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

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
 
What’s the opposite of Wellen’s waves?
Episode 136
What’s the opposite of Wellen’s waves?
Episode 136

April 7, 2014


Hypokalemia

  • Prolonged QT (Due to U waves)
  • ST-segment depression 
  • Biphasic T-waves (Down then up, unike Wellen’s waves)
  • PVC’s, ventricular arrhythmias

Differential for Prolonged QT-intervals

  • Hypokalemia (due to U-wave)

  • Hypomagnesemia
  • Hypocalemia
  • Hypothermia
  • Acute coronary syndromes / ischemia
  • Increased intracranial pressures
  • Nachannel blocking drugs
  • Congenital
 
Quick Bedside Calculation 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), as shown below.

Check out our previous episodes on #Hypokalemia
New T-wave inversions = ACS, right? Hmmm…
Episode 135
New T-wave inversions = ACS, right? Hmmm…
Episode 135

March 31, 2014


PE’s often produce ECG changes that mimic cardiac ischemia & frequently elevate troponins. 
 
Simultaneous TWI’s in anteroseptal & inferior leads = PE until proven otherwise. 
 
ECG findings in Pulmonary Embolism
  • Sinus Tachycardia (only in 30-50%)
  • SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
  • New RBBB or incomplete RBBB
  • Superventricular tachydysrhythmias
  • Ventricular dysrhythmias
  • ST-segment  elevations or depressions
  • New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

Check out more cases here, #PulmonaryEmbolism
Lightheaded 12 YO: Deadly or Benign?
Episode 134

March 24, 2014

Want more
ECG training + CME credit?
 
is now available @ emedhome.com
 

7+ hours of instruction & 10 CME credits! 


Hypertrophic cardiomyopathy
  • Can’t miss cause of #syncope
  • Common cause of sudden death in young males
  • ECG abnormalities are typical
    • ​High voltage
    • Deep narrow Q waves
Want more practice, so that you don’t miss this?
This video has more details about Hypertrophic Cardiomyopathy
Lightheaded 12 YO: Deadly or Benign?
Episode 134

March 24, 2014


Want more
ECG training + CME credit?
 
is now available @ emedhome.com
 

7+ hours of instruction & 10 CME credits! 


Hypertrophic cardiomyopathy
  • Can’t miss cause of #syncope
  • Common cause of sudden death in young males
  • ECG abnormalities are typical
    • ​High voltage
    • Deep narrow Q waves
Want more practice, so that you don’t miss this?
This video has more details about Hypertrophic Cardiomyopathy
22 YO with a STEMI? Maybe…maybe not!
Episode 133

March 17, 2014


Go through the ECG systematically!
Use a stepwise approach or you will miss something
 

Go through the following steps every time:

  1. Rate and Rhythm
  2. Axis
  3. Intervals
  4. Enlargement
  5. Ischemia & Infarction 

​​Recognize abnormalities and consider the differentials that explain them

 

Short QT-Interval Differential

  • Hypercalcemia (STE is not uncommon)
  • Digoxin Toxicity
  • Congenital 
22 YO with a STEMI? Maybe…maybe not!
Episode 133

March 17, 2014


Go through the ECG systematically!
Use a stepwise approach or you will miss something
 

Go through the following steps every time:

  1. Rate and Rhythm
  2. Axis
  3. Intervals
  4. Enlargement
  5. Ischemia & Infarction 

​​Recognize abnormalities and consider the differentials that explain them

 

Short QT-Interval Differential

  • Hypercalcemia (STE is not uncommon)
  • Digoxin Toxicity
  • Congenital 
Pericarditis part deux: You make the call!
Episode 132

March 10, 2014


 

First, make sure you are not missing an acute MI!

  • Do you remember the factors that strongly suggest STEMI? If not, review them here

  • STEMI patients commonly have ventricular arrhythmias and very rarely have atrial dysrhythmias

  • New onset atrial fibrillation or flutter in a patient with ST-elevation favors Pericarditis 

 
Nothing in medicine is 100%…including the ECG 
When in doubt, do serial ECG’s, ECHO, Consult & Cath!

References:

Bainey KR, Bhatt DL. Acute pericarditis: appendicitis of the heart? Mayo Clin Proc. 2009;84(1):5–6. PMID: 19121246

Pericarditis part deux: You make the call!
Episode 132

March 10, 2014


Did You Miss Part I? Start HERE 
 

First, make sure you are not missing an acute MI!

  • Do you remember the factors that strongly suggest STEMI? If not, review them here

  • STEMI patients commonly have ventricular arrhythmias and very rarely have atrial dysrhythmias

  • New onset atrial fibrillation or flutter in a patient with ST-elevation favors Pericarditis 

 
Nothing in medicine is 100%…including the ECG 
When in doubt, do serial ECG’s, ECHO, Consult & Cath!

References:

Bainey KR, Bhatt DL. Acute pericarditis: appendicitis of the heart? Mayo Clin Proc. 2009;84(1):5–6. PMID: 19121246

Pericarditis vs. STEMI, Subtle Clues Part I
Episode 131

March 3, 2014


Young people can have MI’s!
Know the subtle ECG differences between STEMI & Pericarditis 

 

First, make sure you are not missing an acute MI

Look for factors that strongly favor STEMI:

  1. Reciprocal ST-segment depression in any leads (except aVR & V1)
  2. Horizontal or convex upward ST-segment morphology 
  3. STE in lead III> the STE in lead II ​​​​​​​​
Also, look for other factors that favor STEMI:
NO factors that suggest STEMI? Consider pericarditis

Look for factors that strongly favor pericarditis:

  1. Pronounced PR-segment depression in multiple leads
  2. Pericardial friction rub
Also, look for other factors that favor pericarditis:
When in doubt, do serial ECG’s, ECHO, and consider cath!

For more practice, check out previous episodes on this important topic
Pericarditis vs. STEMI, Subtle Clues Part I
Episode 131

March 3, 2014


Young people can have MI’s!
Know the subtle ECG differences between STEMI & Pericarditis 

 

First, make sure you are not missing an acute MI

Look for factors that strongly favor STEMI:

  1. Reciprocal ST-segment depression in any leads (except aVR & V1)
  2. Horizontal or convex upward ST-segment morphology 
  3. STE in lead III> the STE in lead II ​​​​​​​​
Also, look for other factors that favor STEMI:
NO factors that suggest STEMI? Consider pericarditis

Look for factors that strongly favor pericarditis:

  1. Pronounced PR-segment depression in multiple leads
  2. Pericardial friction rub
Also, look for other factors that favor pericarditis:
When in doubt, do serial ECG’s, ECHO, and consider cath!

For more practice, check out previous episodes on this important topic
Beware this really wide complex tachycardia!
Episode 130
February 24, 2014
Bizarre rhythm that is REALLY wide?
Consider tox/metabolic causes and treatment with Ca2+ & NaHCO3-

Differential for Wide QRS

  • Ventricular Ectopy
  • Paced Beats
  • Bundle Branch Block
  • Pre-excitation (WPW)
  • Metabolic/Electrolytes (acidosis, hyperkalemia)
  • Medications - Na2+ channel blocking toxicity (i.e. TCA’s & Anti-arrhythmics)
  • Nonspecific intraventricular conduction delay (ex. from LVH)
 

ECG findings in Hyperkalemia

  • Peaked T-waves
  • Widening of the QRS (often marked)
  • Prolonged PR-interval
  • Flattening and eventual loss for p-waves
  • Tachydysrrhythmias
  • Advanced AV Blocks and sinus pauses
  • Fascicular & Bundle Branch Blocks
  • Pseudo ACS with ST-segment changes
  • Sine wave morphology

Check out this previous video on Regular Really Wide Complex Tachycardia


Beware this really wide complex tachycardia!
Episode 130
February 24, 2014
Bizarre rhythm that is REALLY wide?
Consider tox/metabolic causes and treatment with Ca2+ & NaHCO3-

Differential for Wide QRS

  • Ventricular Ectopy
  • Paced Beats
  • Bundle Branch Block
  • Pre-excitation (WPW)
  • Metabolic/Electrolytes (acidosis, hyperkalemia)
  • Medications - Na2+ channel blocking toxicity (i.e. TCA’s & Anti-arrhythmics)
  • Nonspecific intraventricular conduction delay (ex. from LVH)
 

ECG findings in Hyperkalemia

  • Peaked T-waves
  • Widening of the QRS (often marked)
  • Prolonged PR-interval
  • Flattening and eventual loss for p-waves
  • Tachydysrrhythmias
  • Advanced AV Blocks and sinus pauses
  • Fascicular & Bundle Branch Blocks
  • Pseudo ACS with ST-segment changes
  • Sine wave morphology

Check out this previous video on Regular Really Wide Complex Tachycardia