What is the initial management for acute decompensated heart failure?

Initial Management of Acute Decompensated Heart Failure

Immediately administer IV loop diuretics and provide supplemental oxygen if SpO2 <90%, while simultaneously assessing for acute coronary syndrome and determining whether the patient requires vasodilator therapy based on blood pressure. 1, 2

Immediate Assessment (First 5-15 Minutes)

• Measure oxygen saturation with pulse oximetry and provide supplemental oxygen if SpO2 <90%, targeting 94-96% 1, 2
• Obtain immediate ECG and cardiac biomarkers to identify acute coronary syndrome as a precipitating factor 1, 2
• Measure BNP or NT-proBNP levels to confirm diagnosis in patients with acute dyspnea 1, 2
• Monitor vital signs continuously every 5 minutes until therapy stabilizes, particularly heart rate, respiratory rate, and blood pressure 3, 2
• Assess perfusion status by checking for narrow pulse pressure, cool extremities, altered mentation, and resting tachycardia 2
• Determine volume status through jugular venous distention, hepatojugular reflux, peripheral edema, and recent weight changes 2

Primary Pharmacologic Management

IV Loop Diuretics (First-Line Therapy)

For diuretic-naïve patients or new-onset heart failure:

• Administer 20-40 mg IV furosemide bolus immediately 1, 4

For patients already on chronic oral diuretics:

• Give IV bolus at least equivalent to their oral daily dose 1, 4
• Hold oral furosemide and switch to IV administration during acute decompensation 4

Dose escalation protocol:

• Increase dose until urine output increases and weight decreases by 0.5-1.0 kg daily 4
• If inadequate response, increase by 20 mg increments every 2 hours until desired diuretic effect is achieved 4
• Consider twice-daily dosing or continuous infusion if bolus dosing insufficient 4

IV Vasodilators (For Normotensive/Hypertensive Patients)

Administer IV vasodilators early when systolic blood pressure >110 mmHg:

• IV nitroglycerin is preferred for patients with normal to high blood pressure and provides rapid symptom relief 1, 2, 5
• High-dose nitrates (3 mg IV isosorbide dinitrate every 5 minutes) combined with low-dose furosemide (40 mg IV) reduces myocardial infarctions (37% vs 17%) and intubations (40% vs 13%) compared to low-dose nitrates with high-dose furosemide 3
• Delayed administration of vasodilators is associated with higher mortality, so initiate early 2

Avoid vasodilators when:

• Systolic blood pressure <110 mmHg 1, 2

Respiratory Support

• Start non-invasive ventilation (NIV) as soon as possible in patients with respiratory distress and acute pulmonary edema 1, 2
• CPAP is feasible in pre-hospital settings, while pressure-support positive end-expiratory pressure (PS-PEEP) is preferred in hospital 3
• NIV decreases respiratory distress and may reduce need for mechanical endotracheal intubation 1

Management of Chronic Heart Failure Medications

Continue guideline-directed medical therapy unless contraindicated:

• Continue ACE inhibitors/ARBs during exacerbation unless hemodynamically unstable, as they work synergistically with diuretics 1, 4, 2
• Continue beta-blockers during exacerbation unless hemodynamically unstable 1, 4, 2
• Beta-blockers may be reduced temporarily if patient has signs of low cardiac output, bradycardia, advanced AV block, or cardiogenic shock 2
• Monitor for first-dose hypotension with ACE inhibitors 3

Medications to AVOID or Use with Extreme Caution

Avoid routine use of:

• Morphine/opioids - associated with higher rates of mechanical ventilation, ICU admission, and death 1, 2
• NSAIDs or COX-2 inhibitors - increase risk of heart failure worsening 1

Inotropic agents (dobutamine, milrinone) should NOT be used unless:

• Patient is symptomatically hypotensive (SBP <90 mmHg) with signs of hypoperfusion 1, 2, 6
• Signs of hypoperfusion include: oliguria, cold peripheries, altered mental status, lactate >2 mmol/L, metabolic acidosis, SvO2 <65% 3
• Milrinone is indicated only for short-term IV treatment and requires ECG monitoring due to arrhythmia risk 6

Important caveat regarding nesiritide:

• Should NOT be considered first-line therapy due to lack of clear superiority over nitrates and uncertainty regarding safety 3

Critical Monitoring During Treatment

• Weigh patient daily and maintain accurate fluid balance charts 1
• Monitor symptoms and urine output continuously 1, 4
• Check renal function and electrolytes regularly, treating imbalances aggressively while continuing diuresis 1, 4
• If hypotension or azotemia occurs before treatment goals achieved, slow the rate of diuresis but maintain it until fluid retention eliminated 4

Criteria for ICU/CCU Admission

Triage to ICU/CCU if any of the following present:

• Respiratory rate >25 breaths/min 3, 2
• SaO2 <90% 3, 2
• Use of accessory muscles for breathing 3, 2
• Systolic blood pressure <90 mmHg 3, 2
• Need for intubation or already intubated 3, 2
• Signs of hypoperfusion: oliguria, cold peripheries, altered mental status, lactate >2 mmol/L, metabolic acidosis, SvO2 <65% 3

Special Hemodynamic Scenarios

For cardiogenic shock (SBP <90 mmHg with signs of hypoperfusion):

• Obtain immediate ECG and echocardiography 2
• Rapidly transfer to tertiary care center with 24/7 cardiac catheterization capability and ICU/CCU with mechanical circulatory support availability 2
• Consider fluid challenge (250 mL over 10 minutes) if clinically indicated 2
• Start inotropic agent if SBP remains <90 mmHg after fluid challenge 2

For refractory congestion:

• Consider ultrafiltration if not responding to medical therapy 2
• Consider adding thiazide-type diuretic or spironolactone if adequate diuresis not achieved with IV loop diuretics alone 4

Common Pitfalls to Avoid

• Excessive concern about hypotension and azotemia can lead to underutilization of diuretics and refractory edema 4
• Inappropriate diuretic dosing (too low) undermines efficacy of other heart failure medications and increases risk with beta-blockers 4
• High diuretic doses can lead to volume contraction, increasing risk of hypotension with ACE inhibitors and vasodilators 4
• Stopping beta-blockers during acute decompensation worsens outcomes unless patient is truly hemodynamically unstable 2
• Using inotropes in normotensive patients without evidence of decreased organ perfusion increases mortality 2