FELODIPINE
(fel-o'di-peen)
Plendil
Classifications: cardiovascular agent; calcium channel blocker
Prototype: Nifedipine
Pregnancy Category: C
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2.5 mg, 5 mg, 10 mg sustained release tablets
Calcium antagonist with high vascular selectivity that reduces systolic, diastolic, and mean arterial pressure at rest and
during exercise.
BP reduction is due to a reduction in peripheral vascular resistance (after-load) against which the heart works. This reduces
oxygen demand by the heart and consequently may account for its effectiveness in chronic stable angina.
Mild to moderate hypertension.
Severe hypertension, angina, CHF, pulmonary hypertension.
Hypersensitivity to felodipine and sick sinus rhythm or second- or third-degree heart block except with the use of a pacemaker.
Safety and efficacy in children are not established.
Hypotension, CHF, hepatic impairment; pregnancy (category C), lactation.
Hypertension
Adult: PO 5–10 mg once/d (max: 20 mg/d)
Hepatic Impairment
Start older adults and patients with impaired liver function at 2.5 mg q.d.
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Oral
- Give tablet whole. Do not crush or chew tablets.
- Store at or below 30° C (86° F) in a tightly closed, light-resistant container.
Body as a Whole: Most adverse effects appear to be dose dependent. CV: Tachycardia, palpitations, flushing, peripheral edema. CNS: Dizziness, fatigue, headache. GI: Nausea, flatulence, diarrhea, dyspepsia. Hematologic: Small but significant decreases in Hct, Hgb, and RBC count.
Serum alkaline phosphatase may be slightly but significantly increased. Plasma total and ionized calcium levels rise significantly. Serum gamma-glutamyl transferase may increase.
Drug: Adenosine may cause prolonged bradycardia if it is used to treat patients with toxic concentrations of calcium channel blockers. Carbamazepine, phenobarbital, phenytoin may decrease felodipine bioavailability and serum concentrations. Cimetidine may increase felodipine bioavailability (competes for hepatic metabolism). Concomitant felodipine and digoxin administration produces only transient increases in plasma digoxin concentrations (35–40% increase), which are not sustained with continued administration. This interaction may be
of clinical relevance in patients whose plasma digoxin concentration is in the upper portion of the therapeutic range or in patients with preexisting renal insufficiency.
Absorption: Completely absorbed from GI tract; it undergoes extensive first-pass metabolism with only about 15% of dose reaching systemic
circulation. Onset: <1 h. Peak: 2–4 h. Duration: 20–24 h (sustained release formulation). Distribution: >99% bound to plasma proteins. Metabolism: Metabolized via hepatic cytochrome P-450 mixed function oxidase system. Elimination: 60–70% of metabolites are excreted in urine within 72 h. Half-Life: 10 h.
Assessment & Drug Effects
- Monitor BP carefully, especially at initiation of drug therapy, in patients >64 y, and in those with impaired liver function.
- Anticipate BP reduction with possible reflex heart rate increase (5–10 bpm) 2–5 h after dosing.
- Report sustained hypotension promptly; more common with concurrent beta-blocker therapy.
- Assess for and report reflex tachycardia; may precipitate angina.
- Monitor patients for possible digoxin toxicity when taking concurrent digoxin.
Patient Education
- Report peripheral edema, headache, or flushing to physician. These may necessitate discontinuation of drug.
- Get up from lying down slowly and in stages; there is potential for dizziness and hypotension.
- Do not breast feed while taking this drug without consulting physician.
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Canadian drug name; 
Prototype drug