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James Le Fevre
The Ultimate Killer ECG
(conscious) VF
The ultimate Killer ECG
Asystole (Remember fine VF)
Leads not corrected properly
Brugada Syndrome
Long QT syndrome
Short QT syndrome
Arrhythmogenic right ventricular dysplasia (ARVD)Wolff-Parkinson White Syndrome (WPW)Repetitive Monomorphic Ventricular Tachycardia
Catecholaminergic polymorphic VT
Idiopathic Fascicular Ventricular Tachycardia (Verapamil Sensitive Ventricular Tachycardia)
Inherited Arrythmia Syndromes
Hypertrophic obstructive cardiomyopathy
Aortic dissection
Submassive PE/Massive PE
Intracerebral bleed/SAH
Severe Hyperkalemia
Commotio cordis
Other presentations
Risk Assessment and Disposition
Medical Risk to Our Patient
Medicolegal Risk to Us
Opportunity to Save a Life
Why learn this ?
Lead II• The QTc (Short QT Syndrome/Long QT Syndrome)
Lead V2 (V1-V3)• T Wave Inversion (Brugada/ARVD)• ST Elevation (Brugada)• T wave Notching (LQTS)• Epsilon Waves (ARVD)• QRS > 110ms in V1-V3 (ARVD)
The Money Leads
Brugada Syndrome
A ‘Channelopathy’• Sodium channel mutation
The typical patientBrugada syndrome is genetically determined • Now over 60 different mutations identified• 50% spontaneous
Brugada Syndrome
Unmasked/Augmented by• Fever• Ischaemia• Multiple drugs• Hypokalaemia• Hypothermia• Post DC Cardioversion
Brugada Syndrome
Type I ECG WITH• Documented VF or polymorphic VT
• FHx SCD <45 years of age
• Coved-type ECGs in family members
• Inducible VT (EPS)
• Syncope
• Nocturnal agonal respiration
Brugada Syndrome – Diagnostic Criteria
Type 1‘coved-type’STE > 2mm &TwIType 2STE > 2mmTw +ve/biphasicType 3STE < 2mmAny T wave
Brugada Syndrome
Studies small, evidence level low
Symptomatic Type I – Admit
Asymptomatic Type I – Debatable (Need EPS)
Type 2/3 ECG Patterns – Outpatient EPS/Sodium blocker challenge
Patients with Type 2/3 ECG patterns than convert to Type I with Flecainide have unclear prognosis
Definitive: ICD, Quinidine if ICD not feasible
Brugada Syndrome - Disposition
Take home messages• Look at lead V2 closely in anyone with syncope• The diagnosis is in leads V1-V3
• STE
• T wave changes
• RBBB/IRBBB
Brugada Syndrome
Long QT Syndrome
LQTS may be expected to occur in 1 in 10,000 individuals.
Prolongation of the QT interval on ECG
Propensity for:
Ventricular tachyarrhythmias
Sudden Cardiac death
Collapse
Long QT can also be acquired• (MI / IHD / Drugs / Electrolytes)
Congenital Long QT Syndrome
LQTS is caused by mutations of the genes for cardiac potassium, sodium, or calcium ion channels
Essentially, repolarisation takes longer, the QT interval lengthens and predisposes the individual to polymorphic VT/torsade de pointes/VF and SCD
Depending on the type of mutation present, sudden cardiac death may happen during:
Exercise
emotional stress
during sleep
Congenital Long QT Syndrome
Presenting features• Presentation with cardiac arrest or syncope• After a family member suddenly dies/has an arrhythmia• After a routine ECG is taken
Physical examination• Excessive bradycardia for age• Congenital deafness• Syndromic constellations
Long QT Syndrome – Hx/Exam
Normal QTc range
Upper limit children/adolescents• 0.46
Upper limit women• 0.46
Upper limit men• 0.45
Long QT Syndrome
Diagnosis• List of criteria max score 9, score of >3 gives high probability
• 2-3 = intermediate probability
• Realm of cardiologists
• ECG clues for us
• QTc length most important (≥ 480ms = 3 pts, 460-470ms = 2 pts, 450ms Male = 1 pt
• Macroscopic T-wave electrical alternans (1 Point)
• Notched T-waves (1 Point)
• Low heart rate for age (0.5 Points in children)
•2.5% of healthy people have a long QT
•10-15% of CLQTS patients have a n0rmal QT interval
Long QT Syndrome
Long QT Syndrome
Macroscopic T-wave Alternans (1 Point)
Long QT Syndrome
Long QT Syndrome
Notched T waves (1 Point)
Long QT Syndrome
Notched T waves – 1 Point
Admit if ? Congenital LQTS and symptomatic
Discuss if ? Congenital LQTS and asymptomatic
Treatment – Congenital• Depends on type and risk assessment• Beta blockers• ICD• Educate and Investigate family• (Medic alert bracelet, carry around sheet with drugs that
doctor should avoid, train family in CPR)
Congenital Long QT Syndrome - Disposition
Assess risk based on underlying cause
Generally monitor till resolved
If very long QTc consider Magnesium sulfate prophylactically
Replacing electrolytes is good supportive care
If Torsade de Pointes or polymorphic VT• Magnesium and overdrive pace with isoprenaline
Acquired versus congenital:
Torsades in acquired caused by not enough stimulation
Torsades in congenital caused by too much stimulation
Overdrive pacing in Torsades with Congenital LQTS
is absolutely contraindicated
Acquired Long QT Syndrome - Disposition
Take Home Messages
• Measure the QTc (Take interest if >450 men >460 women, worry if you did not need to measure it to notice it)
• Look for T wave alternans (esp. V1-V3)
• Look for notched T waves
• Look for slow heart rate for age
Long QT Syndrome
Short QT Syndrome
Short QT interval ≤ 320 ms with no change with HR, tall, peaked T wave, structurally normal heart
5 mutations found so far
Autosomal dominant inheritance
Think of this in young people with atrial fibrillation and with syncope/cardiac arrest
Short QT Syndrome
• Genotypes 1-3•Gain of function in potassium efflux channels•QTc <320ms• Genotypes 4-5• Loss of function in L-type Calcium channels• Brugada like•QTc <360ms• Digoxin toxicity can also cause shortened QT and
arrythmia
Short QT Syndrome
A distinctive electrocardiographic feature of the short QT syndrome is the appearance of tall peaked T waves, similar to those encountered with hyperkalemia
Brugada-like in genotypes 4-5
QT interval is fixed independent of heart rate
Short QT Syndrome
QTc < 330 ms in males or <340 ms in female diagnostic
QTc < 360 ms in males or <370 ms in females when supported by symptoms or FHx
Short QT Syndrome – Diagnostic Criteria
QT Syndromes – Diagnostic Criteria
Reproduced from ViskinViskin S. The QT interval: too long, too short or just right. Heart Rhythm.2009 May;6(5):711-5. Epub 2009 Mar 3. [PMID: 19389656] [Full text]
Take Home Message• Be very worried if the QTc is <320ms• Very rare
Short QT Syndrome
Arrhythmogenic Right Ventricular Dysplasia
ARVD is due to a type of cardiomyopathy, which is possibly familial in some patients.
Fibrofatty infiltrated Hypokinetic areas
The prevalence of ARVD is estimated to be 1 case per 5,000 population
The death rate associated with arrhythmia is estimated to be 2.5% per year
More common in men than women (3:1)
More common with Italian/Greek descent
Arrhythmogenic Right Ventricular Dysplasia
Major and Minor criteria• 2 Major OR• 1 Major 2 minors OR• 4 minors
Horribly complicated
Arrhythmogenic Right Ventricular Dysplasia – Diagnostic Criteria
Palpitations
Syncope
Cardiac arrest
Often precipitated by exercise
Family history of SCD
Hayden Roulston has this condition
Arrhythmogenic Right Ventricular Dysplasia – Clinical features
Epsilon wave (specific, sensitivity 30%)
T-wave inversions V1-V3 (85% sensitive)
Prolonged S-wave upstroke of 55ms in V1-3 (95% sensitive)
Localised QRS widening of 110ms in V1-V3
Paroxysmal LBBB VT
Frequent LBBB PVCs (>1000/24Hr typically)
Arrhythmogenic Right Ventricular Dysplasia – ECG Features
Epsilon waves
Arrhythmogenic Right Ventricular Dysplasia
Arrhythmogenic Right Ventricular Dysplasia – Prolonged S wave upstroke in V2
Arrhythmogenic Right Ventricular Dysplasia – Localised QRS > 110ms V1-V3
Epsilon wave
Localised QRS > 110ms
T-wave inversions V1-V3
Arrhythmogenic Right Ventricular Dysplasia – ECG Features
LBBB VT (i.e. has a RV origin)
Echo (sensitive, less specific, cheaper)
MRI (Specific and sensitive but expensive)
Combination Echo/MRI ideal
Histology• Least patient-oriented diagnostic technique
Arrhythmogenic Right Ventricular Dysplasia – Imaging
? ARVD with high risk features (syncope due to cardiac arrest, recurrent arrhythmia, FHx) : Admit
? ARVD asymptomatic (i.e. ECG suggestive) : Discuss
Treatment:• High-risk features: Urgent ICD Placement• No high-risk features: Sotalol• Persistent arrhythmias: Ablation• Heart failure: Standard Rx including transplant
Arrhythmogenic Right Ventricular Dysplasia – Disposition
Take home messages• Look for epsilon waves (Best seen V1-V3)• Beware the young patient with very frequent LBBB extrasystoles• Again, examine V1-V3 closely (TWI, QRS >110)
Arrhythmogenic Right Ventricular Dysplasia
Genetic Predisposition
Mostly due to Calcium ryanodine channel mutations
Thought to affect up to 1 in 10,000 people
Polymorphic VT due to emotional upset/physical activity (and therefore catecholamines)
Estimated to cause up to 15% of SCD in young people
ECG clues• Sinus bradycardia, prominent U-waves
Not a diagnosis that one can make in the emergency department
Catecholaminergic polymorphic VT
Due to extra ‘Accessory pathways’ or connections between the atrium and ventricle
WPW syndrome affects approximately 0.15-0.2% of the general population. Of these individuals, 60-70% have no other evidence of heart disease.
Kent bundle
Risk of SCD much lower than in the other discussed syndromes (0.6%)
Wolff-Parkinson-White syndrome
Broad spectrum of presentations• CP/SOB/SCD/Palpitations/Syncope• Routine ECG diagnosis
Classic:• Shortened PR interval (<0.12)• QRS >0.12• Delta wave• Secondary ST-T changes in opposite direction to delta wave
Wolff-Parkinson-White syndrome
Type A• Upright positive delta wave in all precordial leads with a resultant R greater than S
amplitude in lead V1
Wolff-Parkinson-White syndrome
Type B
• negative delta wave
• QRS complex mostly negative in leads V1 and V2 and becomes positive in transition to the lateral leads resembling a left bundle-branch block
Wolff-Parkinson-White syndrome
WPW - SVTO
RT
HO
DR
OM
IC (9
0%)
WPW - SVTA
NT
IDR
OM
IC (1
0%)
Circus movement tachycardias• Vagal maneuvers• Adenosine is Safe, Diltiazem/verapamil second line• Give calcium if using verapamil• Electricity if unstable• Etomidate +/- fentanyl works well for sedation• Give 100J initially (2J/kg in children)
WPW - Orthodromic
Atrial fibrillation with antidromic WPWAdenosine and other AV blockers absolutely Contraindicated• Sedate and Shock is the safest approach (100J first)• Must slow the abnormal pathway NOT the node (i.e. fundamentally
different to normal AF treatment)• If treated like conventional AF, VF can be the outcome• Procainamide can be used
WPW – Antidromic/AF
No longer considered a specific diagnosis in the ‘electrophysiologic study’ era
Lown-Ganong Levine Syndrome
Take Home Messages• If the tachycardia is wide complex, treat it as such
• If in doubt, consult, and/or use electricity
WPW
Hypertrophic cardiomyopathy (HCM) is a genetic disorder that is typically inherited in an autosomal dominant fashion with variable penetrance and variable expressivity
Presents with SCD, arrythmia, heart failure, dizziness, angina, syncope, palpitations
Hypertrophic cardiomyopathy
Some important physical findings• A fourth heart sound
• Displaced, forceful, enlarged apex beat
• Systolic murmur increased on valsalva
Hypertrophic cardiomyopathy
ECG Findings• ST-T wave abnormalities and LVH
• Axis deviation
• BBB
• Ectopic atrial rhythm
• Q waves anterolaterally
• P wave abnormalities
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy
Review ECG in General• Is the QTc >450 (men) or >460 (women) (LQTS) ?• Is the heart rate too low for age (LQTS) ?• Is the QTc <320 (Short QT Syndrome) ?• Are there frequent LBBB PVCs (ARVD) ?• Think of HOCM (LVH criteria+/-ST-T changes, BBB, Q-waves)• Is the PR <0.12 ? Are there delta waves (WPW) ?
Review Leads V1-V3 looking for:• Is the QRS >110ms in V1-V3 (AVRD) ?• Are there inverted T-waves (Brugada, ARVD) ?• Is there ST elevation (Brugada) ?• Is there macroscopic T-wave alternans (LQTS) ?• Are there notched T-waves (LQTS) ?• Are there epsilon waves (ARVD) ?
Is this a Killer ECG ?
• ? ARVD with high risk features: Admit on monitor, inpatient Echo (+/- MRI)• ? ARVD incidentally on ECG : Consult• ? Long QT Syndrome: Admit on monitor• ? Short QT Syndrome: Admit on monitor, Publish• ? HOCM with symptoms: Admit for inpatient Echo• VT/? VT: Admit on monitor•WPW, orthodromic SVT, no AF, stable: Discharge with
advice and f/u, EPS can help risk stratify for SCD•WPW, antidromic SVT, or AF, or both: Use electricity,
discuss with cardiology first if stable, refer cardiology
Disposition ?
Giving an amp of calcium prior to verapamil and diltiazem in SVT can decrease hypotension without decreasing efficacy of cardioversion
Adenosine in asthma is a relative contraindication, avoid if active wheeze or history of severe asthma, consider starting with 3mg
? 5% of VT is adenosine sensitive, Benefit may well outweigh risk. A response to adenosine does NOT prove SVT with aberrancy
QTc is helpful in differentiating Anterior STEMI from Benign early repolarisation as the QTc increases in Anterior STEMI
Some patients are terrified of how adenosine makes them feel, give them a bit of midazolam first (it may increase the chance of cardioversion also)
A gentle carotid massage can differentiate Aflutter with a 2:1 block from a slow SVT (don’t do if a bruit present, be prepared for a long pause)
Etomidate 2-4mL +/- 25mcg fentanyl iv in an unstable patient for DCCV is a good option
Ketamine is the next best, as Etomidate appears to be in short supply
Handy Tips
QUIZ
ARVD
WPW – Type A
LQTS
HOCM
STEMI
Brugada (Type 2)
Electrical alternans (Tamponade)
Brugada Type II
Hyperkalaemia – Patient about to die
Brugada Type I