No

Calcium Channel Blocker

Spasm following subarachnoid hemorrhage from ruptured intracranial aneurysms in patients who are in good neurological condition postictus

C

Clinical effects on the fetus: Use in pregnancy only when clearly needed and when the benefits outweigh the potential hazard to the fetus. Teratogenic and embryotoxic effects have been demonstrated in small animals. No well controlled studies have been conducted in pregnant women.

Breast milk/lactation: Appears in breast milk at levels higher than maternal plasma levels; no recommendations are currently available on breast-feeding

Hypersensitivity to nimodipine or any component

May cause reductions in blood pressure. Use caution in hepatic impairment. Intestinal pseudo-obstruction and ileus have been reported during the use of nimodipine. Use caution in patients with decreased GI motility of a history of bowel obstruction. Use caution when treating patients with increased intracranial pressure.

1% to 10%:

Cardiovascular: Reductions in systemic blood pressure (1.2% to 8.1%)

Central nervous system: Headache (1.2% to 4.1%)

Dermatologic: Rash (0.6% to 2.4%)

Gastrointestinal: Diarrhea (1.7% to 4.2%), abdominal discomfort (2%)

<1% (Limited to important or life-threatening symptoms): Edema (0.3% to 1.2%), EKG abnormalities (0.6% to 1.4%), tachycardia (0% to 1.4%), bradycardia (0.6% to 1%), depression (0% to 1.4%), acne (0% to 1.4%), nausea (0.6% to 1.4%), hemorrhage, hepatitis, muscle cramps/pain (0.2% to 1.4%), dyspnea (0% to 1.4%), itching, GI hemorrhage, thrombocytopenia, anemia, palpitations, vomiting, flushing, diaphoresis, wheezing, lightheadedness, dizziness, rebound vasospasm, jaundice, hypertension, hematoma, neurological deterioration, congestive heart failure, hyponatremia, disseminated intravascular coagulation, deep vein thrombosis

Case report: DIC

The primary cardiac symptoms of calcium blocker overdose include hypotension and bradycardia. The hypotension is caused by peripheral vasodilation, myocardial depression, and bradycardia. Bradycardia results from sinus bradycardia, second- or third-degree atrioventricular block, or sinus arrest with junctional rhythm. Intraventricular conduction is usually not affected so QRS duration is normal.

In a few reported cases, overdose with calcium channel blockers has been associated with hypotension and bradycardia, initially refractory to atropine but becoming more responsive to this agent when larger doses (approaching 1 g/hour for more than 24 hours) of calcium chloride was administered.

CYP3A3/4 enzyme substrate

Azole antifungals may inhibit the calcium channel blocker's metabolism; avoid this combination. Try an antifungal like terbinafine (if appropriate) or monitor closely for altered effect of the calcium channel blocker.

Calcium may reduce the calcium channel blocker's effects, particularly hypotension.

Calcium channel blockers: The effects of other calcium channel blockers may be potentiated by nimodipine.

Grapefruit juice increases the bioavailability of nimodipine; monitor for altered nimodipine effects.

Protease inhibitor like amprenavir and ritonavir may increase nimodipine's serum concentration.

Rifampin increases the metabolism of the calcium channel blocker; adjust the dose of the calcium channel blocker to maintain efficacy.

Valproic acid increased nimodipine's serum concentration; monitor altered effect of nimodipine.

Nimodipine shares the pharmacology of other calcium channel blockers; animal studies indicate that nimodipine has a greater effect on cerebral arterials than other arterials; this increased specificity may be due to the drug's increased lipophilicity and cerebral distribution as compared to nifedipine; inhibits calcium ion from entering the "slow channels" or select voltage sensitive areas of vascular smooth muscle and myocardium during depolarization

Metabolism: Extensive in the liver

Half-life: 3 hours, increases with reduced renal function

Protein binding: >95%

Bioavailability: 13%

Time to peak serum concentration: Oral: Within 1 hour

Elimination: In feces (32%) and in urine (50% within 4 days)

Adults: Oral: 60 mg every 4 hours for 21 days, start therapy within 96 hours after subarachnoid hemorrhage.

Dosing adjustment in hepatic impairment: Reduce dosage to 30 mg every 4 hours in patients with liver failure.

Nimodipine is primarily used in the treatment of subarachnoid hemorrhage and is not used in the management of essential hypertension or angina.

May cause dizziness; may rarely cause depression

None reported

No information available to require special precautions

Other drugs of this class can cause gingival hyperplasia (ie, nifedipine) but there have been no reports for nimodipine

Take as prescribed, for the length of time prescribed; do not discontinue without consulting prescriber. You may experience headache (if unrelieved, consult prescriber), nausea or vomiting (frequent small meals may help), constipation (increased dietary bulk and fluids may help). Promptly report any chest pain or swelling of hands or feet, respiratory distress, sudden weight gain, or unresolved constipation. Pregnancy/breast-feeding precautions: Inform prescriber if you are or intend to be pregnant. Consult prescriber if breast-feeding.

If the capsules cannot be swallowed, the liquid may be removed by making a hole in each end of the capsule with an 18-gauge needle and extracting the contents into a syringe; if given via NG tube, follow with a flush of 30 mL NS

Capsule, liquid-filled: 30 mg

Ramoska EA, Spiller HA, and Myers A, "Calcium Channel Blocker Toxicity," Ann Emerg Med, 1990, 19(6):649-53.