Introduction to Mechanisms of arrhythmias and anti-arrhythmic drugs Flashcards Preview

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Flashcards in Introduction to Mechanisms of arrhythmias and anti-arrhythmic drugs Deck (32)
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1

What are arrhythmias?

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

2

How can arrhythmias be clinically described?

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

3

What do alterations in impulse formation involve?

Changes in automaticity Triggered activity

4

Abnormalities in impulse conduction arise from?

-Re-entry -Conduction block -Accessory tracts

5

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

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

6

What is the most dominant pacemaking component?

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

7

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

Overdrive suppression

8

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

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

9

Altered automaticity may be?

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

10

When may loss of overdrive suppression occur?

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

11

What is afterdepolarization?

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

12

2 types of after depolarization?

EADS- early afterpolarization DADS- delayed afterpolarisation

13

What might repeated afterpolarizations of either type cause?

arrhythmia

14

When do EADs occur?

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

15

When are EADs most likley to occur?

When HR is slow

16

Where do EADs most often occur?

In purkinje fibers

17

What are EADs associated with?

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

18

When an EAD is sustained this can lead to?

arrhythmia- torsades de pointes (life threatening)

19

Explain re-entry as a defect in impulse conduction?

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

20

Diagram showing re-entry?

Contains the whole slide

21

Types of conduction block?

May be partial (incomplete) or complete

22

Partial Block?

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

23

Explain secondary degree AV block?

Intermitant block

Tissue conducts some bimpulses but not others

24

How many types of secondary block? Describe them

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

25

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

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 

26

What does third degree AV block manifest as?

Bradychardia 

Low cardiac ouput 

27

What is an accessory tract pathway?

Some people have electrical pathways in parallel to the AV node 

28

Common accessory tract pathway?

Bundle of Kent 

29

What happens when a patient has an accessory pathway?

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 

30

What do anti-arrhythmic drugs do?

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