Pharmacological treatment of dysrhythmias

Question 1

The spontaneous electrical dischatge of the SAN is from the combined effect of:

Answer 1

• Decrease in K outflow
• ‘funny’ Na current
• Slow inward Ca current

Question 2

Give an example of slow conducting tissue

Answer 2

Nodal tissue

Question 3

Give an example of fast conducting tissue

Answer 3

ventricles

Question 4

What is a dysrthymia?

Answer 4

Describes conditions where the co-ordinated sequence of electrical acitivty in the heart is disrupted

Question 5

What are the potential causes of dysrythmia?

Answer 5

• Changes in heart cells
• Changes in the conduction of the impulse through the heart
• Combination

Question 6

What are the 4 classifications of dysrhtymia?

Answer 6

• Atrial (supraventricular)
• Junctional (associated with the AV node
• Ventricular
• Tachycardias or bradycardias

Question 7

What 4 broad categories of event do dysrythmias arise from?

Answer 7

• Ectopic pacemaker activity
• Delayed after-depolarisations
• Circus re-entry
• Heart block

Question 8

What are the classes of antidusrhythmic drugs?

Answer 8

1a. sodium channel blockers → disopyramide
1b. sodium channel blockers → lignocaine
1c. sodium channel blockers → flecainide
2. beta-adrenoreceptor blockers → sotalol
3. potassium channel blockers → amiodarone
4. calcium channel blockers → verapamil

unclassificed → adenosine and digoxin

Question 9

What are sodium channel blockers?

Answer 9

Drugs bind the different domains of the voltage gated sodium chennel. They inhibit action potential propagation and they reduced the rate of cardiac depolarisations during phase 0 (fast conducting tissue)

Question 10

Why are sodium channel blockers subdivided into different classes?

Answer 10

a,b and c based on the properties of the drugs un binding to sodium channels in their various states such as open, refractory and resting

Question 11

How does depolarisation change the state of sodium channels?

Answer 11

switches channels from resting to open state → activation

Question 12

How does maintained depolarisation affect sodium channels

Answer 12

Causes them to move to a refractory state → inactivation

Question 13

What type of drugs bind during open and refractory periods?

Answer 13

use-dependent meaning they work more effectively when activity is high (not as good at normal beating rates)

Question 14

Clinical uses of type 1a sodium channel blocker and give and example

Answer 14

Disopyramide

• ventricular dysrhythmias
• prevention of recurrent atrial fibrillation triggered by vagal over activity

Question 15

Clinical uses of type 1b sodium channel blocker and give and example

Answer 15

Lignocaine (given by IV)

• Treatment and prevention of ventricular tachycardia and fibrillation during and immediately after MI

Question 16

Clinical uses of type 1c sodium channel blocker and give and example

Answer 16

Flecainide

• suppressed ventricular ectopic beats
• prevents paroxysmal atrial fibrillation and recurrent tachycardias associated with abnormal conducting pathways

Question 17

What pathway do beta-blockers infiltrate?

Answer 17

signal transduction pathway of beta adrenreceptors

Question 18

What is the action of beta-blockers

Answer 18

Slow HR and decrease CO

Question 19

What does beta1 receptor activation cause?

Answer 19

enhances caclium entry in phase 1 of the cardiac action potential

Question 20

How do beta-blockers affect the refractory period? and what do they prevent?

Answer 20

increase the refractory period of the AV node and prevent recurrent attacks of supraventricular tachycardias

Question 21

Examples of class 2 antidyrhtymic drugs

Answer 21

Sotalol, bisoprolol, atenolol

Question 22

Clinical uses of class 2 anti-dysrhythmic drugs

Answer 22

reduce mortality following MI

Prevent recurrence of tachycardias provoked by increase sympathetic activity

Question 23

What is the action of class 3 anti-dysrhythmic drugs?

Answer 23

potassium channel blockers - prolongs the cardiac AP by prolonging the refractory period

Question 24

What is amiodarone used to treat?

Answer 24

tachycardia associated with Wolff-Parkinson-White syndrome

supraventircular and ventricular tachycarrhytmias

Question 25

What is WPW syndrome?

Answer 25

heart condition featuring episodes of an abnoramlly fast heart rate

Question 26

What is class 4 of antidysrhtymic drugs?

Answer 26

Calcium channel blocker

Verapamil and diltiazem

Question 27

What is the action of CCBs?

Answer 27

Blocks cardiac voltage gated calcium channels

Slows conduction through the SA and AV nodes where the conduction of the AP relied on the slow calcium currents

Shorten the plateau of the cardiac AP and reduce the force of contraction of the heart

Question 28

Clinical uses of class 4 drugs

Answer 28

• Prevent recurrence of SVTs
• reduce ventricular rate when there is atrial fibrillation provided they dont have WPW syndrome
• Ineffective and dangerous in ventricular dysrhytmias

Question 29

What is the difference between verapamil and diltiazem?

Answer 29

more effect on smooth muscle calcium channels and has less bradycardia

Question 30

What phase does each class of drugs affect?

Answer 30

Class 1 = rapid depolarisation (phase 0)

Class 2 = pacemaker potential (phase 4) and plateau (phase 2)

Class III (and Ia) = repolarisation (phase 3)

Class IV = plateau (phase 2)

Question 31

What does adenosine have effects on?

Answer 31

breathing, cardiac and smooth muscle, vagal afferent nerves and platelets

Question 32

What is responsible for the effect on the AV node?

Answer 32

A₁ receptor

Question 33

What is adenosine used for?

Answer 33

Terminate SVTs as it decreases pacemaker activity

Question 34

What is the action of digoxin?

Answer 34

Increase vagal efferent activity to the heart

Reduces sinoatrial firing rate and reduces condutcion volecity of electrical impulses throuigh the AV node