Cardiac Arrhythmias Flashcards by Jasmine Aikman

2 categories of electrical dysfunction in the heart

defect in impulse formation or conduction

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Defects in impulse formation causes of arrhythmias

altered automaticity - escapes, ectopics

triggered activity - early + delayed afterdepolarisations

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defects in impulse conduction causes of arrhythmias

re-entry, conduction block, accessory tracts

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Escape beat/rhythm occurs when

SAN impulse is pathologically low frequency or its conduction is impaired and latent pacemaker causes a beat/s

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ectopic beat/rhythm occurs when

latent pacemaker fires faster than SAN

due to ischaemia, hypokalaemia, ^sympathetics and fibre stretch

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early afterdepolarisation occurs in ____

ass. with

Purkinjes(often during Phase 2/3) can be self perpetuating

prolongation of AP and sotalol (prolonging QT drugs)

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delayed afterdepolarisation caused by ___

ass. with __

transient Na influx

Ca2+ overload due to catecholamines, digoxin, HF

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re-entry occurs when ___

damage of an area causes unidirectional block and so retrograde current not cancelled out and = circus rhythm

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First degree heart block =

PR interval prolonged

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Mobitz type 1 2nd degree heart block

PR gradually increases until QRS dropped

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2nd degree Mobitz Type 2 heart block

PR interval constant but every nth QRS iis dropped

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complete/ 3rd degree heart block

atria and ventricles beat independently

Purkinje pacemaker is slow and unreliable = bradycardia and low CO

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accessory pathway that bypasses AVN =

bundle of Kent

may => tachyarrhythmias

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Atrial arrhythmias =

AF
atrial flutter
ectopic atrial tachy
sinus brady
sinus pauses

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AVN arrhythmias =

AVN re-entry
accessory pathway
AVN block

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Ventricular arrhythmias =

PVC (premature ventricular complex)
VT
VF
asystole

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6 causes of cardiac arrhythmias:

anatomical - congenital, accessory pathways
autonomic - symp/vagal tone
metabolic - hypoxic myocardium (COPD, PE) iscahemic myocardium (MI, angina), electrolyte imbalances
drugs - esp if block K+ channels
inflammation - viral myocarditis
genetic

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Causes of altered automaticity:

ischaemia, catecholamines

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hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia _____ the Phase 4 pacemaker potential slope in nodal cells

increase

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Hypokalaemia cause the pakemaker potential slope in nodal cells to ___
____ ectopics
_____ repolarisation

increases slope
increases ectopics
prolongs repolarisation

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Hypothermia and hyperkalaemia ___ the Phase 4 pacemaker potential slope in nodal cells

decrease

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Hyperkalaemia _____ conduction in nodal cells

slows

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Pause dependant triggered activity causes a _____ in phase ____
= _____ after-depolarisation

after depolarisation in phase 3

early after-depolarisation

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Catechol dependant triggered activity causes a ____ in phase ____
= _____ after-depolarisation

afterdepolarisation in late phase 3 / 4

delayed after-depolarisation

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Triggered activity is behind ____ toxicity, _____ in long QT syndrome and ____kalaemia

digoxin toxicity torsades de pointes in long QT hypokalaemia

conditions that ___ conduction velocity or ____ refractory period promote functional block =>

depress conduction velocity / shorten refractory period | re-entry

eg.s of re-entry arrhythmia causes

WPW - accessory pathways previous MI AVN re-entry

Electrophysiological (EP) study =

induce arrhythmia and study it

24hr Holt ECG is used to diagnose

paroxysmal arrhythmias

used to look for a structural cause behind arrhythmias =

echocardiogram

Use an exercise ECG to see if there is ___

exercise related arrhythmia | myocardial ischaemia eg. Stable angina

Treatment for atrial ectopics =

none - usually asymptomatic / palpitations can give β-blockers if needed avoid stimulants

A bp of less than ___ indicates sinus bradycardia common in _____ STEMI Treatment =

60bpm inferior acute = atropine haemodynamically unstable = pacing

A bp of more than ___ indicates sinus tachycardia | Treatment =

100bpm | β-blockers

Management of acute SVT 1st line = 2nd line =

``` 1st = vagal manoeuvre -> carotid massage (not if stroke risk) 2nd = IV adenosine / verapamil ```

carotid massage is not done for acute SVT if ____

at risk of stroke

Management of chronic SVT:

avoid stimulants β-blockers/verapamil radiofrequency ablation - must have no anti-arrhythmics for 3-5 days before

Anti-arrhythmics that can cause heart block

β-blockers | CCB - verapamil

Acquired complete heart block seen in the elderly due to idiopathic fibrosis and calcification of the conduction system

Lenegre-Lev disease

Treatment for 1st degree heart block

none

Treatment for 2nd degree heart block

dual chamber pacemaker (RA + RV)

Treatment for complete heart block

Dual chamber pacemaker (RA and RV)

RA pacemakers are used in ____

SAN disease with normal AVN

RV pacemakers are used in ____

AF with slow ventricular rate

Transcutaneous pacemakers are given in ____ scenarios until a ____ can be placed

acute - emergencies - painful to place | transvenous pacemaker

PVC - premature ventricular complex are usually ____ but may get ____ as bp drops after beat

asymptomatic brief dizziness If is worse on exertion investigate further

Common causes of PVC -

structural/ischaemic HD LV hypertrophy HF

Treatment of PVC - premature ventricular complexes

β-blockers

broad complex tachycardia are associated with ___ or ____

significant heart disease - coronary artery disease/MI | cardiomyopathy/inherited - eg. Brugada

Treatment of VF:

defibrillate cardiopulmonary resuscitation ICD dual chamber

Treatment of acute VT:

``` DC cardioversion (unstable) anti-arrhythmics - amiodarone / lidocaine (stable) if non-confirmed diagnosis - adenosine ```

In VT _____ must be corrected if are the cause

electrolytes

chronic VT treatment:

ICD - dual chambers (life-threatening) | β-blockers

anatomically AF usually arise from ____

near pulmonary veins in LA

Paroxysmal AF =

Persistent AF =

> 48hrs | can be cardioverted to normal (but doesnt occur spontaneously)

Permanent/chronic AF =

not able to be cardioverted by treatment

Sick sinus syndrome is caused by ___ | causes ____

dysfunction of the SAN causing arrhythmias eg. AF | tachy - brady

Causes of AF:

``` alcohol congenital heart surgery COPD pneumonia pericarditis vagal causes ```

lone/idiopathic AF occurs in ___ of HD w ___ ventricular dysfunction

absence of HD | no ventricular dysfunction

Treatment to terminate AF (rhythm control):

DC cardioversion - 90% effective Flecainide/sotalol/amiodarone - 30% effective β-blockers and CCB can stop VT developing

In AF ECG: HR = ____ Rhythm = ___ Defining characteristic = ___

>300bpm irregularly irregular no p waves - fine f waves

If AF with VT then treat with ___

pacemaker | to stop pseudo-regularisation => coronary hypoperfusion

Treatment for rate control of AF (slow AVN conduction + stop VT developing)

Digoxin, β-blockers and CCB - diltiazem and verapamil

Treatment to chronically stop AF =

anti-arrhythmics | catheter ablation - of near pulm veins/AVN

Given in all cases of AF (except valvular):

anti-coagulation

Torsades de Pointes HR= ECG features = causes=

200-250bpm polymorphic, wide QRS, long QT hypokalaemia, AP prolonged (by drugs), renal impairment (increases drug levels)

Score used to decide whether or not to give anti-coagulants by risk of thrombo-embolism:

CHA2DS2 - VASc | or if have mitral valve disease give anticoag.s

CHA2DS2 - VASc score

``` CCF/LV dysfunction Hypertension Age >=75yo 2 points Diabetes mellitus Stroke 2 points Vascular disease Age 65-74yo Sex = Female ```

Score used to measure haemorrhage risk:

HASBLED

HASBLED factors = | more likely to haemorrhage

``` Hypertension Abnormal renal/liver function Stroke Bleeding Labile INRs Elderly >65yo Drug/alcohol ```

Rapid regular form of ren-entrant atrial tachycardia

Atrial flutter

Usually paroxysmal, caused by macro-re-entry circuit in RA:

atrial flutter

Atrial flutter if chronic can lead to

ECG features for atrial flutter

saw tooth F wave | 2V to 1A beat - so Ventricular rate is slower

Treatment for atrial flutter if doesn't spontaneously resolve:

RF ablation (80-90%) Ia, Ic, III anti-arrhythmics to restor sinus rhythm/slow vent. rate cardioversion warfarin

``` Congenital Long QT syndrome Brugada Syndrome Catecholaminergic Polymorphic Ventricular tachycardia (CPVT) Short QT syndrome Progressive familial conduction disease Familial AF Familial WPW ALL = ```

inherited arrhythmogenic channelopathies

KVLQT1 (K+ channel) defect is main cause of

Long QT syndrome

Long QT causes ___ triggered by adrenergic stimulation

torsades de pointes

Autosomal dominant isolated LQT syndrome =

Romano-Ward syndrome

Autosomal dominant LQT syndrome with extra-cardiac features (2)

``` Andersen-Tawil syndrome (muscle weakness and abnormal features) Timothy syndrome (webbed digits) ```

Autosomal recessive LQT w deafness

Jervell-Lange-Neilson syndrome

___ repolarisating current OR ____ depolarising current increase AP duration

decreasing repol | increasing depol

Increase in the Na+ current in myocytes is a ___ form of LQTS and is 90% penetrant for ____

rare | sudden cardiac death

Brugada syndrome is autosomal ___ 8x more likely in ___ Have a risk of _+_+__

dominant males torsades de pointes, VF, AF

Main channels affected in Brugada syndrome

Na+ (SCNSA) | Ca2+ (CaCN1Ac)

ECG in Brugada syndrome shows: | may only be seen with provocative testing with ___/___ as block Na+ channels

STE and RBBB in V1-3 | flecainide/ajmaline

In Brugada syndrome avoid:

anti-arrhythmics, psychotropics, analgesics, anaestesia

Catecholaminergic polymorphic VT (CPVT) is ___ if inherited due to ___ mutation ___ if inherited due to ___ mutation

autosomal dom - ryanodine (ryR2) receptor | autosomal recessive - cardiac calsequestrin gene (CASQ2)

In CPVT treatment =

avoid exercise β-blockers ICD if necessary (flecainide if can't)

Atrial flutter has regular/irregular QRS complexes

regular - commonly 2:1

Drugs that cause a lengthened QT

``` sotalol quinidine antihistamines macrolides amiodarone phenothiazines tricyclics ```

Low __,___+___ (electrolytes) causes lengthened QT

K+ Ca+ Mg2+

ECG pattern seen in RBBB

MaRRoW M in V1 W in V6

ECG pattern seen in LBBB

WiLLiaM W in V1 M in V6

Causes of RBBB

normal variant PE cor pulmonale

Causes of LBBB

IHD hypertension cardiomyopathy idiopathic fibrosis