Ant arrhythmic drugs

Anti-Arrhythmic Drugs
By:- Dr. Manish Pal Singh,
Associate Professor
1AGRA PUBLIC PHARMACY COLLEGE, ARTONI, AGRA, UP, INDIA
Source*- www.physio-pedia.com

Cardiac Arrhythmia:
❑ Cardiac arrhythmias results from alterations in the orderly sequence of
depolarization followed by repolarization in the heart.
❑ Arrhythmias are the most important cause of sudden cardiac death.
❑ Abnormal automaticity or impaired conduction or both underline cardiac
arrhythmias.
AGRA PUBLIC PHARMACY COLLEGE,
ARTONI, AGRA, UP, INDIA
2
Source*-https://www.ohsu.edu/doernbecher/pediatric-
electrophysiology-and-arrhythmia

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Divided into five phases (0,1,2,3,4)
• Phase 0 – rapid depolarization
• Phase 1 – early repolarization
• Phase 2 – plateau phase
• Phase 3 – rapid repolarization
• Phase 4 – resting phase,
diastolic depolarization
Source*-
https://www.google.com/uFbasicmedicalkey.com

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ARRHYTHMIA
Abnormal
impulse
conduction
Abnormal
impulse
generation
Triggered
activity
Arrhythmia may be occur due to-
• Abnormal pacemaker activity
•Shift of the pacemaker from SA node to another
place in the heart.
• Block at different points in the spread of the
impulses through the heart.
•Abnormal pathways of impulse transmission
through the heart.
•Spontaneous generation of spurious impulses in
almost any part of the heart.

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Abnormal impulse conduction

❑ Conduction Block:-
▪ Due to depression of impulse conduction at AV node & bundle of His,
due to vagal influence or ischemia.
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1st degree heart block – slowed conduction
2nd degree block – some supraventricular
complex not conducted
3rd degree block – no supraventricular complex are conducted
Premature contraction

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Re-Entry Moments- “Circus Movements
Source*- https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.slideshare.net

➢ Due to abnormality of conduction , an impulse may recirculate in the heart and
causes repetitive activation without the need for any new impulse to be
generated.
➢ When the normal cardiac impulses in the normal heart has traveled through the
extent of the ventricles, it has no place to go because all the ventricles muscle is
refractory & can’t conduct the impulse further. Therefore, that impulses dies &
the heart awaits a new AP to begin in the SA node.
➢ Circus movement type:- A premature impulse temporarily blocked in one
direction by refractory tissue, makes a one-way transit around an obstacle finds
the original spot in an advanced state of recovery and rexicites it, setting up
recurrent activation of adjacent myocardium.
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Accessory tract pathway
Source*- https://www.google.com/url
Accessory
pathway in the
heart called
Bundle of Kent

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Important Types of Arrhythmia :-
1. ES (Extra systoles)- premature beats
2. PVST (Paroxysmal supraventricular tachycardia)- Due to circus movement
type of Re-entry or accessory pathway
3. AFL (Atrial flutter)- Due to re entry circuit in right atrium
4. AF (Atrial Fibrillation)- Due to electrophysiological in homogeneity of atrial fibers.
5. Ventricular Tachycardia (VT)- Due to either discharge from ectopic focus or reentry
circuits
6. Torsades de Points- Polymorphic VT with rapid asynchronous complex, twisting
along the baseline on ECG with long QT interval
7. Ventricular fibrillation - Grossly irregular, rapid & fractionated action of ventricles
– resulting in in coordinated contraction of ventricles with loss of
pumping function.

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Source*- https://www.google.com/Fen.wikipedia.org
Approachable Targets of Anti-arrhythmic Drugs

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Targets mechanisms of Anti-arrhythmic Drugs

Classification of Anti-arrhythmic drugs
13Source*- https://www.google.com/Fbpspubs.onlinelibrary.wiley.com
(Na+-channel blocker)
(β blocker)
K+ channel blocker
(Ca+- channel blocker)

CLASS-I- Drugs:
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They act on open Na+
channels or
inactivated only
They ↓ automaticity in non-nodal
tissues (atria, ventricles, and purkinje
fibers)

Subclass- IA:
❑ The oldest anti-arrhythmic drugs- ‘Quinidine & Procainamide’.
❑ They are open state Na+- channel blockers, which suppress A-V conduction &
prolong refractoriness.
❑ Slowing the rate of rise in phase 0
❑ They prolong action potential & ERP
❑ ↓the slope of Phase 4 spontaneous depolarization
❑ ↑ QRS & QT interval
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ADR’s:
• Cinchonism” – tinnitus, vertigo,
• headache, nausea & blurred vision.
• Gastrointestinal intolerance.
• Hypersensitivity reactions.
Drug Interactions:
▪ Quinidine can interact the plasma concentration of digoxin, which may in turn lead
to signs and symptoms of digitalis toxicity.
▪ Cimitidine increases hepatic metabolism of quinidine.
16Source*- https://www.google.com/imgres?imgurl

Subclass- IB:
❑ These drugs block Na+- channels more in the inactivated than in the open state.
❑ They shorten Phase 3 repolarization.
❑ the duration of the cardiac action potential
❑ Prolong phase 4.
❑ Lidocaine used as local anaesthetic drug, in addition it is a popular
antiarrhythmic drug.
❑ Its cardiac action is suppression oof
Of automaticity in ectopic foci.
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18
Source*-
=https%3A%2F%2Fdir.indiamart.com%2Fimpcat%2Flidocaine.
ADR’s:-
Neurological effects- Drowsiness, Slurred speech,
Confusion and convulsions.
Contraindications:-
Lidocaine is contraindicated in the presence of second and
third degree heart block, since it may increase the degree of
block and can abolish the idioventricular Pacemaker
responsible for maintaining the cardiac rhythm.
Drug Interactions:-
Proponolol increases its toxicity.
The myocardial depressant effect of lidocaine is
enhanced by phenytoin administration.

Subclass- IC:
❑ These are most potent Na+- channel blockers with more prominent action on
open state & the longest recovery times.
❑ markedly slow Phase 0 depolarization.
❑ slow conduction in the myocardial tissue
❑ minor effects on the duration of action potential and ERP
❑ reduce automaticity by increasing threshold potential rather than decreasing
slope of Phase 4 depolarization.
❑ They have profound effect on His-Purkinje as well as accessory pathway
conduction.
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❑ Flecainide produce ADR’s like-
• torsades de point,
• Visual disturbances & headache
• Digoxin toxicity
• Contraindiaction- cardiogenic shock
❑ Propafenone produce ADR’s like-
• proarrhythmogenic effect,
• metallic taste & constipation
• Contraindication- Heart failure
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Source*- https://www.google.com/imgres?imgurlt

CLASS-II
❑ Its suppress adrenergically mediated ectopic activity.
❑ Depress phase 4 depolarization
❑ Depress automaticity
❑ Prolong AV conduction
-↑ ERP
-Prolong PR interval
- ↓ HR
❑ ↓ contractility
❑ Use inappropriate sinus tachycardia
Sympathetic mediated arrhythmias
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CLASS-III
❑ K+ channel blockers .
❑ This class is prolongation of repolarization; AP is widened & ERP is increased.
❑ Prolong QT & PR
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AMIDARONE-----
Next PPT

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Iodine –
containing
Block of delayed
rectifier K+
↓HR & AV
nodal
conduction
QT
prolongation
Preferentially
block Na+
channel
Arrhythmic
death in post
MI
ADR- heart block,
pulmonary,
hepatitis, dermatitis
Interaction –
digoxin,
diltiazem &
quinidine
Uses =VF,
VT
& AF

CLASS-IV
❑ The primary action to inhibit L-type Ca++- channel mediated slow channel
inward current.
❑ ↓ Rate of phase 4 in SA / AV node
❑ Slow conduction – prolong ERP
❑ Phase 0 upstroke ↓
❑ The basic action of verapamil is to depress Ca++ mediated depolarization.
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Source*- www.slideshare.net%2Fnasertadvi%2Fantiarrhythmic-drugs

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Source*-
https%3A%2F%2Fwww.diabetesselfmanagement.com%2

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