There are several drugs which are used to treat cardiac arrhythmias. They are categorized by their effects on the cardiac action potential not the type of drug itself.

– All classes I-V are used to treat tachyarrhythmia, whereas the rest are used to treat bradyarrhythmia’s

Class I

Class I drugs affect voltage gated Na+ channels. As drugs with a high affinity only for the resting state would be toxic, these have an affinity for either the activated or inactivated state.


i) Class IA

e.g. Quinidine + Procainamide

These drugs block active Na+ channels, thereby increasing AP duration, the effective refractory period and the duration of the QT interval. 


This is used for rhythm control in SVT as it maintains sinus rhythm

– Also used for ventricular arrhythmias and malaria (similar to quinine)



Side effects

• Cinchonism (ringing of ears + dizziness), GI problems

• It increases digoxin plasma levels –> predisposes digoxin toxicity


This is similar to Quinidine but gives drug-induced SLE


This is a class IA anti-arrhythmic

ii) Class IB

e.g. Lidocaine + Mexiletine

These drugs have higher affinity for inactivated state of the Na+ channel

– They increase refractory period duration in cardiac cells

– As they bind the inactivated state, the have more action in depolarised cells where many sodium channels will be in the refractory period

– This is found in areas affected by MI so it means they can prevent premature beats in this more excitable tissue.

– Hence, used for preventing ventricular arrhythmias and V-fib in MI patients

– Lidocaine is the least cardiotoxic anti-arrhythmic.

iii) Class IC

e.g. Flecainide + Propafenone

These agents block all morphological forms of the Na channel

– Cause widening of QRS complex and prolongation of the PR interval

– They significantly prolong the AP at the AV node

– They need to be used carefully as they are also pro-arrhythmic


This is used to treat AV nodal reciprocating tachycardia

– Also treats arrhythmias associated with accessory pathway such as Wolff-Parkinson-White syndrome

– Used for chemical cardioversion in atrial fibrillation patients without LV dysfunction

Side effects
  • Pro-arrhythmic effects

  • Asthenia

  • Visual disturbances

  • LV dysfunction, heart failure
  • Significant valve disease
  • 2nd or 3rd degree heart block, bundle branch block

Class II – Beta-blockers

e.g. Propranolol + Bisoprolol

These act by inhibiting sympathetic stimulation to the heart, slowing the heart rate

– They are used as rate control to decrease the heart rate in atrial fibrillation

– Also used to prevent tachyarrhythmias in tissue with increased excitability e.g. after heart attack

– Used to prevent tachyarrhythmia due to increased sympathetic activity e.g. hyperthyroidism 

Side effects
  • Bronchoconstriction, fatigue, sleep disturbances/nightmares
  • Coldness of extremities, impotence, decreased hypoglycaemia awareness

Class III


This blocks the outward K+ current which inhibits repolarisation

– It also has class I actions by blocking inward Na+ currents

– It is the most commonly prescribed anti-arrhythmic and first-line drug in ventricular arrhythmias

– Also used as pharmacological cardioversion (rhythm control) in atrial fibrillation

– It has a very long half-life and is given into central veins

Side effects
  • Corneal microdeposits [EYE]
  • Hypo/hyperthyroidism (as made of iodine) [THYROID]
  • Lengthens QT interval, transient fall in BP with IV use [HEART]
  • Lower lobe pulmonary fibrosis [LUNGS]
  • Liver fibrosis/hepatitis [LIVER]
  • Constipation, vomiting, altered taste [GI TRACT]
  • Sleep disorders, movement disorders [NEURO]
  • Blue/grey skin deposits (grey-man syndrome), photosensitivity reaction [SKIN]
  • Thrombophlebitis –> hence given into central veins [VEINS]
  • CYP450 enzyme inhibitor so enhances effect of warfarin + increases digoxin levels [ENZYMES]

Due to these effects, it is important to constantly monitor patients:

– Before starting treatment –> check TFTs, LFTs, serum K+ and CXR

– Then every 6 months –> check TFTs + LFTs


This is a non-selective B-adrenoceptor antagonist that also has class III actions

Used in SVT and ventricular tachycardia 

Side effects
  • Associated with QT interval lengthening leading to torsade de pointes

Class IV

e.g Verapamil + Diltiazem

These are cardioselective L-type Ca channel blockers which act primarily in nodal tissue due to their high use dependence

– They prolong nodal conduction and refractory period –> slows heart rate

– Used as rate control in atrial fibrillation

Side effects
  • Sinus bradycardia (transient asystole) –> reversed by atropine

  • Hypotension  

  • Ankle swelling           

  • Constipation (verapamil)

Class V

e.g. Adenosine

Adenosine binds P1 receptors –> Gi coupled –> less cAMP –> less Ca2+ –> hyperpolarization

– This hyperpolarises the AV node which causes a transient heart block which slows the heart rate

– It is the drug of choice in treating supraventricular tachycardias, and has a half-life of 8 seconds

Side effects
  • Arrhythmia (can cause severe bradycardia and asystole)

  • Chest pain/discomfort and a bad feeling of apprehension

  • NB Contraindicated in asthma as can cause bronchospasm

Other anti-arrhythmics

e.g. Digoxin

Digoxin also increases vagal activity which helps to slow the heart down.

– Therefore, it can be used as an anti-arrhythmic –> used in rate control for atrial fibrillation 


This is a muscarinic antagonist which blocks the parasympathetic effects of ACh

– It shifts the balance towards the sympathetic nervous system

– Used first line to increase heart rate in bradycardia and Ca2+– blocker overdose

Side effects
  • Dry mouth, mydriasis (eye dilation)


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