Arrhythmia Flashcards

1
Q

what is overdrive suppression

A

SAN pacemaking being dominant over latent pacemakers such as AVN and purkinje fibres

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2
Q

how does SAN maintain overdrive suppression

A

discharge of AP faster than other heart structures

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3
Q

if san is low, what may a latent pacemaker due

A

create an escape beat

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4
Q

if latent pacemaker fires faster than SAN it creates a

A

ectopic rhythm

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5
Q

other cardiac myocytes may have the ability to take over pacemaking if there is?

A

tissue damage

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6
Q

what conditions cause latent pacemakers to discharge APs fast

A

ischaemia, hypokalaemia, fibre stretch, increased sympathetic activity

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7
Q

what is an EAD and what may trigger it

A

early afterdepolarisaton which occur during AP
prolongation of AP and drugs prolonging QT interval
bradycardia

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8
Q

What channels mediate EADs, where are they most frequent and what can it lead to

A

calcium channel in phase 2 and sodium in phase 3
purkinje fibres
may lead to torsades de pointes

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9
Q

what are DADs

A

delayed afterdepolarisations occurring after repolarisation

excessive CICR release from SR and sodium influx

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10
Q

where are DADs likely to occur and what may they be triggered by

A

tachycardia, increased and decreased by prolongation and shortening of AP
may be triggered by drugs increasing calcium influx or detention, catecholamines or digoxin

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11
Q

what is re-entry

A

self sustaining electrical circuit repeatedly stimulating myocardium due to lack of opposition AP to negate it

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12
Q

what is conduction block

A

slowing or failure of conduction through AVN

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13
Q

what is first degree AV block

A

slowed conduction to AVN, prolonged PR

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14
Q

what is Type 1 2nd degree AV block

A

PR increases until AV node fails and misses ventricular beat

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15
Q

what is type 2 2nd degree AV block

A

PR interval constant but every Nth ventricular depolarisation missing

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16
Q

what is 3rd degree AV block

A

independent beating of atria and ventricles

ventricular beating controlled by purkinje fibres so bradycardic

17
Q

what is the bundle of kent

A

accessory tract that is parallel to AVN and conducts faster. may form reentry loop with ventricles

18
Q

what is the vaughn williams classification

A

pharmacological classification of drug effects on cardiac AP

19
Q

what do class IA drugs do

A

act on Na channel to slow AP rise and prolong refractory period

20
Q

what do class IB drugs do

A

act on Na channel to prevent premature beats

21
Q

what do class IC drugs do

A

act on Na channel to depress conduction

22
Q

what do class II drugs do

A

beta antagonists

decrease depolarisation rate in SAN and AVN

23
Q

what do class III drugs do

A

K channels - prolong AP duration so increase refractory period

24
Q

what do class IV drugs do

A

Ca channels - slow AVN conduction and SAN conduction to decrease cardiac conduction force

25
Q

what type of tissue do class I drugs act best on

A

ischaemic tissue

26
Q

AF is most common in what demographic

A

older patients

27
Q

how can AF be treated?

A

pharmacologic cardioversion with anti-arrhythmics

DCCV

28
Q

what is paroxysmal AF

A

<48 hours
recurrent
less chance to throw clot

29
Q

what is persistent AF

A

<48 hrs
can be cardioverted to sinus rhythm
unlikely to restore itself

30
Q

what is permanent AF

A

NSR cannot be restored

31
Q

what is lone AF

A

AF with absent heart disease

disease of exclusion

32
Q

what does AF look like on ECG

A

fast atrial rate
irregular irregular rhythm
variable ventricle rate
absent p waves and f waves

33
Q

when should you anticoagulate for AF

A

with >2 cha2ds2-vas with warfarin, NOACS or DOACS

34
Q

treating AF

A

beta blockers/digoxin/verapamil/diltiazem
amiodarone/DCCV
catheter ablation

35
Q

what is atrial flutter

A

rapid and regular atrial tachycardia caused by reentry at right atrium

36
Q

can atrial flutter progress to AF

A

yes!

37
Q

first line treatment of atrial flutter

A

ablation