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Calcium Channel Blocker
Calclium channel blocker that causes vascular smooth muscle relaxation and slows conduction through the AV node. Greater effects on conduction and a lesser effect on vascular smooth muscle than do other agents in the same class.
Mechanism of Action
- Causes vascular dilation and slows conduction through the AV noce.
- Inhibits arrhythmias causes by a reentry mechanism such as with PSVT and decreases the rapid ventricular response seen with atrial tacyarrhythmias.
- Reduces myocardial oxygen demand because of its negative inotropic effects and causes coronary and and peripheral vasodilation.
Onset of Action
- Onset: 5 min
- Peak: 5-15 min
- Duration: 10-60 min
- Half-life: 2-8 hrs
Narrow-complex tachycardias including stable, narrow-complex tachycardias if rhythm remains uncontrolled or unconverted by adenosine or vagal maneuver or if SVT is recurrent and to control ventricular rate in patients with atrial fibrillation or atrial flutter.
- Severe hypotension
- Cardiogenic shock
- Ventricular tachycardia in the prehospital setting
- Wolff-Parkison-White syndrome
- Patients receiving IV B-blockers
- Avoid in patients with heart failure
- constant blood pressure monitoring
- Calcium chloride can be used for Calcium Channel Blocker overdose
- Heart block
2.5-5mg, repeat doseof 5-10mg can be administered 15-30mins later if no conversion
- 0-1yr- 0.1-0.2mg/kg with a max of 2.0mg SIVP
- 1-15yrs- 0.1-0.3mg/kg with a max of 5.0mg SIVP
Route of Administration
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