Non-conducted PAC’s vs. Mobitz II
Episode 99
July 22, 2013
Non-conducted PAC’s vs. Mobitz II
Episode 99
July 22, 2013

How is the heart like a toilet??!!  Watch this week’s video and you will never flush before your toilet is finished repolarizing ever again!

 
  • Non-conducted PACs produce pauses that may mimic Mobitz II
  • Remember that the P-P interval must remain contant in Mobitz blocks
  • Management is very different for PAC’s vs. Mobitz II. True Mobitz II will require invasive procedures whereas non-conducted PAC’s are generally benign
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.


 
Scarbossa’s criteria identifies MI in patients with LBBB 
Episode 94
June 17, 2013

Tombstones, checkmarks, and bundles, oh my!

Criteria for left bundle branch block (LBBB)

  • Widened QRS > 0.12 sec in adults
  • Broad notched or slurred R waves in I and V6 WITHOUT Q-waves
  • Broad S waves in V1, V2, V3, may have a small r wave

LBBB causes ST-segment and T wave changes that make the diagnosis of acute MI difficult. Patients with LBBB can be expected to have ST-segment and T waves that are discordant to the direction of the QRS complex. This is expected and referred to as the “rule of appropriate discordance”. In fact, it is very concerning when the QRS complex and the ST-segment are concordant (point in same direction).

You CAN diagnose MI in LBBB, once you understand Sgarbossa’s criteria.

Sgarbossa’s criteria is used to diagnose MI in the setting of a known chronic LBBB. The following 3 ECG criteria can help diagnose AMI in patients with LBBB.

1. STE ≥ 1mm concordant with QRS deflection in any single lead (odds ratios for AMI of 25.2!)

2. STD ≥ 1mm in V1, V2, OR V3 that is concordant. Does NOT need to be in contiguous leads (odds ratios for AMI of 6.0)

3. Discordant STE ≥ 5mm (lower specificity) or STE >20% of size of QRS.


Everything you nees to know about Scarbossa…
Scarbossa’s criteria identifies MI in patients with LBBB 
Episode 94
June 17, 2013

Tombstones, checkmarks, and bundles, oh my!

Criteria for left bundle branch block (LBBB)

  • Widened QRS > 0.12 sec in adults
  • Broad notched or slurred R waves in I and V6 WITHOUT Q-waves
  • Broad S waves in V1, V2, V3, may have a small r wave

LBBB causes ST-segment and T wave changes that make the diagnosis of acute MI difficult. Patients with LBBB can be expected to have ST-segment and T waves that are discordant to the direction of the QRS complex. This is expected and referred to as the “rule of appropriate discordance”. In fact, it is very concerning when the QRS complex and the ST-segment are concordant (point in same direction).

You CAN diagnose MI in LBBB, once you understand Sgarbossa’s criteria.

Sgarbossa’s criteria is used to diagnose MI in the setting of a known chronic LBBB. The following 3 ECG criteria can help diagnose AMI in patients with LBBB.

1. STE ≥ 1mm concordant with QRS deflection in any single lead (odds ratios for AMI of 25.2!)

2. STD ≥ 1mm in V1, V2, OR V3 that is concordant. Does NOT need to be in contiguous leads (odds ratios for AMI of 6.0)

3. Discordant STE ≥ 5mm (lower specificity) or STE >20% of size of QRS.


Everything you nees to know about Scarbossa…
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.
  T-wave changes of severe hypokalemia
  T-wave changes of severe hypokalemia
Episode 89
May 13, 2013

 
Ever heard of “Reverse-Wellens syndrome” ? Watch this to learn about this dangerous Wellens syndrome mimic.
“Reverse-Wellens” waves deflect downward before going up & are seen in cases of severe hypokalemia that produce U-waves. See below…

Compare this to Wellens waves that may also be biphasic, but deflect upward before going down!
What anatomical distribution of ischemia is associated with the ECG changes of Wellens Syndrome? Review Wellens by watching the videos below!  

Review these previous episodes and master Wellens syndrome…

 
  Dangers of  “Non-specific ST-segment abnormalities” ​
  Dangers of  “Non-specific ST-segment abnormalities” ​
Episode 87
April 29, 2013

 
 
When in doubt, order serial ECG!
Get good at ECG’s and you will save lives!
 
  • ST-segment depression or elevation <1mm are typically interpreted as “Non-specific ST-segment abnormalities” by the ECG machine. Ischemia causes dynamic ECG changes, and this can be an early sign of MI.
  • Beware of STE in aVR! STE in aVR with other ischemic findings is BAD! (LMCA occlusion, proximal LAD occlusion, or triple vessel disease)
 

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

 
Anteroseptal ischemia or Posterior STEMI? ​
Episode 86
April 22, 2013

Syncope leads to cardiac arrest within 15 minutes. What’s the diagnosis? Find out in 15 minutes!​

Always think of the following differentials every time you are looking at an ECG in a patient who presents with syncope:
  1. Acute Coronary Syndrome
  2. Tachy/Brady-dysrhythmias (AV-blocks)
  3. WPW
  4. Brugada syndrome
  5. Hypertrophic cardiomyopathy
  6. Long/Short QT syndrome
  7. Arrhythmogenic RV dysplasia
 
Differential for ST-Depression in Anteroseptal Leads
  • Posterior STEMI
  • Anteroseptal ischemia
  • Miscellaneous
  • RBBB, Hypokalemia, etc.
Posterior Myocardial Infarction
  • ST-segment depression (STD)  instead of ST-elevation (STE)
  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • Mirror image of septal MI in leads V1-V2
  • Large R-waves instead of Q’s
  • Upright T-waves instead of T-wave inversions

ECG changes in leads V1-V3

Septal MI

STE

Inverted

T-waves

Q-waves develop over hours

Posterior MI

STD

Upright

T-waves

Tall R’s develop over hours

 

 



 
Anteroseptal ischemia or Posterior STEMI? ​
Episode 86
April 22, 2013

Syncope leads to cardiac arrest within 15 minutes. What’s the diagnosis? Find out in 15 minutes!​

Always think of the following differentials every time you are looking at an ECG in a patient who presents with syncope:
  1. Acute Coronary Syndrome
  2. Tachy/Brady-dysrhythmias (AV-blocks)
  3. WPW
  4. Brugada syndrome
  5. Hypertrophic cardiomyopathy
  6. Long/Short QT syndrome
  7. Arrhythmogenic RV dysplasia
 
Differential for ST-Depression in Anteroseptal Leads
  • Posterior STEMI
  • Anteroseptal ischemia
  • Miscellaneous
  • RBBB, Hypokalemia, etc.
Posterior Myocardial Infarction
  • ST-segment depression (STD)  instead of ST-elevation (STE)
  • Usually associated with Inferior MI due to RCA or circumflex occlusion
  • Mirror image of septal MI in leads V1-V2
  • Large R-waves instead of Q’s
  • Upright T-waves instead of T-wave inversions

ECG changes in leads V1-V3

Septal MI

STE

Inverted

T-waves

Q-waves develop over hours

Posterior MI

STD

Upright

T-waves

Tall R’s develop over hours

 

 


Everything you need to freshen up your skills on this topic…

 
When pericarditis isn’t pericarditis
Episode 84
April 8, 2013

Young patients can and will have MIs. Don’t miss the diagnosis!

Pericarditis vs. STEMI
  • First, make sure you are not missing an acute MI by looking for factors strongly associated with AMI. 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? If yes, it’s likely a STEMI
 
  • If the answer to all three 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
When in doubt, do serial EKG’s!


 
When pericarditis isn’t pericarditis
Episode 84
April 8, 2013

Young patients can and will have MIs. Don’t miss the diagnosis!

Pericarditis vs. STEMI
  • First, make sure you are not missing an acute MI by looking for factors strongly associated with AMI. 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? If yes, it’s likely a STEMI
 
  • If the answer to all three 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
When in doubt, do serial EKG’s!

Everything you every wanted to know about diffuse ST-segment elevation, covered in these related episodes