PHARMACOLOGY - Antiarrhythmic Drugs

Question 1

What is a supraventricular arrhythmia?

Answer 1

A supraventricular arrhythmia is an arrhythmia which originates in the atria

Question 2

What is a ventricular arrhythmia?

Answer 2

A ventricular arrhythmia is an arrhythmia which originates in the ventricles

Question 3

What are the two main classifications of drugs used to treat tachyarrythmias?

Answer 3

Vaughan Williams antiarrhythmic drugs
Digoxin

Question 4

What are the four classifications of Vaughan Williams antiarrhythmic drugs?

Answer 4

Class 1 - Sodium channel blockers
Class 2 - β blockers
Class 3 - Potassium channel blockers
Class 4 - Calcium channel blockers

Question 5

What is the mechanism of action of Vaughan Williams class 1 antiarryhthmics?

Answer 5

Vaughan Williams class 1 antiarryhthmics block sodium channels in cardiac muscle cells which inhibits the influx of sodium into the cells and thus slows the rate of depolarisation and contraction

Question 6

What are the two main subclasses of class 1 antiarrhythmic drugs?

Answer 6

Class 1a: Immediate dissociation
Class 1b: Fast dissociation

Question 7

When is the use of class 1a antiarrhythmics indicated?

Answer 7

Class 1a antiarrythmics are used for haemodynamically significant or life-threatening arrhythmias

Question 8

Give an example of a class 1a antiarrythmic

Answer 8

Quinidine

Question 9

When specifically is quinidine used for treating horses?

Answer 9

Quinidine is used to treat atrial fibrillation in horses

Question 10

What are the three potential side effects of class 1a antiarrhythmics?

Answer 10

Hypotension
Increased QRS duration
Ventricular tachycardia

Question 11

When is the use of class 1b antiarrhythmics indicated?

Answer 11

Class 1b antiarrythmics are used for haemodynamically significant or life-threatening arrhythmias

Question 12

Give an example of a class 1b antiarrhythmic

Answer 12

Lidocaine

Question 13

What is lidocaine used for other than as an antiarrhythmic?

Answer 13

Local anaesthetic

Question 14

What is the mechanism of action for Vaughan Williams class 2 antiarryhthmics?

Answer 14

Vaughan Williams class 2 antiarryhthmics block β receptors in cardiac muscle cells which reduces sympathetic activity which will decrease myocardial contractility and slow atrioventricular (AV) node conduction which will decrease heart rate

Question 15

When is the use of Vaughan Williams class 2 antiarryhthmics indicated?

Answer 15

Vaughan Williams class 2 antiarryhthmics are used for the the treatment of supraventricular and ventricular arrhythmias and to treat hypertrophic cardiomyopathy

Question 16

What are the five potential side effects of Vaughan Williams class 2 antiarryhthmics?

Answer 16

Worsen congestive heart failure
Lethargy
Depression
Bradycardia
Bronchospasm

Question 17

What is the mechanism of action for Vaughan Williams class 3 antiarryhthmics?

Answer 17

Vaughan Williams class 3 antiarryhthmics block potassium channels in cardiac muscle cells which will inhibit potassium efflux out of the cell and thus slow down repolarisation and prolong action potential duration, which will prolong myocardial contraction

Question 18

Give an example of a Vaughan Williams class 3 antiarryhthmic

Answer 18

Amiodarone

Question 19

What are the four potential side affects of Vaughan Williams class 3 antiarryhthmics?

Answer 19

Elevated liver enzymes
Gastrointestinal (GI) disturbances
Pulmonary fibrosis
Thyroid effects

Question 20

What is the mechanism of action for Vaughan Williams class 4 antiarryhthmics?

Answer 20

Vaughan Williams class 4 antiarryhthmics block L-type calcium channels on pacemaker cells in nodal tissue and cardiac muscle cells. In pacemaker cells inhibiting the influx of calcium will slow the rate in which the cells depolarise and prolong the action potential duration, decreasing the heart rate. In cardiomyocytes, this will inhibit the influx of calcium into the cell during the plateau phase, which will shorten the plateau phase, decreasing the action potential duration which will decrease myocardial contractility

Question 21

When is the use of Vaughan Williams class 4 antiarryhthmics indicated?

Answer 21

Vaughan Williams class 4 antiarryhthmics are used to treat supraventricular arrhythmias and hypertrophic cardiomyopathy

Question 22

Give an example of a Vaughan Williams class 4 antiarryhthmic drug

Answer 22

Verapamil

Question 23

What are the four pharmacodynamic effects of digoxin?

Answer 23

Antiarrhythmic
Increases baroreceptor activity
Positive inotropic effect
Diuretic

Question 24

What is the mechanism of action of digoxin as an antiarrhythmic?

Answer 24

Digoxin stimulates parasympathetic activity which will slow atrioventricular (AV) node conduction and will thus decease heart rate

Question 25

When is the use of digoxin as an antiarryhthmic indicated?

Answer 25

Digoxin is used to treat supraventricular arrhythmias

Question 26

How does digoxin increase the activity of baroreceptors?

Answer 26

Digoxin stimulates the parasympathetic nervous system and thus there will be decreased sympathetic activity and circulating catecholamines which will increase baroreceptor activity

Question 27

How does digoxin have a positive inotropic effect?

Answer 27

Digoxin inhibits the Na+/K+ ATPase pump on cardiac muscle cells, which will increase intracellular sodium levels which will disrupt the normal Na+/Ca2+ counter-transport mechanism leading to an increase in intracellular calcium which will enhance myocardial contractility

Question 28

How does digoxin have a diuretic effect?

Answer 28

Digoxin inhibits the Na+/K+ ATPase pump on the renal tubular epithelial cells which will inhibit the reabsorption of sodium and subsequently water into the bloodstream, resulting in diuresis

Question 29

(T/F) Digoxin has a wide therapeutic index

Answer 29

FALSE. Digoxin has a narrow therapeutic index

Question 30

Why should digoxin be given orally?

Answer 30

Digoxin has a 60-75% bioavailability when given orally

Question 31

(T/F) Digoxin is plasma protein bound

Answer 31

TRUE.

Question 32

Why does digoxin have such a long half life?

Answer 32

Digoxin has a high volume of distribution and will accumulate within skeletal muscle

Question 33

What is the half life of digoxin in dogs?

Answer 33

24 - 30 hours

Question 34

What is the half life of digoxin in cats?

Answer 34

36 hours

Question 35

How long does it take for digoxin to reach steady state?

Answer 35

Seven days

Question 36

How is digoxin eliminated?

Answer 36

Digoxin is eliminated by the kidneys

Question 37

What are the six signs of digoxin toxicity?

Answer 37

Enhanced borborygmi Depression Anorexia Vomiting Diarrhoea Fatal arrhythmia

Question 38

Which three factors can predispose a patient to digoxin toxicity?

Answer 38

Hypokalaemia Cachexia Impaired renal function

Question 39

Which breed of dog is predisposed to digoxin toxicity?

Answer 39

Dobermans

Question 40

Why does hypokalaemia increase the risk of digoxin toxicity?

Answer 40

Hypokalaemia increases the risk of digoxin toxicity as digoxin binds to same the binding side as potassium on the Na+/K+ ATPase pump so when there is low potassium in the blood, this will create more binding sites for digoxin which will increase the risk of digoxin toxicity

Question 41

How can cachexia increase the risk of digoxin toxicity?

Answer 41

Cachexia reduces skeletal muscle mass and thus if there is reduced skeletal muscle there will be more circulating digoxin as it cannot accumulate as well in skeletal muscle

Question 42

Which five methods can be used to prevent digoxin toxicity?

Answer 42

Start on a low dose Dose based on body surface area rather than weight Avoid loading doses Reduce starting dose if patient is predisposed to toxicity Monitor digoxin serum levels

Question 43

How should you treat an acute overdose of digoxin?

Answer 43

Activated charcoal Digibind

Question 44

What is digibind?

Answer 44

Digibind is an antibody which will directly chelate digoxin

Question 45

What are the three main classifications of drugs used to treat bradyarrythmias?

Answer 45

Anticholinergic drugs β-agonists Methylxanthines

Question 46

What is the mechanism of action for anticholinergic drugs as antiarrhythmics?

Answer 46

Anticholinergics inhibit the binding of acetylcholine to muscarinic receptors on cardiac muscle cells, which will thus decrease the parasympathetic activity and increase myocardial contractility

Question 47

What are the four potential side effects of anticholinergic drugs?

Answer 47

Constipation Tachycardia Urinary retention Dry mucous membranes

Question 48

What is the mechanism of action for β-agonists as antiarrhythmics?

Answer 48

β-agonists stimulate β adrenergic receptors on cardiac muscle cells which will increase sympathetic activity and thus increase myocardial contractility

Question 49

What is the mechanism of action for methylxanthines as antiarrhythmics?

Answer 49

Methylxanthines are phosphodiesterase (PDE) inhibitors. Phosphodiesterases (PDE) are enzymes which catalyse the hydrolysis of cAMP and thus inhibiting this action, there will be increased and prolonged cAMP, increasing calcium influx and myocardial contractility