Arrhythmias · mediated arrhythmias Clinical Presentation Recommendation Class Level of Evidence...
Transcript of Arrhythmias · mediated arrhythmias Clinical Presentation Recommendation Class Level of Evidence...
Arrhythmias:Supraventricular and Ventricular Tachycardias
Dr Sajad Ahmed HayatConsultant Electrophysiologist
University Hospitals Coventry & [email protected]
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