Arrhythmias:Supraventricular and Ventricular Tachycardias

Dr Sajad Ahmed HayatConsultant Electrophysiologist

University Hospitals Coventry & WarwickshireSajad.Hayat@uhcw.nhs.uk

Disclosure

Honorarium from Sanofi and

Bayer

Why is it important?

• Tachyarrhythmias are common

• Emergency

• Anxiety

• SOME are life threatening

• Want to pass the KBA

Question

What is this tachyarrhythmia?

1. Ventricular tachycardia

2. AVNRT with aberrant conduction

3. Supraventricular tachycardia with an accessory pathway (pre-

excitation/WPW)

4. Atrial flutter with aberrant conduction

5. Don’t know

BCT differential diagnosis

• VT

• SVT with aberrant conduction

– AVNRT/AVRT/AT/Atrial flutter with BBB

• SVT with anterograde conduction over an accessory pathway

– antidromic AVRT

– pre-excited AF

VT versus SVT?

• Various electrocardiographic criteria

• Most likelihood of VT

• Safer to assume VT rather than SVT with aberrancy especially

in the acute setting

• Other strategies to differentiate

ECG features- a simple approach

• AV dissociation?

ECG features- a simple approach

• AV dissociation?

• Capture/fusion beats?

ECG features- a simple approach

• AV dissociation?

• Capture/fusion beats?

• Does it look like BBB (left or right)?

– Sharp onset, axis change in precordial leads (i.e. non-concordant)

ECG features- a simple approach

• AV dissociation?

• Capture/fusion beats?

• Does it look like BBB (left or right)?

– Sharp onset, axis change in precordial leads (i.e. non-concordant)

• Negative/positive concordance – more in keeping with VT

• AV dissociation?

• Capture/fusion beats?

• Does it look like BBB (left or right)?

– Sharp onset, axis change in precordial leads (i.e. non-concordant)

• Negative/positive concordance

• QRS very broad? >140ms if RBBB pattern or >160ms if LBBB

ECG features- a simple approach

• AV dissociation?

• Capture/fusion beats?

• Does it look like BBB (left or right)?

– Sharp onset, axis change in precordial leads (i.e. non-concordant)

• Negative/positive concordance

• QRS very broad? >140ms if RBBB pattern or >160ms if LBBB

• Unusual axis:

– North West Axis (+ve aVR, -ve inf)

– RBBB with LAD or LBBB with RAD

ECG features- a simple approach

• AV dissociation?

• Capture/fusion beats?

• Does it look like BBB (left or right)?

– Sharp onset, axis change in precordial leads (i.e. non-concordant)

– Negative/positive concordance

• QRS very broad? >140ms if RBBB pattern or >160ms if LBBB

• Unusual axis:

– North West Axis (+ve aVR, -ve inf)

– L RBBB with LAD or LBBB with RAD

• Other features?

ECG features- a simple approach

ECG features- a simple approach

Rules and more rules….

Use of adenosine

• Blocking AV node may help

• Need to use high dose

• Resus facilities available

Don’t forget the sinus rhythm ECG

• Often helpful

• BBB

• Pre-excitation

• Presence of myocardial infarction

Question

Patient is haemodynamically stable, C/O palpitations. What would you like to do

next?

1. Sedate & DC cardiovert

2. Give amiodarone

3. Give adenosine

4. Give another drug (beta blocker, digoxin, verapamil)

5. Don’t know

Case history

• Hx of paroxysmal AF

• Prescribed beta blocker – poorly tolerated

• Given flecainide

• Organised AF to flutter, and slowed flutter rate so can conduct through AV

node 1:1 atrium to ventricle BUT with bundle branch block

• TAKE A GOOD HISTORY

Treatment of VT

• Monomorphic VT

• Polymorphic VT

REMEMBER........

• Never wrong to cardiovert electrically (but get a 12-lead ECG if patient not compromised)

Monomorphic VTHaemodynamically Stable

• ‘Scar’ related

• Haemodynamically stable – can use medical therapy

– ALS – amiodarone

– IV 150-300 mg CENTRALLY over 10-60 minutes, then 0.9-1.2g over 24

hours and every 24 hours (need about 6g iv to fully load)

– Load orally (can use 400 mg tds for ‘rapid’ loading)

• IV β-blocker– Fast/short acting e.g. metoprolol – take 10 mg and give 2.5 mg every

1-2 minutes

– Can give another 10 mg

– If effective then give oral as much as BP will tolerate, and then change to od preparation

• Lignocaine

– IV loading: 1-1.5mg/kg slow bolus

– Then 1-4mg/min infusion

– Negatively inotropic – mexiletine is the best oral equivalent

Monomorphic VTHaemodynamically Stable

Monomorphic VT

Amiodarone Lignocaine(1,2)

Sotalol(1)

Procainamide(2)

n 32% 31% 16% 15%

Termination<15 mins

15% 18% 69% 79%

Hypotension 15% 7% 6% 7%

1. Ho et al. 1994

2. Gorgels et al. 1996

REMEMBER........

• Never give verapamil to a patient with broad complex

tachycardia

• Sedation can be very effective (↓adrenaline drive + prepares

for DCCV)

Monomorphic VT

• Recurrent episodes can occur

• Consider Mg2+ bolus and infusion (little evidence)

• Temporary pacing wire - overdrive pacing and/or pacing at 80-

100 bpm to suppress ectopics triggering VT

• Get help if you need it

• All patients need further assessment:

• Echocardiography

• Coronary angiography

• CMR

• Increasing use of VT ablation when recurrent despite medical

therapy

• Candidate for an ICD

Monomorphic VT

Polymorphic VT

• Normally related to prolonged QT

• Acquired (drug related) or congenital (LQTS)

• Identify the culprit drug

• LQTS – QT may be normal on ECG

Polymorphic VT

REMEMBER........

• Never give amiodarone (or any other QT prolonging anti-arrhythmic)

• CARDIOVERSION

• Identify any culprit drug and stop

• Magnesium (8-20mmol) IV stat

• Correct all electrolytes

• Bradycardia induced (R on T) – consider pacing

Polymorphic VT

Other VTs

• Normal heart

– RVOT tachycardia

– Fascicular VT

– CPVT

• Dilated/Valvular or Ischaemic heart disease

– Bundle branch re-entry VT

RVOT tachycardia

• LBBB pattern

• Strongly positive inferior complexes (inferior axis)

• May see similar morphology ectopy on non-tachycardia ECG

• Normal LV function

• β-blocker, verapamil, ablation

• DD ARVC

Fascicular VT

• RBBB pattern

• Left axis (often ‘straight up’)

• Relatively narrow QRS (AVL)

• Rare and therefore do not over-diagnose

Bundle branch re-entry VT

• Intraventricular conduction delay on SR ECG (± AV delay)

• Often LBBB (similar to SR ECG)

• Dilated LV (non-ischaemic > ischaemic)

• Ablation potentially curative

• BUT patient profile may warrant ICD

Summary

• Systematically assess the ECG

• If in doubt treat broad complex tachycardia as VT

• Cardioversion is the safest treatment

• Don’t give verapamil (however tempted!)

Supraventricular tachycardias

• Sinus node

– IST/sinus node re-entry

• Atrial tissue

– Atrial flutter – macro re-entrant

– Atrial tachycardia – focal/micro re-entrant

• Junctional re-entrant tachycardia

– AVNRT

– AVRT

Narrow Complex Tachycardia (QRS <120ms)

Regular?

AFAT/AFl with variable conductionMAT

P waves visible?

Ps > Vs?

AT/A Flutter Assess RP Interval

AVNRT

Yes No

Yes

No

Yes No

Short (RP<PR) Long (RP>PR)

ISTAT

PJRTAtypical AVNRT

RP <70ms RP >70ms

AVRTAtypical AVNRT

AT ESC guidelines 2003

ECG - A 25 yr old male presents to A&E with palpitations

What is the most likely diagnosis?

1. Atrioventricular re-entrant tachycardia

2. Atrioventricular nodal re-entrant tachycardia

3. Atrial tachycardia

4. Ventricular tachycardia

5. Permanent junctional re-entrant tachycardia

The patient has been seen by the A&E team and is on oxygen, has IV access, external defib pads on and is able to talk. His blood pressure is 86/50mmHg. What is your next step?

1. Check and correct electrolytes

2. BP is <90mmHg proceed to DCCV

3. Attempt vagal maneuvers

4. IV atropine

5. IV adenosine

Patient has experienced symptoms before 2-3/year. What is the best evidence approach to longer term management according to ESC guidelines?

1. Ablation of the fast pathway

2. Regular treatment with flecainide

3. Pill in the pocket flecainide

4. Ablation of the slow pathway

5. No medical therapy or intervention

Recommendations for long-term treatment of patients with recurrent AVNRT

Clinical Presentation Recommendation Class Level of Evidence

Poorly tolerated AVNRT with hemodynamic intolerance Catheter ablation I B

Verapamil, diltiazem, β-blockers, sotalol, amiodarone

Flecainide,* propafenone*IIa C

Recurrent symptomatic AVNRT Catheter ablation I B

Verapamil I B

Diltiazem, β-blockers I C

Recurrent AVNRT unresponsive to β or Ca2+-channel blocker and patient declines RF ablation

Flecainide,* propafenone,* sotalol IIa B

Amiodarone IIb C

AVNRT with infrequent or single episode in patients who desire complete control of arrhythmia

Catheter ablation I B

ECG clues for AVNRT

Pseudo–R wave in lead V1 and/or a pseudo–S wave in inferior leads

Responses of narrow complex tachycardias to adenosine

IV adenosine

No change in rate Gradual slowing then reacceleration

of rate

Sudden termination

Persisting atrial tachycardia with

transient high grade AV block

• Inadequate dose delivery

• Consider fascicular VT

• Sinus tachycardia• Focal AT• Non-paroxysmal

junctionaltachycardia

• AVNRT• AVRT• Sinus node re-

entry• Focal AT

• Macro re-entrant atrial tachycardia

• Micro re-entrant atrial tachycardia

TREATMENT

• Vagal manoeuvres/carotid massage (caution in the elderly)

• Adenosine common to all (terminates nodal dependent)– It needs to be given into a large vein

– Makes patient feel unwell

– Give 12 mg initially (unless small, then 6 mg) and then 18 mg or 24 mg if no effect

– The only true contraindication is severe asthma (brittle – requiring ITU)

• If haemodynamically compromised then cardiovert electrically

Narrow Complex Tachycardia

AVNRT• Most common regular SVT

• 75 % ♀

• Typical and atypical types – mainly EP lab diagnosis

• Dual pathways in AV node (may occur in up to 25% of patients in EP lab)

Treatment

• Vagal manoeuvres

• Medication – acutely adenosine, later beta blockers, calcium channel

blockers, flecainide or amiodarone

• DC cardioversion rarely necessary

• Electrophysiology study & ablation – 0.5-1% risk of PPM

REMEMBER........

• Recurrence rates are high and ablation is curative in over 90-95% so refer all AVNRT patients to an electrophysiologist

ECG - A 17 yr old female presents to A&E with palpitations

ECG – She is given adenosine and tachycardia terminates

What is the most likely diagnosis?

1. Orthodromic atrioventricular re-entrant tachycardia

2. Atrioventricular nodal re-entrant tachycardia

3. Atrial tachycardia

4. Antidromic atrioventricular re-entrant tachycardia

5. Permanent junctional re-entrant tachycardia

What is the best evidence approach to longer term management according to ESC guidelines?

1. Amiodarone

2. Flecainide

3. Sotalol

4. Ablation of the accessory pathway

5. Verapamil

Recommendations for long-term therapy of accessory pathway–mediated arrhythmias

Clinical Presentation Recommendation Class Level of Evidence

WPW syndrome (pre-excitation and symptomatic arrhythmias), well tolerated

Catheter ablation I B

Flecainide, propafenoneSotalol, amiodarone, blockers

IIa C

Verapamil, diltiazem, digoxin III C

WPW syndrome (with AF and rapid-conduction or poorly tolerated AVRT)

Catheter ablation I B

AVRT, poorly tolerated (no pre-excitation)

Catheter ablation I B

Flecainide, propafenone, sotalol, amiodarone IIa C

β-blockers, IIb C

Verapamil, diltiazem, digoxin III C

Pre-excitation, asymptomatic None I C

Catheter ablation IIa B

Pre-excitation (WPW)

• Sudden death occurs rarely (0.1%)• Other factors that influence risk: presence of multiple bypass tracts, family history of

premature sudden death• Sudden cardiac death is unusual without preceding symptoms

Treatment• Vagal manoeuvres• Medication (adenosine, beta blockers, flecainide or amiodarone)• Cardioversion (pre-excited AF)• Electrophysiology study & ablation

Catheter ablation of SVT (not AF)

• Day case procedure

• Sedation

• High ‘cure’ rates (90-95%)

• Serious risk < 1:2000

• Risk of PPM 1:1-200

• No driving 1 week

• Redo rate 5-10%

ECG

Atrial tachycardia

• Often sudden onset/offset

• P wave may look abnormal (look at inferior leads - inverted P waves

suggesting low atrial focus)

• May not see P waves clearly if 1:1 AV conduction

• Response to adenosine: AV block but P waves continue at same rate

(rarely can terminate tachycardia)

Atrial tachycardia

• The least common form of SVT

• Affects children, young women and the elderly

• Can present with very rapid ventricular rates but syncope and

hypotension are unusual

• Can be incessant and lead to a tachycardia induced

cardiomyopathy

Atrial tachycardia

• Beta blockers will control the rate but won’t terminate AT

• AT is best suppressed with class I anti-arrhythmics such as flecainide (N.B. patients

with impaired LV function)

• Verapamil can be effective

• Amiodarone works but

– Not a good long-term drug

– Makes ablation very difficult

• Ablation has a 75%-80% cure rate and is recommended for patients who:

– Can’t take drugs to suppress or find that drugs are ineffective

ECG - adenosine

Atrial flutter

• Often sudden onset/offset

• P wave may have characteristic ‘sawtooth’ appearance – no

‘isoelectric’ (flat) period in several leads

• Response to adenosine: AV block and unmasks flutter waves

• Has a thromboembolic risk similar to AF (and often co-exists)

REMEMBER........

• Recurrence rates are high and ablation is curative in over 90-95% so refer all flutter patients to an electrophysiologist

Summary

• Narrow complex tachycardia is common

• Often benign

• Management driven by frequency/severity of symptoms

• Catheter ablation curative in many