Antiarrhythmic drugs

Question 1

class II drugs- beta blockers

Answer 1

• reduces the heart rate, conduction velocity and intracellular calcium overload
• effective for delayed after depolarization
  non-selective ones are usually for the adrenaline-induced hypokalemia related arrthymia in high stress state e.g. acute MI, resuscitation from cardiac arrest

Question 2

Class III drugs: potassium channel blockers

Answer 2

e.g. dofetilide, amiodarone, dronedarone, sotalol
reduce the rate of repolarization, increase duration of AP and effective refractory periods
reduce re-entry and automaticity

Question 3

Dofetilide

Answer 3

• potent potassium channel blocker

- risk of torsades de pointes (cautious with renal failure and renal cation channel blocker people, hypokalemic)

Question 4

Amiodarone

Answer 4

• broad spectrum of action (all four classes)
• low risk of torsades de pointes
  side effects: due to presence of iodine group -> hepatic hypersensitivity, pulmonary fibrosis
• pro-arrhythmia: bradycardia and heart block
• drug interaction: CYP3A4

Question 5

Dronedarone

Answer 5

• same as amiodarone, but no iodine
• absorption increases when taken with food
• liver toxicity

Question 6

Sotalol

Answer 6

• for paediatric age group
• class III with class II action, due to a racemic mixture of l and d-sotalol (l is the one)
• risk of torsades de pointes and left ventricular depression

Question 7

Class 4- CCBs

Answer 7

• cardiac selective ones
• reduce heart rate, the conduction velocity and the calcium overload (block DAD)
• diltiazem, verapamil

side effects:
heart failure (reduce force of contraction and AV block)
hypotension, maybe peripheral oedema

contraindicated in ventricular tachycardia

Question 8

Adenosine

Answer 8

• activate the presynaptic purinergic receptor, reduces the NE release and thus automaticity
• binds to A1 receptor on SA and AV, inhibit adenylyl cyclase, reduce intracellular calcium overload
• activate the K channels on SA and AV nodes, increase the maximum diastolic potential, increase duration of reaching threshold from phase 4 -> reduce automaticity

side effects:

• hypotension
• chest pain and short of breath (bronchospasm)

Question 9

cardiac glycosides- digoxin

Answer 9

• parasympathomimetic effect to reduce the heart rate and conduction velocity
• pro-arrhythmia: inhibit the Na K atpase therefore reduce the expulsion of ca by na ca exchanger -> DAD

Question 10

Muscarinic receptor antagonist- atropine

Answer 10

• block the parasympathetic output to SA and AV node, increases the heart rate and conduction velocity
• reduce vagal influence
• used for AV block

side effects: dry mouth, tachycardia

Question 11

Class 1a drugs- Na channel blockers

Answer 11

• intermediate kinetics (reduce automaticity and conduction velocity)
• block K channels (effective refractory period increases)
  e.g. procainamide, quinidine, disopyramide
  side effects: pro-arrhythmia (EAD, torsades de pointes; anticholinergic- tachycardia)
  reduces the force of contraction (disopyramide>quinidine>procainamide)

Question 12

Class 1b drug

Answer 12

• rapid dissociation within normal heart beat, block premature beats
• preferably bind to inactivated channels and act on depolarised cells
  side effect: CNS disturbances
  e.g. lidocaine, mexiletine

Question 13

Class 1c drug

Answer 13

slow dissociation, reduce conduction velocity
side effect: pro-arrhythmia, heart failure (worsened in propafenone - beta block effect)
- propafenone, encainide, flecainide