ECG Masterclass Diagnosis and Management of Tachyarrhythmias Dr Sajad Ahmed Hayat Consultant Electrophysiologist University Hospitals Coventry & Warwickshire Sajad.Hayat@uhcw.nhs.uk
Why is it important? Tachyarrhythmias are common Emergency Anxiety (for both patient and healthcare professional!) 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 Mahaim fibres
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
AV dissociation? ECG features - a simple approach
AV dissociation? Capture/fusion beats? ECG features - a simple approach
AV dissociation? Capture/fusion beats? ECG features - a simple approach 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 Unusual axis: ECG features - a simple approach North West Axis (+ve avr, -ve inf) RBBB with LAD or LBBB with RAD
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
REMEMBER... Treat as VT and you won t go wrong Don t forget the history
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 slows 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)
Scar related Monomorphic VT Haemodynamically Stable Haemodynamically stable can use medical therapy ALS amiodarone (NO data) 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)
Lignocaine Monomorphic VT Haemodynamically Stable IV loading: 1-1.5mg/kg slow bolus. Then 1-4mg/min infusion. Negatively inotropic mexiletine is the best oral equivalent. 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
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 Mg 2+ bolus and infusion (little evidence). Temporary pacing wire - overdrive pacing and/or pacing at 80-100 bpm to suppress ectopics causing VT Get help if you need it.
Monomorphic VT All patients need further assessment: Echocardiography Coronary angiography Increasing use of VT ablation when recurrent despite medical therapy Candidate for an ICD
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)
Polymorphic VT CARDIOVERSION Identify any culprit drug and stop Magnesium (8-20mmol) iv stat Correct all electrolytes Bradycardia induced (R on T) - pace
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
Fascicular VT
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 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) No P waves visible? Yes Ps > Vs? Yes Regular? No AF AT/AFl with variable conduction MAT Yes AT/A Flutter No Assess RP Interval Short (RP<PR) Long (RP>PR) RP <70ms AVNRT RP >70ms AVRT Atypical AVNRT AT IST AT PJRT Atypical AVNRT 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.
ECG clues for AVNRT Pseudo R wave in lead V1 and/or a pseudo S wave in inferior leads
You are asked to see the patient in A&E. 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. IV Amiodarone. 4. IV atropine. 5. IV adenosine.
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 junctional tachycardia AVNRT AVRT Sinus node reentry Focal AT Macro re-entrant atrial tachycardia Micro re-entrant atrial tachycardia
TREATMENT Narrow Complex Tachycardia 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 12mg initially (unless small, then 6mg) and then 18mg or 24 mg if no effect The only true contraindication is severe asthma (brittle requiring ITU) If haemodynamically compromised then cardiovert electrically
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* Recurrent symptomatic AVNRT Catheter ablation I B Recurrent AVNRT unresponsive to β or Ca 2+ -channel blocker and patient declines RF ablation AVNRT with infrequent or single episode in patients who desire complete control of arrhythmia IIa Verapamil I B Diltiazem, β-blockers I C Flecainide,* propafenone,* sotalol IIa B Amiodarone IIb C Catheter ablation I B C
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. Atrioventricular re-entrant tachycardia 2. Atrioventricular nodal re-entrant tachycardia 3. Atrial tachycardia 4. Atrioventricular nodal re-entrant tachycardia with bystander accessory pathway 5. Permanent junctional re-entrant tachycardia
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 accessory pathway. 5. No medical therapy.
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 WPW syndrome (with AF and rapid-conduction or poorly tolerated AVRT) AVRT, poorly tolerated (no preexcitation) Catheter ablation I B Flecainide, propafenone Sotalol, amiodarone, blockers Verapamil, diltiazem, digoxin III C IIa Catheter ablation I B Catheter ablation I B Flecainide, propafenone, sotalol, amiodarone IIa β-blockers, IIb C Verapamil, diltiazem, digoxin III C Pre-excitation, asymptomatic None I C Catheter ablation IIa B C C
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
Indications for RF ablation of AVRT Symptomatic AVRT AF (and fast V rates) Patients with AVRT Asymptomatic patients with ventricular pre-excitation whose livelihood, profession, insurability, or mental well-being may be influenced by unpredictable tachyarrhythmias or in whom such tachyarrhythmias would endanger the public safety should have an RF ablation procedure Patients with a family history of sudden cardiac death
Catheter ablation of SVT (not AF) Daycase 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%
Question What is the diagnosis? 1. AV re-entrant tachycardia (AVRT) 2. Sinus tachycardia 3. Atrial flutter 4. AV nodal re-entrant tachycardia (AVNRT) 5. Atrial tachycardia
Sinus rhythm/tachycardia Gradual onset/offset Normal looking P wave Response to adenosine: AV block but P waves continue at same rate (or do slow occasionally and transiently) Look for other causes e.g. PE etc.
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)
Atrial flutter If haemodynamically compromised DCCV If stable then rate/rhythm control Rate control often difficult (β-blocker + another agent) Rhythm control chemical vs. electrical Like AT class I very effective BUT caution 1:1 conduction, amiodarone toxic DCCV electively but need to consider anticoagulation issues <48 hours nil needed >48 hours TOE guided + anticoagulation or 4 weeks anticoagulation first
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 similar Often driven by symptoms Catheter ablation curative in many