Pharmacological Treatment of Dysrhythmias

Question 1

What is a long QT interval (>0.4 - 0.44) caused by?

Answer 1

A mutation in K+ channels

Question 2

What phases are not included in the SA node?

Answer 2

Phase 1 and 2

Question 3

How are dysrhythmias classifiedin terms of where the abnormality arises?

Answer 3

• Atrial (supraventricular)
• Junctional (assciated with AV node)
• Ventricular

Question 4

What are the 1a class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 4

Sodium channel blockers e.g disopyramide

Question 5

What are the 1b class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 5

Sodium channel blockers e.g lignocaine

Question 6

What are the 1c class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 6

Sodium channel blockers e.g flecainide

Question 7

What are the 2 class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 7

b-adrenoreceptor blockers e.g sotalol

Question 8

What are the 3 class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 8

Potassium channel block e.g amiodarone

Question 9

What are the 4 class of antidysrhythmic drugs (Vaughan Williams) system?

Answer 9

Calcium channel blockers e.g verapamil

Question 10

Name 2 unclassified antidysrhythmic drugs

Answer 10

Adenosine and digoxin

Question 11

How do the class1 dysrhtmic drugs operate?

Answer 11

• They inhibit the action potential and they reduce the rate of cardiac depolarisation during phase 0
• Use-dependant

Question 12

What is the clinical use of class 1a antidysrhtmics (disopyramide)?

Answer 12

• Ventricular dysrhythmias, prevention of recurrent atrial fibrilation triggered by vagal over-activity.

Question 13

What is the clinical use of class 1b antidysrhythmics (lignocaine)?

Answer 13

Treatment and prevention of ventricular tachycardia and fibrilation during and immediately after MI

Question 14

What is the clinical use of class 1c antidysrhythmics (Flecainide)?

Answer 14

Suppresses ventricular ectopic beats. Prevents paroxysmal atrial fibrilation and recurrent tchycardias associated with abnormal conducting pathways.

Question 15

How do class 2 antidysrhythmics work?

Answer 15

• They block Beta 1 receptors
• B1 receptors enhance calcium entry in phase 2 of the cardiac action potential so blocking them reduces this
• Beta blockers increase the refractory period of the AV node so prevent recurrent attacks of supraventricular tachycardias
• Slowing HR by blocking SA node will decrease occurence of dysrhythmias

Question 16

What drug can be considered a class 2 and 3 antidysrhythmic?

Answer 16

sotalol

Question 17

How do class 3 drugs (amiodarone) work?

Answer 17

• They are potassium channel blockers

- They prolong the cardiac action potential by prolonging the refractory period

Question 18

What drug is WPW syndrome treated with?

Answer 18

Amiodarone (class 3) (K+ channel blocker)
Also effective in many other supraventricular and ventricular tachyarrhythmias

Question 19

`What conditions are treated with Sotalol?

Answer 19

It is used in supraventricular dysrhythmias and suppresses ventricular ectopic beats and short runs of ventricular tachycardia

Question 20

How do class 4 antidysrhythmics work?

Answer 20

• Blocks cardiac voltage-gated L-type calcium channels
• Slow conduction through SA and AV nodes where the conduction of the AP relies on the slow calcium currents
• They shorten the plateau of the cardiac AP and reduce the force of contraction of the heart

Question 21

How does adenosine work?

Answer 21

• A1 receptor is responsible for thr effect on the AV node
• These receptors are linked to the same cardiac potassium channels that are activated by ACh. and so it hyperpolarises cardiac conducting tissue and slows the HR. It decreases pacemaker activity
• Used to terminate SVTs

Question 22

How does digoxin work?

Answer 22

• Increase vagal efferent activity to the heart
• The parasympathomimetic action of digoxin reduces SA firing rate (decreasing HR) and reduces conduction velocity of electrical impulses through the AV node
• Toxic concentrations disturb sinus rhythm. Inhibition of Na/K+ pump cause depolarisation - ectopic beats