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MODULE 10 - Cardiovascular System > PHARMACOLOGY - Antiarrhythmic Drugs > Flashcards

PHARMACOLOGY - Antiarrhythmic Drugs Flashcards

1
Q

What is a supraventricular arrhythmia?

A

A supraventricular arrhythmia is an arrhythmia which originates in the atria

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2
Q

What is a ventricular arrhythmia?

A

A ventricular arrhythmia is an arrhythmia which originates in the ventricles

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3
Q

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

A

Vaughan Williams antiarrhythmic drugs
Digoxin

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4
Q

What are the four classifications of Vaughan Williams antiarrhythmic drugs?

A

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

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5
Q

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

A

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

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6
Q

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

A

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

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7
Q

When is the use of class 1a antiarrhythmics indicated?

A

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

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8
Q

Give an example of a class 1a antiarrythmic

A

Quinidine

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9
Q

When specifically is quinidine used for treating horses?

A

Quinidine is used to treat atrial fibrillation in horses

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10
Q

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

A

Hypotension
Increased QRS duration
Ventricular tachycardia

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11
Q

When is the use of class 1b antiarrhythmics indicated?

A

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

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12
Q

Give an example of a class 1b antiarrhythmic

A

Lidocaine

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13
Q

What is lidocaine used for other than as an antiarrhythmic?

A

Local anaesthetic

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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

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

A

Worsen congestive heart failure
Lethargy
Depression
Bradycardia
Bronchospasm

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17
Q

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

A

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

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18
Q

Give an example of a Vaughan Williams class 3 antiarryhthmic

A

Amiodarone

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19
Q

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

A

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

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20
Q

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

A

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

21
Q

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

A

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

22
Q

Give an example of a Vaughan Williams class 4 antiarryhthmic drug

A

Verapamil

23
Q

What are the four pharmacodynamic effects of digoxin?

A

Antiarrhythmic
Increases baroreceptor activity
Positive inotropic effect
Diuretic

24
Q

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

A

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

25
Q

When is the use of digoxin as an antiarryhthmic indicated?

A

Digoxin is used to treat supraventricular arrhythmias

26
Q

How does digoxin increase the activity of baroreceptors?

A

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

27
Q

How does digoxin have a positive inotropic effect?

A

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

28
Q

How does digoxin have a diuretic effect?

A

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

29
Q

(T/F) Digoxin has a wide therapeutic index

A

FALSE. Digoxin has a narrow therapeutic index

30
Q

Why should digoxin be given orally?

A

Digoxin has a 60-75% bioavailability when given orally

31
Q

(T/F) Digoxin is plasma protein bound

A

TRUE.

32
Q

Why does digoxin have such a long half life?

A

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

33
Q

What is the half life of digoxin in dogs?

A

24 - 30 hours

34
Q

What is the half life of digoxin in cats?

A

36 hours

35
Q

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

A

Seven days

36
Q

How is digoxin eliminated?

A

Digoxin is eliminated by the kidneys

37
Q

What are the six signs of digoxin toxicity?

A

Enhanced borborygmi
Depression
Anorexia
Vomiting
Diarrhoea
Fatal arrhythmia

38
Q

Which three factors can predispose a patient to digoxin toxicity?

A

Hypokalaemia
Cachexia
Impaired renal function

39
Q

Which breed of dog is predisposed to digoxin toxicity?

A

Dobermans

40
Q

Why does hypokalaemia increase the risk of digoxin toxicity?

A

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

41
Q

How can cachexia increase the risk of digoxin toxicity?

A

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

42
Q

Which five methods can be used to prevent digoxin toxicity?

A

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

43
Q

How should you treat an acute overdose of digoxin?

A

Activated charcoal
Digibind

44
Q

What is digibind?

A

Digibind is an antibody which will directly chelate digoxin

45
Q

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

A

Anticholinergic drugs
β-agonists
Methylxanthines

46
Q

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

A

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

47
Q

What are the four potential side effects of anticholinergic drugs?

A

Constipation
Tachycardia
Urinary retention
Dry mucous membranes

48
Q

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

A

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

49
Q

What is the mechanism of action for methylxanthines as antiarrhythmics?

A

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

MODULE 10 - Cardiovascular System (16 decks)

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