Arrhythmias Flashcards by Courtney Macdonald

ECG features of left bundle branch block

Wide QRS, deep S wave in V1, broad notched R wave in V6

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Features of left anterior fasicular block

Left axis deviation and Initial R wave in inferior leads

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Features of Left posterior fasicular block

Right axis deviation and initial R wave in 1 and aVL and q wave in inferior leads

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ECG features of right bundle branch block

Wide QRS, rSR in V1, deep S wave in V6

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Explain difference between two types of AV junctional re-entrant tachycardias

AVNRT- AV node is dissociated into 2 pathways which can both conduct impulses

AVRT- caused by an accessory pathway between atria and ventricles which can set up a re-entrant circuit with the AV node

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What is direction of conduction in most AVNRT tachycardias?

Antegrade via slow pathway, retrograde via fast pathway (slow-fast type = 80-90%)

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Explain reason for delta wave in sinus rhythm?

Conduction occurs via both accessory and AV nodal pathways. Accessory pathway is fast to conduct so impulse gets rapidly to ventricle (short PR and slurred upstroke) but then activation of ventricles is slow due to not being through usual conducting system. By this time the conduction has occurred through the slower AV node and ventricles get activated quickly via His-Purkinjie system so you see a normal QRS (fusion beat)

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What are the two patterns of AVRT?

Orthodromic - antegrade conduction via AV node and retrograde via accessory (narrow complex)

Antidromic - antegrade conduction via accessory pathway and retrograde via AV node (large wide complexes with delta wave)

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What are the two types of WPW?

Type A - v1 is positive, left sided accessory pathway

Type B - V1 is negative

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Differences between AVRNT and AVRT on ECG

Hard to tell, can look at p wave
In AVNRT the p wave immediately follows or I superimposed on the QRS because the circuit is short
In AVRT inverted p waves occur halfway between the QRS complexes usually superimposed on the T waves

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Features of pre-excited AF

Irregular
Different QRS morphologies - wide delta waves, normal QRS
Axis stable
Can deteriorate into VT or VF (more likely if faster rate

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Treatments for AV junctional re-entrant tachycardias

Vagal stimulation
Adenosine
Verapamil, flecainide, sotalol, disopyramide
Pacing
Cardioversion

Prevention = ablation (high success-90%)

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Lifetime risk of AF

Increases with age, lifetime = 26%

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Causes of AF

Heart disease - ischaemia, heart failure, surgery, pericarditis, valvular disease, hypertension
Extrinsic - hyperthyroid, alcohol, Obesity, sleep apnoea, extreme exercise, infection, PE
Genetic

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What makes up CHA2DS2-VASc?

C - cardiac failure
H - hypertension
A - over 75 = 2 points
D - diabetes
S - previous stroke or TIA = 2 points
V - vascular disease (MI, peripheral vascular disease, significant aortic plaque)
A - between 65-74
S- female

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Stroke risk in AF

In general 5% per year
Risk stratified
Score 2 = 2.2%, score 5 = 10%

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Difference between rate and rhythm control in AF?

Rate control is non inferior to rhythm control as per AFFIRM and RACE trials
But most rhythm control pts didn’t maintain sinus rhythm and a secondary analysis showed sinus rhythm was associated with better outcomes

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What anti coagulation is needed for cardioversion?

Safe without OAC if

Role of flecainide in AF?

Pharmacological cardioversion
Can use as “pill in pocket”
Should ideally combine with b-blocker to prevent fast ventricular rate if AF organised into atrial flutter
Use in structurally normal heart (can otherwise cause ventricular tachyarrhythmias)

Treatment of atrial flutter?

Catheter ablation (90% success)
Cardioversion
Drugs are less effective, often need higher doses and combination therapy

Causes of wide complex tachycardia

SVT with aberrancy
SVT with pre-excitation
SVT with pacemaker
SVT with rate related bundle branch block
Polymorphic VT
Monomorphic VT
Torsades de pointes
Ventricular fibrillation
Interference

Differentiating VT from wide complex tachycardia

Concordance - across chest leads, same polarity
AV dissociation - independent p waves
Capture beat - normal QRS
Fusion beat - fusion of normal QRS and wide complex
Axis - extreme axis suggests VT

ECG changes in ARVC

T wave inversion V1-V3
Epsilon wave in V1
VT has LBBB morphology

ECG changes in RVOT-VT

LBBB morphology

Right axis deviation

ECG changes in fasicular tachycardia

Most common in left posterior fasicle: RBBB morphology, Left axis deviation If left anterior fasicle (rare) get RBBB and right axis deviation

What is torsades de pointes?

Polymorphic VT that occurs in patients with prolonged QT interval Causes: drugs, genetic, metabolic , bradycardia

What are common types of long QT syndrome, what triggers the arrhythmia, and how is the ECG different?

LQT1 - potassium channel, swimming, broad T wave LQT2 - potassium channel, loud noises, menstruation and post partum, long and notched T wave LQT3 - sodium channel, occur during sleep, long isoelectric ST segment

What is Brugada syndrome and what does ECG show?

Primary electrical disorder of sodium channel ECG - down sloping ST elevation with inverted T waves in V1-V3 and partial RBBB Risk is ventricular fibrillation

Causes of diseased AV node

``` Idiopathic fibrosis Myocardial infarction Aortic valve disease Congenital Cardiac surgery Haemochromotosis ```

What is bifasicular block?

Bifasicular : 2 of 3 fascicles are blocked, most common is RBBB and left anterior fasicular block Trifasicular block: all 3 fascicles are blocked

When is a mobitz type 1 AV block not considered benign?

When it occurs in older people during the day (has similar prognosis in this setting to Mobitz type 2) Usually it is vagally mediated, occurring in sleep in young people

What is a stokes Adams attack?

Syncope due to transient asystole or ventricular tacyarrythmia Sudden loss of consciousness with no warning followed by immediate recovery

Most common gene mutation in Brugada syndrome

SCN5a - mutation in cardiac sodium channel that causes decreased intercellular sodium

What inheritance is Brugada syndrome?

Autosomal dominant

What is the difference between Brugada pattern on ECG and Brugada syndrome?

Syndrome is when you have associated symptoms

What is the significance of type 2 Brugada ECG pattern?

Not a diagnostic for brigade pattern | Can give Flecainide to see if converts to Type 1 = Brugada pattern

What are the gene mutations in LQT 1,2 + 3

``` 1 = KCNQ1 (decrease in function of K channel so K doesn't move out of cell = longer plateau phase of action potential) 2 = KCNH2 (as above) 3 = SCN5a (sodium channel mutation) ```

When do you do genetic testing for long QT?

Strong suspicion with ECG changes and symptoms Screen family members with an index patient with a proven mutation Ay symptomatic patients with significantly prolonged QT in the absence of other causes

What is the mutation in catecholaminergic VT and when does it usually present?

Presents in childhood, VT on exercise, stress or emotion | Mutation in cardiac ryanadine receptor calcium release channels

What is the inheritance of catecholaminergic polymorphic VT

Autosomal dominant

What are some indications for pacing?

Symptomatic sinus node disease High degree AV block (even if asymptomatic) Symptomatic tacy-Brady syndrome Bifasicular block with symptoms (10% will progress to complete heart block if symptoms are present) Symptomatic recurrent neurocardiogenic syncope with prominent cardio-inhibition Other symptomatic AV blocks that are not to a high degree

What are the differences between CHB due to inferior MI and anterior MI

Inferior MI - usually due to odema, often resolves, good prognosis Anterior MI - indicates large amount of ischemia and CHB is due to necrosis of conducting system, worse outcomes, often need pacing

What is a side effects of ventricular only pacing

Increased rates of AF | Increased admissions with CHF