Introduction to Mechanisms of arrhythmias and anti-arrhythmic drugs Flashcards
What are arrhythmias?
Are disturbances of heart rate, or rhythm (regularity of beats) – can be caused by changes in impulse formation, or impulse conduction
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
What do alterations in impulse formation involve?
Changes in automaticity Triggered activity
Abnormalities in impulse conduction arise from?
-Re-entry -Conduction block -Accessory tracts
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
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)
What is it known as when the SA node is dominant over other latent pacemakers?
Overdrive suppression
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
Altered automaticity may be?
Physiological -Pathophysiological- latent pacemakers take over SA node and there is loss of overdrive suppression
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
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
2 types of after depolarization?
EADS- early afterpolarization DADS- delayed afterpolarisation
What might repeated afterpolarizations of either type cause?
arrhythmia
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
When are EADs most likley to occur?
When HR is slow
Where do EADs most often occur?
In purkinje fibers
What are EADs associated with?
Prolongation of the AP and drugs(sotalol) prolonging the QT interval
When an EAD is sustained this can lead to?
arrhythmia- torsades de pointes (life threatening)
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
Diagram showing re-entry?
Contains the whole slide
Types of conduction block?
May be partial (incomplete) or complete
Partial Block?
Slowed conduction= tissue conducts all impulses just more slowly than usual eg first degree AV block
Explain secondary degree AV block?
Intermitant block
Tissue conducts some bimpulses but not others
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
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
What does third degree AV block manifest as?
Bradychardia
Low cardiac ouput
What is an accessory tract pathway?
Some people have electrical pathways in parallel to the AV node
Common accessory tract pathway?
Bundle of Kent
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
What do anti-arrhythmic drugs do?
Generally inhibit specific ion channels (or activate/block specific receptors) with the intention of suppressing abnormal electrical activity
What is the Vaughn Williams classification?
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
