6th March 2024

Antiarrhythmic Medication

The mainstay in arrhythmia management is antiarrhythmic medication. Electrical cardioversion is used where there is haemodynamic compromise or electively to return to sinus rhythm, for instance, in AF. Alternatively, electrophysiological studies may be performed to identify arrhythmias and ablate areas along the conductive pathway to eliminate the arrhythmia.

Antiarrhythmic drugs target ion channels in cardiac myocytes and/or nodal cells to manipulate the cardiac action potential and negate arrhythmias. Since parasympathetic and sympathetic activity also influence cardiac conductivity, drugs that affect their activity can also be used. There are numerous ways to categorise antiarrhythmics but the Vaughan-Williams classification system remains the most prevalent:

• Class I: Na⁺ Channel Blockers. They work by reducing conduction velocity at phase 0 but can also affect phase 3 of non-nodal repolarisation and thereby change the corrected QT interval. These drugs can be further subclassified by the degree to which they block Na+ channels as well as their effect on the QTc interval. All class I drugs can be used in VT, however only Ia and Ic can be used in AF/flutter and SVT, this is because Ib drugs have little influence on atrial myocytes.
  • Ia: Moderate Na blockade, QTc prolongation – e.g., Quinidine, procainamide, disopyramide. These drugs are limited by their pro-arrhythmic effects.
  • Ib: Weak Na blockade, QTc shortening – e.g., Lidocaine and mexiletine – only used for ventricular arrhythmias. They have a greater influence on myocytes following ischaemia, so they are useful in post-MI arrhythmias.
  • Ic: Strong Na blockage, no effect on QTc – Flecainide and propafenone. They should be avoided in patients with ischaemic heart disease or structural heart disease as they are found to cause increased mortality.
• Class II: Beta blockers – e.g., bisoprolol, metoprolol and atenolol. They reduce sympathetic influence by blocking beta-adrenoreceptors in the heart. There is reduced SA node firing and AV node conduction, which reduces rate and conduction velocity, respectively. Side effects include bradycardia, AV block, bronchospasm, fatigue, and reduced exercise tolerance due to negative chronotropy.
• Class III – K+ channel blockers – e.g., amiodarone, dronedarone, sotalol, ibutilide, dofetilide. They affect potassium efflux, thus prolonging the QT interval. Amiodarone is commonly used in clinical practice for VT, VF, AF and flutter and has additional class I, II, and IV action. Side effects include thyroid dysfunction, deranged LFTs and pulmonary fibrosis.
• Class IV – Ca²⁺ channel blocker (non-dihydropyridines) – diltiazem and verapamil. They block L-type calcium channels which reduces both rate and velocity of conduction, most effective at nodal cells. Side effects include AV block, bradycardia and reduced contractility, therefore contraindicated in heart failure.

Other antiarrhythmics include adenosine, digoxin and atropine. For MRCP part 1, you will be expected to identify an abnormal rhythm from an ECG on clinical description and select appropriate treatment options. Table 1 summarises common conditions where these medications are used.

Table 1: Showing mode of action of common conditions in which these medications are used.