## Drug of Choice for Vasospasm Prevention in Subarachnoid Hemorrhage **Key Point:** Nimodipine is the ONLY calcium channel blocker with proven efficacy in reducing vasospasm-related morbidity and mortality following subarachnoid hemorrhage (SAH). ### Mechanism of Nimodipine 1. **Selective cerebral vasodilation** — preferentially dilates cerebral arteries over systemic vessels 2. **Reduces vasospasm incidence** — prevents or delays arterial narrowing (typically occurs days 4–14 post-SAH) 3. **Neuroprotection** — may have additional cytoprotective effects beyond vasodilation ### Dosing & Administration - **Oral:** 60 mg every 4 hours for 21 days (standard regimen) - **IV:** Reserved for patients unable to take oral medication; requires careful hemodynamic monitoring - **Timing:** Initiate as soon as possible after SAH diagnosis (ideally within 96 hours) ### Evidence Base **High-Yield:** Multiple RCTs (including landmark CONSCIOUS-1 trial) demonstrate nimodipine reduces delayed cerebral ischemia (DCI) and improves neurological outcomes in SAH patients. ### Comparison with Other Calcium Channel Blockers | Drug | Cerebral Selectivity | Vasospasm Prevention | Clinical Use in SAH | |------|----------------------|----------------------|---------------------| | Nimodipine | High (dihydropyridine) | ✓ Proven | **Standard of care** | | Verapamil | Low (non-DHP) | ✗ Not proven | Contraindicated (bradycardia, AV block) | | Diltiazem | Low (non-DHP) | ✗ Not proven | Not recommended | | Amlodipine | Moderate (dihydropyridine) | ✗ Not proven | No role in acute SAH | **Clinical Pearl:** Nimodipine is the ONLY agent with Class I evidence recommendation in international guidelines (American Heart Association, European Stroke Organization) for SAH management. ### Monitoring During Nimodipine Therapy - Systemic hypotension (most common side effect) - Headache, flushing, reflex tachycardia - Monitor BP, HR, and neurological status regularly - Dose reduction if systolic BP drops >20 mmHg [cite:Harrison 21e Ch 296]
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