Anti-arrhythmic drugs • Cardiac arrhythmias are commonly seen during myocardial ischemia, digoxin treatment and anesthesia. • Anti-arrhythmic drugs are used to prevent and treat cardiac arrhythmias. To treat bradyarrhythmias Atropine and Isoproterenol (pacemaker) To treat tachyarrhythmias Antiarrhythmic drugs
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Anti-arrhythmic drugs Cardiac arrhythmias are commonly seen during myocardial ischemia, digoxin treatment and anesthesia. Anti-arrhythmic drugs are used.
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Anti-arrhythmic drugs
• Cardiac arrhythmias are commonly seen during myocardial ischemia, digoxin treatment and anesthesia.
• Anti-arrhythmic drugs are used to prevent and treat cardiac arrhythmias.To treat
bradyarrhythmias
Atropine and Isoproterenol (pacemaker)
To treat tachyarrhythmias
Antiarrhythmic drugs
Anti-arrhythmic drugs
Anti-arrhythmic drugs
• The electrical impulse that triggers cardiac contraction originates in SA node and travels through atria and AV node and then propagates over purkinje system and invades all parts of ventricles.
• Arrhythmias are caused by 1. Abnormalities in the generation or2. Abnormalities in the conduction of
Abnormal generation of impulse :• Enhanced automaticity : beta receptor
stimulation
• Atrial and ventricular cells may have pacemaker activity in hypokalemic conditions.
• After-depolarization is of two types -- 1. Early After Depolarization that occur during late phase 2 or phase 3 as in bradycardia or 2. Delayed After Depolarization that occur during phase 4 when intracellular load is high (digoxin toxicity).
Abnormal conduction of impulse : Re-entry
• There has to be an obstacle to homogenous conduction (anatomic or physiological).
• Normally electrical excitation becomes extinguished at the end of the circuit due to collision of impulse.
• An unidirectional block prevents anterograde impulse but retrograde impulse is propagated.
Anti-arrhythmic drugs
Anti-arrhythmic drugs
Class I Mechanism of action Examples Comments
Ia Na channel blockers that ↑ APD
Quinidine Procainamide
Large block OPEN Na & K Channels, hence both QRS & QT affected.
Ib Na channel blockers that may slightly ↓ APD
Lidocaine Mexiletine Phenytoin
High affinity for INACTIVATED than open Na channels with rapid unbinding during diastole, hence little effect on QRS; also blocks the small Na plateau current which may slightly shortens the APD.
Ic Na channel blockers that do not change APD
Propafenone Flecainide
Large block of OPEN Na channels & very slow unbinding during diastole markedly prolong QRS.
Anti-arrhythmic drugs
Class I : Sodium channel blockers: – State dependent blocking action
(high affinity for open/inactivated channel) causes
effective refractory period (ERP).– Rate dependent blocking action
(greatest at fast heart rates)
Anti-arrhythmic drugs
Anti-arrhythmic drugs
CLASS IA : Quinidine • Cinchona bark, dextro isomer of
quinine.• It blocks the sodium channel and
also potassium channel.• It has anti-muscarinic (decrease the AV
node refractory period, which can result in a rapid acceleration of ventricular rate) and alpha blocking action.
Anti-arrhythmic drugs
CLASS IA : Quinidine • It is bitter and irritant.• Quinidine is also an inhibitor of the
cytochrome P450 type 2D6.• It ↑↑ plasma digoxin by displacing it from
tissue binding sites and decreasing its excretion.
• Used (rarely because of proarrhythmic effects) in the treatment of supraventricular tachycardia (after AV block) and ventricular tachycardia
Anti-arrhythmic drugs
CLASS IA : Quinidine : Adverse effects :
• GIT : Diarrhea, nausea, vomiting and cinchonism – ringing in ears.
• Precipitate torsades de pointes by prolonging QT interval
Anti-arrhythmic drugs
Class IA : Procainamide • Used for the treatment of
ventricular tachycardia (second/third choice after amiodarone & lidocaine).
• Chronic use result in a positive anti-nuclear antibody (ANA) titer and SLE like syndrome (arthralgia and arthritis) especially in slow acetylators.
Anti-arrhythmic drugs
Class IA : Procainamide • Procainamide is converted to N-
acetylprocainamide (NAPA), which blocks potassium channels (prolongs APD, but does not block Na channels).
• NAPA accumulation has been implicated in producing torsade de pointes in patients with renal failure.
Anti-arrhythmic drugs
CLASS IB : Lidocaine: Least cardiotoxic :• Block Na channels: preference for
INACTIVATED channels in partially depolarized cells of ischemic area.
• High first pass metabolism – not given orally
• Used in treatment of ventricular arrhythmia and also in digoxin induced arrhythmias.
• Main toxicity is neurological – drowsiness, confusion and nystagmus.
Anti-arrhythmic drugs
CLASS IC : Flecainide• This is a class of potent Na channel
blocker • Drugs of this class have negative inotropic
effect and highly pro-arrhythmogenic especially in setting of myocardial infarction.
• Flecainide is indicated for life threatening ventricular fibrillation and refractory or symptomatic supraventricular arrhythmia.
Anti-arrhythmic drugs
• CLASS II : Beta blockers : Propranolol, Metoprolol, Carvedilol• CLASS III : Agents widening APD :
K channel blockers : Amiodarone, Sotalol, Ibutilide• CLASS IV : CCB : Verapamil, Diltiazem
Anti-arrhythmic drugs
CLASS II : BETA BLOCKERS :• Propranolol, Metoprolol, Esmolol,
Carvedilol• These diminish phase 4 depolarization –
decreasing automaticity• Prolong AV conduction• Prevent re-infarction & sudden death in
patients with a history of CHF or MI• Used for the control of ventricular rate in
patients with atrial fibrillation
Anti-arrhythmic drugs
BETA BLOCKERS
Anti-arrhythmic drugs
CLASS III : POTASSIUM CHANNELBLOCKERS : Amiodarone• It is an iodine containing highly
lipophilic anti-arrhythmic with multiple actions
o Block K channels o Block inactivated Na + channelso Inhibit Ca channels
Anti-arrhythmic drugs
Class III : Amiodarone :• Used in wide range of ventricular and atrial