Drugs to treat arrhythmias II Flashcards
Class III MOA
no effect on
phase 0, but they markedly prolong phase
3 and increase the
QT interval.
Why is the use of Amiodiorone limited?
Use is limited due to side effects (incl. tachy arrhythmia)
But it is one of the safest antiarrhythmic agent after B-blockers for oral use
Indications of amiodarone
prophylaxis and treatment of supra ventricular and ventricular arrhythmias
Explain Amiodarone structure
Amiodarone is an organic iodine compound that is structurally related to thyroid hormone
Oral absorption, bioavailability and distribution of Amiodarone
Slow oral absorption with bioavailability of 20-55%
Wide distribution in fat, muscles and Liver.
How long does the therapeutic effect of Amiodarone take?
Therapeutic response may take 3 weeks, with peak effect reached in
1-5 months
After withdrawal of tx with amiodarone, how long do antiarrhythmic effects persist?
Antiarrhythmic effect persist for 10 – 150 days after withdrawal of
long-term treatment
Onset of action of amiodarone
IV 10-15 minutes
Metabolism and excretion of Amiodarone
Extensive hepatic metabolism with biliary excretion (renal excretion
negligible)
Contraindications of Amiodarone (40
Cardiac bradycardia/block, hyperthyroidism, sensitivity to iodine,
hypokalemia
Pregnancy and lactation
Cautions of Amiodarone
Heart failure, hepatic impairment
Drug interactions of Amiodarone
May interact with other drugs for months after
discontinuation of treatment
* Other antiarrhythmics, b-blockers, digoxin, drugs causing QT prolongation,
phenytoin, simvastatin, warfarin, grapefruit juice
Amiodarone adverse effects
May take several weeks to appear and continue for months after
discontinuation of treatment
* Torsades de Pointes
* Hyper/hypothyroidism (thyroid function monitoring necessary)
* Neurotoxicity (including peripheral neuropathies)
* Photosensitivity (warn to avoid exposure to sunlight)
* GI
* Uncommon: pulmonary fibrosis & hypersensitivity pneumonitis
Effects of Class II and Class IV antidysrhythmic drugs
Class II drugs (β-adrenoceptor antagonists) and Class IV drugs (calcium channel blockers) slow phase 4 depolarization in the SA node and increase the PP
interval.
They also slow the atrioventricular (AV) node conduction velocity and increase
the PR interval.
MOA of propranolol (5)
Inhibit sympathetic activation of cardiac automaticity and conduction,
* Slow the heart rate,
* Decrease the AV node conduction velocity, and
* Increase the AV node refractory period,
* Little effect on ventricular conduction and repolarization.