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Killer ECGs

Killer ECGs



By James Le Fevre, ED Registrar - how to detect conditions in ED associated with sudden cardiac death

By James Le Fevre, ED Registrar - how to detect conditions in ED associated with sudden cardiac death



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  • Risk assessment of the well-looking patient with a symptom that may be relatively benign but can be deadly A large part of EM practice Medical risk versus medico-legal risk Opportunity to genuinely save a life
  • Brugada syndrome is most common in people from Asia Brugada syndrome is 8-10 times more prevalent in men than in women Second leading cause of death in males <40 after trauma Mean age of sudden death is 41 Previously described as SUNDS (Sudden unexplained nocturnal death syndrome in SEA)
  • frequency of gene mutation is equal, therefore, higher penetrance in men Brugada syndrome most commonly affects otherwise healthy men aged 30-50 years
  • Fever can
  • Major Criteria Right ventricular dysfunction Severe dilatation and reduction of RV ejection fraction with little or no LV impairment Localized RV aneurysms Severe segmental dilatation of the RV Tissue characterization Fibrofatty replacement of myocardium on endomyocardial biopsy Conduction abnormalities Epsilon waves in V1 - V3. Localized prolongation (>110 ms) of QRS in V1 - V3 Family history Familial disease confirmed on autopsy or surgery Minor Criteria Right ventricular dysfunction Mild global RV dilatation and/or reduced ejection fraction with normal LV. Mild segmental dilatation of the RV Regional RV hypokinesis Tissue characterization Conduction abnormalities Inverted T waves in V2 and V3 in an individual over 12 years old, in the absence of a right bundle branch block (RBBB) Late potentials on signal averaged EKG. Ventricular tachycardia with a left bundle branch block (LBBB) morphology Frequent PVCs (> 1000 PVCs / 24 hours) Family history Family history of sudden cardiac death before age 35 Family history of ARVD
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Killer ECGs Killer ECGs Presentation Transcript

  • 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-ParkinsonWhite Syndrome (WPW) Repetitive MonomorphicVentricularTachycardia Catecholaminergic polymorphicVT Idiopathic FascicularVentricularTachycardia (Verapamil Sensitive VentricularTachycardia) 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) LeadV2 (V1-V3) • TWave Inversion (Brugada/ARVD) • ST Elevation (Brugada) • T wave Notching (LQTS) • EpsilonWaves (ARVD) • QRS > 110ms inV1-V3 (ARVD) The Money Leads
  • Brugada Syndrome
  • A ‘Channelopathy’ • Sodium channel mutation The typical patient Brugada 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 ECGWITH • DocumentedVF or polymorphicVT • FHx SCD <45 years of age • Coved-type ECGs in family members • InducibleVT (EPS) • Syncope • Nocturnal agonal respiration Brugada Syndrome – Diagnostic Criteria
  • Type 1 ‘coved-type’ STE > 2mm & TwI Type 2 STE > 2mm Tw +ve/biphasic Type 3 STE < 2mm AnyT wave Brugada Syndrome
  • Studies small, evidence level low SymptomaticType I – Admit AsymptomaticType I – Debatable (Need EPS) Type 2/3 ECG Patterns – Outpatient EPS/Sodium blocker challenge Patients withType 2/3 ECG patterns than convert toType I with Flecainide have unclear prognosis Definitive: ICD, Quinidine if ICD not feasible Brugada Syndrome - Disposition
  • Take home messages •Look at leadV2 closely in anyone with syncope • The diagnosis is in leadsV1-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 polymorphicVT/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 • MacroscopicT-wave electrical alternans (1 Point) • NotchedT-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 IfTorsade de Pointes or polymorphicVT • 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 inTorsades 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 forT wave alternans (esp.V1-V3) • Look for notchedT 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, peakedT 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 peakedT 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 Viskin Viskin 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 RightVentricular 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 RightVentricular Dysplasia
  • Major and Minor criteria • 2 Major OR • 1 Major 2 minors OR • 4 minors Horribly complicated Arrhythmogenic RightVentricular Dysplasia – Diagnostic Criteria
  • Palpitations Syncope Cardiac arrest Often precipitated by exercise Family history of SCD Hayden Roulston has this condition Arrhythmogenic RightVentricular Dysplasia – Clinical features
  • Epsilon wave (specific, sensitivity 30%) T-wave inversionsV1-V3 (85% sensitive) Prolonged S-wave upstroke of 55ms inV1-3 (95% sensitive) Localised QRS widening of 110ms inV1-V3 Paroxysmal LBBBVT Frequent LBBB PVCs (>1000/24Hr typically) Arrhythmogenic RightVentricular Dysplasia – ECG Features
  • Epsilon waves Arrhythmogenic RightVentricular Dysplasia
  • Arrhythmogenic RightVentricular Dysplasia – Prolonged S wave upstroke inV2
  • Arrhythmogenic RightVentricular Dysplasia – Localised QRS > 110msV1-V3 Epsilon wave Localised QRS > 110ms T-wave inversions V1-V3
  • Arrhythmogenic RightVentricular 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 RightVentricular 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 RightVentricular Dysplasia – Disposition
  • Take home messages • Look for epsilon waves (Best seenV1-V3) • Beware the young patient with very frequent LBBB extrasystoles • Again, examineV1-V3 closely (TWI, QRS >110) Arrhythmogenic RightVentricular Dysplasia
  • Genetic Predisposition Mostly due to Calcium ryanodine channel mutations Thought to affect up to 1 in 10,000 people PolymorphicVT 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 polymorphicVT
  • 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 leadV1 Wolff-Parkinson-White syndrome
  • Type B • negative delta wave • QRS complex mostly negative in leadsV1 andV2 and becomes positive in transition to the lateral leads resembling a left bundle-branch block Wolff-Parkinson-White syndrome
  • 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 antidromicWPW Adenosine 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 LeadsV1-V3 looking for: • Is the QRS >110ms inV1-V3 (AVRD) ? • Are there invertedT-waves (Brugada, ARVD) ? • Is there ST elevation (Brugada) ? • Is there macroscopicT-wave alternans (LQTS) ? • Are there notchedT-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% ofVT 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 HandyTips
  • WPW – Type A
  • LQTS
  • HOCM
  • Brugada (Type 2)
  • Electrical alternans (Tamponade)
  • BrugadaType II
  • Hyperkalaemia – Patient about to die
  • BrugadaType I