Carvedilol is a 3rd-generation beta-blocker with combined β1, β2, and α1 blockade.
It reduces heart rate, contractility, and systemic vascular resistance.
Classification: • 3rd Generation (Vasodilating) • Nonselective β-blocker • α1-blocking properties • No intrinsic sympathomimetic activity (ISA)
Blocks:
• β1 receptors → ↓ Heart rate, ↓ contractility • β2 receptors → Potential bronchospasm risk • α1 receptors → Vasodilation (↓ SVR)
Net Effects:
• ↓ Cardiac output • ↓ Systemic vascular resistance • ↓ Blood pressure • ↓ Myocardial oxygen demand
Because of α1 blockade, carvedilol lowers afterload more than pure β1 blockers.
• Proven mortality benefit • Reduces hospitalizations • Part of guideline-directed medical therapy (GDMT)
Evidence-based HFrEF beta-blockers:
• ★ Carvedilol • ★ Metoprolol Succinate • ★ Bisoprolol
• Effective due to combined α and β blockade • Not first-line for uncomplicated HTN
• Reduces remodeling • Improves survival
• Used to reduce variceal bleeding risk • Decreases portal pressure
• Start low • Titrate slowly • Initiate only when patient is euvolemic • Do NOT start during acute decompensation
• Bradycardia • Hypotension • Dizziness • Fatigue • Bronchospasm (β2 blockade) • Masked hypoglycemia
Orthostatic hypotension more common than with pure β1 blockers due to α1 blockade.
• Severe bradycardia • High-grade AV block (without pacemaker) • Cardiogenic shock • Acute decompensated heart failure
Use caution in: • Asthma • Severe hypotension
Carvedilol: • β1 + β2 + α1 blockade • Reduces SVR • More blood pressure lowering • More orthostasis risk
Metoprolol: • β1 selective • No α1 blockade • Less orthostasis
Both reduce mortality in HFrEF (succinate form for metoprolol).
✔ Mortality-reducing in HFrEF ✔ Provides afterload reduction via α1 blockade ✔ Start low, titrate slowly in HF ✔ Avoid in acute decompensated HF ✔ More orthostatic hypotension than metoprolol
Related:
→ Beta-Blockers Overview → Heart Failure Module → Hypertension Module → Return to Cardiovascular Modules