Which pharmacological feature best distinguishes epinephrine from norepinephrine in clinical use?

## Distinguishing Epinephrine from Norepinephrine ### Receptor Selectivity and Vascular Effects **Key Point:** The critical difference lies in β₂-adrenergic receptor activation. Epinephrine has significant β₂ activity, while norepinephrine lacks clinically relevant β₂ effects. | Feature | Epinephrine | Norepinephrine | |---------|-------------|----------------| | **α₁ activity** | Moderate | Strong | | **β₁ activity** | Strong | Moderate | | **β₂ activity** | Strong | Negligible | | **Vascular effect** | Biphasic: low dose → vasodilation (β₂); high dose → vasoconstriction (α₁) | Predominantly vasoconstriction (α₁) | | **Skeletal muscle blood flow** | Increases (β₂-mediated) | Decreases or unchanged | | **Blood pressure response** | Low dose: ↓ MAP; high dose: ↑ MAP | Consistently ↑ MAP | ### Clinical Implications **High-Yield:** In anaphylaxis and acute asthma, epinephrine is the drug of choice because: 1. β₂ activity relaxes bronchial smooth muscle 2. β₂-mediated vasodilation in skeletal muscle improves perfusion 3. α₁ activity counteracts hypotension Norepinephrine causes pure vasoconstriction without bronchodilation, making it unsuitable for anaphylaxis but useful in septic shock where vasoconstriction alone is desired. **Clinical Pearl:** Epinephrine's β₂ effect on skeletal muscle vessels is why it is preferred in anaphylaxis — the vasodilation improves tissue perfusion despite systemic vasoconstriction at higher doses. Norepinephrine's lack of β₂ activity means it causes uniform vasoconstriction, potentially worsening tissue perfusion in distributive shock. **Mnemonic:** **EPI-β₂** — Epinephrine has β₂ activity; **NE-α only** — Norepinephrine is predominantly α. [cite:KD Tripathi 8e Ch 12]