class antiarrhythmic drugs
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1
ANTIARRHYTHMICS
Dr. RAGHU PRASADA M SMBBS,MDASSISTANT PROFESSOR DEPT. OF PHARMACOLOGYSSIMS & RC.
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Normal Sinus Rhythm
Heart rhythm is determined by SA node = Cardiac Pacemaker
Sinus rhythm Specialised pacemaker
cells spontaneously generate APs
APs spread through the conducting pathways
Normal sinus rate 60-100 beats/min
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Cardiac Action Potential
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
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0 1 2 3 4
• Effective refractory period• absolute refractory period• relative refractory period
1
0
2
3
4
ARP RRP
Cardiac Action Potential
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What is an Arrhythmia ?
Irregular rhythm
Abnormal Rate
Conduction abnormality
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What causes an arrhythmia?
Changes in automaticity of the PM Ectopic foci causing abnormal APs Reentry tachycardias Block of conduction pathways Abnormal conduction pathways (WPW) Electrolyte disturbances and DRUGS Hypoxic/Ischaemic tissue can undergo spontaneous
depolarisation and become an ectopic pacemaker
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ECG showing
wave segments
Contraction of atria
Contraction of ventricles
Repolarization of ventricles
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Vaughan-Williams Classification
Class Mechanism Example
I Na channel blockersMembrane Stabilisers
Lignocaine
II Beta Blockers Metoprolol
III K channel blockers Amiodarone
IV Ca channel blockers Verapamil
Other Digoxin. Adenosine.MgSO4. Atropine
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Class I
IA IB IC
They ↓ automaticity in non-nodal tissues (atria, ventricles, and purkinje
fibers)
They act on open Na+ channels or
inactivated only
“use dependence”
Have moderate K+ channel blockade
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IA – Quinidine, Procainamide, Disopyramide Slowing the rate of rise in phase 0 They prolong action potential & ERP ↓ the slope of Phase 4 spontaneous depolarization ↑ QRS & QT interval Slow rate of dissociation with open Na+ channels
Vmax
APD
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Antimalarial, antipyretic, skeletal muscle relaxant & atropine like action.
A/E ▪ quinidine syncope from
ventricular tachycardia▪ Diarrhoea▪ “Cinchonism” – tinnitus,
vertigo, headache, nausea & blurred vision.
200-400 mg orally tds
C/I
AV block
QT prolongatio
n- Torsades de pointes Digoxin,
enzyme inducer
Myasthenia gravis
IA – QUINIDINE
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IB – Lidocaine, Mexiletine, Phenytoin & Tocainide They shorten Phase 3 repolarization ↓ the duration of the cardiac action
potential Prolong phase 4 They show rapid association &
dissociation with inactiated Na+ channels
Vmax
APD
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IB – Lidocaine
Used IV because of extensive 1st pass metabolism No vagolytic effects Least cartiotoxic CNS side effects LD – 150-200mg for 15mins MD – 1-4mg/min Used for VT Propranolol ↑ its toxicity
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IC – Flecainide, Encainide, Propafenone & moricizine
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.
Vmax
«APD
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Class II drugs – Propranolol, Metoprolol, Esmolol, Acebutolol
Depress phase 4 depolarization
depress automaticity prolong AV conduction
↑ ERPProlong PR interval HR
contractility
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Class II drugs
Propranolol Esmolol
Resistant v arrhythmia SVT
10 – 80 mg TDS LD 500mg / kg / min for 1 min
1 – 3 mg in 50ml 5%D – 1 min MD 50mg / kg / min for 4 min
Contraindication
Asthma
Sinus Bradycardia
AV block
Severe CHF
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Class III drugs - Amiodarone , Dronedarone, Vernakalant, Ibutilide, Bretylium, Dofetilide
K+ channel blockers AP / ERP without
affecting Phase 0 / 4 Prolong QT & PR APD
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Amiodarone
Iodine – containing
Block K+ Na+ , Ca++
& β
HR & AV nodal
conduction
QT prolongatio
n
Uses =VF, VT & AF
Arrhythmic
death in post MI
LD-150mg slow IV
MD-1mg/min for
6hrs
A/E – heart block, pulmonary, hepatitis, dermatitis, corneal
deposits & thyroidism
Interaction – digoxin, diltizem & quinidine
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class III
Dronedarone-Without iodine, short t1/2, AF Oral 400mg twice daily
Vernakalant-Na+ & K+, atrial ERP, A/D faster, AF
Azimilide-Block both rapid & slow k+ channel
Tedisamil
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Class IV – Verapamil, Diltiazem
Mechanism-block L-type calcium channels.• Rate of phase 4 in SA / AV node• Slow conduction – prolong ERP• Phase 0 upstroke
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Verapamil
Stronger action on heart than smooth muscle Used in supraventricular arrhythmia 80-120mg three times a day A/E – ankle oedema, constipation C/I – AV block, LVF, hypotention & WPW It digoxin toxicity
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Uses
Sympathetically mediated
arrhythmia
Sinus tachycardia
AES
Supraventricular arrhythmia – AF /
PSVT
Ventricular arrhythmia – QT
VPC WPW
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