62 year old male CC: Chest pain

62 year old male presents to the emergency department complaining of chest discomfort.

Past medical history is significant for dyslipidemia and ulcerative colitis. Also prior history of significant tobacco use.

Maternal history of CAD. Maternal and paternal history of CVA.

The patient’s only medication is Lipitor but he took an aspinin en route to the hospital.

Onset: Patient states the pain started that morning and became progressively worse since lunch time
Provoke: Nothing makes the pain better or worse
Quality: Sharp and nonpleuritic
Radiate: The pain radiates down the right arm to the bicep
Severity: 7/10
Time: Patient states he experienced a similar pain in his right upper chest several days prior while playing tennis. He stopped exercising and the pain resolved.

The pain makes the patient feel “a little clammy.” He denies shortness of breath. He states that he feels “a little dizzy” but denies palpitations. He had a negative stress test 3-4 years ago.

He has a known history of left bundle branch block.

The patient’s skin is warm and dry.

Breath sounds clear bilaterally. No JVD. Neuro exam normal.

Vital signs:

Resp: 18
Pulse: 60
BP: 140/72
SpO2: 98 on RA

A 12-lead ECG is captured and presented to the ED physician within 5 minutes of arrival.

An “old” ECG is pulled from the computer system for comparison.

What is your impression?

*** UPDATE ***

After oxygen and nitroglycerin the patient reports a significant decrease in pain.

An additional 12-lead ECG is captured.

There is now slightly less ST-elevation in leads V3 and V4.

Remember that a secondary ST-segment abnormality (as opposed to a primary ST-segment abnormality) should not “improve” with oxygen and nitroglycerin!

In other words, if this ST-elevation was caused just by the LBBB, it shouldn’t be “getting better”. Changing ST-segments suggest the dynamic supply vs. demand characteristics of ACS!

Now, let’s go back to the initial 12-lead ECG. Is the ST-elevation in the anterior leads cause for concern?

Go back and read Identifying AMI in the presence of left bundle branch block (or paced rhythm).

Remember, discordant ST-elevation = or > 5 mm is the least specific of Sgarbossa’s criteria! That’s why we use the modified rule that I learned from Dr. Stephen Smith of Dr. Smith’s ECG Blog.

That criterion states that discordant ST-elevation should not be more than 0.2 (or 20%) the depth of the S-wave in the setting of left bundle branch block (ST/QRS ratio).

Using that criterion, how does this ECG measure up? Let’s take a look.

The patient was ultimately cathed and angiography revealed 100% occlusion of the LAD.

Final thought:

Does it get any more difficult that that? If Dr. Smith’s decision rule works this great, shouldn’t we be shouting it from the rooftops?

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part I

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part II

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)

7 Comments

  • Christopher says:

    Comparing the two I see that P-mitrale is now present, so LAE (look at the data, the P axis also shifted). Change in the shape/size of the ST segment in the inferior leads, and flattening in the high lateral leads of the ST segment. Morphological changes in II, aVF, aVR, and V5 perhaps explainable through lead placement.Following Sgarbossa's 3 criteria:1. >=1mm STE concordant? No.2. >=1mm STD V1-V3? No.3. >=5mm STE discordant? Yes.The STE in V2-V4 appears to have increased over time and appears to be greater than would be expected for the S-waves.The criteria support calling the MI in the face of LBBB. Patient presentation also supports this.Differentials I'm considering include cholecystitis, liver problems, chest/rib pain, and atypical presentation of an AMI.

  • Christopher says:

    Typo: *looking at the data, the P axis also shifted.Also, it looks like there is new notching present, which I seem to recall having some significance.

  • Tom B says:

    Great reply, Christopher! Speaking of how much ST-elevation is appropriate for the size of the S-wave, what is our cut-off?Remember, the least specific of Sgarbossa's criteria is discordant ST-elevation = or > 5 mm! I'll give you the answer (since it's changed recently).According to recent data out of Hennepin County Medical Center (with credit to Dr. Stephen Smith of Dr. Smith's ECG Blog) the cut-off is 0.2 (or 20%) the depth of the S-wave! So would this ECG qualify based on the modified criteria?Tom

  • Christopher says:

    Using a lil image wizardry it appears the ST segment is >=5mm STE and >20% the size of the preceding S-wave.The image below shows two areas (green 20% of the preceding S-wave).LBBB 20% of S-wave

  • Tom B says:

    Well done, Christopher! I'll add the update and my own graphic now. After all, the case has been up for at least 10 minutes! LOL! :)Tom

  • Terry says:

    Thanks Tom this Sgarbossa criteria has been a real eye opener for me. Can't tell you how many times I have said or been told you can't dx an MI with a BBB or all new LBBB is an MI until proven otherwise. Keep up the good work.

  • Tom B says:

    Terry -I completely understand! That's an important myth to "bust"! It's unfortunate that we indoctrinate paramedics this way, but the reality is that it's misunderstood by many ED physicians.One of the ways the "myth" got started is the fact that AMI used to be diagnosed with Q-waves on the 12-lead ECG, and LBBB can obscure Q-waves.Now that we're in the reperfusion era, it's ST-elevation that is important, and of course LBBB also causes ST-elevation whether acute STEMI is present or not, so it does change the "rules" and it makes the dx more challenging (but as you've seen, certainly not impossible).The final complication is that previous studies that led to the creation of "new LBBB" as a criterion for reperfusion therapy were based on a rise and fall of cardiac biomarkers, not an acute occlusive thrombus in an epicardial coronary artery confirmed by angiography! In other words, the studies combined STEMI and NSTEMI. That's why the work done in Minneapolis is so important. You may recall that almost half of LBBB had no culprit artery in the Larson study! That's one of the reasons I pay attention when they come up with a modified criterion that works! Tom

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