15 yo girl with anxiety? Check the ECG!
Episode 146

June 16, 2014


15 yo girl with anxiety? Check the ECG!
Episode 146

June 16, 2014


ECG Differentials for syncope / palpitations:
  • Ischemia
  • Tachy / Bradycardias & AV-blocks
  • Intervals
    • WPW / Pre-excitation
    • Long / Short QT syndromes
  • Hypertrophic cardiomyopathy
  • Brugada syndrome
  • Arrhythmogenic RV dysplasia

WPW Syndrome 

Ventricular pre-excitation
  • 0.1-3% of the population
  • Classic triad
    • Shortened PR interval
    • Widened QRS interval
    • Delta wave (Not always present!)​
  • ​Predisposition to atrial tachydysrhythmias 
  • ​​WPW can be intermittent
 

Don’t hesitate to get ECGs on young patients!

Look in all 12 leads and suspect WPW if you notice a short PR-interval.


For more syncope cases, check out… #Syncope

33yo with reflux? Just slap yourself!
Episode 145

June 9, 2014


AMI in Pregnancy

     Pregnancy increases risk of AMI 3-4X
  • Slight overall risk
  • 3rd trimester to 6 weeks post-partum
  • Maternal mortality = 5-11%
  • Fetal mortality = 9%
  • ​Increased with pregnancy at older ages
  • Increased atherosclerosis and risk factors
     Most common causes
         1.  Coronary artery dissection (35-50%)
  • Usually anterior wall
  • Hormonal changes to vessel wall
  • Shear forces
  • Underlying disease (i.e. connective tissue disorders)
         2.  ​​Plaque rupture due to atherosclerosis (40%)
 
ECG changes in Pregnancy
  • Axis changes (LAD or RAD)
  • Small Q in III
  • Non-specific TWI’s
  • Increased R/S ration in V1-V2
​Treatment
  • Coordinate with OB and Cardiology
  • Usual Care (ASA probably ok)
  • PCI > Thrombolytics 
    • Concern for hemorrhage peripartum
    • Concern for coronary artery dissection
    • Thrombolytics: placental transfer is low
    • Heparin is ok
Young women do get MI’s!

33yo with reflux? Just slap yourself!
Episode 145

June 9, 2014


AMI in Pregnancy

     Pregnancy increases risk of AMI 3-4X
  • Slight overall risk
  • 3rd trimester to 6 weeks post-partum
  • Maternal mortality = 5-11%
  • Fetal mortality = 9%
  • ​Increased with pregnancy at older ages
  • Increased atherosclerosis and risk factors
     Most common causes
         1.  Coronary artery dissection (35-50%)
  • Usually anterior wall
  • Hormonal changes to vessel wall
  • Shear forces
  • Underlying disease (i.e. connective tissue disorders)
         2.  ​​Plaque rupture due to atherosclerosis (40%)
 
ECG changes in Pregnancy
  • Axis changes (LAD or RAD)
  • Small Q in III
  • Non-specific TWI’s
  • Increased R/S ration in V1-V2
​Treatment
  • Coordinate with OB and Cardiology
  • Usual Care (ASA probably ok)
  • PCI > Thrombolytics 
    • Concern for hemorrhage peripartum
    • Concern for coronary artery dissection
    • Thrombolytics: placental transfer is low
    • Heparin is ok
Young women do get MI’s!

Reference:

Sahni G. Chest Pain Syndromes in Pregnancy. Cardiology Clinics. 2012;30(3):343–367. PMID: 22813362

A “bread and butter” case with some “toast and jam” for pearls
Episode 144

June 2, 2014


Upcoming Conference & Workshop:
International Conference on Emergency Medicine 
June 10, 2014 in Hong Kong
Differential for Narrow & Irregular Tachycardias
 
1. Atrial Fibrillation
  • No distinct regular atrial activity
  • Causes an irregularly irregular rhythm
  • "Lumpy bumby" with no clear P waves that map out
  • Treatment is cardioversion in unstable patients

​2. Atrial flutter with variable conduction

  • Regular atrial activity (flutter waves) at ~ 300 bpm
  • Variable ventricular conduction causes an irregular rhythm
  • P waves may be subtle and easy to miss (look closely at V1)
  • Treatment is cardioversion in unstable patients

3. Multifocal atrial tachycardia (MAT)

  • Clear atrial activity that is irregular (no dominant atrial focus)
  • Causes an irregularly irregular rhythm (some P waves may not be conducted)
  • At least 3 morphologically distinct P waves
  • Variable intervals (P-P, P-R, R-R)
  • Aberrant conduction may be present
  • Ventricular rate usually 100-150
  • ​When rate < 100, called “wandering atrial pacemaker”
  • Most often associated with pulmonary disease (acute or chronic)
  • Beta blockers, Theophylline, HypoMg2+ and HypoK+ may be contributing factors
  • Not a destabilizing rhythm, treat the underlying cause

Never shock sinus tachycardia or MAT!


Still hungry? How about some more narrow complex tachycardia ?
A “bread and butter” case with some “toast and jam” for pearls
Episode 144

June 2, 2014


Upcoming Conference & Workshop:
International Conference on Emergency Medicine 
June 10, 2014 in Hong Kong
Differential for Narrow & Irregular Tachycardias
 
1. Atrial Fibrillation
  • No distinct regular atrial activity
  • Causes an irregularly irregular rhythm
  • "Lumpy bumby" with no clear P waves that map out
  • Treatment is cardioversion in unstable patients

​2. Atrial flutter with variable conduction

  • Regular atrial activity (flutter waves) at ~ 300 bpm
  • Variable ventricular conduction causes an irregular rhythm
  • P waves may be subtle and easy to miss (look closely at V1)
  • Treatment is cardioversion in unstable patients

3. Multifocal atrial tachycardia (MAT)

  • Clear atrial activity that is irregular (no dominant atrial focus)
  • Causes an irregularly irregular rhythm (some P waves may not be conducted)
  • At least 3 morphologically distinct P waves
  • Variable intervals (P-P, P-R, R-R)
  • Aberrant conduction may be present
  • Ventricular rate usually 100-150
  • ​When rate < 100, called “wandering atrial pacemaker”
  • Most often associated with pulmonary disease (acute or chronic)
  • Beta blockers, Theophylline, HypoMg2+ and HypoK+ may be contributing factors
  • Not a destabilizing rhythm, treat the underlying cause

Never shock sinus tachycardia or MAT!


Still hungry? How about some more narrow complex tachycardia ?
Answers to the 2014 UMEM ECG Competition
Episode 143

May 26, 2014


SPOILER ALERT:

Test your skills & take the test the before watching this!


Did you miss a few questions?
 
Study the linked content & learn from mistakes
to make sure you don’t miss when it really counts. 
 
Your patients deserve it!

Answers:

  1. B. Pathological Q-waves are at least 40 ms (1mm) in duration (width). They can develop within a couple hours of onset of MI. 

  2. D. ST elevation in II,III,aVF, & V1 + ST depression in lead V2 is highly suggestive of inferior & right ventricular MI. What if V2 has ST depression but V1 & V3 are isoelectric? Do you remember how to diagnose RV MI? How about posterior MI?

  3. A. You can diagnose MI in patients with left bundle branch block. Concordant ST depression ≥ 1mm in V1, V2, or V3 is specific for an acute MI. Make sure you are aware of the Modified Sgarbossa Rule

  4. A. Sometimes ST depression needs to be treated just like ST elevation! Know that de Winter T-waves are suggestive of an acute proximal LAD lesion. 

  5. C. Wellens syndrome is specific for an obstructed LAD lesion. Patients may be asymptomatic, but may benefit from non-emergent catheterization. Check out these other can’t miss cases of Wellens syndrome and make sure you know what’s the opposite of Wellens waves

  6. D. New T-wave inversions in aVL can be the first sign of an inferior STEMI. Subtle reciprocal changes can preceed ST elevations in MI. 

  7. D. Hyperkalemia can cause advanced AV blocks and sinus pauses. When dealing with a bizarre rhythm that is not responding to ACLS, consider hyperkalemia & treat with empiric Ca2+ and NaHCO3-

  8. A. Pericarditis does not give you the check mark sign & PR depression is NOT specific for pericarditis! Know the differences in ECG findings of STEMI vs Pericarditis. 

  9. B. Simultaneous T-wave inversions in anteroseptal and inferior leads = PE until proven otherwise. Do you know the other ECG findings in PE

  10. B. High ventricular voltages and deep narrow Q waves are concerning for hypertrophic cardiomyopathy. Get a doppler echo to make the diagnosis. What else must you look for on the ECG of patients with syncope?

  11. D. Toxic and metabolic derangements can cause really…really wide QRS complexes. Do you remember the differential for wide complex & regular tachycardias

  12. A. Hypercalcemia and Digoxin toxicity may cause short QT intervals. Are you using a systematic and stepwise approach to reading your ECG’s?

  13. D. Accelerated idioventricular rhythms are associated with reperfusion of STEMI. Consider AIVR in patients who are s/p thrombolytics with rhythms that are too slow to be VT. 

  14. D. Procainamide should be your drug of choice in stable patients with atrial fibrillation with WPW. AV nodal blockade can cause ventricular fibrillation and death!

  15. C. Atrial flutter is the most commonly missed tachydysrhythmia. It can cause a regular or irregular rhythm based on its pattern of conduction. Do you know the tips and tricks to avoid misdiagnosing it?

  16. B. In type I, 2nd degree AV block, each atrial impulse has longer and longer conduction time until it fails to conduct to the ventricle. Are you confident in your treatment of unstable bradycardia

  17. B. Patients with syncope and suspected Brugada syndrome need admission for EP testing. 

  18. A. Don’t rule out ventricular tachycardia and call it SVT based on age. Have you heard about the Mattu 2-step algorithm for wide complex tachycardia? Use it to make sure you do not miss this deadly diagnosis. 

  19. C. In type II, 2nd degree AV block, some but not all impulses are transmitted to the ventricles WITHOUT progressive PR interval lengthening. Watch difficult rhythm interpretation made easy for more practice. 

  20. D. The terminal QRS vector in aVR and V6 should always be opposite one another. If the vectors point in the same direction, consider misplaced leads and repeat the ECG! Using a systematic approach and knowing the causes of right axis deviation should have made you consider lead misplacement. 


 
Answers to the 2014 UMEM ECG Competition
Episode 143

May 26, 2014


SPOILER ALERT:

Test your skills & take the test the before watching this!


Did you miss a few questions?
 
Study the linked content & learn from mistakes
to make sure you don’t miss when it really counts. 
 
Your patients deserve it!

Answers:

  1. B. Pathological Q-waves are at least 40 ms (1mm) in duration (width). They can develop within a couple hours of onset of MI. 

  2. D. ST elevation in II,III,aVF, & V1 + ST depression in lead V2 is highly suggestive of inferior & right ventricular MI. What if V2 has ST depression but V1 & V3 are isoelectric? Do you remember how to diagnose RV MI? How about posterior MI?

  3. A. You can diagnose MI in patients with left bundle branch block. Concordant ST depression ≥ 1mm in V1, V2, or V3 is specific for an acute MI. Make sure you are aware of the Modified Sgarbossa Rule

  4. A. Sometimes ST depression needs to be treated just like ST elevation! Know that de Winter T-waves are suggestive of an acute proximal LAD lesion. 

  5. C. Wellens syndrome is specific for an obstructed LAD lesion. Patients may be asymptomatic, but may benefit from non-emergent catheterization. Check out these other can’t miss cases of Wellens syndrome and make sure you know what’s the opposite of Wellens waves

  6. D. New T-wave inversions in aVL can be the first sign of an inferior STEMI. Subtle reciprocal changes can preceed ST elevations in MI. 

  7. D. Hyperkalemia can cause advanced AV blocks and sinus pauses. When dealing with a bizarre rhythm that is not responding to ACLS, consider hyperkalemia & treat with empiric Ca2+ and NaHCO3-

  8. A. Pericarditis does not give you the check mark sign & PR depression is NOT specific for pericarditis! Know the differences in ECG findings of STEMI vs Pericarditis. 

  9. B. Simultaneous T-wave inversions in anteroseptal and inferior leads = PE until proven otherwise. Do you know the other ECG findings in PE

  10. B. High ventricular voltages and deep narrow Q waves are concerning for hypertrophic cardiomyopathy. Get a doppler echo to make the diagnosis. What else must you look for on the ECG of patients with syncope?

  11. D. Toxic and metabolic derangements can cause really…really wide QRS complexes. Do you remember the differential for wide complex & regular tachycardias

  12. A. Hypercalcemia and Digoxin toxicity may cause short QT intervals. Are you using a systematic and stepwise approach to reading your ECG’s?

  13. D. Accelerated idioventricular rhythms are associated with reperfusion of STEMI. Consider AIVR in patients who are s/p thrombolytics with rhythms that are too slow to be VT. 

  14. D. Procainamide should be your drug of choice in stable patients with atrial fibrillation with WPW. AV nodal blockade can cause ventricular fibrillation and death!

  15. C. Atrial flutter is the most commonly missed tachydysrhythmia. It can cause a regular or irregular rhythm based on its pattern of conduction. Do you know the tips and tricks to avoid misdiagnosing it?

  16. B. In type I, 2nd degree AV block, each atrial impulse has longer and longer conduction time until it fails to conduct to the ventricle. Are you confident in your treatment of unstable bradycardia

  17. B. Patients with syncope and suspected Brugada syndrome need admission for EP testing. 

  18. A. Don’t rule out ventricular tachycardia and call it SVT based on age. Have you heard about the Mattu 2-step algorithm for wide complex tachycardia? Use it to make sure you do not miss this deadly diagnosis. 

  19. C. In type II, 2nd degree AV block, some but not all impulses are transmitted to the ventricles WITHOUT progressive PR interval lengthening. Watch difficult rhythm interpretation made easy for more practice. 

  20. D. The terminal QRS vector in aVR and V6 should always be opposite one another. If the vectors point in the same direction, consider misplaced leads and repeat the ECG! Using a systematic approach and knowing the causes of right axis deviation should have made you consider lead misplacement. 


 
3 patients died because their MD’s didn’t watch this video…
Episode 142

May 19, 2014


Download & test your skills with the 2014 UMEM ECG Competition 

Answers revealed on next weeks video! 


PE’s often produce ECG changes that mimic cardiac ischemia!
 
Simultaneous TWI’s in AS & Inf leads = PE until proven otherwise. 
 
ECG findings in Pulmonary Embolism
  • Sinus Tachycardia 
  • SIQIII or SIQIIITIII (Rightward Axis)
  • New RBBB or incomplete RBBB
  • Superventricular tachydysrhythmias
  • Ventricular dysrhythmias
  • ST-segment elevations or depressions
  • New TWI’s, especially in anteroseptal +/- inferior leads
    • Acute Pulmonary HTN = PE until proven otherwise!

Check out more cases here, #PulmonaryEmbolism
 
3 patients died because their MD’s didn’t watch this video…
Episode 142

May 19, 2014


Download & test your skills with the 2014 UMEM ECG Competition 

Answers revealed on next weeks video! 


PE’s often produce ECG changes that mimic cardiac ischemia!
 
Simultaneous TWI’s in AS & Inf leads = PE until proven otherwise. 
 
ECG findings in Pulmonary Embolism
  • Sinus Tachycardia 
  • SIQIII or SIQIIITIII (Rightward Axis)
  • New RBBB or incomplete RBBB
  • Superventricular tachydysrhythmias
  • Ventricular dysrhythmias
  • ST-segment elevations or depressions
  • New TWI’s, especially in anteroseptal +/- inferior leads
    • Acute Pulmonary HTN = PE until proven otherwise!

Check out more cases here, #PulmonaryEmbolism
 
John Doe has a seizure. What good is an ECG?
Episode 141

May 12, 2014


Download the 2014 UMEM ECG Competition and test yourself!

Answers coming soon. 


Be systematic and consider the differentials when you find an abnormality!

 
Causes of Rightward Axis Deviation
  • Right ventricular hypertrophy
  • Pulmonary HTN - Acute (PE) & chronic lung disease (COPD)
  • Left posterior fascicular block
  • Lateral MI (from Q-waves in lead I)
  • Ventricular ectopy (VT)
  • Hyperkalemia
  • Na2+ channel blocker toxicity
  • Lead misplacement / Dextrocardia
  • Normal thin adults with horizontally positioned hearts
Causes of QRS prolongation
  • BBB (LBBB or RBBB) or paced rhythm
  • Pre-excitation (WPW)
  • Ventricular ectopy
  • Metabolic/Electrolytes (acidosis, hyperkalemia)
  • Nonspecific intraventricular conduction delay (eg. LVH)
  • Na2+ channel blocker toxicity ​
Na2+ channel blocker toxicity
  • Tachycardia (usually)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1 (sometimes)
  • Prolonged QRS
  • Prolonged QTc

Think of cocaine (Na2+ channel blocker) toxicity in pts. with fever & HTN 

 
John Doe has a seizure. What good is an ECG?
Episode 141

May 12, 2014


Download the 2014 UMEM ECG Competition and test yourself!

Answers coming soon. 


Be systematic and consider the differentials when you find an abnormality!

 
Causes of Rightward Axis Deviation
  • Right ventricular hypertrophy
  • Pulmonary HTN - Acute (PE) & chronic lung disease (COPD)
  • Left posterior fascicular block
  • Lateral MI (from Q-waves in lead I)
  • Ventricular ectopy (VT)
  • Hyperkalemia
  • Na2+ channel blocker toxicity
  • Lead misplacement / Dextrocardia
  • Normal thin adults with horizontally positioned hearts
Causes of QRS prolongation
  • BBB (LBBB or RBBB) or paced rhythm
  • Pre-excitation (WPW)
  • Ventricular ectopy
  • Metabolic/Electrolytes (acidosis, hyperkalemia)
  • Nonspecific intraventricular conduction delay (eg. LVH)
  • Na2+ channel blocker toxicity ​
Na2+ channel blocker toxicity
  • Tachycardia (usually)
  • Right Axis Deviation
  • Tall R wave in aVR
  • Tall R in V1 (sometimes)
  • Prolonged QRS
  • Prolonged QTc

Think of cocaine (Na2+ channel blocker) toxicity in pts. with fever & HTN 

 
Need some more practice with AV blocks?
Episode 140

May 5, 2014


Take Home Points

  1. Find out what the atrium is doing (map out p-waves)

  2. Find out what the ventricle is doing
  3. Figure out the relationship between them (PR-interval) 
The answer usually lies in the PR-interval!
 
  • ​Check out more cases of AV block by watching this previous episode

  • Biphasic T-waves (i.e. Wellens syndrome) are indicative of ischemia.

  • New biphasic T-waves in the inferior leads, may be indicative of RCA lesions. 

Need some more practice with AV blocks?
Episode 140

May 5, 2014


Take Home Points

  • When interpreting difficult rhythms, always do these three things:
  1. Find out what the atrium is doing (map out p-waves)

  2. Find out what the ventricle is doing
  3. Figure out the relationship between them (PR-interval) 
The answer usually lies in the PR-interval!
 
  • ​Check out more cases of AV block by watching this previous episode

  • Biphasic T-waves (i.e. Wellens syndrome) are indicative of ischemia.

  • New biphasic T-waves in the inferior leads, may be indicative of RCA lesions. 

What’s a better predictor of ACS than the ECG?
Episode 139

April 28, 2014



References:

Body R, Carley S, Wibberley C, et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010;81(3):281–286. PMID: 20036454

Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629. PMID: 16304077

Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263. PMID: 9786377

What’s a better predictor of ACS than the ECG?
Episode 139

April 28, 2014


Most important predictors of ACS

  • History is still the key predictor!
    • ​Chest pain associated with the following is concerning
      • ​Radiation
      • Diaphoresis
      • Vomiting
      • Exertion
  • ​​​​Get serial ECGs when history is concerning or patient has persistant pain

References:

Body R, Carley S, Wibberley C, et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010;81(3):281–286. PMID: 20036454

Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629. PMID: 16304077

Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263. PMID: 9786377

2 patients, 20 mins, tons of pearls!
Episode 138

April 21, 2014



You can find several more cases of STEMI vs. Pericarditis here!
2 patients, 20 mins, tons of pearls!
Episode 138

April 21, 2014


STEMI vs. Pericarditis

  • Clinical signs & symptoms are often unreliable
  • First troponin can also be unreliable
  • ECG machine interpretation is not to be trusted!
  • Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that rule-in STEMI:

  • Reciprocal ST depression in any leads (except aVR & V1)
  • Horizontal or convex upward ST-segment morphology 
  • STE in lead III> the STE in lead II ​​​​​​​​
  • R-T sign or “check mark sign
  • Q-waves that you know are new

Look for the factors that rule in STEMI before thinking pericarditis! 

Step 2. Factors that suggest pericarditis:

  • Pronounced PR depression in multiple leads 
  • Spodick sign
  • Pericardial friction rub
  • Pericardial effusion 

When in doubt…CATH!

 

You can find several more cases of STEMI vs. Pericarditis here!
"Kitchen syncope" revealed!
Episode 137

April 14, 2014


Want more
ECG training + CME credit?
 
The Advanced ECG Workshop
is available at emedhome.com

7+ hours of video & 10 CME credits! 

Want to go to Hong Kong?

The International Conference on Emergency Medicine

is in Hong Kong on July 10, 2014

Go to www.icem2014.org for more info

AV Blocks…the key to the diagnosis is the PR-interval!

  • Lengthening of the PR = Mobitz I
  • Constant PR = Mobitz II (Usually has wide QRS)

"Kitchen syncope" revealed!
Episode 137

April 14, 2014


Want more
ECG training + CME credit?
 
The Advanced ECG Workshop
is available at emedhome.com

7+ hours of video & 10 CME credits! 

Want to go to Hong Kong?

The International Conference on Emergency Medicine

is in Hong Kong on July 10, 2014

Go to www.icem2014.org for more info

AV Blocks…the key to the diagnosis is the PR-interval!

  • Lengthening of the PR = Mobitz I
  • Constant PR = Mobitz II (Usually has wide QRS)