Management of Decompensated Heart Failure
Immediately initiate intravenous loop diuretics at a dose equal to or exceeding the patient's chronic oral daily dose (or 20-40 mg IV furosemide if diuretic-naïve), while continuing ACE inhibitors/ARBs and beta-blockers in most patients unless hemodynamically unstable. 1
Initial Diagnostic Assessment
The diagnosis requires rapid determination of three key elements: 2
- Volume status: Assess jugular venous pressure, peripheral edema, pulmonary rales, and weight gain 1
- Adequacy of perfusion: Evaluate blood pressure, heart rate, peripheral perfusion, mental status, and urine output 1
- Precipitating factors: Identify medication/dietary non-compliance (most common cause at 42-47%), acute coronary syndrome, uncontrolled hypertension, arrhythmias (especially atrial fibrillation present in >30%), infections, or worsening renal function 2, 3
Obtain cardiac troponin and ECG immediately to identify acute MI, which is present in up to 20% of decompensated heart failure admissions and represents a critical reversible cause. 2, 1
Measure BNP or NT-proBNP if the diagnosis is uncertain, but interpret results in the context of all clinical data rather than in isolation. 2, 1
Immediate Pharmacologic Management
Diuretic Therapy (First-Line for Volume Overload)
Begin IV loop diuretics without delay in the emergency department for patients with significant fluid overload—early intervention is associated with better outcomes. 2
- For patients on chronic oral diuretics: Start with IV dose at least equal to (or 1-2 times) their total daily oral dose 1, 2
- For diuretic-naïve patients: Initiate furosemide 20-40 mg IV 1
- Administer as bolus or continuous infusion based on response, uptitrating dose and/or adding synergistic diuretic agents (thiazides, metolazone) if inadequate response 2
Critical Medication Continuation
Continue ACE inhibitors/ARBs during hospitalization in the majority of patients, especially those with concomitant hypertension, as oral therapy should be continued or even uptitrated. 2, 1
Continue beta-blockers in most patients, as continuation is well tolerated and results in better outcomes. 2, 1
- Withhold or reduce beta-blockers only in: patients recently started or uptitrated on beta-blockers, or those with marked volume overload 2
Reduce or temporarily discontinue ACE inhibitors/ARBs/aldosterone antagonists in patients with worsening azotemia until renal function improves. 2
Vasodilator Therapy (Adjunctive)
In patients with systolic blood pressure >110 mmHg and severe congestion, consider IV nitroglycerin or nitroprusside as adjunct to diuretics for relief of dyspnea, though these agents have not been shown to improve long-term outcomes. 2, 1
- Nitroglycerin may develop tachyphylaxis within 24 hours 2
- Nitroprusside requires arterial line monitoring due to hypotension risk and potential for thiocyanate/cyanide toxicity with prolonged use 2
Management of Low Cardiac Output States
For patients with signs of hypoperfusion (cool extremities, altered mental status, worsening renal function) despite adequate or low blood pressure, consider inotropic support. 2, 1
Dobutamine is indicated when low cardiac output rather than elevated pulmonary pressure is the primary problem, though it should only be used for short-term support (experience does not extend beyond 48 hours). 4, 5
Milrinone reduces left atrial congestion more effectively than dobutamine and is better tolerated in patients receiving beta-blockers. 5
Hold diuretics temporarily until perfusion is restored, then resume once systolic blood pressure ≥90 mmHg and perfusion improves. 1
Daily Monitoring Requirements
Inadequate monitoring leads to premature discharge—registry data confirm patients are frequently discharged after losing only a few pounds despite remaining hemodynamically compromised. 2
- Daily weights at the same time each day 1
- Daily electrolytes, BUN, and creatinine during active IV diuresis 1
- Fluid intake and output with running totals 1
- Blood pressure monitoring including orthostatic measurements 1
Serial natriuretic peptide measurements and routine Swan-Ganz catheterization have not been shown to improve outcomes in hospitalized heart failure patients. 2
Evaluation for Underlying Coronary Disease
Coronary angiography is underutilized in decompensated heart failure—registry data show opportunities to diagnose important coronary artery disease are frequently missed. 2
For newly discovered heart failure, ensure coronary structure and function are well delineated while simultaneously beginning treatment, as coronary artery disease plays an important causative role. 2
Refractory Congestion
Consider ultrafiltration for patients with obvious volume overload not responding to escalated diuretics, though this requires careful patient selection and monitoring for catheter-related complications. 2, 1
Invasive hemodynamic monitoring may guide therapy in patients with respiratory distress or unclear volume status, though routine use has not improved outcomes. 1
Essential Supportive Care
Provide VTE prophylaxis for all hospitalized heart failure patients to prevent venous thromboembolic disease. 2, 1
Avoid NSAIDs and COX-2 inhibitors, as they worsen fluid retention and increase decompensation risk. 6
Common Pitfalls
Premature discontinuation of guideline-directed medical therapy causes more harm than good—the majority of patients should have oral therapy continued or uptitrated during hospitalization. 2, 6
Inadequate decongestion is extremely common—patients may improve symptomatically but remain hemodynamically compromised with persistent elevated filling pressures, which predicts increased risk of readmission and death. 2
Failure to identify precipitating factors leads to recurrent decompensation—medication/dietary non-compliance is the most common cause and must be addressed before discharge. 3