Antidysrhymic drugs Lecture 9

Question 1

What is dysrhythmias?

Answer 1

Disorders of rate or rhythm of the heart

Can be atrial, junctional or ventricular

Causes Tachycardia or bradycardia

Drugs can affect heart function by direct methods (affecting force of contraction and rate/rhythm)

Question 2

What is automaticity

Answer 2

• Ectopic pacemakers i.e. when develop more rapid pacemaker potential than the SA node
• Only an issue when it allows for re-entry to occur

Question 3

What is re-entry?

Answer 3

• Waves of electrical activity in the middle reach each other and come to a stop
• Causes an ordered progression of the depolarisation wave
• However damage can render some of the cardiac muscle different in its electrical properties
• Can cause a uni-directional block, which allows current to flow back and re-excite the tissue

Question 4

What is accessory pathway re-entry?

Answer 4

-Re-entry can occur at the AV node but unlikely as this node only lets through signals at certain points

Get transient depolarisations during repolarisation resulting in AP outside of the SA node control

Wolff-Parkinson-White syndrome

• Signals are let through more points in the AV node
• The signal can re-enter and re-excite the atria before it is ready to be excited again
• It can lead to signals getting to the ventricles before the normal AV node delay causing early excitation
• THis changes the QRS complex (as ventricles depolarise over a longer period of time)

Question 5

What is a heart block?

Answer 5

• Problem with waves of depolarisation not getting through the AV node
• If this progresses pathologically you can get second-degree AV block, with much more severe delay between APs
• Third degree leads to far more failures than APs

Question 6

Describe class 1 antiarhythmic drugs

Answer 6

Lignocaine, flecainide, lidocaine

Voltage-gated Na channel blockers

-Major impact on phase 0, reducing excitability of cardiomyocytes

Question 7

Describe class 2 antiarhythmic drugs

Answer 7

Beta blockers - Propranolol

Decreases sympathetic effects in the heart

Decreases the slope of the pacemaker potential

Increases AV conduction time

Question 8

Describe class 3 antiarhythmic drugs

Answer 8

Amiodarone (Ca), sotalol (beta blocker function)

Prolongs the cardiac action potential Via K channel blockage

Question 9

Describe class 4 antiarhythmic drugs

Answer 9

Verapamil, diltiazem

L type Ca channel blockers - only works on L-type in the heart and not vasculature.

Affects AV node by decreasing activty

Question 10

Describe adenosine as an antiarhythmic drug

Answer 10

Non-classified

Adenosine

Binding of adenosine to receptors in SA/AV nodes causes:

• Opening of K+ channels
• Closing of Ca2+ channels
• Depresses AV node activity, increasing refractory period

Question 11

Describe digoxin as an antiarhythmic

Answer 11

Cardiac glycosides eg digoxin

Increases vagal activity to the heart, decreases AV conduction rate and dcreases ventricular rate

Therapeutic considerations for the drugs:

Antidysrhythmics can cause dysrhythmia if given at wrong dose or wrong type of drug.