Untitled Quiz

Anti-arrhythmic Drugs

• The heart is a specialized muscle that contracts regularly and continuously, pumping blood to the body and lungs.
• The pumping action is caused by a flow of regular electrical impulses that repeat in a cycle.
• The heart's natural pacemaker is the SA node.
• The SA node sends out regular electrical impulses from the atrium, causing it to contract and pump blood into the ventricle.
• The electrical impulse is then conducted to the ventricles through the AV node.
• The impulse spreads into the ventricles, causing the muscle to contract and pump out the blood.

Action Potential of Cardiac Muscles

• The action potential of cardiac muscles is a complex process involving various phases.
• Phase 4: The membrane potential is stable at -90mV.
• Phase 0: Rapid influx of sodium ions through fast sodium channels.
• Phase 1: A rapid repolarization due to the closing of sodium channels and opening of potassium channels.
• Phase 2: A plateau phase caused by slow calcium channels opening and potassium channels remaining open.
• Phase 3: Repolarization due to the closing of calcium channels and increase in potassium efflux.

Potential Terms

• ERP: Effective Refractory Period – the time needed before a second action potential can be produced.
• RRP: Relative Refractory Period – the time after the ERP when a second action potential can be produced but with a larger stimulus.
• APD: Action Potential Duration – the time it takes for the cardiac action potential to complete.

Normal Sinus Rhythm

• Describes a normal heart rhythm.
• Shown in a graph of electrical activity of the heart (ECG).

Arrhythmia

• An abnormal heart rhythm.
• Heartbeats can be slow, rapid, or irregular.
• Rapid arrhythmias (over 100 bpm) are called tachycardia.
• Slow arrhythmias (under 60 bpm) are called bradycardia.
• Irregular rhythms are called fibrillations (e.g., atrial fibrillation, ventricular fibrillation).

Vaughan William Classification of Anti-arrhythmic Drugs

• Anti-arrhythmic drugs are classified into four classes based on their electrophysiological effects.
• Class I: Sodium channel blockers (Ia, Ib, Ic)
• Class II: Beta-adrenoceptor blockers.
• Class III: Potassium channel blockers.
• Class IV: Calcium channel blockers.

Class Ia Anti-arrhythmics (Quinidine, Procainamide, Disopyramide)

• Block Na+ channels with a moderate rate of dissociation.
• Block K+ channels.
• Prolong phase 0 and 3, and APD & ERP.
• Decrease slope of phase 4.
• Decrease conduction velocity (CV).

Class Ib Anti-arrhythmics (Lidocaine, Phenytoin, Mexiletine, Tocainide)

• Block Na+ channels with a fast rate of dissociation.
• Activate K+ channels.
• Shorten the action potential duration (APD) and effective refractory period (ERP).
• Decreases conduction velocity (CV) especially in ventricular arrhythmias.

Class Ic Anti-arrhythmics (Propafenone, Moricizine, Flecainide)

• Block Na+ channels with a slow rate of dissociation.
• Have no effect on K+ channels.
• No effect on phase 3.
• No effect on APD and ERP.
• Markedly decrease conduction velocity (CV).

Quinidine

• Anti-arrhythmic anti-malarial drug
• Well absorbed orally and 90% bound to plasma proteins.
• Metabolized in liver by hydroxylation.
• Has anticholinergic (atropine-like) effect.
• Has α-blocking effect but antagonized by depressed action on SAN and AVN.
• Side effects include cardiotoxicity, GIT issues, CNS issues, and hypersensitivity.
• Drug-drug interactions include enzyme inducers and inhibitors.

Procainamide

• Weak anticholinergic effect.
• No α-blocking effect.
• Well absorbed orally.
• Metabolized in liver by acetylation to form N-acetylprocainamide (NAPA).
• Side effects include cardiotoxicity (similar to quinidine), GIT issues, CNS issues, and hypersensitivity. Includes SLE (if slow acetylation).

Disopyramide

• Has more anticholinergic effect.
• No α-blocking effect.
• Well absorbed orally.
• 30% metabolized in liver to form mono-N-dealkylated metabolite.
• Side effects include cardiotoxicity (similar to quinidine) and GIT issues.

Lidocaine

• Anti-arrhythmic local anesthetic drug.
• Given intravenously (IV) to avoid first-pass metabolism.
• Therapeutic uses include ventricular arrhythmias (MI, digitalis toxicity, open heart surgery).
• Side effects are less cardiotoxicity and extracardiac (paresthesia, tremor, dizziness).

Phenytoin

• Anti-arrhythmic anti-epileptic drug.
• Therapeutic uses include ventricular arrhythmias (MI, digitalis toxicity, open heart surgery).

Mexiletine

• Well absorbed orally.
• Therapeutic uses include ventricular arrhythmias (MI, digitalis toxicity, open heart surgery).

Tocainide

• Well absorbed orally.
• Therapeutic uses include ventricular arrhythmias (MI, digitalis toxicity, open heart surgery).

Propranolol

• Beta blocker that blocks β-receptors, slowing heart rate and restoring normal rhythm
• Used in supraventricular & prophylactic post-MI ventricular arrhythmias

Esmolol

• Beta blocker that blocks β-receptors, slowing heart rate and restoring normal rhythm
• Used in supraventricular & prophylactic post-MI ventricular arrhythmias

Metoprolol

• Beta blocker that blocks β-receptors, slowing heart rate and restoring normal rhythm
• Used in supraventricular & prophylactic post-MI ventricular arrhythmias

Pindolol

• Beta blocker that blocks β-receptors, slowing heart rate and restoring normal rhythm
• Used in supraventricular & prophylactic post-MI ventricular arrhythmias

Amiodarone

• Anti-arrhythmic anti-anginal drug.
• Broad-spectrum activity (class I, II, III, IV).
• Contains iodine, blocks T4 to T3 conversion.
• Has vasodilating effect on coronary & peripheral vessels
• Slow onset of action.
• Long half-life (t1/2).
• Side effects include hypo/hyperthyroidism, pulmonary fibrosis, and corneal microdeposits.

Sotalol

• Class II and III activity (i.e., some β-blocker and some K+ blocker effects).

Bretylium

• Anti-arrhythmic antihypertensive drug.

Verapamil

• Class IV calcium channel blocker.
• Slows heart rate (HR) and restores normal rhythm.
• Used in supraventricular tachycardia.
• Side effects include hypotension, heart block, peripheral edema, constipation, and drug interactions (digoxin toxicity).

Diltiazem

• Class IV calcium channel blocker.
• Slows HR and restores normal rhythm.
• Used in supraventricular tachycardia.

Bepridil

• Class IV calcium channel blocker.
• Slows HR and restores normal rhythm.
• Used in supraventricular tachycardia.

Digoxin

• Acts by inhibiting Na/K ATPase, increasing ERP and decreasing CV.
• Toxic concentrations can cause ectopic beats and ventricular arrhythmias.

Adenosine

• Stimulates adenosine receptors in the AVN, blocking Ca channels, stimulating K channels, decreasing AVN activity and CV.
• Widely used to treat supraventricular tachycardia (SVT).

Magnesium Sulfate

• Stimulates Na/K ATPase and blocks Ca channels.
• Used in digitalis-induced arrhythmias, if hypomagnesemia is present.