What are the signs, symptoms, and treatment of acute decompensated congestive heart failure?

Acute Decompensated Congestive Heart Failure: Signs, Symptoms, and Treatment

Clinical Presentation and Recognition

Acute decompensated heart failure (ADHF) presents with rapid onset or worsening of dyspnea at rest, orthopnea, paroxysmal nocturnal dyspnea, or progressive fatigue developing over hours to weeks, requiring urgent hospitalization for intravenous therapy. 1, 2

Cardinal Signs of Congestion

• Bibasilar pulmonary rales (often widespread throughout lung fields) indicate pulmonary edema 1, 2
• Elevated jugular venous pressure ≥15 cm H₂O with positive hepatojugular reflux 1, 2
• Rapid weight gain >2 kg within 3 days due to fluid retention 2, 3
• Worsening peripheral edema progressing to ascites in severe cases 1, 2
• Respiratory distress with use of accessory muscles and respiratory rate >25/min 4, 5

Signs of Hypoperfusion

• Cold extremities with delayed capillary refill 1, 2
• Altered mental status or confusion 1, 2
• Oliguria (<0.5 mL/kg/h) indicating renal hypoperfusion 1, 4
• Low-normal blood pressure with compensatory tachycardia 1, 2

Distinguishing ADHF from Stable Heart Failure

• Stable chronic heart failure maintains unchanged symptoms for ≥1 month on current oral therapy 2
• ADHF represents deterioration from baseline requiring treatment escalation, most commonly intravenous diuretics 2
• ADHF accounts for approximately 80% of heart failure hospitalizations and carries significantly worse prognosis than stable disease 1, 2

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Immediate Diagnostic Assessment

Perform a 12-lead ECG, chest X-ray, and measure BNP/NT-proBNP within the first hour while simultaneously initiating treatment. 1, 4

Essential Initial Tests

• ECG monitoring to detect ST-segment elevation myocardial infarction, arrhythmias (especially atrial fibrillation), and ischemic changes 1, 4
• Chest radiography reveals pulmonary venous congestion, interstitial edema, Kerley B lines, pleural effusions, and cardiomegaly (though 20% may appear normal despite significant edema) 2, 4, 5
• Echocardiography should be performed as soon as possible to assess left and right ventricular systolic and diastolic function, valvular abnormalities, and mechanical complications 1
• Laboratory panel: electrolytes (especially potassium), creatinine, estimated GFR, glucose, complete blood count, liver enzymes, and cardiac troponin 1, 4

Blood Pressure Classification Guides Therapy

• Hypertensive ADHF: systolic BP >140 mmHg 4, 5
• Normotensive ADHF: systolic BP 90-140 mmHg 4, 5
• Hypotensive/cardiogenic shock: systolic BP <90 mmHg with signs of hypoperfusion 1, 4

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Immediate Treatment Algorithm

First-Line Therapy for All Patients (Within First Hour)

Administer intravenous loop diuretics immediately as the cornerstone of ADHF treatment to achieve rapid decongestion. 1, 4, 5

Loop Diuretic Dosing

• For patients already on chronic oral loop diuretics: give IV furosemide at 2-2.5 times the total daily oral dose 4, 5
• For diuretic-naïve patients: start with IV furosemide 20-40 mg as initial bolus 1, 4, 5
• Administer within the first 60 minutes of presentation 4
• Critical pitfall: Under-dosing is a common error; the IV dose must match or exceed the patient's chronic oral regimen to prevent treatment failure 4, 5

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Vasodilator Therapy (When Systolic BP ≥110 mmHg)

Add intravenous nitroglycerin immediately in combination with loop diuretics for rapid relief of dyspnea and pulmonary congestion in patients with adequate blood pressure. 1, 4, 5

• Nitroglycerin is the preferred first-line vasodilator 1, 4, 5
• Nitroprusside may be used when blood pressure is markedly elevated and low cardiac output coexists 1, 4, 5
• Nesiritide is an alternative when nitroglycerin is contraindicated or ineffective 1, 4, 5
• Absolute contraindication: systolic BP <110 mmHg 4, 5
• Early vasodilator use is associated with lower mortality in observational studies, whereas delayed administration correlates with higher mortality 4, 5

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Oxygen and Respiratory Support

• Provide supplemental oxygen only when SpO₂ <90%; routine oxygen in non-hypoxemic patients offers no benefit 4, 5
• Target SpO₂ 94-96% with face mask or CPAP 1
• Initiate non-invasive ventilation (CPAP/BiPAP) when respiratory rate >25/min or SpO₂ <90% despite supplemental oxygen, or when overt respiratory distress is present 4

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Continuation of Guideline-Directed Medical Therapy

Continue ACE-inhibitors/ARBs and beta-blockers in normotensive patients unless true hemodynamic instability (cardiogenic shock) is present. 4, 5

• ACE-inhibitors/ARBs should be maintained and dose escalation considered when tolerated 4, 5, 6
• Beta-blockers are continued unless cardiogenic shock, severe bradycardia (<50 bpm), or marked volume overload exists 4, 5
• Mineralocorticoid receptor antagonists provide additional diuretic benefit and should be continued in normotensive patients 4, 5
• Common pitfall: Unnecessary discontinuation of these agents due to modest blood pressure reductions worsens long-term outcomes; modest BP reductions do not impair decongestion 4, 5

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Therapies to AVOID in Normotensive Patients

Inotropes (Class III – Harmful)

Parenteral inotropes (dobutamine, milrinone, dopamine) must NOT be used without documented hypoperfusion; they are reserved exclusively for severe systolic dysfunction with hypotension (SBP <90 mmHg) and signs of low organ perfusion. 4, 5

• Inotropes increase mortality and arrhythmias when given to normotensive patients 4, 5
• There is no evidence supporting dobutamine for pulmonary edema in patients with normal or high blood pressure 5

Other Contraindicated Therapies

• Routine morphine administration is discouraged because it is linked to higher rates of mechanical ventilation, ICU admission, and death 4, 5
• Vasopressors have no role when SBP >110 mmHg and low-output signs are absent 4, 5

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Management of Cardiogenic Shock (SBP <90 mmHg with Hypoperfusion)

Identify cardiogenic shock when systolic BP <90 mmHg with signs of hypoperfusion: oliguria <0.5 mL/kg/h, altered mentation, cold extremities, or lactate >2 mmol/L. 4

Immediate Interventions

• Give a fluid challenge (≥200 mL saline or Ringer's lactate over 15-30 minutes) if overt fluid overload is not present 4
• Dobutamine may be used to increase cardiac output 4, 6, 7
• Levosimendan is an alternative calcium sensitizer, especially in patients already on oral beta-blockers 4, 7
• Norepinephrine is preferred over dopamine for vasopressor support 4

Mechanical Circulatory Support

• Intra-aortic balloon pump (IABP) is indicated when acute left-sided heart failure does not respond rapidly to fluids, vasodilators, and inotropes 4
• Consider short-term mechanical circulatory support (ECMO, Impella) in refractory shock, guided by age, comorbidities, and neurological status 4
• Transfer all cardiogenic shock patients promptly to a tertiary care center with 24/7 cardiac catheterization and dedicated ICU 4

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Management of Specific Precipitating Factors

Acute Coronary Syndrome

• Perform invasive revascularization within ≤2 hours when ACS coexists with acute heart failure 1, 4
• Coronary angiography is often required as acute coronary syndromes are a frequent cause of ADHF 1

Severe Arrhythmias

• For atrial fibrillation with rapid ventricular response: beta-blockers are first-line for rate control; IV cardiac glycosides may be added when rapid control is needed 4, 5
• Electrical cardioversion for arrhythmias causing hemodynamic compromise 4
• Treat symptomatic bradycardia with atropine 0.25-0.5 mg IV (repeat as needed); if unresponsive, proceed to temporary pacing 4

Common Precipitants to Address

• Discontinue NSAIDs immediately (e.g., etoricoxib) as they promote sodium and water retention, impair renal function, and antagonize ACE-inhibitor effects 2
• Treat uncontrolled hypertension aggressively as it is a frequent trigger 2
• Address medication non-adherence, dietary sodium excess, infections (especially pneumonia), and worsening renal function 1, 2

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Escalation for Persistent Congestion

• If congestion persists after 24-48 hours of maximized loop-diuretic therapy, switch to continuous IV furosemide infusion after an initial loading dose 4, 5
• Ultrafiltration should be considered for refractory congestion that does not respond to optimized medical therapy 1, 4, 5

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Monitoring During Hospitalization

Measure blood pressure every 5 minutes until vasodilator and diuretic doses are stabilized. 1

• Continuous monitoring: pulse oximetry, arterial BP, continuous ECG, respiratory rate, and urine output 1, 4
• Daily laboratory checks: electrolytes (especially potassium), creatinine, BUN 4, 5
• Daily weights and intake/output measurements 4
• Pulmonary artery catheterization is indicated in selected patients with persistent symptoms despite therapy, worsening renal function, or when vasoactive agents are required 1, 4, 5
• Routine invasive hemodynamic monitoring is NOT recommended in normotensive patients who are clinically responding to diuretics and vasodilators 4, 5

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Prognostic Implications and Follow-Up

Acute decompensation carries markedly worse prognosis than stable CHF: 30-50% of patients experience death or rehospitalization within 60 days, and 45-50% are rehospitalized within 12 months. 1, 2

Post-Discharge Management

• Management by a specialist heart-failure team (experienced cardiologist or trained staff) improves outcomes and shortens hospitalization 1, 4
• Enroll patients in a disease-management program and arrange follow-up within 1-2 weeks (ideally within 72 hours) after discharge 4
• Permanently discontinue NSAIDs; use acetaminophen or topical analgesics for pain control 2
• Implement strict sodium restriction (<2 g/day) and daily weight monitoring 2
• Optimize guideline-directed medical therapy before discharge: titrate ACE-inhibitor (or ARB), beta-blocker, and aldosterone antagonist to target doses 2, 6