Its major indication is in the treatment of sustained life-threatening ventricular arrhythmias, such as recurrent ventricular tachycardia and fibrillation.

It may inhibit atrioventricular conduction and sinus node function,

It prolongs the action potential and refractory period in myocardium and inhibits adrenergic stimulation.

The most commonly used antiarrhythmic drug to treat supraventricular and ventricular arrhythmias.

Potent atrial antifibrillatory agent.

Clas III antiarrhythmic broad spectrum antiarryhtmic agent inhibiting characteristics of all 4 Vaugn Williams classes.

Considered the most effective antiarrhythmic agent.

Oral bioavailability averages approximately 50%.

Highly lipophilic with a large volume of distribution with a delayed onset of action from 2 days to 3 weeks for oral therapy and long elimination half life.

Metabolized by hepatic cytochrome p450 system and excreted in the feces.

Renal excretion is less than 1%.

Active metabolite is N-desethylamiodrone, which has a longer half life.

Use is limited by toxicity due its high iodine content causing pulmonary fibrosis, thyroid disease as well as by liver disease.


Widely used in AF for conversion and maintenance of normal sinus rhythm and rate control.

Despite common use for AF it not FDA approved for this purpose.

In atrial fibrillation the drug’s long half-life and large volume of distribution may take days to weeks of oral dosing to achieve efficacy.

It’s efficacy to maintain sinus rhythm in atrial fibrillation exceeds other antiarrhythmic drugs.

Antiarrhymic agent of choice for ventricular arrhythmias, refractory ventricular fibrillation/pulseless ventricular tachycardia, when patient is unresponsive to CPR, defibrillation, and vasopressor therapy.

Approved for the treatment of life-threatening, recurrent ventricular arrhythmias, such as ventricular fibrillation or ventricular tachycardia associated with instability, and oral dosing may require a high dose load to achieve efficacy.

Half-life averages 26-107 days, and approximately 61 days for active metabolite, N-desethylamiodarone.

Use requires baseline monitoring, and periodic monitoring.

Plasma levels are 0.5-2.5 microgm/ml, but levels do no correlate well with efficacy or toxicity.

Adverse reactions: pulmonary toxicity, hepatotoxicity, hyperthyroidism, hypothyroidism, blue- gray skin discolorization in sun-exposed skin, corneal deposits, and CNS effects of ataxia and neuropathy.

The most widely prescribed antiarrhythmic drug.

Each 100 mg tablet provides 10 times the average daily iodine content in the American diet.

It has a long half-life of 100 days, due to its lipophilic nature.

It decreases the conversion of T4 to T3, inhibits the binding of T3 to its nuclear receptors, is directly toxic to thyroid follicular cells resulting in a destructive thyroiditis.

There is an inversely proportional effect of dietary iodine intake on thyroid function in amiodarone induced thyroid dysfunction.

With underlying thyroid disease and excessive iodine after  amiodarone ingestion, can result in hypothyroidism or hyperthyroidism.

Amiodarone can cause increased thyroid hormone synthesis due to its high iodine content, and due to destructive thyroiditis releasing thyroid.

Incidence of pulmonary toxicity 1-27% with common manifestations of cough, dyspnea on exertion, fever or pleuritic chest pain.

Pulmonary functions including measurement of diffusing capacity should be done as baseline before initiating therapy.

Subclinical hypothyroidism with small increases in serum TSH concentrations and low-normal serum T4 concentrations occurs in about 20% of patients treated with amiodarone.

Hypothyroidism is seen in approximately 10-20% of patients.

About 3% of treated patients in the U.S. become hyperthyroid, between four months and three years after initiation of amiodarone.

Has a combination of beta-blockade, calcium channel blockade, and class III antiarrhthymic effects.

Thyroid dysfunction, including hyper and hypothyroidism can occur with the use of immune checkpoint inhibitors.

Drug interactions with warfarin, and digoxin.

In patients with acute onset of AF and impaired ventricular function amiodarone or digoxin are recommended because of minimal negative inotropic effects.

May be an increased mortality in patients with severe acute or chronic heart failure.

In a meta-analysis of the use of this agent for persistent AF to achieve sinus rhythm: 12 randomized control studies with 5060 patients revealed the agent to be more effective than a placebo or rate control drug achieving sinus rhythm and it was not associated with increased mortality or increased hospitalizations (Doyle).

Meta-analysis showed a 10-19% reduction in mortality in high risk patients, while other studies show a neutral effect on survival, but is associated with the 2-5 times increase in the risk of pulmonary and thyroid toxicity.

Implantable cardioverter-defibrillators are superior to this drug to improve survival in patients with sustained ventricular tachycardia or ventricular fibrillation due to a nonreversible cause and in patients at high risk for sudden cardiac death.

The antiarrhythmic drug of choice in patients with ventricular tachycardia or ventricular fibrillation who are not otherwise candidates for an implantable cardioverter-defibrillator.

The drug has minimal negative inotropic effects and has low proarrhythmic potential.

Concomitant antiarrhythmic treatment, most commonly amiodarone, is used to treat atriam and ventricular arrhythmias in 30-70% of patients with an implantable cardio-defibrillator.

When combined with a beta blocker reduces frequency of implantable cardioverter-defibrillator shocks.

Can suppress symptomatic, nonsustained ventricular tachycardia.

Typical dosing is 200 to 400 mg daily.

Amiodarone can be used intravenously (150 mg IV bolus; then 1 mg/minute for 6 hrs followed by 0.5 mg/minute for 18 hrs or by mouth 400 mg 3 times daily for 7 days followed by 400 mg twice daily for 1 week as a loading dose.

The patients should be closely followed for amiodarone toxicity, including QT prolongation, hepatic, and thyroid function abnormalities.

During therapy, intracytoplasmic lamellar deposits occur in the cornea, lens, retina, and optic nerve.

The most common symptom, reported by 1.4-40.0% of patients, is colored rings around lights.

The most common ocular finding is corneal epithelial opacities resembling a cat’s whiskers in 70-100% of patients; however, lens opacities have been reported in 50-60% of patients.

Neither type of deposit impairs visual acuity, and their presence is not contraindicative to continued amiodarone treatment.

Retinopathy has, rarely, been reported in association with amiodarone treatment.

It is lipid soluble, allowing it to reach many tissues in the body.

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