The normal heart beats regularly at 60–100 beats per min (bpm), which is controlled by the sinoatrial (SA) node located in the right atrium. Tachycardia describes a heart that beats more rapidly (>100 bpm). Bradycardia describes a situation where the heart beats more slowly (<60 bpm). Electrical signals generated in the SA node travel through a conduction pathway in the wall of the atria (causing atrial contraction) before reaching and depolarising the AV node. The electrical signal delays while passing through the AV node, which allows the ventricles to fill with blood from the atria. The signal then spreads rapidly through the ventricles via the His bundle–branches in specialised Purkinje fibres. These rapidly-conducting fibres mean that the ventricular muscle contracts simultaneously, raising the pressure that expels blood from the left and right ventricles to supply the systemic and pulmonary circulations. 

Arrhythmias are abnormalities of the heart rhythm, which occur when the electrical signals coordinating the regular heartbeats are disordered. Mechanisms of arrhythmias are abnormal automaticity, triggered activity and re-entry.

Antiarrhythmic drugs

Antiarrhythmic drugs suppress the causative mechanisms mainly by

1) increasing the threshold potential for depolarisation,

2) decreasing the conduction velocity, and

3) prolonging the refractory period.

Antiarrhythmic drugs are divided into four groups according to the Vaughan Williams classification.

Class I drugs inhibit Na+ channels to increase the threshold potential and decrease the conduction velocity in the atrial and ventricular tissues where Na+ entry generates the action potential upstroke phase.

Class IV drugs exert similar effects in the SA and AV node by inhibiting Ca2+ channels since Ca2+ entry generates the action potential upstroke phase in the nodal cells. The increase of the threshold potential suppresses the automaticity and the triggered activity. The decrease of the conduction velocity could block re-entry to terminate some arrhythmias.

Class III drugs prolong the refractory period by inhibiting K+ channels and some class I drugs prolong it by slowing recovery from the inactivation of Na+ channels. The prolongation of the refractory period could also block re-entry to terminate arrhythmias.

Class II drugs are beta-adrenoceptor antagonists (β-blockers) and slow firing of the SA and AV node, which causes slowing of the heart rate and AV conduction velocity. Class II drugs also suppress catecholamine-induced increase of Ca2+ currents, Na+ currents and K+ currents (IKs: slow component of the delayed rectifier K+ currents).


Arrhythmias can be divided into three types: premature contraction, tachyarrhythmia and bradyarrhythmia. Premature contraction and tachyarrhythmia are originated either from the atria or the ventricles, and bradyarrhythmia is caused by dysfunction of the SA node. The following are common arrhythmias and their treatments.

I.       Premature contractions
1. Supraventricular premature contractions (SVPCs). SVPCs do not usually require treatment unless they affect quality of life (QOL). Reduction of caffeine and alcohol intake is recommended. Symptomatic SVPCs are sometimes treated with β-blockers. Class I drugs can be used for patients with SVPCs without organic heart diseases.

2. Ventricular premature contractions (VPCs)

  • Without organic heart diseases (Idiopathic VPCs). Asymptomatic or mildly symptomatic VPCs do not require treatment. Life style changes including reduction of caffeine intake are usually sufficient. Symptomatic VPCs that impair patients’ QOL are treated with β-blockers, class IV drugs and class I drugs depending on their pathophysiology.
  • With organic heart diseases. Symptomatic or frequent VPCs are treated with β-blockers and amiodarone (a class III drug having multiple actions on ion channels and receptors), which improves cardiac function by reducing VPCs.

II.      Tachyarrhythmias
1. Paroxysmal supraventricular tachycardia (PSVT). AV nodal re-entry tachycardia (AVNRT) and AV reciprocating reentry tachycardia (AVRT) are major PSVT. If the episodes are not self-limited, these arrhythmias are acutely treated with drugs that slow AV nodal conduction - adenosine, β-blockers and verapamil (a class IV, non-dihydropiridine Ca2+ channel blocker). Adenosine is not approved in Japan and ATP is used instead. Adenosine (or ATP) is rapidly injected intravenously. For pharmacological prophylactic therapy, β-blockers and verapamil are used, but catheter ablation is the first-line therapy that could provide a permanent cure.  

2. Atrial fibrillation (AF). AF is the most commonly encountered arrhythmia in clinical practice. Abnormal automaticity and formation of re-entry circuits in the atrium and pulmonary vein play a pivotal role in onset and maintenance of AF. In general, the paroxysmal form of AF progresses to the persistent or permanent form of AF after repetitive occurrence. When AF occurs because the atria excite chaotically and irregularly, the ventricles cannot respond to every atrial beat. Therefore. the ventricular responses are irregular and heart rate may increase to ≥150–200 bpm, which impairs the pump function of the heart and can increase the chances of heart failure. In addition, the chaotic and ineffective contraction of the atria increases the potential for clot formation in the atria, which can increase the risk of stroke and systemic thromboembolism. Therefore, the heart rate needs to be reduced by rate control or rhythm control, and the clot formation needs to be prevented by anticoagulation therapy. AF patients can be treated with drugs or catheter ablation.

  • Anticoagulation therapy. In AF patients, risk of thromboembolism needs to be assessed when starting anticoagulation therapy. For anticoagulation therapy, warfarin and novel direct oral anticoagulants (DOACs) are used. Warfarin is a vitamin K antagonist, which takes time to have a therapeutic effect, and has higher risk for bleeding than the novel DOACs. There are two kinds of DOACs, direct thrombin inhibitors (e.g. dabigatran) and factor Xa inhibitors (e.g. rivaroxaban, apixaban). Their onset of therapeutic effect is earlier (within a day) and they have less bleeding risk.
  • Rate control therapy. Drugs used for rate control therapy are β-blockers, non-dihydropyridine Ca2+ blockers (e.g. verapamil, diltiazem) and digoxin. β-blockers are normally the first line drugs, because they can be used for AF patients with or without heart failure. Non-dihydropyridine Ca2+ blockers are used only for AF patients without heart failure. Digoxin is for AF patients with heart failure.
  • Rhythm control (sinus rhythm maintenance) therapy. Drugs used for rhythm control therapy are class I drugs (except lidocaine and mexiletine) and multiple channel blockers, amiodarone and bepridil.

3. Atrial flutter. Atrial flutter is a macro-re-entrant tachyarrhythmia and, in contrast to AF, the atria beat regularly. The atrial beat is so rapid (240–440 bpm) that the ventricles usually cannot respond to every beat. If AV conduction ratio is 2:1, the heart rate is 150 bpm when the atrial rate is 300 bpm. Similar to AF, sinus rhythm restoration, rate control therapy and anticoagulation are considered.

  • Anticoagulation therapy. Warfarin and novel DOACs are used. Anticoagulation therapy is recommended in atrial flutter patients because it is known that risks of thromboembolism are comparable to AF.
  • Rate control therapy. Similar to AF, β-blockers, non-dihydropyridine Ca2+ blockers (e.g. verapamil, diltiazem) and digoxin are used to control heart rate. While non-dihydropyridine Ca2+ blockers are used for patients with hemodynamically stable atrial flutter, digoxin can be used for patients who are hemodynamically unstable.
  • Rhythm control (sinus rhythm restoration) therapy. Class III drugs which prolong the refractory period and class I drugs which slow the conduction velocity are used to stop atrial flutter. When sinus rhythm restoration therapy is attempted, caution should be taken not to lead to a rapid 1:1 ventricular response: it is preferable to use β-blockers and non-dihydropyridine Ca2+ blockers to delay AV conduction.

4. Ventricular tachycardia (VT)

  • Without organic heart diseases (idiopathic VT). Idiopathic VT can originate from various areas, most frequently from the outflow tract. In patients with idiopathic VT, a β-blocker and verapamil (class IV) are useful. Class I drugs can sometimes be effective.
  • With organic heart diseases. If the patient is hemodynamically unstable with VT, direct-current cardioversion should be performed. For pharmacological treatment, amiodarone and sotalol are frequently used, and lidocaine may be considered.

5. Ventricular fibrillation (VF). Ventricular fibrillation (VF), chaotic and irregular excitement in the ventricles, is the main cause of sudden cardiac death. Electrical cardioversion is the only therapy to immediately stop VF.  

III.     Bradyarrhythmias
Bradyarrhythmias are rhythm disturbances including sinus node dysfunction and AV conduction disturbances. In general, pacemaker implantation is indicated for patients with symptomatic bradyarrhythmias. No treatment is necessary for asymptomatic bradycardia. Atropine and sympathomimetics can be used to treat bradycardia until pacemaker implantation.

Dr. Kuniaki Ishii

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