Heart failure is a clinical syndrome of impaired forward flow and maladaptive neurohormonal activation.
It is not primarily a pump failure problem — it is a neurohormonal disease.
Core equation:
CO = HR × SV
Stroke Volume depends on:
• Preload • Afterload • Contractility
In heart failure:
• ↓ Contractility (HFrEF) • ↑ Afterload • ↑ Preload • ↑ Neurohormonal activation (RAAS + SNS)
• EF ≤ 40% • Systolic dysfunction • Proven mortality-reducing therapies exist
• EF ≥ 50% • Diastolic dysfunction • Limited mortality-reducing therapies
• EF 41–49% • Treated similar to HFrEF
Compensatory systems become maladaptive:
1. Sympathetic activation
2. RAAS activation
3. Aldosterone excess
4. Ventricular remodeling
Modern therapy blocks these pathways.
Chronic neurohormonal activation causes:
GDMT prevents remodeling.
All patients with HFrEF should receive:
These therapies reduce mortality and hospitalization.
Preferred:
Alternative:
• ACE Inhibitor • ARB
Effects:
• ↓ Afterload • ↓ Aldosterone • ↓ Remodeling • ↓ Mortality
Only three reduce mortality:
Effects:
• ↓ Sympathetic drive • ↓ Remodeling • ↓ Sudden cardiac death
Effects:
• ↓ Aldosterone-mediated fibrosis • ↓ Remodeling • ↓ Mortality
Monitor potassium closely.
Effects:
• ↓ HF hospitalization • ↓ Mortality • Benefit independent of diabetes status
Hydralazine + Isosorbide Dinitrate
• Particularly beneficial in Black patients
• If HR ≥70 on maximally tolerated beta-blocker
• Soluble guanylate cyclase stimulator
Diuretics DO NOT reduce mortality.
Used for congestion relief:
Effect:
No strong mortality-reducing therapies except:
Management focuses on:
Related:
→ Hypertension Module → Dysrhythmias Module → Return to Cardiovascular Modules