Can’t miss cases of Wellens Syndrome
Episode 103
August 19, 2013

If you love Wellens ECGs, here’s 4 cases and 16 minutes of love!

​Wellens Syndrome
  • T-wave abnormality in precordial leads (V2-V3, +/-V4)
  • Specific for obstructed LAD lesion
  • High risk for extensive anterior wall MI and death
    • 2 types
      • Type 1-Deeply symmetric TWI
      • Type 2- Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).
  • ST changes are often absent and patient can be chest pain free!
  • Look carefully at the ECG when the machine tells you there are “non-specific ST abnormalities”
  • Cardiac biomarkers often initially normal
  • Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
  • Do not diagnose in the presence of large amplitude QRS complexes
  • When in doubt get serial ECG’s!

Knowing how to diagnose Wellens saves lives. Make sure you know about it. These previous episodes will help, check them out…

 
Can’t miss cases of Wellens Syndrome
Episode 103
August 19, 2013

If you love Wellens ECGs, here’s 4 cases and 16 minutes of love!

​Wellens Syndrome
  • T-wave abnormality in precordial leads (V2-V3, +/-V4)
  • Specific for obstructed LAD lesion
  • High risk for extensive anterior wall MI and death
    • 2 types
      • Type 1-Deeply symmetric TWI
      • Type 2- Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).
  • ST changes are often absent and patient can be chest pain free!
  • Look carefully at the ECG when the machine tells you there are “non-specific ST abnormalities”
  • Cardiac biomarkers often initially normal
  • Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
  • Do not diagnose in the presence of large amplitude QRS complexes
  • When in doubt get serial ECG’s!

Knowing how to diagnose Wellens saves lives. Make sure you know about it. These previous episodes will help, check them out…

 

Everything you want to know about 2nd degree AV Blocks

Episode 98​
July 15, 2013

​​When is 2nd degree AV block not the same as Mobitz? Here’s all you want to know about 2nd degree AVB!

 
2nd Degree AV Block

Atrial impulses fail to conducts to the ventrcles. (ie P:QRS >1)

  • Type I (Mobitz I, Wenckebach)

    • Each atrial impulse has longer and longer conduction time until it fails to conduct to the ventricle.

    • Block usually at level of AV node, producing narrow QRS’s

    • May sometimes also have wide QRS’s in patient’s with pre-existing bundle branch block or intraventricular conduction delay

    • At least 2 consecutive P-QRS complexes demonstrate progressive PR-interval lengthening before a non-conducted P-wave

    • P-P interval remains constant​

  • Type II (Mobitz II)

    • Some but not all impulses are transmitted to the ventricles WITHOUT progressive PR lengthening.

    • Typically due infranodal block, producing wide QRS’s (can also sometime be narrow!)

    • At least 2 consecutive P-QRS complexes demonstrate constant PR-intervals before the non-conducted P wave

    • P-P interval remains constant

What if there are not any consecutive P-QRS complexes before the non-conducted P?

  • If there is a fixed 2:1 ratio throughout, you can’t tell if the PR-interval is lengthening, hence can’t differentiate between Type I & II

  • Just call it “2nd degree AV block with fixed 2:1 block”

 
Advanced (high-grade) AV Block
  • P:QRS conduction ratio of is 3:1 or higher
  • Produces extremely slow ventricular rates
  • Can be Mobitz I or II, may be able to differentiate based on width of QRS

Right Bundle Branch Block

3-Step approach to diagnosing AV blocks 

 

Everything you want to know about 2nd degree AV Blocks

Episode 98​
July 15, 2013

​​When is 2nd degree AV block not the same as Mobitz? Here’s all you want to know about 2nd degree AVB!

 
2nd Degree AV Block

Atrial impulses fail to conducts to the ventrcles. (ie P:QRS >1)

  • Type I (Mobitz I, Wenckebach)

    • Each atrial impulse has longer and longer conduction time until it fails to conduct to the ventricle.

    • Block usually at level of AV node, producing narrow QRS’s

    • May sometimes also have wide QRS’s in patient’s with pre-existing bundle branch block or intraventricular conduction delay

    • At least 2 consecutive P-QRS complexes demonstrate progressive PR-interval lengthening before a non-conducted P-wave

    • P-P interval remains constant​

  • Type II (Mobitz II)

    • Some but not all impulses are transmitted to the ventricles WITHOUT progressive PR lengthening.

    • Typically due infranodal block, producing wide QRS’s (can also sometime be narrow!)

    • At least 2 consecutive P-QRS complexes demonstrate constant PR-intervals before the non-conducted P wave

    • P-P interval remains constant

What if there are not any consecutive P-QRS complexes before the non-conducted P?

  • If there is a fixed 2:1 ratio throughout, you can’t tell if the PR-interval is lengthening, hence can’t differentiate between Type I & II

  • Just call it “2nd degree AV block with fixed 2:1 block”

 
Advanced (high-grade) AV Block
  • P:QRS conduction ratio of is 3:1 or higher
  • Produces extremely slow ventricular rates
  • Can be Mobitz I or II, may be able to differentiate based on width of QRS
 

Mastered AV blocks to make sure your patients get the best care possible. If not, check out these previous episodes…

AV blocks & Rabbit ears for RBBB vs. PVC

Right Bundle Branch Block

3-Step approach to diagnosing AV blocks 

 
AV blocks & Rabbit ears for RBBB vs. PVC
Episode 97
July 8, 2013

Virtually a full review of AV blocks from a single patient…in 14 minutes!​

When interpreting rhythms, always do these three things:
1. Find out what the atrium is doing
2. Find out what the ventricle is doing
3. Figure out the relationship between the atrium and ventricle (PR-interval)

The answer usually lies in the PR-interval!

1st Degree AV Block = “delay” > 200ms at AV node or His bundle.

When the P:QRS>1, consider 2nd and 3rd degree AV Blocks

2nd Degree AV Block = Not every atrial impulse goes through to the ventrcles. (ie P:QRS >1)

  • Mobitz Type I (Wenckebach) -Each atrial impulse has longer and longer delay until it fails to conduct to the ventricle. Progressive PR-interval lengthening before a dropped beat.

  • Mobitz Type II - typically due to block below AV node in His bundle. Some but not all impulses are transmitted to the ventricles WITHOUT progressive PR lengthening.

3nd Degree AV Block = P waves march out normally at 60-100 bpm with no relation to the ventricular rate which is typically slower than sinus or the atrial rate.
 

RBBB vs PVC’s

Wide QRS complexes, with large R waves in V1 can be caused by both RBBB and PVC’s. An RSR’ pattern or the “rabbit ear appearance” is typically seen in V1 with RBBB. PVC’s from a left ventricular source will also have dominant R waves in V1. One way to differentiate between RBBB and a PVC is to pay attention to the morphology of the QRS complex.

 
  • RBBB - typically has a small R wave (left rabbit ear) and a tall R’ (right rabbit ear).
  • PVC’s - will have a larger R wave (left rabbit ear) and a smaller R’ (right rabbit ear) or a “hitched” downslope to the wave.
 

Extra Pearl

R wave > 15mm in setting of RBBB + Rightward Axis = Right ventricular hypertropy (RVH)


Bunny ears not enough? Want more? Check out these related episodes…
 
 
 
AV blocks & Rabbit ears for RBBB vs. PVC
Episode 97
July 8, 2013

Virtually a full review of AV blocks from a single patient…in 14 minutes!​

When interpreting rhythms, always do these three things:
1. Find out what the atrium is doing
2. Find out what the ventricle is doing
3. Figure out the relationship between the atrium and ventricle (PR-interval)

The answer usually lies in the PR-interval!

1st Degree AV Block = “delay” > 200ms at AV node or His bundle.

When the P:QRS>1, consider 2nd and 3rd degree AV Blocks

2nd Degree AV Block = Not every atrial impulse goes through to the ventrcles. (ie P:QRS >1)

  • Mobitz Type I (Wenckebach) -Each atrial impulse has longer and longer delay until it fails to conduct to the ventricle. Progressive PR-interval lengthening before a dropped beat.

  • Mobitz Type II - typically due to block below AV node in His bundle. Some but not all impulses are transmitted to the ventricles WITHOUT progressive PR lengthening.

3nd Degree AV Block = P waves march out normally at 60-100 bpm with no relation to the ventricular rate which is typically slower than sinus or the atrial rate.
 

RBBB vs PVC’s

Wide QRS complexes, with large R waves in V1 can be caused by both RBBB and PVC’s. An RSR’ pattern or the “rabbit ear appearance” is typically seen in V1 with RBBB. PVC’s from a left ventricular source will also have dominant R waves in V1. One way to differentiate between RBBB and a PVC is to pay attention to the morphology of the QRS complex.

 
  • RBBB - typically has a small R wave (left rabbit ear) and a tall R’ (right rabbit ear).
  • PVC’s - will have a larger R wave (left rabbit ear) and a smaller R’ (right rabbit ear) or a “hitched” downslope to the wave.
 

Extra Pearl

R wave > 15mm in setting of RBBB + Rightward Axis = Right ventricular hypertropy (RVH)


Bunny ears not enough? Want more? Check out these related episodes…
 
 
 
Review of Wellens Syndrome
Episode 96
July 1, 2013

Wellens Syndrome

  • T-wave abnormality in precordial leads (V2-V3, +/-V4)
  • Specific for obstructed proximal LAD lesion
  • High risk for extensive anterior wall MI and death
  • 2 types
    • Type 1-Deeply symmetric TWI
    • Type 2- Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).

  • ST changes are often absent and patient can be chest pain free
  • Cardiac biomarkers often initially normal
  • Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
  • Do not diagnose in the presence of large amplitude QRS complexes
  • When in doubt get serial ECG’s!

Wellens, make sure you know about it. These will help…


 
Review of Wellens Syndrome
Episode 96
July 1, 2013

Wellens Syndrome

  • T-wave abnormality in precordial leads (V2-V3, +/-V4)
  • Specific for obstructed proximal LAD lesion
  • High risk for extensive anterior wall MI and death
  • 2 types
    • Type 1-Deeply symmetric TWI
    • Type 2- Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).

  • ST changes are often absent and patient can be chest pain free
  • Cardiac biomarkers often initially normal
  • Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
  • Do not diagnose in the presence of large amplitude QRS complexes
  • When in doubt get serial ECG’s!

Wellens, make sure you know about it. These will help…


 
Lumen stenosis and size is not as important as plaque vulnerability 
Episode 95
June 24, 2013

Size isn’t everything! Here’s the most important video of the year! (no joke)

Plaque vulnerability based on 3 major factors

  1. Fibrous cap
  2. Lipid core
  3. Inflammatory cells

Recent stress testing and catheterizations are NOT predictive of new plaque rupture!

  • Small plaques may be more unstable and more prone to rupture
  • Infarct related arteries often have non-obstructing plaque, before rupture and MI
  • Angiography can not distinguish stable vs. unstable plaque composition, and give no information about the fibrous cap or lipid core

Key point: Nothing will risk stratify you to zero! You can’t always rely in the recently negative stress test or “unremarkable” cath.  History of presenting illness is the most important information and should guide your management.


Must read references:

Libby, P. (2013). Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. New England Journal of Medicine, 368(21), 2004–2013.

 
References:

Virmani, R., Burke, A. P., Farb, A., & Kolodgie, F. D. (2006). Pathology of the Vulnerable Plaque. Journal of the American College of Cardiology, 47(8), C13–C18.


 
Lumen stenosis and size is not as important as plaque vulnerability 
Episode 95
June 24, 2013

Size isn’t everything! Here’s the most important video of the year! (no joke)

Plaque vulnerability based on 3 major factors

  1. Fibrous cap
  2. Lipid core
  3. Inflammatory cells

Recent stress testing and catheterizations are NOT predictive of new plaque rupture!

  • Small plaques may be more unstable and more prone to rupture
  • Infarct related arteries often have non-obstructing plaque, before rupture and MI
  • Angiography can not distinguish stable vs. unstable plaque composition, and give no information about the fibrous cap or lipid core

Key point: Nothing will risk stratify you to zero! You can’t always rely in the recently negative stress test or “unremarkable” cath.  History of presenting illness is the most important information and should guide your management.


Must read references:

Libby, P. (2013). Mechanisms of Acute Coronary Syndromes and Their Implications for Therapy. New England Journal of Medicine, 368(21), 2004–2013.

 
References:

Virmani, R., Burke, A. P., Farb, A., & Kolodgie, F. D. (2006). Pathology of the Vulnerable Plaque. Journal of the American College of Cardiology, 47(8), C13–C18.


 
  ECG findings in Thoracic Aortic Dissection
Episode 93
June 10, 2013

Just a simple inferior STEMI? Don’t be too sure….

About 4-8% of Thoracic Aortic Dissection’s (TAD)
will present with ECG signs of STEMI
  • Usually inferior ST-elevation or diffuse ischemia with ST-depression
  • Typical for inferior STEMI’s to have reciprocal changes in leads I & aVL
  • Consider posterior and right ventricular extension of infarction with inferior STEMI
  • Not all chest pain (CP) = ACS, don’t forget to consider TAD
    • CP + new neurological SSx → TAD
    • CP + new diastolic murmur → TAD
    • CP + new renal failure → TAD
    • CP + new ischemic extremities → TAD
    • Remember that TAD can dissect backward and cause hemorrhagic pericardial effusions…careful with that heparin gtt!


  ECG findings in Thoracic Aortic Dissection
Episode 93
June 10, 2013

Just a simple inferior STEMI? Don’t be too sure….

About 4-8% of Thoracic Aortic Dissection’s (TAD)
will present with ECG signs of STEMI
  • Usually inferior ST-elevation or diffuse ischemia with ST-depression
  • Typical for inferior STEMI’s to have reciprocal changes in leads I & aVL
  • Consider posterior and right ventricular extension of infarction with inferior STEMI
  • Not all chest pain (CP) = ACS, don’t forget to consider TAD
    • CP + new neurological SSx → TAD
    • CP + new diastolic murmur → TAD
    • CP + new renal failure → TAD
    • CP + new ischemic extremities → TAD
    • Remember that TAD can dissect backward and cause hemorrhagic pericardial effusions…careful with that heparin gtt!


  Check mark sign in STEMI
Episode 92
June 3, 2013

Ever hear of the ‘check-mark sign’? Well, now you have. And it might help you save a life.

  • QR-T complex or “Check mark sign” - a finding associated with STEMI.
    • Limited ST-segment, because immediately after the R wave there is a small downslope (s-wave) that quickly transitions to the T-wave
    • Uncommon, but can be helpful when other rules do not help distinguish between STEMI and Pericarditis
    • Be careful when diagnosing pericarditis in cases where the ECG shows check mark sign
  • Young patients DO have MI’s
  • Don’t trust ECG computer interpretations. You should be the expert!

Pericarditis vs. STEMI Algorithm - covered in previous episodes (links below)

  • First, make sure you are not missing an acute MI by looking for factors strongly associated with STEMI. Ask yourself:
  1. Is there reciprocal ST-segment depression in any leads (except for aVR and V1)? If yes, it’s a STEMI. If not,…

  2. Is the ST-segment morphology convex or horizontal? If yes, it’s a STEMI. If not,…

  3. Is the STE in lead III> the STE in lead II? If yes, it’s a STEMI.

  4. Are there new Q waves? (Need old ECG) If yes, it’s likely a STEMI

  5. Is there a QR-T or check mark sign? If yes, it’s likely a STEMI

  • If the answer to all these questions is NO, then you should consider the possibility of it being pericarditis. Factors associated with pericarditis:
  1. Is there pronounced PR-segment depression in all leads? If so, it’s possibly pericarditis. (But could also be due to cardiac ischemia, so make sure you are not missing an MI first by answering the first 3 questions!)
  2. Is there a pericardial friction rub? If so, it’s possibly pericarditis


  Check mark sign in STEMI
Episode 92
June 3, 2013

Ever hear of the ‘check-mark sign’? Well, now you have. And it might help you save a life.

  • QR-T complex or “Check mark sign” - a finding associated with STEMI.
    • Limited ST-segment, because immediately after the R wave there is a small downslope (s-wave) that quickly transitions to the T-wave
    • Uncommon, but can be helpful when other rules do not help distinguish between STEMI and Pericarditis
    • Be careful when diagnosing pericarditis in cases where the ECG shows check mark sign
  • Young patients DO have MI’s
  • Don’t trust ECG computer interpretations. You should be the expert!

Pericarditis vs. STEMI Algorithm - covered in previous episodes (links below)

  • First, make sure you are not missing an acute MI by looking for factors strongly associated with STEMI. Ask yourself:
  1. Is there reciprocal ST-segment depression in any leads (except for aVR and V1)? If yes, it’s a STEMI. If not,…

  2. Is the ST-segment morphology convex or horizontal? If yes, it’s a STEMI. If not,…

  3. Is the STE in lead III> the STE in lead II? If yes, it’s a STEMI.

  4. Are there new Q waves? (Need old ECG) If yes, it’s likely a STEMI

  5. Is there a QR-T or check mark sign? If yes, it’s likely a STEMI

  • If the answer to all these questions is NO, then you should consider the possibility of it being pericarditis. Factors associated with pericarditis:
  1. Is there pronounced PR-segment depression in all leads? If so, it’s possibly pericarditis. (But could also be due to cardiac ischemia, so make sure you are not missing an MI first by answering the first 3 questions!)
  2. Is there a pericardial friction rub? If so, it’s possibly pericarditis


Digoxin Toxicity & AV block: Will IV calcium cause “stone heart”?
Episode 91
May 28, 2013
Digoxin Toxicity & AV block: Will IV calcium cause “stone heart”?
Episode 91
May 28, 2013

Potassium, digoxin, calcium, AVBs, stone heart…so much to discuss this week!

  • When considering AV blocks, always pay attention to the PR segments to help distinguish between Mobitz I, Mobitz II, & AVD/CHB.
  • Hyperkalemia can cause just about anything, including AV blocks!
  • Calcium in probably safe in digoxin toxicity.
  • Levine et al. in their retrospective review of 129 patients who had digoxin toxicity, found that IV calcium did not seem to cause malignant dysrhythmias or increase mortality. They found no support for the historical belief that calcium is contraindicated for these hyperkalemic patients.
  Impressive Syndrome
  Impressive Syndrome
Episode 90
May 21, 2013

Impressive horses, syphilis, and strokes…all in 14 minutes!
 
Hyperkalemia is the syphilis of electrocardiography. It is the great imitator!
 
  • Hyperkalemia can cause STE and mimic STEMI’s & is the most rapid killer in DKA
  • Renal patients with systemic complaints should get an ECG and hyperkalemia should be considered
  • Bizarre Rhythm? Wide QRS? Think Tox/metabolic…get Calcium & Bicarb ready!
  • Hyperkalemic periodic paralysis, aka. Impressive Syndrome - Inherited autosomal dominant condition that affects Na+ channels in muscle and the ability to regulate K+ in the blood. 


 
  When STE in aVR = Left main coronary artery stenosis
Episode 88
May 6, 2013

aVR - the forgotten 12th lead

  • BEWARE OF STE in aVR for patients with acute coronary syndromes
  • STE in aVR with other ischemic findings on ECG is BAD! (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
    • ST-elevation in aVR not applicable in setting of SVT or in asymptomatic patients without ischemic symptoms
  • aVR STE > 1.0mm should make you worry
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • STE of aVR in very tachycardic rhythms (i.e. SVT), and in the setting of severe hypertension and LVH may be a normal variant or have no clinical significance.

Learn more about the forgotten lead, aVR! This episode is loaded with important references you can share with your cardiologist as needed…

References:
 
 
 
 
 
 
 
 
  When STE in aVR = Left main coronary artery stenosis
Episode 88
May 6, 2013

aVR - the forgotten 12th lead

  • BEWARE OF STE in aVR for patients with acute coronary syndromes
  • STE in aVR with other ischemic findings on ECG is BAD! (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
    • ST-elevation in aVR not applicable in setting of SVT or in asymptomatic patients without ischemic symptoms
  • aVR STE > 1.0mm should make you worry
  • LMCA occlusion may require CABG, so avoid drugs like clopidogrel
  • 70% mortality without immediate PCI
  • Medical therapy including lytics does not improve mortality
  • Emergent PCI may decrease mortality to 40%
  • Time delay to PCI is the only predictor of survival
  • STE of aVR in very tachycardic rhythms (i.e. SVT), and in the setting of severe hypertension and LVH may be a normal variant or have no clinical significance.

Learn more about the forgotten lead, aVR! This episode is loaded with important references you can share with your cardiologist as needed…

References: