excessive oxygen can suppress ventilation and lead to hypercapnia through increased ventilation-perfusion mismatch; monitor acid-base balance closely. 1

• Non-invasive ventilation can mask worsening hemodynamics; monitor closely for acute decompensation requiring intubation. 2

• Propofol for sedation (if intubation is needed) can induce hypotension and cardiac depression; midazolam is preferred in patients with acute heart failure or cardiogenic shock. 1

• Acute respiratory therapies (bronchodilators, antibiotics, corticosteroids) are administered to over half of heart failure patients but should be reserved for those with documented pulmonary infection or bronchospasm, as indiscriminate use is associated with worse outcomes. 4

Disposition and Ongoing Management

• Patients who still show signs of respiratory distress after initial ED management require ICU-level monitoring with continued non-invasive ventilation and hemodynamic support. 1

• Once stabilized, initiate or optimize guideline-directed medical therapy (ARNI/ACE-inhibitor, beta-blocker, mineralocorticoid receptor antagonist, SGLT2 inhibitor) before discharge to prevent readmission. 1, 5

• Measure BNP/NT-proBNP and troponin on admission for prognostic stratification, and obtain a pre-discharge natriuretic peptide level to refine post-discharge risk. 5