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58 year old male CC: Chest pain

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Here’s an interesting case sent in by a faithful reader who wishes to remain anonymous.

EMS is called to the residence of a 58 year old male complaining of chest discomfort.

On arrival the patient is found sitting on the edge of the bed. He is anxious but alert and oriented to person, place, time, and event.

He was awakened from sleep by chest discomfort.

Onset: 30 minutes ago while sleeping
Provoke: Nothing makes the pain feel better or worse
Quality: Severe pressure or “ache”
Radiate: The pain does not radiate
Severity: 10/10
Time: He has had chest pain before but “not this bad”

Past medical history: HTN, dyslipidemia

Medications: Lipitor, Norvasc, ASA

Vital signs are assessed.

RR: 24
Pulse: 136
NIBP: 160/98
SpO2: 94 on RA

Breath sounds: basilar rales

The patient admits to mild dyspnea. He states that he has “gained a little weight” recently and his doctor was getting ready to put him “on a water pill.”

Temp: 99.1
BGL: 138

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is given 324 mg of aspirin, 0.4 mg NTG SL spray and placed on CPAP.

Another 12-lead ECG is captured.

The patient is loaded for transport and another rhythm strip is captured.

What do think is going on with this patient’s heart rhythm?

What do you think is wrong with this patient?

You are 15 minutes away from the local non-PCI hospital and 60 minutes away from a STEMI receiving center.

Where would you transport this patient and why?

*** UPDATE ***

This 12-lead ECG was captured en route to the hospital.

And finally this rhythm strip.

Does this shed any light on the mechanism behind the wide complexes?

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

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There has been a lot of discussion lately about identifying AMI in the presence of LBBB (see Dr. Bearemy’s “My Emergency Medicine Blog” here and a recent thread on the EKG Club). I’ve also been receiving a lot of emails offlist, so I think a full discussion is in order.

In my recent post Who benefits the most from reperfusion therapy? I posted a graph that demonstrates how patients with new bundle branch block benefit the most from reperfusion therapy.

*** Important Update ***

Recent evidence suggests that new (meaning previously undetected) LBBB patients do not “rule-in” for AMI at any greater rate than any other group of patients! That’s why it’s so important for health care practitioners to understand Sgarbossa’s criteria! Those are the patients who need immediate reperfusion therapy in the cardiac cath lab!

*** End Update ***

The problem is that in many prehospital 12 lead programs (and regional STEMI systems), patients with LBBB or a QRS duration > 0.12 sec (120 ms) are excluded! In other words, patients with wide QRS are taken to the local community hospital without interventional capability. Or, the cath lab is not activated while EMS is still in the field.

Why would you exclude the very patients who stand to benefit the most from prompt, expertly performed PCI at a cardiac center?

Simple.

It’s too difficult to figure out whether or not the BBB is new! The ECG diagnosis of STEMI can be difficult in the setting of BBB.

In False Positive Cardiac Cath Lab Activations I reviewed Larson, Menssen, Sharkey et all, False-Positive” Cardiac Catheterization Laboratory Activation Among Patients With Suspected ST-Segment Elevation Myocardial Infarction, JAMA 2007;298(23):2754-2760.

I quoted:

Patients with new or presumably new left bundle-branch block had an inordinately high prevalence of false positive catheterization laboratory activation (almost half did not have a culprit artery). Patients with a previous myocardial infarction or previous coronary bypass surgery had a significantly higher prevalence of no culprit artery, likely because of abnormal baseline ECG results.

This is obviously a big problem, and subjecting all patients with LBBB and signs and symptoms of ACS to an emergent cath or the risks associated with thrombolytic therapy is not the answer, as some authors have suggested.

If only there was some kind of algorithm that could help distinguish between patients with LBBB and acute STEMI from patients with LBBB who are not experiencing acute STEMI.

But there is such an algorithm! It’s been around for over 10 years!

The GUSTO investigators Sgarbossa et al., Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. N Eng J Med 1996; 334(8):481-487 published an algorithm which has come to be known as “Sgarbossa’s Criteria”.

The criteria seems complicated but it’s really not. Like anything else, it’s a tool. A very important tool for a critical subset of patients.

The original paper contains a flow chart from which the patient receives a score. I’m not going to publish the flow chart, because it’s not something you need to memorize.

Here is the criteria. A patient is presumed to be experiencing an evolving AMI if any of the following are present.

  1. ST segment elevation = or > 1 mm that is concordant with the QRS complex.
  2. ST segment depression = or > 1 mm in leads V1, V2, or V3.
  3. ST segment elevation = or > 5 mm that is discordant with the QRS complex.

It is the last criterion that has caused the most controversy and requires qualification.

However, before we address the third criterion, we have to dispose of a common misunderstanding.

What do we mean by concordant and discordant? The short answer is, concordant means “the same direction” and discordant means “the opposite direction”.

The rule of appropriate T wave discordance

In the presence of abnormal ventricular depolarization (left bundle branch block, right bundle branch block, paced rhythm, ventricular rhythms) the T wave should be deflected opposite the terminal deflection of the QRS complex (appropriate T wave discordance).

What is the terminal deflection?

The terminal deflection is the last deflection, or wave, of a QRS complex.

Please take the time to learn this! It is extremely important!

Take a look at the following image.

You will notice that each of these QRS complexes is labeled according to the waves are present. If the wave is large, it gets a capital letter. If the wave is comparatively small, it gets a lowercase letter.

I could talk about this image for a long time, but for now, I just want you to notice that an Rs complex is positively deflected while an rS complex is negatively deflected, even though both of them contain only an R and an S wave. But the terminal deflection of each is negative, because they both end in an S wave!

Why is this important?

When teaching Sgarbossa’s Criteria, students always get confused as to whether or not the ST segments and T waves should be deflected opposite the main deflection of the QRS complex or opposite the terminal deflection.

Well, guess what?

With LBBB, the terminal deflection is the main deflection!

So why are we splitting hairs?

Because if you learn to think in terms of the terminal deflection, you can use the rule of appropriate T wave discordance for RBBB, too!

Let’s start by looking at a patient with a normal LBBB.

I have no idea why the GE-Marquette 12SL interpretive algorithm is giving the “data quality prohibits interpretation” message for this ECG. There’s a little bit of artifact in the inferior leads, but it’s not that bad!

This is a normal looking LBBB. We know the frontal plane axis is around 0 degrees, because the QRS complex is isoelectric in lead aVF. Therefore, the perpendicular lead in the hexaxial reference system is lead I. Since lead I is positively deflected, we can place the frontal plane axis at 0 degrees. A physiological left axis deviation (0 to -30) is normal for left bundle branch block.

To put it another way, a negative QRS complex in lead III is normal for LBBB, but it should be upright and monomorphic in lead I.

Now, let’s look at the QRS complexes and the T waves.

You will notice that in every lead, the T wave is deflected opposite the QRS complex! This is “appropriate T wave discordance” in the presence of left bundle branch block.

To help illustrate this point, consider the following graphic.

The blue arrow shows the direction of the terminal deflection of the QRS complex (which is also the main deflection in the setting of LBBB). The red arrows shows the direction of the ST segment and the T wave.

This is what we mean by “appropriate T wave (and ST segment) discordance” with LBBB. Note that with RBBB, the T wave should be discordant, but the ST segment should remain isoelectric. This is why RBBB is usually not listed as a STE-mimic.

With LBBB, there is also a discordant shift of the ST segment, which is why it’s one of the most common STE-mimics! ST segment elevation in the right precordial leads (V1-V3) is a normal finding for LBBB!

In Part II, we’ll look at the “rule of appropriate T wave discordance” as it applies to RBBB and talk more about Sgarbossa’s Criteria.

See also:

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

80 year old male CC: Chest pain

Excessive discordance as a marker of acute STEMI in LBBB

80 year old male CC: Chest pain – Conclusion

“New” LBBB – What’s the big deal?

Sgarbossa’s Criteria – New Graphic

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)

62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)

58 year old female CC: Chest pain

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

Computerized interpretive statements and bundle branch blocks

6 comments

Here’s an ECG that I’ve used in my 12 lead class for many years. It’s usually good for a laugh!


I show this ECG right after I teach students to identify LBBB on the 12 lead ECG.

I explain that it was captured on an emergency call for a 80 year old male who was out jogging when he became acutely ill. EMS finds the man sitting down on a bike path. He is alert and oriented to person, place, time, and event; but he’s cool, pale, and diaphoretic with absent radial pulses. He states to the EMS crew that he has a history of high blood pressure. His medications include Norvasc, a daily aspirin, and a statin.

At this point I ask them to identify the heart rhythm.

No one speaks up right away. No one wants to look stupid in front of the class (one of the things you find out about adult learners).

Finally, I prompt them.

Do you see any P waves?

“No,” they all say in unison.

Is it regular or irregular?

“It’s regular.”

What’s the rate?

Someone says, “32.”

So what is it?

“Junctional.”

Hmmm……..

Are the QRS complexes wide or narrow?

“Wide.”

So what is it?

“Junctional with left bundle branch block.”

Before you learned how to read a 12 lead ECG and identify LBBB, what did you call slow, regular rhythms without P waves and wide QRS complexes?

“Idioventricular rhythm.”

Okay…. so what’s changed?

My point is simple. Wide complex rhythms are ventricular until proven otherwise. Granted, this rule of thumb is typically used for rhythms that are wide and fast. However, the rule is equally valid for rhythms that are wide and slow!

“But the computerized message at the top says it’s a left bundle branch block.”

Yes, it does. It also says “undetermined rhythm.”

The computer is saying, “I don’t know what rhythm this is, but the morphology matches LBBB.”

Is it possible that this rhythm is junctional with LBBB? Yes! It’s possible. But do you assume that it’s junctional? No. You assume the worst. You assume that it’s an idioventricular rhythm.

Then I pose a challenge to the class. Is there an experiment you could perform to help determine if the rhythm is junctional or ventricular? What I’m looking for is a student to say, “Well, you could try o.5 mg Atropine.”

If the rhythm responds to Atropine, there’s a good chance it isn’t ventricular. If it doesn’t respond to Atropine, it really doesn’t prove anything.

A few years back I asked my hypothetical question, and a hand went up in the back of the class (that should have been my first clue that I was dealing with a trouble-maker). I was really hoping he was going to suggest 0.5 mg Atropine. So I called on him.

With a dead-pan look on his face he says, “If the Lidocaine kills him, it was ventricular.”

Touché.