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Antiarrhythmic medicines work in numerous ways to bring the heart to its normal rhythm. These agents are a group of pharmaceuticals that are used to suppress fast rhythms of the heart.

Antiarrhythmic medicines work in numerous ways to bring the heart to its normal rhythm. These agents are a group of pharmaceuticals that are used to suppress fast rhythms of the heart and are often effective or partially effective in treating most varieties of tachycardias. Tachycardia or tachyarrhythmia can be explained as a heart rhythm in which the heart beats faster than 100 beats per minute.

It can be classified into two main types – a) supraventricular tachycardias that start in the upper part of the heart and include atrial fibrillation, atrial flutter and Wolff-Parkinson-White syndrome b) ventricular tachycardia that starts in the lower part of the heart. Untreated ventricular tachycardia can often worsen and lead to ventricular fibrillation, which can result in cardiac arrest.

The presenting features of arrhythmias are palpitations or the symptoms of reduced cardiac outflow that include chest discomfort, dyspnea, lightheadedness or dizziness and shortness of breath. Arrhythmias range in severity from a minor trouble to a potentially fatal problem. They are more common in the elderly and can have intense effects on quality of life.

Causes of tachycardia

Most tachycardias are associated with the underlying heart diseases such as coronary artery disease, heart failure or heart surgery, heart valve abnormalities, high blood pressure, inflammation of the pericardium or abnormalities in the pumping action of the heart; other medical disorders, such as hyperthyroidism and other metabolic disturbances, chronic lung disease, excessive consumption of tea, coffee or alcohol, or electrolyte imbalances; complications developing from anti-arrhythmic medications and abnormal electrical signals in the heart that short-circuit the normal electrical system. 

Classification of anti-arrhythmic drugs

Anti-arrhythmic drugs can be classified clinically into:

a) Drugs that act on supraventricular arrhythmias, e.g. adenosine, cardiac glycosides, verapamil and beta-blockers.
b) Drugs that act on both supraventricular and ventricular arrhythmias, e.g. amiodarone, disopyramide, beta-blockers, flecainide, propafenone, procainamide and quinidine.
c) Drugs that act on ventricular arrhythmias e.g. lidocaine and moracizine.

Anti-arrhythmic drugs can also be classified based on their dominant cellular electrophysiologic effects:

a)    Class I: Membrane-stabilizing e.g. quinidine, lidocaine, flecainide
b)    Class II: Reduce adrenergic input, e.g. beta blockers
c)    Class III: Potassium blockers, e.g. amiodarone, sotalol
d)    Class IV: Calcium channel blockers, e.g. verapamil (but not dihydropyridines).

Sotalol has both Class II and Class III actions. Digoxin and adenosine do not fit into this classification. Digoxin works on arrhythmias by slowing the heartbeat slightly. It also makes the heart contract a little more forcefully, which is why it was originally prescribed to patients with congestive heart failure, a disease where the heart does not contract strongly enough. It is vagotonic, thus prolongs AV nodal conduction and AV nodal refractory periods. Adenosine slows or blocks AV nodal conduction and can terminate tachyarrhythmias that depend upon AV nodal conduction for their perpetuation.

Class I drugs

Class I drugs act by sodium channel blockade and are subdivided into three types (IA, IB and IC) depending on the effect of the agents on their precise effects on depolarisation and repolarisation - IA slow depolarisation and conduction, and prolong repolarisation – thus lengthens the action potential, IB have little effect on phase 0 in normal fibres and shorten repolarisation – thus shortens the action potential, and IC have little effect on repolarisation but profoundly depress both phase 0 depolarisation and conduction.

Class Ia and Ic are primarily indicated for supraventricular tachycardias (SVTs) and all classes of sodium channel blockers are indicated for ventricular tachycardias (VTs). The most upsetting adverse effect associated with Class I drugs is precipitation of proarrhythmia, which is a high drug dose-related arrhythmia considered to be worse in comparison to the arrhythmia being treated with the drug. The anti-cholinergic effects of IA drugs can produce side-effects that include tachycardia, dry mouth, urinary retention, blurred vision and constipation.

Quinidine produces adverse effects that include enhancement of digitalis toxicity, especially if hypokalemia is present and precipitation of torsades de pointes (especially in patients with long-QT syndrome) because of the delay in repolarization. Disopyramide produces negative inotropic effects; procainamide is a negative inotrope and a proarrhythmic. Ib drugs such as lidocaine cause CNS toxicity at levels above 5 micrograms/ml. Ic compounds can cause increased risk of sudden death in patients with a past history of heart attack, and are proarrhythmics as well.

Class II drugs

Class II agents are conventional beta blockers which act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. They are also known to decrease the AV nodal conduction. Clinically recommended beta-blockers can be classified into two categories: 1) non-selective blockers (block both b1 and b2 receptors), or 2) relatively selective b1 blockers (cardio-selective beta-blockers).

These agents are particularly useful in the treatment of hypertension, angina, myocardial infarction, supraventricular tachycardias (such as sinus tachycardia, AV nodal re-entry, atrial fibrillation, and atrial flutter) and heart failure. Class II drugs include atenolol, esmolol, sotalol, timolol, propranolol, and metoprolol among others.

They are generally well tolerated; adverse effects include lassitude, sleep disturbance, and GI upset. Another important side-effect of beta-blockers is impotence (or erectile dysfunction) in men. These drugs are contraindicated in patients with asthma because non-selective beta blockers can cause bronchoconstriction. They are also contraindicated in patients with heart failure, sinus bradycardia and partial AV block.

Class III drugs

Class III agents predominantly block the potassium channels, thereby prolonging action potential duration. Because the action potential is prolonged, rate of automaticity is reduced. The predominant effect on the ECG is QT-interval prolongation. These agents do not affect the sodium channel, so conduction velocity is not significantly decreased.

The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. Class III drugs have a risk of ventricular proarrhythmia, particularly torsades de pointes VT. Common side-effects of these drugs include edema in legs, hypotension, abnormally slow heart rhythms, constipation, headache, or light-headedness.

Class IV drugs

Class IV drugs are the slow nondihydropyridine Ca channel blockers, which decrease heart rate, myocardial force generation and AV nodal conduction velocity, and prolong refractoriness. Thus these drugs are ineffective in heart failure. Class IV drugs include verapamil and diltiazem. These drugs are used primarily to treat SVTs. Ca channel blockers can cause flushing, headache, excessive hypotension, edema and reflex tachycardia.

It is important to check your pulse if you are taking an antiarrhythmic medicine. Immediately contact your doctor if your heart rhythm becomes too slow (less than 50 beats per minute) or irregular while you are on an antiarrhythmic medicine.
 

  • www.aolhealth.com/drugs/antiarrhythmic-medications-for-fast-heart-rates
  • heartdisease.about.com/od/palpitationsarrhythmias/a/arrhythmiadrugs.htm
  • www.patient.co..uk/showdoc/40024974/
  • www.merck.com/mmpe/sec07/ch075/ch075a.html