Management of acute heart failure
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Management of Acute Heart Failure (AHF)
Definition & Overview
AHF encompasses a wide spectrum — from gradual decompensation of chronic heart failure (exertional dyspnea, leg swelling) to acute pulmonary edema. Triggers include medication non-adherence, excess salt/fluid intake, renal failure, poorly controlled hypertension, acute MI, dysrhythmias (especially AF), and substance abuse (cocaine, ethanol).
Core ED therapy remains: nitrates + diuretics + positive-pressure ventilation. — Tintinalli's Emergency Medicine, p. 409
Initial Assessment
Diagnosis
- No single finding is highly sensitive AND specific
- Most sensitive symptom: dyspnea on exertion (84%)
- Most specific symptoms: paroxysmal nocturnal dyspnea, orthopnea, edema (76–84%)
- S3 gallop: highest positive likelihood ratio (4.0) but poor interrater reliability
- BNP / NT-proBNP: useful in undifferentiated dyspnea; correlates with filling pressures and ventricular stretch; guides diagnosis and prognosis
- BNP < 100 pg/mL makes AHF unlikely; > 500 pg/mL is supportive
- NT-proBNP cutoffs: < 300 (rule out); age-adjusted for rule-in
Imaging & ECG
- CXR: pulmonary venous congestion, cardiomegaly, interstitial edema are most specific — but up to 20% of AHF cases have normal CXR
- ECG: identifies ischemia, MI, AF as precipitants
- Point-of-care ultrasound (POCUS): B-lines on lung US (≥3 per zone in ≥2 zones bilaterally) indicate pulmonary edema; LV function assessment aids management
Classification (Tintinalli)
| Profile | Hemodynamics | Clinical Features |
|---|---|---|
| Warm & Wet | Normal BP, ↑ filling pressures | Typical congestion, most common |
| Cold & Wet | Low CO, ↑ filling pressures | Hypoperfusion + congestion |
| Cold & Dry | Low CO, low filling pressures | Cardiogenic shock |
| Warm & Dry | Compensated | Euvolemic |
Treatment
1. Oxygen & Ventilatory Support
- Supplemental O₂ for SpO₂ < 90–92%
- Non-invasive positive pressure ventilation (NPPV) — CPAP or BiPAP — is a cornerstone of AHF management:
- Reduces work of breathing, improves oxygenation, reduces need for intubation
- CPAP particularly effective in acute pulmonary edema
- Intubation reserved for refractory hypoxia, respiratory failure, or altered mental status
2. Diuretics
First-line therapy for volume-overloaded (wet) patients:
- IV furosemide — most commonly used loop diuretic; high IV doses preferred in acute setting
- Reduces preload by venodilation (within minutes) and natriuresis
- Toxicity: hypovolemia, hypokalemia, ototoxicity (at high doses)
- Recent evidence: addition of acetazolamide to high-dose furosemide provides additive benefit
- SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin): increasingly used in both acute and chronic HF; inhibit sodium/glucose reabsorption + cardiac Na⁺/H⁺ exchanger; reduce hospitalizations and mortality — Katzung, p. 211
- Thiazides (e.g., hydrochlorothiazide): much less efficacious; used for mild chronic HF only
3. Vasodilators
Used primarily in hypertensive AHF or high SVR presentations:
- Nitroglycerin (NTG):
- Venodilator at low doses → reduces preload
- Mixed venous/arterial dilator at high doses → reduces afterload
- IV or sublingual routes; titrate to effect
- Avoid in hypotension (SBP < 90 mmHg) or right ventricular infarction
- Sodium nitroprusside: potent arterial + venous dilator; reduces afterload significantly; requires ICU monitoring; risk of thiocyanate toxicity with prolonged use
- Nesiritide (recombinant BNP): approved for AHF but does not improve mortality vs. standard therapy — Tintinalli, p. 409
- Afterload reduction improves ejection fraction but improved survival has not been clearly demonstrated — Katzung, p. 211
4. Inotropes & Vasopressors
Reserved for low-output / cardiogenic shock (Cold & Wet / Cold & Dry profiles):
| Drug | Mechanism | Use |
|---|---|---|
| Dobutamine | β₁ agonist → ↑ contractility, ↓ SVR | AHF with low CO, hypotension |
| Dopamine | Dose-dependent: DA → β₁ → α₁ | Severe hypotension; less preferred |
| Levosimendan | Calcium sensitizer + K⁺-ATP channel opener | Europe-approved; non-inferior to dobutamine; positive inotropy without ↑O₂ demand |
| Norepinephrine | α₁/β₁ agonist | Cardiogenic shock with vasodilation |
| Milrinone | PDE-3 inhibitor → ↑ cAMP | AHF in patients on chronic β-blocker therapy |
Prompt onset and short duration make dobutamine/dopamine most practical in the acute setting. — Katzung, p. 211
5. Hypertensive AHF
A distinct subtype requiring aggressive vasodilation:
- IV nitroglycerin or nitroprusside (titrate to BP)
- High-dose loop diuretics if fluid overloaded
- NPPV strongly indicated
- Avoid excessive diuresis if patient is not truly volume overloaded (redistributive edema pattern)
6. Electrolyte & Metabolic Issues
- Hyponatremia (dilutional): may benefit from vasopressin antagonists
- Conivaptan (V1a/V2 antagonist): IV, approved for euvolemic hyponatremia
- Tolvaptan (V2 antagonist): oral; may benefit AHF + hyponatremia
- Neither agent reduces mortality — Katzung, p. 211
- Monitor and replace potassium (loop diuretics cause kaliuresis → risk of arrhythmias)
7. Treating the Underlying Cause
- Acute MI: emergent revascularization (PCI/thrombolysis) is the priority; AHF may persist post-revascularization
- Atrial fibrillation: rate control or cardioversion
- Hypertension: aggressive BP reduction
- Infection/anemia/thyroid dysfunction: treat precipitating cause
8. Anticoagulation
- Consider if AHF precipitated by or complicated by AF, pulmonary embolism, or LV thrombus
9. Mechanical Circulatory Support
For refractory cardiogenic shock:
- Intra-aortic balloon pump (IABP)
- Impella (percutaneous LV assist device)
- ECMO (extracorporeal membrane oxygenation) — bridge to recovery or transplant
Monitoring & Risk Stratification
Key indicators of high risk (guide admission decisions):
- BUN, creatinine elevation (renal hypoperfusion)
- Troponin elevation (myocardial injury)
- Low systolic BP (< 90 mmHg)
- SpO₂ < 90% despite O₂
- Elevated NT-proBNP
- Hyponatremia
The ADHERE model (BUN, SBP, creatinine) predicts in-hospital mortality and can guide ICU vs. ward disposition. — Tintinalli, p. 415
Disposition
- Majority of ED AHF patients are admitted — ED physicians drive most disposition decisions
- True low-risk patients (normalized vitals, rapid response to therapy, no troponin elevation, no new ischemia) may be candidates for observation or short-stay unit
- Hospitalization is an inflection point — those admitted have higher mortality than matched non-hospitalized patients
Summary Table: Drug Classes in AHF
| Class | Drug(s) | Key Role |
|---|---|---|
| Loop diuretics | Furosemide (IV) | Volume removal; first-line |
| SGLT2 inhibitors | Dapagliflozin, empagliflozin | Diuresis + cardiac benefit |
| Nitrates | NTG, nitroprusside | Preload/afterload reduction |
| Natriuretic peptide | Nesiritide | Vasodilation (no mortality benefit) |
| Inotropes | Dobutamine, levosimendan | Low CO states |
| Vasopressors | Dopamine, norepinephrine | Severe hypotension |
| PDE-3 inhibitors | Milrinone | Low CO + β-blocker use |
| Vasopressin antagonists | Conivaptan, tolvaptan | Dilutional hyponatremia |
| Ventilatory support | CPAP/BiPAP | Pulmonary edema |
Sources: Tintinalli's Emergency Medicine: A Comprehensive Study, pp. 409–416 | Katzung's Basic and Clinical Pharmacology (16th ed.), pp. 210–212 | Braunwald's Heart Disease (11th ed.)
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