Treatment of Arrhythmias

Question 1

Describe the pacemaker potential in cardiac tissue

Answer 1

It is the slow depolarisation that occurs between two depolarisation events.

Question 2

Describe the underlying physiology of arrhythmias and what this may be caused by

Answer 2

It is conditions were co-ordinated sequence of electrical activity is disrupted. Could be due to changes in cardiac cells, conduction of the impulse through heard or a combo of these.

Question 3

Describe the classification of arrhythmias

Answer 3

Artial (supreventricuclar), Junctional (AV node) or ventricular. Then are they tachycardia or bradycardias.

Question 4

What are the four categories of events that can cause arrhythmias

Answer 4

• Ectopic pacemaker activity (electrical activity from cells that should be generating pacemaker)
• Delayed after-depolarisation
• Circus re-entry
• Heart block

(watch youtube vids explaining)

Question 5

What are the classes of antidysrhythmic drugs and give an example of each

Answer 5

1a - sodium channel blockers (SCB) eg, Disopyramide
1b - SCB, eg, Lignocaine
1c - SCB, eg, Flecainide
2 - B-adrenoceptor blocker, eg, Sotalol,
3 - Potassium channel blockers eg, amiodarone
4 - Calcium channel blocker, eg, Verapamil
Unclassified - Adenosine and digoxin

Question 6

Describe the mechanism of Class 1

Answer 6

Mechanism - Inhibit action potential propagation and the reduce rate of cardiac depolarisation during phase 0.

Question 7

How are the subdivisions of class 1 drugs determined?

Answer 7

Its based on their properties in binding to the sodium channels in their various states eg, open, refractory and resting.

Question 8

Why are the class 1 drugs viewed as use-dependant

Answer 8

As they bind to open and refractory states. So it means they work more effectively if there is high activity so more effective against abnormal high frequency activity not normal beating rates.

Question 9

Describe the clinical used of class 1 antidysrhythmic drugs

Answer 9

1a - Ventricular arrhythmias and prevention of recurrent AF
1b - Treatment and prevention of VT and fibrillation in MI
1c. Supress ventricular ectopic beats and prevents paroxysmal AF and recurrent tachycardias

Question 10

Describe what occurs with beta 1 adrenoceptor activation

Answer 10

• Increases rate of depolarisation of pacemaker cells.

- Enhances activity of calcium entry in phase 2 of cardiac action potential

Question 11

Describe the mechanism of Beta 1 adrenoceptor blockers

Answer 11

• Decreases rate of depolarisation of pacemaker cells.
• Prevents enhancement of calcium entry.
• Increase refractory period of the AV node, preventing supraventricular attacks of tachycardia.

Question 12

Name examples and uses of beta-blockers

Answer 12

Sotalol, atenolol. Reduce the mortality following MIs to and prevent recurrence of tachycardia provoked by increased sympathetic activity.

Question 13

Name and example of a class 3 drug and its mechanism

Answer 13

Amiodarone - Prolongs the cardiac action potential by prolonging refractory period

Question 14

What are the clinical uses of class 3 drugs?

Answer 14

Treat the tachycardia associated with Wolff-Parkinson-White syndrome (episodes of tachycardia) and can be effective in other atrial/ventricular tachycardias. Sotalol combines the activity of class 3 with class 2 drugs.

Question 15

Name examples of class 4 drugs and their mechanism

Answer 15

Verapamil and Diltiazem. They block voltage gated L-type calcium channels. In cardiac nodal tissue this slows conduction through SA and AV nodes. It also shortens the plateau of the cardiac AP and reduce force of contraction

Question 16

What are the clinical uses of class 4 drugs?

Answer 16

Used to prevent recurrent supraventricular tachycardias and reduce ventricular rate in AF. However ineffective and dangerous ventricular arrhythmias.

Question 17

Name the two unclassified drugs

Answer 17

Adenosine and Digoxin

Question 18

What is the mechanism and clinical use of adenosine

Answer 18

Binds to A1 receptors which is responsible for effect on AV node. These receptors are linked to cardiac potassium channels so it hyperpolarises cardiac conduction tissue and slows the HR, decreases pacemaker activity. Clinically it is used to terminate SVTs

Question 19

Describe the mechanism of Digoxin

Answer 19

Increases vagal efferent activity to the heart, this parasympathetic action reduces SA firing rate, decreasing HR and reduces conduction velocity of electrical impulses through AV node.

Question 20

What occurs with toxic concentrations of digoxin?

Answer 20

It disturbs sinus rhythm due to inhibition of the sodium-potassium ATPase pump. This causes depolarisation and ectopic beats.