Propranolol
Inderal
Non-selective β (β1 + β2) antagonist
Non-selective β blockade + membrane-stabilizing (Na-channel) activity at high dose. Lipophilic → crosses BBB.
Indications
- •Thyroid storm (also blocks peripheral T4→T3)
- •Rate control
- •Migraine/essential tremor/performance anxiety
- •Pheochromocytoma (only AFTER α-blockade)
- •Portal HTN variceal prophylaxis
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| IV (acute) | 0.5–1 mg IV slow, repeat q5 min (titrate carefully) | — |
| Thyroid storm | 60–80 mg PO q4h or 1–3 mg IV | — |
Pharmacokinetics
IV onset 2–5 min. Hepatic (high first-pass). Lipophilic → CNS effects.
Hemodynamic effects
↓ HR/BP/contractility (both β1 + β2 block → can worsen bronchospasm + mask hypoglycemia strongly).
Respiratory effects
Bronchospasm (non-selective β2 block) — avoid in asthma/COPD.
Side effects
- !Bronchospasm
- !Bradycardia, AV block
- !Masks + prolongs hypoglycemia
- !Fatigue, depression, vivid dreams (CNS)
Contraindications
- ×Asthma/reactive airway
- ×Decompensated HF
- ×Pheochromocytoma before α-blockade (unopposed α → crisis)
- ×Cocaine ischemia
Clinical pearls
- ★Thyroid storm agent of choice — also inhibits peripheral T4→T3 conversion.
- ★In pheochromocytoma, NEVER give a β-blocker before α-blockade (unopposed α-vasoconstriction → hypertensive crisis).
Other drugs in Cardiac / BP
- Epinephrine
α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.
- Norepinephrine
Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.
- Phenylephrine
Pure α1 agonist → vasoconstriction. No β activity.
- Dexmedetomidine
α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.
- Vasopressin
Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.
- Esmolol
Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.
- Magnesium Sulfate
Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).
Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert