Cardiac Arrhythmias Flashcards
2 categories of electrical dysfunction in the heart
defect in impulse formation or conduction
Defects in impulse formation causes of arrhythmias
altered automaticity - escapes, ectopics
triggered activity - early + delayed afterdepolarisations
defects in impulse conduction causes of arrhythmias
re-entry, conduction block, accessory tracts
Escape beat/rhythm occurs when
SAN impulse is pathologically low frequency or its conduction is impaired and latent pacemaker causes a beat/s
ectopic beat/rhythm occurs when
latent pacemaker fires faster than SAN
due to ischaemia, hypokalaemia, ^sympathetics and fibre stretch
early afterdepolarisation occurs in ____
ass. with
Purkinjes(often during Phase 2/3) can be self perpetuating
prolongation of AP and sotalol (prolonging QT drugs)
delayed afterdepolarisation caused by ___
ass. with __
transient Na influx
Ca2+ overload due to catecholamines, digoxin, HF
re-entry occurs when ___
damage of an area causes unidirectional block and so retrograde current not cancelled out and = circus rhythm
First degree heart block =
PR interval prolonged
Mobitz type 1 2nd degree heart block
PR gradually increases until QRS dropped
2nd degree Mobitz Type 2 heart block
PR interval constant but every nth QRS iis dropped
complete/ 3rd degree heart block
atria and ventricles beat independently
Purkinje pacemaker is slow and unreliable = bradycardia and low CO
accessory pathway that bypasses AVN =
bundle of Kent
may => tachyarrhythmias
Atrial arrhythmias =
AF atrial flutter ectopic atrial tachy sinus brady sinus pauses
AVN arrhythmias =
AVN re-entry
accessory pathway
AVN block
Ventricular arrhythmias =
PVC (premature ventricular complex)
VT
VF
asystole
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
Causes of altered automaticity:
ischaemia, catecholamines
hyperthermia, hypoxia, hypercapnia, cardiac dilation, hypokalaemia _____ the Phase 4 pacemaker potential slope in nodal cells
increase
Hypokalaemia cause the pakemaker potential slope in nodal cells to ___
____ ectopics
_____ repolarisation
increases slope
increases ectopics
prolongs repolarisation
Hypothermia and hyperkalaemia ___ the Phase 4 pacemaker potential slope in nodal cells
decrease
Hyperkalaemia _____ conduction in nodal cells
slows
Pause dependant triggered activity causes a _____ in phase ____
= _____ after-depolarisation
after depolarisation in phase 3
early after-depolarisation
Catechol dependant triggered activity causes a ____ in phase ____
= _____ after-depolarisation
afterdepolarisation in late phase 3 / 4
delayed after-depolarisation
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
AF
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
