Pharmacology: Antiarrhythmics Exam 2023 Questions and
Answers with complete solution
What's the principle of antiarrhythmic drugs?
Antiarrhythmic drugs exert their effects by decreasing the automaticity of ectopic
pacemakers more than that of the SA node. They also reduce conduction and
excitability and increase the refractory period to a greater extent in depolarized tissue
than in normally polarized tissue.
What kind of drugs are Class I antiarrhythmics?
These are sodium channel blockers.
What kind of drugs are Class II antiarrhythmics?
These are beta blockers.
What kind of drugs are Class III antiarrhythmics?
These are potassium channel blockers.
What kind of drugs are Class IV antiarrhythmics?
These are calcium channel blockers.
Which antiarrhythmics are in group IA?
1. Quinidine
2. Procainamide
3. Disopyramide
Which antiarrhythmics are in group IB?
1. Lidocaine
2. Mexiletine
Which antiarrhythmics are in group IC?
1. Flecainide
2. Propafenone
Which antiarrhythmics are in group II?
1. Propranolol
2. Metoprolol
3. Esmolol
Which antiarrhythmics are in group III?
1. Amiodarone
2. Sotalol
3. Dofetilide
Which antiarrhythmics are in group IV?
1. Verapamil
2. Diltiazem
What is the drug of choice for ventricular tachycardia?
Lidocaine is the drug of choice for the termination of ventricular tachycardia and the
prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia.
What are class IA antiarrhythmics used for?
They are used to treat atrial fibrillation, supraventricular and ventricular
tachyarrhythmias.
What are class IC antiarrhythmics used for?
, They treat life-threatening supraventricular tachyarrhythmias and ventricular
tachyarrhythmias; they can also be used in prevention of paroxysmal atrial fibrillation
and the maintenance of normal sinus rhythm in patients with symptomatic atrial
fibrillation.
How do the different Class I antiarrhythmics differ in kinetics?
Class IB have fast kinetics, class IC have slow kinetics, and class IA have intermediate
kinetics.
What is the mechanism of action for Class I antiarrhythmics?
They all bind/block the fast Na+ channels that are responsible for phase 0
depolarization, which decreases automaticity, shifting the threshold to more positive
potentials and decreasing the slope of phase 4 depolarization. The block of Na+
channels leaves fewer channels available to open in response to membrane
depolarization, thereby raising the threshold for action potential firing and slowing the
rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+
channels for depolarization, Class I drugs do not have any direct effect on nodal tissue.
Why are Class IC antiarrhythmics the most potent?
Class IC drugs express their effects at all heart rates due to their slow kinetics, making
them the most potent of all the class I drugs.
Describe the pharmacokinetics of quinidine.
Quinidine forms active metabolites from breakdown with CYP 3A4. It is also an
inhibitor of CYP 2D6, 3A4 and the P-glycoprotein pump.
Describe the pharmacokinetics of procainamide.
A percentage of procainamide is acetylated to N-acetylprocainamide (NAPA), this
metabolite has class III activity and thus prolongs duration of action potential.
Describe the pharmacokinetics of lidocaine.
Lidocaine can only be given IV due to extensive first-pass metabolism. Mexiletine can
be used both orally and IV.
What are the general adverse effects of Class IA antiarrythmics?
The anticholinergic effects of IA drugs produce the typical side effects of tachycardia,
dry mouth, urinary retention, blurred vision and constipation. Diarrhea, nausea,
headache and dizziness are also common side effects of many Class I drugs.
What are the adverse effects of quinidine?
By increasing the refractory period quinidine can precipitate arrhythmias such as
torsades de pointes. It can also enhance digoxin toxicity by decreasing its renal
clearance. Other side effects of quinidine include cinchonism (blurred vision, tinnitus,
headache, psychosis); nausea, vomiting, diarrhea and abdominal cramps,
thrombocytopenic purpura and hemolytic anemia.
What are the adverse effects of procainamide?
The chronic use of procainamide is associated with a high incidence of adverse effects
including a reversible lupus-like syndrome, GI intolerance, aggravation of underlying
HF, induction of ventricular arrhythmias and CNS effects such as depression,
hallucinations and psychosis.
What are the adverse effects of disopyramide?
Disopyramide has pronounced negative inotropic effects and may induce hypotension &
cardiac failure without pre-existing myocardial dysfunction. It is also associated with
severe antimuscarinic effects.
Answers with complete solution
What's the principle of antiarrhythmic drugs?
Antiarrhythmic drugs exert their effects by decreasing the automaticity of ectopic
pacemakers more than that of the SA node. They also reduce conduction and
excitability and increase the refractory period to a greater extent in depolarized tissue
than in normally polarized tissue.
What kind of drugs are Class I antiarrhythmics?
These are sodium channel blockers.
What kind of drugs are Class II antiarrhythmics?
These are beta blockers.
What kind of drugs are Class III antiarrhythmics?
These are potassium channel blockers.
What kind of drugs are Class IV antiarrhythmics?
These are calcium channel blockers.
Which antiarrhythmics are in group IA?
1. Quinidine
2. Procainamide
3. Disopyramide
Which antiarrhythmics are in group IB?
1. Lidocaine
2. Mexiletine
Which antiarrhythmics are in group IC?
1. Flecainide
2. Propafenone
Which antiarrhythmics are in group II?
1. Propranolol
2. Metoprolol
3. Esmolol
Which antiarrhythmics are in group III?
1. Amiodarone
2. Sotalol
3. Dofetilide
Which antiarrhythmics are in group IV?
1. Verapamil
2. Diltiazem
What is the drug of choice for ventricular tachycardia?
Lidocaine is the drug of choice for the termination of ventricular tachycardia and the
prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia.
What are class IA antiarrhythmics used for?
They are used to treat atrial fibrillation, supraventricular and ventricular
tachyarrhythmias.
What are class IC antiarrhythmics used for?
, They treat life-threatening supraventricular tachyarrhythmias and ventricular
tachyarrhythmias; they can also be used in prevention of paroxysmal atrial fibrillation
and the maintenance of normal sinus rhythm in patients with symptomatic atrial
fibrillation.
How do the different Class I antiarrhythmics differ in kinetics?
Class IB have fast kinetics, class IC have slow kinetics, and class IA have intermediate
kinetics.
What is the mechanism of action for Class I antiarrhythmics?
They all bind/block the fast Na+ channels that are responsible for phase 0
depolarization, which decreases automaticity, shifting the threshold to more positive
potentials and decreasing the slope of phase 4 depolarization. The block of Na+
channels leaves fewer channels available to open in response to membrane
depolarization, thereby raising the threshold for action potential firing and slowing the
rate of depolarization. Because nodal tissue action potentials do not rely on fast Na+
channels for depolarization, Class I drugs do not have any direct effect on nodal tissue.
Why are Class IC antiarrhythmics the most potent?
Class IC drugs express their effects at all heart rates due to their slow kinetics, making
them the most potent of all the class I drugs.
Describe the pharmacokinetics of quinidine.
Quinidine forms active metabolites from breakdown with CYP 3A4. It is also an
inhibitor of CYP 2D6, 3A4 and the P-glycoprotein pump.
Describe the pharmacokinetics of procainamide.
A percentage of procainamide is acetylated to N-acetylprocainamide (NAPA), this
metabolite has class III activity and thus prolongs duration of action potential.
Describe the pharmacokinetics of lidocaine.
Lidocaine can only be given IV due to extensive first-pass metabolism. Mexiletine can
be used both orally and IV.
What are the general adverse effects of Class IA antiarrythmics?
The anticholinergic effects of IA drugs produce the typical side effects of tachycardia,
dry mouth, urinary retention, blurred vision and constipation. Diarrhea, nausea,
headache and dizziness are also common side effects of many Class I drugs.
What are the adverse effects of quinidine?
By increasing the refractory period quinidine can precipitate arrhythmias such as
torsades de pointes. It can also enhance digoxin toxicity by decreasing its renal
clearance. Other side effects of quinidine include cinchonism (blurred vision, tinnitus,
headache, psychosis); nausea, vomiting, diarrhea and abdominal cramps,
thrombocytopenic purpura and hemolytic anemia.
What are the adverse effects of procainamide?
The chronic use of procainamide is associated with a high incidence of adverse effects
including a reversible lupus-like syndrome, GI intolerance, aggravation of underlying
HF, induction of ventricular arrhythmias and CNS effects such as depression,
hallucinations and psychosis.
What are the adverse effects of disopyramide?
Disopyramide has pronounced negative inotropic effects and may induce hypotension &
cardiac failure without pre-existing myocardial dysfunction. It is also associated with
severe antimuscarinic effects.
