💊 Flecainide

Flecainide is a Class Ic antiarrhythmic agent, according to the Vaughan Williams classification. It primarily acts by blocking fast sodium channels in the heart.

Flecainide potently blocks fast voltage-gated sodium channels in myocardial cells, particularly in the atria, ventricles, and His-Purkinje system. This significantly slows the upstroke of the action potential (phase 0) and decreases conduction velocity, without significantly affecting the action potential duration or refractory period. This leads to a dose-dependent widening of the QRS complex on the ECG.

Flecainide is primarily used for the treatment of paroxysmal supraventricular tachycardias (PSVT), including AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT). It is also indicated for the maintenance of sinus rhythm in patients with symptomatic paroxysmal atrial fibrillation or flutter, particularly in patients with structurally normal hearts. It can be used for certain ventricular arrhythmias in patients without structural heart disease.

Absolute contraindications include structural heart disease (e.g., ischaemic heart disease, heart failure, significant left ventricular hypertrophy), as this significantly increases the risk of proarrhythmia. Other contraindications include second- or third-degree AV block (unless a pacemaker is in situ), sick sinus syndrome (unless a pacemaker is in situ), and known hypersensitivity to flecainide.

Common adverse effects include dizziness, visual disturbances (blurred vision, spots), and nausea. More serious adverse effects include proarrhythmia, particularly ventricular tachycardia or fibrillation, especially in patients with underlying structural heart disease. It can also exacerbate heart failure and cause bradycardia or AV block. A significant increase in QRS duration is a marker of toxicity.

Patients should have a baseline ECG to assess PR and QRS duration, and regular ECGs during treatment to monitor for QRS widening (indicating toxicity) and PR prolongation. Electrolytes, particularly potassium, should be monitored and corrected if abnormal. Renal and hepatic function should be assessed, as flecainide is metabolised by the liver and excreted by the kidneys.

Always confirm patient allergies and thoroughly review their cardiac history for any structural heart disease or ischaemia before prescribing. Be aware of interactions with other antiarrhythmics, cimetidine (increases flecainide levels), and drugs that prolong the QT interval. Counsel patients about potential dizziness and visual disturbances, advising caution with driving, and to report any new or worsening palpitations.

Flecainide is highly effective for rhythm control in atrial fibrillation in patients with structurally normal hearts. Its use is strictly contraindicated in patients with ischaemic heart disease or heart failure due to a significant increase in mortality (CAST trial). It can be used as a 'pill-in-the-pocket' approach for self-termination of AF in carefully selected patients. ECG monitoring for QRS widening is crucial.

SBA questions often highlight the absolute contraindication of structural heart disease due to the increased risk of proarrhythmia. They might also focus on its use in 'pill-in-the-pocket' strategies for atrial fibrillation in selected patients. The ECG changes (QRS widening) and common side effects like visual disturbances are also frequently tested.