anti arrhthymic drugs

1. Spurthi BS
Doctor of Pharmacy (PharmD)
Mallige college of pharmacy

9. Contractionof
atria
Contractionof
ventricles
Repolarization of
ventricles

10. Class Mechanism Example
IA Na channel blockers
Moderately decrease dv/dt
QUINIDINE
PROCAINAMIDE
DISOPYRAMIDE
IB Na channel blockers
Little decrease in dv/dt
LIGNOCAINE
MEXILETINE
TOCAINIDE
PHENYTOIN
IC Na channel blockers
Marked decrease in dv/dt
FLECAINIDE
PROPAFENONE
ENCAINIDE
MORICIZINE

11. Class Mechanism Example
II Beta Blockers METOPROLOL
III K channel blockers AMIODARONE
DRONIDARONE
SOTOLOL
DOFETILIDE
IBUTILIDE
IV Ca channel blockers VERAPAMIL
Other Digoxin. Adenosine.
MgSO4. Atropine

16. Slowing the rate of rise in phase 0
They prolong action potential and ERP
↓ the slope of Phase 4 spontaneous depolarization
↑ QRS & QT interval
Slow rate of dissociation with open Na+ channels

17. 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 prolongation
- Torsades de pointes
Digoxin,
enzyme
inducer
Myasthenia gravis

18. They shorten Phase 3 repolarization
↓ the duration of the cardiac action potential
Prolong phase 4
They show rapid association & dissociation
with inactivated Na+ channels

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

20. 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.

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

24. 19

25. 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

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

27. Iodine – containing
Block K+ Na+ , Ca++
& β
HR & AV nodal conduction, QT prolongation
 Arrhythmic death in post
MI Uses
VF, VT & AF
LD-150mg slow IV
MD-1mg/min for 6hrs
A/E – heart block, pulmonary, hepatitis,
dermatitis, corneal deposits & thyroidism
Interaction – digoxin, Diltiazem & quinidine

28. Dronedarone-
Without iodine, short t1/2, AF Oral
400mg twice daily
Vernakalant
-Na+& K+, atrial ERP, A/D faster, AF
Azimilide-
block both rapid and slow K+ channel
Tedisamil

29. 24

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

31. Stronger action on heart than smooth
muscle Used in supraventricular
arrhythmia
80-120mg three times a
day Uses
Sympathetically mediated
arrhythmia Sinus tachycardia
Supraventricular arrhythmia – AF /
PSVT Ventricular arrhythmia – QT
VPC, WPW
A/E – ankle oedema, constipation
C/I – AV block, LVF, hypotension &
WPW It  digoxin toxicity

32. Inhibits Na K/ATPase pump
Contractility increases as intracellular Ca, Na
increases and loss of intracellular K+
Digoxin toxicity- renal insufficiency, ischemia,
hypokalemia, calcium channel blockers, beta
blockers, cyclosporine and furosemide
Normal levels- 0.5-2ng/ml
Treatment of toxicity-charcoal. Correct
potassium, calcium IV, DIGIBIND antibodies

33. Naturally occurring nucleoside
Given rapid IV for reentrant supra
ventricular arrhythmias
Used to produce controlled hypotension for
surgeries
Diagnosis of coronary artery disease
It activates ACH sensitive K+ CURRENT IN
atrium, sinus and AV node decreases action
potential duration and causes hyperpolarisation