NISOLDIPINE
(ni-sol'di-peen)
Nisocor, Sular
Classifications: cardiovascular agent; calcium channel blocker; antihypertensive
Prototype: Nifedipine
Pregnancy Category: C
|
10 mg, 20 mg, 30 mg, 40 mg sustained release tablets
Structurally similar to nifedipine. Inhibits calcium ion influx across cell membranes of cardiac muscle and vascular smooth
muscle, which results in vasodilation, inotropism, and negative chronotropism.
Inhibits vasoconstriction in the peripheral vasculature (10 times as potent than nifedipine). Significantly reduces total
peripheral resistance, decreases blood pressure, and increases cardiac output. It is also a potent coronary vasodilator.
Hypertension, angina.
CHF.
Hypersensitivity to nisoldipine or other calcium blockers; systolic BP <90 mm Hg, advanced aortic stenosis, advanced heart
failure, cardiogenic shock, severe hypotension, sick sinus syndrome; pregnancy (category D).
Liver dysfunction; older adult; paroxysmal atrial fibrillation; digital ischemia, ulceration, or gangrene; nonobstructive
hypertrophic cardiomyopathy; Duchenne muscular dystrophy; lactation.
Hypertension, Angina
Adult: PO 10–20 mg/d in 2 divided doses (max: 40 mg/d), may need to reduce dose in patients with liver disease (cirrhosis, chronic
hepatitis)
|
Oral
- Give drug with food to decrease GI distress, but do not give with grapefruit juice or a high fat meal.
- Ensure that sustained release form is not chewed or crushed. It must be swallowed whole.
- Discontinue drug gradually to prevent adverse effects.
- Consider dosage reductions in older adults; initiate therapy at lower doses and follow with gradual increases.
- Store at 15°–30° C (59°–86° F).
CNS: Dizziness, anxiety, tremor, weakness, fatigue, headache. CV: Hypotension, lower extremity edema, palpitations, orthostatic hypotension. GI: Abdominal pain, cramps, constipation, dry mouth, diarrhea, nausea. Skin: Flushing, rash, erythema, urticaria. Urogenital: Urinary frequency. Respiratory: Pulmonary edema (patients with CHF), wheezing, dyspnea. Body as a Whole: Myalgia.
Drug: May cause significant increase in digoxin level in patients with CHF. beta blockers may cause hypotension and bradycardia. Phenytoin may significantly decrease nisoldipine levels.
Absorption: Rapidly absorbed from GI tract; 4–8% reaches systemic circulation; absorption not affected by food. Peak Effect: 1–3 h. Duration: 8–12 h for hypertension, 7–8 h for angina. Distribution: 99% protein bound. Metabolism: Extensively metabolized in liver. Elimination: 70–75% excreted in urine as metabolites. Half-Life: 2–14 h.
Assessment & Drug Effects
- Monitor blood pressure carefully during period of drug initiation and with dosage increments.
- Monitor cardiovascular status especially heart rate, frequency of angina attacks, or worsening heart failure.
- Assess for and report edematous weight gain.
- Monitor digoxin levels closely with concurrent use and watch for S&S of digoxin toxicity (see Appendix F).
Patient & Family Education
- Do not discontinue the drug abruptly.
- Report symptoms of orthostatic hypotension or other bothersome adverse effects to physician.
- Do not drive or engage in potentially hazardous activities until response to drug is known.
- Do not breast feed while taking this drug without consulting physician.
1%)
Canadian drug name; 
Prototype drug