ANTI-ARRYTHMIC DRUGS INTRODUCTION: A Heart arrhythmia is an irregular heartbeat. Arrhythmias occur when the electrical signals that coordinate the heart's beats don't work properly.

1. PRESENTED BY:
Allsun Sweetline. M.S
II yr BDS

2. INTRODUCTION
ACTION POTENTIAL
CLASSIFICATION
DRUG CHOICE

4. A Heart arrhythmia is an
Arrhythmias occur when
the electrical signals that
coordinate the heart's beats
don't work properly.

5. TOO SLOW TOO FAST

14. The ultimate goal of antiarrhythmic drug therapy:
 Restore normal sinus rhythm and conduction
 Prevent more serious and possibly lethal arrhythmias from
occurring.
Antiarrhythmic drugs are used to:
● Stop an irregular, extra electrical impulse in your heart.
● Prevent abnormally fast electrical impulses from traveling along
heart tissues.

19. Quinidine, often used as an anti-
malarial, is also used as an
antiarrhythmic by prolongating atrial
RP and minimising RP disparity of
atrial fibers.
Never drug of choice because it can
precipitate arrhythmia

20. Very important pharmacokinetics of Quinidine are
1. Inhibition of CYP2D6 and 3A4, and P- Glycoprotein
2. Forms active metabolism
Side effects
1. Toxic doses: ventricular tachy (worsen by hyper-K+)
2. Cinchonism (blurred vision, tinnitus, headache,
psychosis)
4. Can cause Torsades de pointes

21. Precautions before giving QUINIDINE
● 1st give testing dose
● Digoxin (digitalize the heart)
● Give anti coagulant
● Shouldn't give QUINIDINE for Old standing
atrial fibrillation more than 6 months

23. ● Orally active drug similar to quinidine
● Has a ganglion blocking effect but doesn’t have
α blocking activity
Mechanism of action:
1. Block Na+ channels in activated state
2. Block K+ channels
3. Prolonged action potential duration and
refractory period

24. The only clinical application of procainamide is during
life-threatening arrhythmias (with no other medication
around)
Prolonged use may cause systemic lupus erythematous
A toxic dose of Procainamide can lead to
1. Asystole
2. Induction of ventricular arrhythmias

26. ● The effects of disopyramide are very similar to those of quinidine
and cardiac antimuscarinic effects are even more marked than
those of quinidine.
● Therapeutic Use
○ Can suppress ventricular arrhythmias and is longer acting
than other drugs in its class.
○ Disopyramide's atropine-like activity accounts for most of its
symptomatic adverse effects.

27. Toxicity
● Cardiac
○ As a result of its negative inotropic effect, it may precipitate
heart failure
○ It should not be used in patients with heart failure.
● Extracardiac
○ Atropine-like activity accounts for most of its symptomatic
adverse effects:urinary retention ,dry mouth,blurred vision,
constipation, and worsening of preexisting glaucoma.

32. Lidocaine is only administered IV (extensive first-
pass metabolism)
t½ 1 to 1.5 hrs
Particularly useful in treating ventricular
arrhythmias
Mechanism of action:
○
Sodium channel blockage
○
Does not prolong and may shorten action
potential

33. Lidocaine is the drug of choice for
1. Termination of ventricular
tachycardia
2. Prevention of ventricular
fibrillation after cardioversion
in setting of acute ischemia

34. Toxic doses of can lead to
1. convulsions
2. coma
Mexiletine only differs from Lidocaine in that
it can be administered orally

38. •Flecainide aggravates CHF due to its negative
inotropic effects
•Treatment with Flecainide, can lead to
1. Life-threatening arrhythmias
2. Ventricular tachycardia

39. ● Clinical applications of Flecainide
○
1. Severe symptomatic ventricular
arrhythmia
2. Premature ventricular contraction
3. Ventricular tachy resistant to others
4. Severe symptomatic supraventricular
arrhythmias

40. Adverse effect
● Premature ventricular contractions.
● Atrial fibrillation (AF)
● Wolf Parkinson White (WPW) syndrome
● Also shown to have
● teratogenic effect

43. ● Propafenone has similar adverse effects to Flecainide
● Propafenone is used for life-threatening ventricular
arrhythmias & maintenance of normal sinus rhythm in
patients with symptomatic A-fib

44. Adverse effect
● Dizziness
● Blurred vision
● Nausea

49. ● Amiodarone is related structurally to
thyroxine (contains iodine)
● Dominant effect of Amiodarone is to block
K+ channels (also blocks Na+ channels &
weak Ca++ channel blocker, inhibits (α &β
receptors)adrenergic stimulation
● Due to the numerous actions of
Amiodorone, it also has the capacity to
induce many side effects

50. ●
Amiodarone can be used for ventricular
and supraventricular subtypes of
arrhythmias
●
About 50% of patients would rather live
with their arrhythmia than be on
Amiodarone (due to its adverse effects)

51. Cause
Corneal microdeposits

52. ● Clinical uses
○ Unique wide spectrum anti-arrythmic
drug
○ Recurrent ventricular fibrillatrion
○ Recurrent haemodynamically unstable
ventricular tachycardia

54. ● Sotalol is a beta-blocker that is a Class III antiarrhythmic because it
1. Inhibits rapid outward K+ current
2. Prolongs repolarization & duration of AP
3. Legnthens refractory period
● Clinical applications of Sotalol
1. Treatment of life-threatening ventricular arrhythmias
2. Maintenance of sinus rhythm in patients with atrial fibrillation
● Sotalol is not used for asymptomatic arrhythmias because of its pro-
arrhythmic effects