Introduction to Mechanisms of arrhythmias and anti-arrhythmic drugs

Question 1

What are arrhythmias?

Answer 1

Are disturbances of heart rate, or rhythm (regularity of beats) – can be caused by changes in impulse formation, or impulse conduction

Question 2

How can arrhythmias be clinically described?

Answer 2

Arrhythmias are clinically described in terms of -rate bradycardias (HR ˂ 60 b.p.m. during the day; ˂ 50 b.p.m. at night) tachycardias (HR ˃ 100 b.p.m.) -site of origin supraventricular (atria and the AV node) ventricular

Question 3

What do alterations in impulse formation involve?

Answer 3

Changes in automaticity Triggered activity

Question 4

Abnormalities in impulse conduction arise from?

Answer 4

-Re-entry -Conduction block -Accessory tracts

Question 5

Do components of the cardiac conduction system (apart from SA node) possess automaticity?

Answer 5

Yes. They demonstrate a (slower) spontaneous phase 4 depolarization and thus possess automaticity

Question 6

What is the most dominant pacemaking component?

Answer 6

SA node It is normally highest - 70-80bpm dominant over latent pacemakers (AV node and purkinje fibers) (50-60 and 70-80bpm)

Question 7

What is it known as when the SA node is dominant over other latent pacemakers?

Answer 7

Overdrive suppression

Question 8

What must happen in order for SA node to exert its normal control of rate and rhythm?

Answer 8

Must discharge action potentials at a frequency greater than that of any other heart structure

Question 9

Altered automaticity may be?

Answer 9

Physiological -Pathophysiological- latent pacemakers take over SA node and there is loss of overdrive suppression

Question 10

When may loss of overdrive suppression occur?

Answer 10

If the SA node firing frequency is pathologically low or if conduction of impulse from SA node is impaired –a latent pacemaker may initiate an impulse that generates an escape beat- a run of such impulses may give rise to an escape rhythm- series of escape beats -May occur if a latent pacemaker fires at an intrinsic rate faster than the SA node rate- latent pacemaker fires ecoptic beat or ecoptic rhythm these can result in ischaemia, hypokalaemia, increased sympathetic activity -Can occur in response to tissue damage - post MI

Question 11

What is afterdepolarization?

Answer 11

A normal action potential may trigger abnormal oscillations in membrane potential termed afterdepolarizations (ADs) that occur during, or after, repolarization ADs of amplitude sufficient to reach threshold cause premature action potentials and beats

Question 12

2 types of after depolarization?

Answer 12

EADS- early afterpolarization DADS- delayed afterpolarisation

Question 13

What might repeated afterpolarizations of either type cause?

Answer 13

arrhythmia

Question 14

When do EADs occur?

Answer 14

Occur during the inciting AP within -Phase 2 (terminal plateau) mediated by Ca++ channels- when Na+ channels are still inactivated - Phase 3 (repolarization) - mediated by Na+ channels - when partial recovery of Na+ channels from inactivation has occured

Question 15

When are EADs most likley to occur?

Answer 15

When HR is slow

Question 16

Where do EADs most often occur?

Answer 16

In purkinje fibers

Question 17

What are EADs associated with?

Answer 17

Prolongation of the AP and drugs(sotalol) prolonging the QT interval

Question 18

When an EAD is sustained this can lead to?

Answer 18

arrhythmia- torsades de pointes (life threatening)

Question 19

Explain re-entry as a defect in impulse conduction?

Answer 19

Self sustaining circuit (may be 2 parallel conducting pathways) stimulates an area of myocardium repeatedly/rapidly. -Re-entrant circuit requires uni-directional block= anterograde conduction prohibited, retrograde conduction allowed, slowed retrograde conduction velocity

Question 20

Diagram showing re-entry?

Answer 20

Contains the whole slide

Question 21

Types of conduction block?

Answer 21

May be partial (incomplete) or complete

Question 22

Partial Block?

Answer 22

Slowed conduction= tissue conducts all impulses just more slowly than usual eg first degree AV block

Question 23

Explain secondary degree AV block?

Answer 23

Intermitant block

Tissue conducts some bimpulses but not others

Question 24

How many types of secondary block? Describe them

Answer 24

2

Mobitz type 1- PR interval gradually increases from cycle to cycle until AV node failscompletely and a ventricular beat is missed

Monitz type 2- PR interval is constant but every nth ventricular depolarization is missing

Question 25

Describe complete block and give the other term it can be reffered to as?

Answer 25

Third degree AV block

No impulses are conducted through the affected area

Atria nd ventricles beat independantly

Ventricular pacemaker is now th epurkinje fibers - fire relatively slow and unreliablely

Question 26

What does third degree AV block manifest as?

Answer 26

Bradychardia

Low cardiac ouput

Question 27

What is an accessory tract pathway?

Answer 27

Some people have electrical pathways in parallel to the AV node

Question 28

Common accessory tract pathway?

Answer 28

Bundle of Kent

Question 29

What happens when a patient has an accessory pathway?

Answer 29

Impulse is sent through bundle of kent more quickly than that through the AV node

Ventricles recieve impulse from both the normal and accessory pathways

This can set up a condition for a re-entrant loop - predisposing to tachyarrhythmias

Question 30

What do anti-arrhythmic drugs do?

Answer 30

Generally inhibit specific ion channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity

Question 31

What is the Vaughn Williams classification?

Answer 31

How anti-arrhythmic drugs are classified pharmacologically based upo their effects upon cardiac APs

Classifies 4 classes with class divided into a,b and c