Anti-Arrhythmic Drugs

Question 1

What are the different normal variations in sinus rhythm?

Answer 1

sinus tachycardia
- heart rate is too fast = more than 100bpm

sinus bradycardia
- heart rate is too slow = less than 50bpm

sinus arrhythmia

• R-R intervals vary between beats
• can have multiple P waves

Question 2

What are the two main types of arrhythmia?

Answer 2

supraventricular - originates in the atrial tissues

ventricular - originates in the ventricles

Question 3

What are the main causes of arrhythmia?

Answer 3

abnormalities in the conduction - rate, direction and path
abnormalities in automaticity - rate of discharge
damage to the SA node

Question 4

What are the three main mechanisms of abnormalities of conduction?

Answer 4

rate - slowed conduction/spread of depolarisation

direction - unidirectional block in the conducting pathway

path - anatomical abnormalities may produce an accessory pathway to allow conduction from the ventricle to the heart (can bypass some paths, results in tachycardia)

Question 5

What are the mechanisms is abnormalities of automaticity?

Answer 5

change in the rate of discharge from the SAN can result in

early after depolarisation - membrane potential oscillations during plateau/repolarisation phase

delayed after depolarisation - spontaneous depolarisation after AP depolarisation

Question 6

What is ectopic focus? What is its effects?

Answer 6

ectopic focus are abnormal pacemaker sites outside of the SAN
- can lead to dys-synchronisation of the heart beat = due to premature beats outside of the SAN function

Question 7

What are the factors affecting choice of pharmacological treatment?

Answer 7

identification of the cause of the arrhythmia

identification of the site within the heart that is the initiator of the arrhythmia

Question 8

What are the different classes of anti-arrhythmic drugs?

Answer 8

Class II - beta blockers = affect membrane potential
Class I - sodium channel blockers = affect depolarisation
Class IV - calcium channel antagonists = affect the plateau
Class III - potassium channel blockers = affect repolarisation

adenosine
digoxin

Question 9

What is Class I of the anti-arrhythmic drugs?

Answer 9

sodium channel blockers

Ia - treats ventricular dysrhythmia, atrial fibrillation = quinidine, procainamide

Ib - treats ventricular tachycardia and fibrillation, digitalis induced arrhythmia = lignocaine, tocainide

Ic - treats resistant ventricular tachycardia, paroxysmal atrial fibrillation = flecainide

Question 10

What is Class II of anti-arrhythmic drugs?

Answer 10

beta blockers - atenolol, propranolol

blocks the effects of catecholamines (adrenaline/noradrenaline) at the beta-1 adrenoceptors
- decreases sympathetic activity

decreases rate of automaticity - less firing from the SAN
prolongs refractoriness - prolongs depolarisation

treats supraventricular tachycardia

Question 11

What is Class III of the anti-arrhythmic drugs?

Answer 11

potassium channel blockers - bretylium, sotalol, amiodarone

prolongs the refractory period

prevents delayed after depolarisations (occur after phase 3)

treats Wolff-Parkinson White Syndrome (accessory pathway bypasses the AVN resulting in fast HR)

Question 12

What is Class IV of the anti-arrhythmic drugs?

Answer 12

calcium channel antagonists

• verapamil, diltiazem
• nifedipine and dihydropyridine derivatives are only used in hypertension as they have no anti-arrhythmic effects

treats supraventricular arrhythmia

Question 13

How does adenosine act?

Answer 13

acts on receptors on the AV node

has negative chronotropic and dromotropic effects

• chronotropic = reduces heart rate
• dromotropic = reduces conduction velocity

decreases AP duration

• prolongs the PR interval = holds the impulse at the AVN
• transient complete AV block = slows impulse

Question 14

What are the side effects of adenosine?

Answer 14

flushing 
dyspnoea - shortness of breath
bronchospasm = is contraindicated in asthmatics 
vomiting 
headaches
characteristic feeling of impending doom

Question 15

How does digoxin act?

Answer 15

inhibits the Na/K ATPase pump

• reversible inhibition
• increases force of contraction as intracellular sodium increases

AVN inhibition

• has vagomimetic effects = stimulates the parasympathetic nervous system by increasing vagal activity
• slows conduction of electrical impulses at the AVN therefore decreasing heart rate

treats atrial flutter, atrial fibrillation and heart failure

Question 16

What are the effects of digoxin toxicity?

Answer 16

increased frequency of ventricular ectopics
paroxysmal atrial tachycardia with AV block
marked ST segment depression - ischaemia
can cause ventricular tachycardia or ventricular fibrillation