67 yo DOE. Piece of cake!
Episode 159
67 yo DOE. Piece of cake!
Episode 159

September 15, 2014


Large PE’s commonly cause T-wave inversions.

New TWI’s in anteroseptal & inferior leads = PE until proven otherwise. 


Check out more cases here #PulmonaryEmbolism
Patient found down with WCT
Episode 158
Patient found down with WCT
Episode 158

September 8, 2014


Causes of QRS prolongation
  • Ventricular ectopy
  • BBB (LBBB or RBBB) or paced rhythm
  • Pre-excitation (WPW)
  • Metabolic/Electrolytes (acidosis, hyperkalemia)
  • Medication toxicity ​
  • Nonspecific intraventricular conduction delay (eg. LVH)
​What about the causes of Really Wide QRS complexes?
  • Think of toxicologic and metabolic (hyperkalemia & severe acidosis) causes
  • Consider Calcium and Sodium Bicarbonate therapy before antiarrhythmics

Do your remember your differentials for Right Axis Deviation? How about the classic findings of TCA toxicity?

Knowledge + advocacy saves lives
Episode 157
Knowledge + advocacy saves lives
Episode 157

September 1, 2014


YOU MUST BE THE EXPERT AT READING ECG’s!

Don’t assume that your consultants know more than you!

Knowledge of ECGs & advocacy for patients will save lives! 


Want to make sure you never miss these type of cases? Check out these links and save a life…

aVR, the forgotten lead you need to remember

Why Brugada syndrome needs an EP study

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