Treatment of dysrhythmias

Question 1

The spontaneous electrical discharge of the SAN is from the combined effect of what?

Answer 1

• Decrease in potassium outflow
• Funny sodium current
• Slow inward calcium current

Question 2

What could dysrhythmias be due to and how can they be classified?

Answer 2

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

Broadly classified as:

• Atrial (supraventricular)
• Junctional (associated with AVN)
• Ventricular
• Tachycardia/bradycardia

Question 3

What four broad categories of event can dysrhythmias be due to?

Answer 3

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

Question 4

List the classifications of anti-dysrhythmic drugs?

Answer 4

1a - sodium channel blockers (all class 1) - disopyramide
1b - lignocaine
1c - flecainide
2- BB - sotalol
3 - potassium channel blockers - amiodarone
4 - CCBs - verapamil

Unclassified - adenosine/dig

Question 5

How do class 1 drugs work?

Answer 5

Inhibit AP propagation and they reduce the rate of cardiac depolarisation during phase 0
Class subdivisions based on properties of drugs in binding to sodium channels in various states such as open, refractory and resting
- These drugs bind to the open and refractory states of channels and so viewed as use-dependent - work more effectively if high activity and so are more effective against abnormal high frequency activity and not so much against normal beating rates

Question 6

What are clinical uses of class 1 drugs?

Answer 6

1a - disopyramide (resembles quinidine) - vent dysrhythmias, prevention of recurrent AF triggered by vagal over activity

1b - lignocaine (IV) - tx and prevention of vent tachy and fibrillation during and immediately after MI

1c - flecainide - suppresses vent ectopic beats. Prevents paroxysmal AF and recurrent tachy associated with abnormal conducting pathways

Question 7

How do class 2 drugs work and what is their clinical use?

Answer 7

BB’s block beta-1 receptors of heart and decrease CO, increases rate of depolarisation of pacemaker cells so blocking them decreases this, also enhances calcium entry in phase 2 of cardiac AP so blocking reduces this
Enhance the refractory period of AVN so prevent recurrent attacks of supravent tachy
Basically increased symp drive and influence tend to promote dysrhythmias and so reducing influence will slow heart and decrease their occurrence

Sotalol, bisoprolol and atenolol reduce mortality post-MI and prevent recurrence of tachy provoked by increased symp activity

Question 8

How do class 3 drugs work and what is their clinical use?

Answer 8

Amiodarone prolongs cardiac AP by prolonging refractory period
Used for tachycardia associated with the Wolff-Parkinson-White syndrome - features episodes of an abnormally fast HR. Episodes can lest for seconds-days. They may occur regularly or just once in a while. The combination of WPW syndrome and AF can be life-threatening
Also effective in many other supraventricular and ventricular tachycardias.

Sotalol combines class 3 with class 2 actions - used in supravent dysrhythmias and suppresses vent ectopic beats and short runs of vent tachy

Question 9

How do class 4 drugs work and what are the clinical uses?

Answer 9

Verapamil and diltiazem block cardiac VG L-type calcium channels
They slow conduction through the SAN and AVN where the conduction of the Ap relies on the slow calcium currents
They shorten the plateau the cardiac AP and reduce the force of contraction of heart

Used to prevent recurrence of SVTs and to reduce the vent rate in patients with AF provided they don’t have WPW syndrome. It is ineffective and dangerous in vent dysrhythmias

Diltiazem has more effect on SM calcium channels than verapamil and has less bradycardia

Question 10

Adenosine

Answer 10

a1 receptor responsible for effect on AVN
These receptors are linked to same cardiac potassium channels that are activated by ACh and so hyperpolarises cardiac conducting tissue and slows HR, decreases pacemaker activity

Used to terminate SVTs

Question 11

Digoxin

Answer 11

Increase vagal efferent activity to heart
parasympathetic action reduces SAN firing rate (decreases HR) and reduces conduction velocity of electrical impulses through the AVN

Toxic concentrations disturb sinus rhythm. Inhibition of sodium/potassium pump causes depolarisation - ectopic beats