Antiarrhythmic Drugs Free Pharmacology Note – 2021

Antiarrhythmic Drugs are used to treat Arrhythmia. Arrhythmia is a problem with the rate or rhythm of the heartbeat. During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm. In this Note, we are going to discuss Classification, Mechanism of Action, Adverse effect, therapeutic effect, and drug interactions of Antiarrhythmic drugs.

What is Arrhythmia and What is Antiarrhythmic Drugs ?

Arrhythmia is a common disorder of cardiac excitation. During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm. A heartbeat that is too fast is called tachycardia and A heartbeat that is too slow is called bradycardia.

There are four types of Arrhythmia and they are

• Atrial fibrillation,
• Bradycardia
• Tachycardia
• Ventricular arrhythmia

Symptoms of Arrhythmia includes

• Shortness of breath
• Feeling tired or light-headed
• Rapid thumping in chest or palpitations
• Chest pain
• Losing consciousness

Antiarrhythmic drugs are used to control or correct cardiac rhythm. The ultimate goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction. When it is not possible to revert to normal sinus rhythm, drugs may be used to prevent more serious and possibly l lethal arrhythmias from occurring. Antiarrhythmic drugs are used to: decrease or increase conduction velocity, alter the excitability of cardiac cells by changing the duration of the effective refractory period, suppress abnormal automaticity

Classifications of Antiarrhythmatics

The classification of these drugs are given in the below table

Class	Mechanism	Example
I. Sodium Channel Blockers	Reduce phase 0 slope and peak of action potential.
IA. Moderate	A moderate reduction in phase 0 slope; increase APD; increase ERP	Quinidine, Procainamide
IB. Weak	A small reduction in phase 0 slope; reduce APD; decrease ERP.	Lidocaine, Phenytoin
IC. Strong	Pronounced reduction in phase 0 slope; no effect on APD or ERP	Flecainide, Flecainide
II. β-Blockers	Block sympathetic activity; reduce rate and conduction.	Propranolol and Metoprolol
III. Potassium Channel Blocker	Delay repolarisation (phase 3) and thereby increase action potential duration and effective refractory period	Amiodaron and Bretylium.
IV. Calcium Channel Blockers	Block L-type calcium -channels; most effective at SA and AV nodes; reduce the rate and conduction	Verapamil, Diltiazem, and Nifedipine

Antiarrhythmic Drugs – Sodium Channel Blockers

Sodium channel blockers are the most widely used antiarrhythmic agents. They
act by blocking myocardial Na+ion channels. They are mainly used for the
treatment of supraventricular, nodal, and ventricular arrhythmias, especially after
MI and DC shock.

Mechanism of Action

Antiarrhythmic activity of sodium channel blockers is due to:

• A decrease in the inflow of sodium during phase 0 slows the maximum rate of depolarisation
• Decrease in excitability and conduction velocity
• Prolongation of the effective refractory period
• Decrease in the slope of phase 4 spontaneous depolarization (automaticity).

Therapeutic Uses

Therapeutic uses of the Sodium Channel Blockers are given below:

• Treatment of supraventricular, nodal, and ventricular arrhythmias, especially after MI and DC shock.
• After treatment of atrial flutter and fibrillation to maintain sinus rhythm.

Adverse Effect

The adverse effects of sodium channel blockers are marked depression of AV conduction, hypotension, bradycardia, anorexia, nausea, and vomiting.

Moderate (Class IA)

These drugs slow the rate of rising of action potential and prolong the duration of the action potential. They block Na+ ion channels and prolong the repolarisation time.

Quinidine: Quinidine binds to open and inactivated Na+ ion channels to prevent the influx of Na+ ions; thus slowing down the rapid upstroke during phase 0. It also reduces the slope of phase 4 spontaneous depolarisation and inhibits potassium channels. These actions result in
slow conduction velocity and increased refractoriness.

Procainamide: Procainamide stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.

Weak (Class IB)

The characteristic effects of these drugs are reduced rate of rising of action potential and reduced or unchanged APD ( Action Potential Duration). The drugs of Class IB rapidly associate and dissociate from the sodium channels. Thus, their actions are manifested when the cardiac cells are depolarised or firing rapidly.

Lidocaine: It is a local anesthetic that shortens phase 3 repolarisation and decreases the duration of action potential . Lidocaine is useful in treating ventricular arrhythmias. It was the drug of choice for the emergency treatment of cardiac arrhythmias. It does not slow down conduction, thus has a little effect on the AV junction arrhythmia. Lidocaine in higher doses causes cardiac and CNS manifestations. SA nodal arrest and hypotension may also occur. Paraesthesia, tremor (facial twitching), vomiting, lightheadedness, slurred speech, and convulsions also occur commonly.

Phenytoin: It is an antiepileptic drug used in tonic-clonic seizures. It
produces unique cardiac electrophysiological effects, thus is used in digoxin-induced arrhythmia.

Strong (Class IC)

Drugs of this class are powerful blockers of fast Na +
ion channels, and thus reduce upstroke of AP in normal and diseased myocardium. There is delayed inactivation of slow Na+ ion channels during the downslope of AP, and this results in the prolongation of APD. In addition, there is inhibition of delayed rectifier K+ current (less K +
efflux), so the APD is prolonged in His Bundle and Purkinje fiber system.

Flecainide: It blocks Na+ and K+ ion channels in normal and ischemic myocardium, thus slowing down the recovery of blocked Na+ ion channels. It further slows down the conduction of electrical impulses in the heart, i.e., reduces excitability.

Propafenone: It blocks fast Na+ ion channels and gives a mild βblocking action (1/10 of propranolol) and class -IV action (Ca ++ ion channel blockage). QT interval does not change but QRS and PR intervals are prolonged. It is effective orally and is metabolized by CYP 2D6 (in persons with CYP 2D6 deficiency, it is slowly metabolized).

Antiarrhythmic Drugs – β -Blockers

The β-blockers or β-adrenergic receptor blockers produce some important electrophysiological effects. They are highly effective in arrhythmias in which excess catecholamine plays a role after MI, CHF, pheochromocytoma, anxiety, anesthesia and postoperative period, exercise, and mitral valve prolapse. Excess of cAMP is considered to be responsible for causing ischemia induced
ventricular fibrillation.

Mechanism of Action

Reduction in intracellular Ca ++ ions leads to reduced phase 2 of AP. There is a reduction in SA nodal automaticity, slowing of conduction, and prolongation of ERP (Effective Refractive Period ) in the AV node. They counteract catecholamine-induced after depolarisations (arrhythmias) by reducing cAMP and Ca ++ ion accumulation.
Beta-blockers are also effective prophylactically in suppressing supraventricular tachycardia because they suppress the automaticity of ectopic foci and slow AV nodal conduction, thereby reducing ventricular response in atrial fibrillation. They reduce cardiac contractility and blood pressure.

Therapeutic Uses

At present beta-blockers are considered to be better antiarrhythmic agents because they improve survival, have a broader spectrum of antiarrhythmic action, and are comparatively safer. In addition , they act synergistically with many other antiarrhythmic agents reducing their arrhythmogenic potential.

Adverse Effect

Some common adverse effects of β-blockers are:

• Worsening of CHF
• Bronchospasm
• Cardiac conduction blocks
• Bradycardia
• Peripheral vasospasm
• Insomnia
• Hypotension

Antiarrhythmic Drugs – Potassium Channel Blockers

Class III agents block K+ ion channels, thus the outward potassium current during
re-polarisation of cardiac cells diminishes. These agents prolong the duration of action potential without altering phase 0 of depolarisation or the resting membrane potential. They prolong the effective refractory period and increase refractoriness. All class III drugs have the potential to induce arrhythmias.

Mechanism of Action

Blocking of K+ ion channels in phase 3 of the action potential reduce the efflux
of K+ ions from the myocyte; thus slowing down the repolarisation rate of the
cell and increasing the length of the plateau phase of the action potential. These
actions result in an increase of the refractory period of atrial, ventricular and
Purkinje cells as well as the increase of the QT interval.

Therapeutic Uses

Potassium channel blockers are used to treat:

• Recurrent ventricular fibrillation
• Unstable ventricular tachycardia
• Atrial fibrillation

Adverse Effects

Common adverse effects of potassium channel blockers are pulmonary fibrosis, photosensitivity, corneal micro-deposits, hypothyroidism, and peripheral neuropathy, AV block, bradycardia, ventricular arrhythmia s, bronchospasm, and severe hypotension.

Antiarrhythmic Drugs – Calcium Channel Blockers

The drugs included in CCBs are verapamil, diltiazem, and bepridil (blocks Na+ ion channels also).

Mechanism of Action

CCBs block the slow in ward calcium channels, and slow down the conduction
through the AV node

Therapeutic Uses

CCBs are used to treat atrial fibrillation and flutter, prinzmetal and variant angina
and unstable or chronic stable angina pectoris, and hypertension.

Adverse Effects

CCBs give rise to dizziness, hypotension, bradycardia, edema, constipation, AV
block, ventricular systole, ventricular fibrillation, and nausea.

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