Nimodipine
Nimotop · Nymalize
Dihydropyridine calcium channel blocker (cerebroselective)
Lipophilic DHP CCB with CNS penetration → improves neurologic outcomes after aneurysmal SAH (mechanism beyond vasospasm — likely neuroprotective).
Indications
- •Aneurysmal subarachnoid hemorrhage — improve neurologic outcome (NOT to treat vasospasm per se)
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| SAH | 60 mg PO/NG q4h × 21 days (ORAL only — IV caused deaths) | — |
Pharmacokinetics
Oral. Hepatic first-pass. Given enterally.
Hemodynamic effects
Can cause hypotension — hold/reduce if it compromises cerebral perfusion pressure.
Side effects
- !Hypotension
- !IV administration is CONTRAINDICATED / has caused deaths (must be PO/NG)
Contraindications
- ×IV administration (fatal)
- ×Significant hypotension
Clinical pearls
- ★ORAL/NG ONLY — never give IV (deaths from accidental IV use → the syringe is often labeled 'ORAL/NG only').
- ★Improves SAH outcomes even though it doesn't reliably reverse angiographic vasospasm.
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
