Verapamil
Verapamil
Chemical
Synthetic papaverine derivative
Use
- Hypertension
- Angina
- SVT
Presentation
Tablets
Racemic mixture → solution for injection
L isomer = inhibits Ca2+ influx across slow (L type) Ca2+ channels
D isomer = no Ca2+ blocking activity; mimics LA at fast Na+ channels
Dose
PO: 250 – 480mg (divided doses)
IV: 5 – 10mg over 30 sec
→ PO dose much higher than IV dose due to extensive 1st pass metabolism
Route
PO: 240 – 480mg
IV: 5 – 10mg → then can infuse 5mcg/kg/min to sustain effect
Onset
IV peak effect 3 mins
DoA
20 mins
MoA
- Competitive antagonist at L-type Ca2+ channels
- ↓Ca2+ influx into vascular smooth m. & myocytes
- Inhibits contraction
Verapamil’s predominant effect is at AV node, but also SA node, myocardium, peripheral vessels
PD
CVS:
- Class & antiarrhythmic
- ↓automaticity (↓Ph 4 depolarisation)
- ↓conduction velocity
- ↑refractory period
- AV conduction slowed
- – ve inotrope
- Vasodilation arterioles → ↓BP
- Potent CA vasodilation
CNS: Cerebral vasodilation
GU: ↑RBF 2° ↓ vascular resistance
PK
A
20% OBA
Significant 1st pass
D
>90% PPB (all CCBs)
VD 5L/kg
M
Demethylation & dealkylation in liver
Norverapamil = activity
E
70% metabolites excreted in urine
16% metabolites excreted in faeces
t ½ B 6hrs
Adverse Effects
- Hypotension
- Profound -ve inotropy with overdose
Multiple drug interactions
- Potentiate NMBD
- Volatiles → -ve inotropy
- ↑risk LA toxicity with verapamil
- ↑[Digoxin] levels ∴↑ risk toxicity
- Huge additive -ve chrono & inotropic effect in conjunction with β blockers