1C class antiarrythmic drug that blocks sodium channels and slows conductance in atrial and ventricular tissues by increasing the effective refractory period.

Trade names Tambocor

Bioavailability 95%

Protein binding 40%

Metabolism CYP2D6

Biological half-life 20 hours with a range 12-27 hours.

Excretion by renal mechanisms.

class Ic antiarrhythmic agent used to prevent and treat tachyarrhythmias.

It is used to treat a variety of cardiac arrhythmias including paroxysmal atrial fibrillation, paroxysmal supraventricular tachycardia and ventricular tachycardia.

Regulates the flow of sodium in the heart, and causes prolongation of the cardiac action potential.

Because of the action of flecainide on the His-Purkinje system, it is used in the treatment of many types of supraventricular tachycardias, including AV nodal re-entrant tachycardia (AVNRT) and Wolff-Parkinson-White syndrome (WPW).

Limited use in the treatment of certain forms of ventricular tachycardia.

Useful in the treatment of ventricular tachycardias that are not in the setting of an acute ischemic event.

It has use in the treatment of right ventricular outflow tract tachycardia and in the suppression of arrhythmias in arrhythmogenic right ventricular dysplasia.

Has increased mortality when used to suppress ventricular extrasystoles in the setting of acute myocardial infarction.

The administration of flecainide may help reveal the ECG findings that are characteristic of Brugada syndrome.

The Cardiac Arrhythmia Suppression Trial (CAST) demonstrated that patients with structural heart disease (such as a history of MI or left ventricular dysfunction, and also patients with ventricular arrhythmias, should not take this drug.

There is a risk of proarrhythmia is increased when flecainide is co-administered with other class Ic antiarrhythmics, such as encainide, and with hypokalemia.

Risk of proarrhythmia is not necessarily associated with the length of time an individual is taking the drug

Dosing may need to be adjusted in individuals who develop either liver failure or renal failure.

Because of the negative inotropic effects, should be used with caution withatients with depressed ejection fraction, as it may worsen congestive heart failure.

Should be avoided in people with ischemic heart disease and the elderly.

As with all class I antiarrhythmic agents, it captures thresholds of pacemakers.

Due to the narrow therapeutic index should be alert for signs of toxicity before life-threatening arrhythmias occur like torsades de pointes.

Signs of toxicity include marked prolongation of the PR interval and widening of the QRS duration on ECG, and there may be signs and symptoms attributable to overt heart failure secondary to sudden decreased myocardial contractility.

Treatment of flecainide induced cardiac toxicity involves increasing its excretion, blocking its effects in the heart, and instituting of cardiovascular support to avoid impending lethal arrhythmias.

Agents to avoid arrhythmias include administration of a beta-sympathomimetic agent, a sodium load often in the form of hypertonic sodium bicarbonate.

Has a very high affinity for lung tissue and is associated with drug-induced interstitial lung disease.

Flecainide works by blocking the sodium channel in the heart, slowing the upstroke of the cardiac action potential, and slows conduction of the electrical impulse within the heart.

Reduces cardiac excitability.

Its greatest effect is on the His-Purkinje system and ventricular myocardium.

Causes decreased contractility of the myocardium, which leads to a decrease in the ejection fraction.

The effect of flecainide on the sodium channels of the heart increases as the heart rate increases.

Is useful to break a tachyarrhythmia.

Flecainide also inhibits ryanodine receptor 2, a major regulator of sarcoplasmic release of stored calcium ions.

It can reduce calcium sparks and thus arrhythmogenic calcium waves in the heart.

Flecainide has high bioavailability.

Peak serum concentrations can be seen 1 to 6 hours after ingestion of an oral dose.

The plasma half-life is about 20 hours, and can range from 12 to 27 hours.

A steady state equilibrium is typically achieved in 3 to 5 days.

Primarily eliminated by the kidneys, with the remainder metabolized by the cytochrome P450 2D6 isoenzyme in the liver.

Impaired renal function or urine pH will greatly affect its elimination.

Interacts with numerous drugs and can potentiate the effects of other myocardial depressants and AV node blocking agents.

Can decrease the metabolism or elimination of many drugs that use the cytochrome P450 enzyme system.


Interactions with flecainide include:







Long-term effects Edit

In the long term, it is safe in patients with a healthy heart with no signs of left ventricular hypertrophy, ischemic heart disease or heart failure.


Can place on site

The degree of sodium channel blockade increases with increased in heart rate and the drug is frequently used in the management of atrial tachyarrhythmias.

Causes QRS widening at toxic doses with rapid heart rates.

Duration of QRS is used as a guide adjust dosage.

Can lead to organization atrial fibrillation into slow atrial flutter owing to decreased atrial tissue conductance.

Atrial flutter rates are in the range of 300 BPM, but in the presence of this drug can be significantly slower.

When administered with nodal blocking agent slow flutter can be conducted to the ventricle in a one to one ratio resulting in extremely rapid ventricular rate.

Effects greatly enhanced with higher heart rates and can result in significant I ntraventricular conduction delays , causing a wide complex QRS.

Patients on flecainide can present with wide complex tachycardia, with a broad abnormal looking QRS.

Use of the drug in the presence of structural heart disease can result in ventricular arrhythmias manifesting as monomorphic sinusso ideal wide QRS tachycardias for as polymorphic ventricular tachycardia or fibrillation.

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