Amlodipine
Norvasc · Amlodipin Sandoz · Amlodipine Teva
A cornerstone drug for hypertension and stable angina, and the easiest calcium channel blocker to use: once-daily dosing, a half-life of almost two days, and no dose adjustment in renal impairment. Unlike verapamil and diltiazem, amlodipine has no clinically significant negative inotropic effect and can therefore be used in heart failure with reduced ejection fraction when blood pressure or angina requires it. The slow onset makes the drug unsuitable for acute blood pressure reduction.
The effect builds over days to a week — never uptitrate based on a single blood pressure reading, as the risk of cumulative hypotension is significant. In overdose, refractory vasoplegic shock may require high-dose insulin-glucose and calcium.
Dosing in adults
| Indication | Regimen | Comment |
|---|---|---|
| Hypertension | 5 mg × 1, if needed 10 mg × 1 after 1–2 weeks | evaluate effect no sooner than one week |
| Stable and vasospastic angina | 5–10 mg × 1 | monotherapy or added to beta-blocker |
| Hypertension in heart failure (HFrEF) | 5–10 mg × 1 | prognostically neutral but safe in reduced EF |
| Elderly or frail patient | 2,5–5 mg × 1 | start low, orthostatic hypotension and fall risk |
| Children and adolescents 6–17 years, hypertension | 2,5 mg × 1, may be increased to 5 mg after 4 weeks | doses above 5 mg have not been studied in children |
No dose adjustment at any degree of renal impairment — metabolites are inactive and elimination is virtually independent of renal function. Not dialysed; high protein binding makes the drug difficult to remove.
Clearance decreases and AUC increases by 40–60 %. Start with 2,5 mg daily and titrate slowly; no maximum dose has been established in severe hepatic impairment.
From 6 years of age in hypertension: 2,5 mg × 1, may be increased to 5 mg × 1 after 4 weeks. Data for children under 6 years are limited.
Do not use amlodipine for acute blood pressure reduction: the effect takes hours to days and repeated doses in the emergency department cause delayed, prolonged hypotension. Ankle oedema is also haemodynamic, not a sign of fluid retention — it does not respond to furosemide but to dose reduction or addition of RAAS blockade.
Pharmacokinetics
- BIOAVAIL.
- 64–80 %, independent of food
- t½
- 35–50 h
- Tmax
- 6–12 h
- PROTEIN BINDING
- 97,5 %
- METABOLISM
- CYP3A4, inactive metabolites
- EXCRETION
- Renal as metabolites, approximately 10 % unchanged
- STEADY STATE
- after 7–8 days
- INOTROPY
- no clinically significant negative effect