Why you should care when things are totally RAD
Episode 156

August 25, 2014


Don’t ignore the AXIS!

Can’t Miss Causes of Rightward Axis Deviation in the ED
  • Na2+ channel blocker toxicity
  • Pulmonary HTN - Consider PE
Other Causes of Rightward Axis Deviation
  • Hyperkalemia
  • Ventricular ectopy (VT)
  • Lateral MI (from Q-waves in lead I)
  • Left posterior fascicular block
  • Right ventricular hypertrophy
  • Dextrocardia
Na2+ channel blocker toxicity
  • Tachycardia (usually)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1 (sometimes)
  • Prolonged QRS
  • Prolonged QTc
Why you should care when things are totally RAD
Episode 156

August 25, 2014


Don’t ignore the AXIS!

Can’t Miss Causes of Rightward Axis Deviation in the ED
  • Na2+ channel blocker toxicity
  • Pulmonary HTN - Consider PE
Other Causes of Rightward Axis Deviation
  • Hyperkalemia
  • Ventricular ectopy (VT)
  • Lateral MI (from Q-waves in lead I)
  • Left posterior fascicular block
  • Right ventricular hypertrophy
  • Dextrocardia
Na2+ channel blocker toxicity
  • Tachycardia (usually)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1 (sometimes)
  • Prolonged QRS
  • Prolonged QTc
Another syncope case with a diagnostic ECG
Episode 155

August 18, 2014


Low Voltage Definition
  • QRS amplitudes in limb leads all < 5 mm or in all chest leads < 10mm (specific definition)
  • QRS amplitudes in I+II+III < 15 mm or V1+V2+V3 < 30 mm (sensitive definition)
Low Voltage QRS Differential
  • “Low Power/Weak Battery”
    • Infiltrative diseases (Amyloid, Sarcoid, etc.)
    • End stage cardiomyopathy
    • Myxedema (severe hypothyroidism)
  • Conduction blockage
    • Fluid/Effusion (pericardial or pleural)
    • Fat (obesity)
    • Air (COPD, PTX)

Don’t rely only on electrical alternans to diagnose pericardial effusions.

Low voltage + Tachycardia = Pericardial effusion until proven otherwise!

Another syncope case with a diagnostic ECG
Episode 155

August 18, 2014


Think of these differentials everytime you interpret the ECG of patients with syncope:
Low Voltage Definition
  • QRS amplitudes in limb leads all < 5 mm or in all chest leads < 10mm (specific definition)
  • QRS amplitudes in I+II+III < 15 mm or V1+V2+V3 < 30 mm (sensitive definition)
Low Voltage QRS Differential
  • “Low Power/Weak Battery”
    • Infiltrative diseases (Amyloid, Sarcoid, etc.)
    • End stage cardiomyopathy
    • Myxedema (severe hypothyroidism)
  • Conduction blockage
    • Fluid/Effusion (pericardial or pleural)
    • Fat (obesity)
    • Air (COPD, PTX)

Don’t rely only on electrical alternans to diagnose pericardial effusions.

Low voltage + Tachycardia = Pericardial effusion until proven otherwise!

Rodney Dangerfield makes an encore performance!
Episode 154

August 11, 2014


aVR - the forgotten 12th lead
ST-segment elevation (STE) in aVR with other ischemic findings is BAD!
(i.e. LMCA occlusion, proximal LAD occlusion, or triple vessel disease)
 
In the setting of ACS, STE in aVR…
  • + STE in aVL = LMCA occlusion
  • + STE in V1 = LMCA or proximal LAD occlusion
  • STE in aVR > STE V1 = LMCA occlusion
  • STE in aVR> 1.0mm should make you worry!

Some literature indicates…

  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • Immediate transfer for PCI if necessary!

This is not yet in the ACC/AHA guidelines for emergent cath lab activation!

Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID: 21146650
Rodney Dangerfield makes an encore performance!
Episode 154

August 11, 2014


aVR - the forgotten 12th lead
ST-segment elevation (STE) in aVR with other ischemic findings is BAD!
(i.e. LMCA occlusion, proximal LAD occlusion, or triple vessel disease)
 
In the setting of ACS, STE in aVR…
  • + STE in aVL = LMCA occlusion
  • + STE in V1 = LMCA or proximal LAD occlusion
  • STE in aVR > STE V1 = LMCA occlusion
  • STE in aVR> 1.0mm should make you worry!

Some literature indicates…

  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • Immediate transfer for PCI if necessary!

This is not yet in the ACC/AHA guidelines for emergent cath lab activation!

Remember: STE of aVR in very tachycardic rhythms (i.e. SVT), or in the setting of severe hypertension & LVH/RVH may be a normal variant and may have no clinical significance. Hence, the rule does not apply to asymptomatic patients without ST changes indicative of ischemia!


Want more practice/references? Check out these previous episodes & learn to respect aVR:


Reference:
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID: 21146650
Brugada Part II: 2014 revelations
Episode 153

August 4, 2014


If you interpret ECG’s in patients with syncope…
You have to know how to diagnose Brugada syndrome!
  • Consider Brugada syndrome in patients presenting after syncope
  • Diagnosis of the syndrome requires ECG findings + clinical findings
  • Coved STE is most concerning
  • Discussion/referral to electrophysiologist can be life saving

In case you missed it, start by watching last weeks episode: Brugada Part I

Brugada ECG Abnormalities in V1-V2
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type" (lower mortality)
  • ​Moving leads (V1-V2) one interspace higher may increase the abnormality

Diagnosis of the syndrome requires 2 parts:
  1. Typical ECG abnormality (especially coved type) +
  2. Clinical characteristics, one of the following:
  • ​History of VT/VF
  • FHx of sudden cardiac death
  • FHx of coved-type ECG
  • Agonal respirations during sleep
  • Inducibility of VT/VF during EP study

For the fellow ECG Nerds:

  • First onset of symptoms (VT,VF, syncope, sudden death) ~ 40 years old
    • ​41 +/- 15 years on average of VF episodes
    • Arrhythmias reported from 2-84 years
    • Is reported cause of SIDS & sudden cardiac death in young children
    • ​​Arrhythmic events tend to occur at rest or sleep
    • Vagal tone and fever thought to increase VF episodes
  • Mortality ~10%/yr without internal cardioverter-defibrillator (ICD)
    • Mortality & VF episode rates are highest in Type I (coved) pattern
    • Also associated with supraventricular arrhythmias (A.fib & SVT)
    • Antidysrhythmics have no effect on prognosis
    • Best treatment is ICD placement

References:

Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease:description of six cases. Am Heart J. 1989;6:1203-9. PMID: 2589161

Hoogendijk MG, Opthof T, Postema PG, et al. The Brugada ECG Pattern: A Marker of Channelopathy, Structural Heart Disease or Neither? Towards a Unifying Mechanism of the Brugada Syndrome. Circ Arrhythm Electrophysiol. 2010;3:283–290. PMID: 20551422

Mizusawa Y, Wilde AA. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;3:606-16. PMID: 22715240

Brugada Part II: 2014 revelations
Episode 153

August 4, 2014


If you interpret ECG’s in patients with syncope…
You have to know how to diagnose Brugada syndrome!
  • Consider Brugada syndrome in patients presenting after syncope
  • Diagnosis of the syndrome requires ECG findings + clinical findings
  • Coved STE is most concerning
  • Discussion/referral to electrophysiologist can be life saving

In case you missed it, start by watching last weeks episode: Brugada Part I

Brugada ECG Abnormalities in V1-V2
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type" (lower mortality)
  • ​Moving leads (V1-V2) one interspace higher may increase the abnormality

Diagnosis of the syndrome requires 2 parts:
  1. Typical ECG abnormality (especially coved type) +
  2. Clinical characteristics, one of the following:
  • ​History of VT/VF
  • FHx of sudden cardiac death
  • FHx of coved-type ECG
  • Agonal respirations during sleep
  • Inducibility of VT/VF during EP study

For the fellow ECG Nerds:

  • First onset of symptoms (VT,VF, syncope, sudden death) ~ 40 years old
    • ​41 +/- 15 years on average of VF episodes
    • Arrhythmias reported from 2-84 years
    • Is reported cause of SIDS & sudden cardiac death in young children
    • ​​Arrhythmic events tend to occur at rest or sleep
    • Vagal tone and fever thought to increase VF episodes
  • Mortality ~10%/yr without internal cardioverter-defibrillator (ICD)
    • Mortality & VF episode rates are highest in Type I (coved) pattern
    • Also associated with supraventricular arrhythmias (A.fib & SVT)
    • Antidysrhythmics have no effect on prognosis
    • Best treatment is ICD placement

References:

Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease:description of six cases. Am Heart J. 1989;6:1203-9. PMID: 2589161

Hoogendijk MG, Opthof T, Postema PG, et al. The Brugada ECG Pattern: A Marker of Channelopathy, Structural Heart Disease or Neither? Towards a Unifying Mechanism of the Brugada Syndrome. Circ Arrhythm Electrophysiol. 2010;3:283–290. PMID: 20551422

Mizusawa Y, Wilde AA. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;3:606-16. PMID: 22715240

A near-disaster in the stress test lab
Episode 152

July 28, 2014


Brugada Syndrome

  • A hereditary sodium channelopathy associated with sudden cardiac death (SCD) in patients with structurally normal hearts
  • More common cause of SCD than previously recognized
  • Most common in young males
  • First onset of symptoms (syncope, sudden death) ~ 40 years old
  • Mortality about 10% per year if not treated with internal cardioverter-defibrillator (ICD)
  • Syndrome characterized by
    • ​ECG abnormalities in leads V1-V2
    • Polymorphic or monomorphic VT
    • Structurally normal heart
    • Familial occurence in about half of patients
  • ​Discuss/refer to electrophysiologist
ECG Findings in V1-V2​
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type"

A near-disaster in the stress test lab
Episode 152

July 28, 2014


Brugada Syndrome

  • A hereditary sodium channelopathy associated with sudden cardiac death (SCD) in patients with structurally normal hearts
  • More common cause of SCD than previously recognized
  • Most common in young males
  • First onset of symptoms (syncope, sudden death) ~ 40 years old
  • Mortality about 10% per year if not treated with internal cardioverter-defibrillator (ICD)
  • Syndrome characterized by
    • ​ECG abnormalities in leads V1-V2
    • Polymorphic or monomorphic VT
    • Structurally normal heart
    • Familial occurence in about half of patients
  • ​Discuss/refer to electrophysiologist
ECG Findings in V1-V2​
  • RBBB or incomplete RBBB pattern
  • ST-segment elevation - 2 types
    • ​​"Coved-type" (most common & concerning)
    • "Saddle-type"

Should you workup trauma with an ECG??
Episode 151

July 21, 2014


Upcoming ECG CME:
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Quick Estimation of QT interval

T-waves should typically end before the midpoint of the R-R interval. Beware of a prolonged QT-interval when the T-wave ends after the midpoint of the R-R interval (half way between the R-waves).

Differential for Prolonged QTc

  • Hypokalemia
  • Hypomagnesemia
  • Hypocalemia
  • Hypothermia
  • Acute coronary syndromes / ischemia
  • Increased intracranial pressures
  • Medications (many)
  • Congenital

Prolonged QTc

  • Check lytes & medications
  • Beware of torsades 
    • Can present as seizures
    • ​Treat with Mg2+, shock, overdrive pacing

Check out more cases on prolonged-QT intervals & hypokalemia:
Should you workup trauma with an ECG??
Episode 151

July 21, 2014


Upcoming ECG CME:
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Quick Estimation of QT interval

T-waves should typically end before the midpoint of the R-R interval. Beware of a prolonged QT-interval when the T-wave ends after the midpoint of the R-R interval (half way between the R-waves).

Differential for Prolonged QTc

  • Hypokalemia
  • Hypomagnesemia
  • Hypocalemia
  • Hypothermia
  • Acute coronary syndromes / ischemia
  • Increased intracranial pressures
  • Medications (many)
  • Congenital

Prolonged QTc

  • Check lytes & medications
  • Beware of torsades 
    • Can present as seizures
    • ​Treat with Mg2+, shock, overdrive pacing

Check out more cases on prolonged-QT intervals & hypokalemia:
See how cereal saves lives!
Episode 150

July 14, 2014


Some patients with STEMI will have non-diagnostic INITIAL ECGs. 
 
Have a low threshold to get serial ECGs!
 
Repeat the ECG with persistent or changing pain. 
 

Here are links to more cases where serial ECGs made a difference:


Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: A report from the American Heart Association Mission: Lifeline program. Am Heart J. 2013;165(1):50–56. PMID: 23237133

See how cereal saves lives!
Episode 150

July 14, 2014


Some patients with STEMI will have non-diagnostic INITIAL ECGs. 
 
Have a low threshold to get serial ECGs!
 
Repeat the ECG with persistent or changing pain. 
 

Here are links to more cases where serial ECGs made a difference:


Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: A report from the American Heart Association Mission: Lifeline program. Am Heart J. 2013;165(1):50–56. PMID: 23237133

Posterior STEMI or anterior ischemia?
Episode 149

July 7, 2014


Upcoming Conference:

October 15-17, 2014
Baltimore, MD

Differential for ST-Depression in Anteroseptal Leads
  1. Posterior STEMI
  2. Anteroseptal ischemia
  3. Miscellaneous
    • RBBB, Hypokalemia, etc.

Posterior Myocardial Infarction

  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • 4% of STEMI’s are isolated PMI’s with increased M&M compared to Isolated inferior MI’s
  • Mirror image of septal MI in leads V1-V2
    • Large R-waves instead of Q’s
    • ST-segment depression (STD)  instead of ST-elevation (STE)
    • Upright T-waves instead of T-wave inversions

ECG Changes in Leads V1-V2 (-V3)

Septal STEMI
ST-segment
Elevation
Inverted
T-waves
Q-waves
develop over hours
Posterior STEMI
(Mirror image)
ST-segment
Depression 
Upright
T-waves
Tall R’s
develop over hours

In doubt? Get posterior leads when there’s ST-depression in septal leads! 

Posterior STEMI or anterior ischemia?
Episode 149

July 7, 2014


Upcoming Conference:

October 15-17, 2014
Baltimore, MD

Differential for ST-Depression in Anteroseptal Leads
  1. Posterior STEMI
  2. Anteroseptal ischemia
  3. Miscellaneous
    • RBBB, Hypokalemia, etc.

Posterior Myocardial Infarction

  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • 4% of STEMI’s are isolated PMI’s with increased M&M compared to Isolated inferior MI’s
  • Mirror image of septal MI in leads V1-V2
    • Large R-waves instead of Q’s
    • ST-segment depression (STD)  instead of ST-elevation (STE)
    • Upright T-waves instead of T-wave inversions

ECG Changes in Leads V1-V2 (-V3)

Septal STEMI
ST-segment
Elevation
Inverted
T-waves
Q-waves
develop over hours
Posterior STEMI
(Mirror image)
ST-segment
Depression 
Upright
T-waves
Tall R’s
develop over hours

In doubt? Get posterior leads when there’s ST-depression in septal leads! 

How to evaluate fast and wide
Episode 148

June 30, 2014


Upcoming ECG CME:
 
"Cruisin’ with Cardiograms"
Sept 14-21, 2014
 
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Causes of QRS prolongation

  • Ventricular ectopy

  • BBB (LBBB or RBBB) or paced rhythm

  • Tox/Metabolic (Na2+ channel blocker toxicity, acidosis, hyperkalemia)

  • Pre-excitation (WPW)

  • Nonspecific intraventricular conduction delay (eg. LVH)

Atrial Fibrillation with WPW

  • Very rapid, irregularly irregular tachycardia 

  • Rates may approach 250-300 bpm or higher

  • Changing QRS complex shape and width

  • Often misdiagnosed as SVT, VT, or A.fib with aberrancy

  • AV nodal blockade (BB’s, CCB’s, Amiodarone, etc.) can cause ventricular fibrillation and death

  • Amiodarone has AV nodal blockade properties & may have proarrhythmic effects in Afib with WPW (can accelerate ventricular rate and precipitate Vfib)


References:
 

Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602

Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217

Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745

Tijunelis  MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. CJEM. 2005 Jul;7(4), 262–265. PMID: 17355684

How to evaluate fast and wide
Episode 148

June 30, 2014


Upcoming ECG CME:
 
"Cruisin’ with Cardiograms"
Sept 14-21, 2014
 
Emergency Cardiology in Las Vegas 
Oct 2-5, 2014

Causes of QRS prolongation

  • Ventricular ectopy

  • BBB (LBBB or RBBB) or paced rhythm

  • Tox/Metabolic (Na2+ channel blocker toxicity, acidosis, hyperkalemia)

  • Pre-excitation (WPW)

  • Nonspecific intraventricular conduction delay (eg. LVH)

Atrial Fibrillation with WPW

  • Very rapid, irregularly irregular tachycardia 

  • Rates may approach 250-300 bpm or higher

  • Changing QRS complex shape and width

  • Often misdiagnosed as SVT, VT, or A.fib with aberrancy

  • AV nodal blockade (BB’s, CCB’s, Amiodarone, etc.) can cause ventricular fibrillation and death

  • Amiodarone has AV nodal blockade properties & may have proarrhythmic effects in Afib with WPW (can accelerate ventricular rate and precipitate Vfib)


References:
 

Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602

Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217

Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745

Tijunelis  MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. CJEM. 2005 Jul;7(4), 262–265. PMID: 17355684

Something you better know if your patient speaks Italian!
Episode 147

June 23, 2014


ECG Differentials for Syncope:

  • Ischemia
  • Dysrhythmias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia​ (ARVD)

ARVD - Epsilon waves

Background

  • Not common except in certain populations
    • ​General population: 1/1,000-1/10,000
    • Italy: 40/10,000
      • Most common cause of sudden death in young
  • Familial (autosomal dominant)
  • Male > Female
  • Caused by progressive replacement of RV myocardium by fibrofatty tissue that interferes with impulse conduction

Clinical 

  • Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  • Usually manifests between puberty - 60 years of age
  • Often have FHx of premature sudden death in family members < 35 years old
  • ECG findings are imperfect
  • ECHO, MRI, MDCT, and endomyocardial biopsy used for diagnosis

ECG findings

  • Leads V1-V3
    • ​Epsilon waves
    • TWI’s 
    • Slight prolongation of QRS
  • LBBB-type VT or many PVC’s

Management

  • Consult electrophysiology
  • Active ventricular dysrhythmias
    • Stable: Beta blockers, Class III antiarrhythmics
    • ICD placement in patients with cardiac arrest, syncope, VT
  • ​​Heightened concern if
    • Young, especially males
    • Family Hx of early sudden death
    • Many PVC’s
    • LBBB-type VT
    • Epsilon Waves with TWI in V1-V3

Reference:

Basso C, Corrado D, Marcus FL, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet. 2009 Aril 11;373(9671):1289-300. PMID:19362677

Something you better know if your patient speaks Italian!
Episode 147

June 23, 2014


ECG Differentials for Syncope:

  • Ischemia
  • Dysrhythmias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia​ (ARVD)

ARVD - Epsilon waves

Background

  • Not common except in certain populations
    • ​General population: 1/1,000-1/10,000
    • Italy: 40/10,000
      • Most common cause of sudden death in young
  • Familial (autosomal dominant)
  • Male > Female
  • Caused by progressive replacement of RV myocardium by fibrofatty tissue that interferes with impulse conduction

Clinical 

  • Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  • Usually manifests between puberty - 60 years of age
  • Often have FHx of premature sudden death in family members < 35 years old
  • ECG findings are imperfect
  • ECHO, MRI, MDCT, and endomyocardial biopsy used for diagnosis

ECG findings

  • Leads V1-V3
    • ​Epsilon waves
    • TWI’s 
    • Slight prolongation of QRS
  • LBBB-type VT or many PVC’s

Management

  • Consult electrophysiology
  • Active ventricular dysrhythmias
    • Stable: Beta blockers, Class III antiarrhythmics
    • ICD placement in patients with cardiac arrest, syncope, VT
  • ​​Heightened concern if
    • Young, especially males
    • Family Hx of early sudden death
    • Many PVC’s
    • LBBB-type VT
    • Epsilon Waves with TWI in V1-V3

Reference:

Basso C, Corrado D, Marcus FL, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet. 2009 Aril 11;373(9671):1289-300. PMID:19362677