Class antiarrhythmic drugs

1. Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.
1

2. 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

3. 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

4. 0 1 2 3 4
•Effective refractory period
•absolute refractory period
•relative refractory period
1
0
2
3
4
ARP RRP

5. Irregular rhythm
Abnormal Rate
Conduction abnormality

6. 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/Ischaemictissue can undergo spontaneous
depolarisationand become an ectopic pacemaker

7. Contraction of
atria
Contraction of
ventricles
Repolarizationof
ventricles

8. ClassMechanism Example
I Na channel blockers
Membrane Stabilisers
Lignocaine
II Beta Blockers Metoprolol
IIIK channel blockers Amiodarone
IV Ca channel blockers Verapamil
OtherDigoxin. Adenosine.
MgSO4. Atropine

9. Class I
IA IB IC
They ↓automaticity in non-nodal tissues
(atria, ventricles, and purkinjefibers)
They act on open Na
+
channels or inactivated
only
“use
dependence”
Have moderate K
+
channel
blockade

10. 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

11. Antimalarial, antipyretic, skeletal
muscle relaxant & atropine like
action.
A/E
▪quinidinesyncope from
ventricular tachycardia
▪Diarrhoea
▪“Cinchonism” –tinnitus,
vertigo, headache, nausea &
blurred vision.
200-400 mg orally tds
C/I
AV block
QT prolongation
-Torsadesde
pointes
Digoxin, enzyme
inducer
Myasthenia
gravis

12. They shorten Phase 3 repolarization
↓the duration of the cardiac action potential
Prolong phase 4
They show rapid association & dissociation with
inactiatedNa
+
channels
Vmax
APD

13. Used IV because of extensive 1st pass metabolism
No vagolyticeffects
Least cartiotoxic
CNS side effects
LD –150-200mg for 15mins
MD –1-4mg/min
Used for VT
Propranolol↑ its toxicity

14. markedly slow Phase 0 depolarization
slow conductionin 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

15. Depress phase 4
depolarization
depress automaticity
prolong AV conduction
↑ERP
Prolong PR interval
HR
contractility

16. Propranolol Esmolol
Resistantv 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

17. K+ channel blockers
AP / ERP without affecting
Phase 0 / 4
Prolong QT & PR APD

18. Iodine –containing
Block K
+
Na
+
, Ca
++
&
β
HR & AV nodal
conduction
QT prolongation
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

19. Dronedarone-Without iodine, short t1/2, AF
Oral 400mg twice daily
Vernakalant-Na
+
& K
+
, atrialERP, A/D faster, AF

Azimilide-Block both rapid & slow k+ channel

Tedisamil

20. Mechanism-block L-type calcium channels.
•Rate of phase 4 in SA / AV node
•Slow conduction –prolong ERP
•Phase 0 upstroke

21. Stronger action on heart than smooth muscle
Used in supraventriculararrhythmia
80-120mg three times a day
A/E –ankle oedema, constipation
C/I –AV block, LVF, hypotention& WPW
It digoxin toxicity

22. Sympathetically
mediated arrhythmia
Sinus tachycardia
AES
Supraventricular
arrhythmia –AF /
PSVT
Ventricular
arrhythmia –QT
VPC WPW