Digoxin
Lanoxin
Cardiac glycoside (positive inotrope + AV-nodal blocker)
Inhibits the Na⁺/K⁺-ATPase → ↑ intracellular Na⁺ → ↑ Ca²⁺ via Na/Ca exchange → ↑ contractility. Also ↑ vagal tone → AV-nodal slowing (rate control).
Indications
- •Rate control in AF (esp. with heart failure/hypotension — doesn't drop BP)
- •Heart failure (adjunct)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Loading (AF) | 0.25 mg IV q6h ×2–3 doses (~0.5–1 mg total), then 0.125–0.25 mg daily | — |
Pharmacokinetics
Onset 15–30 min IV, peak effect hours. Long half-life ~36 h. RENALLY cleared (accumulates in renal failure). Narrow therapeutic index (0.5–2 ng/mL).
Hemodynamic effects
Rate control WITHOUT hypotension (unlike CCB/β-blocker) — useful in the hemodynamically fragile.
Side effects
- !Toxicity: N/V, visual changes (yellow-green halos), ANY arrhythmia (classically PAT with block, bidirectional VT)
- !HYPOKALEMIA + hypomagnesemia + hypercalcemia POTENTIATE toxicity
- !Bradyarrhythmias
Contraindications
- ×WPW with AF (accelerates accessory pathway → VF)
- ×2nd/3rd-degree block
- ×Hypokalemia (potentiates)
- ×VT/VF
Reversal / antidote
Digoxin immune Fab (DigiFab) for life-threatening toxicity
Clinical pearls
- ★The rate-control agent that does NOT lower BP — favored in AF with HF/hypotension.
- ★HYPOKALEMIA dramatically worsens toxicity (both compete at Na/K-ATPase) — check K⁺ before/after cardioversion; avoid calcium (stone heart) in dig toxicity.
- ★Antidote = digoxin immune Fab.
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
