Crushing Chest pain, Tachycardia, and Very Elevated Blood Pressure in a 40-something Man.

A 40-something male called 911 for 2 hours of crushing, non-radiating, chest pain at about 11 AM.   He reported a similar episode last year when his blood pressure was very out of control and that again he has not taken his BP meds for 2 months.  He stated he had drunk 12 cans of Mountain Dew (high caffeine content) overnight. 

On exam, he was very anxious,  holding his chest, breathing normally.  Chest pain was worse with palpation.  

His BP was 250/150 with a heart rate of 150.

Here are 2 prehospital ECGs, 6 minutes apart:

Heart rate 156.  ST Elevation. Large T-waves

The computer read both ECGs as "Early Repolarization"  

What do you think?

There is definitely anterior ST Elevation.  

There is also STE in I and aVL, with reciprocal STD in inferior leads.  

There is also extreme tachycardia and elevated BP.  

Tachycardia can exacerbate pre-existing normal ST Elevation.  Moreover, both tachycardia and hypertension can result in demand ischemia.  Tachycardia is not seen in ACS unless there is a severe complication such as cardiogenic shock.  Therefore, if there is ACS here, there is also another underlying pathology contributing to tachycardia and elevated BP (toxic, volume depletion, and more).  The combination of untreated hypertension, anxiety, and caffeine could be the source of all this.

Exception!!!  The STE in I and aVL, with inferior reciprocal ST depression, should not be present due to tachycardia!!  Because of this, I think this ECG is all but diagnostic of OMI. 

Management?  I would first want to find the etiology of the tachycardia and hypertension, correct it with supportive care to normalize BP and heart rate, and then record another ECG.  But I would not waste any time.

The patient received aspirin, sublingual NTG, fluids, and reassurance.  The patient became much less anxious.

On arrival in the ED, the BP was 164/105 with a pulse of 113.  He was not placed in a critical care area or made high priority, as there were dozens of very ill patients present in the ED.  

An ECG was ordered.  Due to severe overcrowding, the ECG was not recorded for 57 minutes.  

Here it is:

QTc is 418.  The computer called non-specific changes

What do you think? 

 

This was immediately recognized by our very astute emergency physicians as diagnostic of LAD occlusion.  There is minimal ST Elevation in I, aVL V2, V3, V4, with hyperacute T-waves in V2-V4 and some inferior ST depression.

The cath lab was activated.

If you don't immediately recognize this as anterior (LAD) OMI, you can use the 4-variable formula or the simplified formula, both explained in detail at this post. 

The 4-variable formula value is (using 418 for QTc, 3.0mm for STE60V3, 11.5mm for RAV4, and 11.5mm for QRSV2) = 20.10, which is diagnostic of LAD occlusion.  The most accurate cutpoint is 18.2, but any value over 19.0 is very specific for LAD occlusion.

Initial hs troponin I (which returned much later) was 141 ng/L.  This value by itself does not help to distinguish type 1 from type 2 MI, or even from non-MI acute or chronic myocardial injury, much less to diagnose OMI vs. NOMI.  In a U.S. population, taking all patients with an initial value over 200 ng/L (which includes many with much higher troponins) the PPV for any MI (type 1 or 2 MI, but not for OMI) was about 70% and for type 1 MI was about 50%.  Thus, the PPV at 200 ng/L is less than 50% for type 1 MI and even less for OMI.

16 minutes later, before leaving for the cath lab, this was recorded:

Evolution of hyperacute T-waves, making it more obvious, but still not meeting STEMI criteria.

And another 16 minutes later:

This is the first ECG that was called STEMI by the computer algorithm (because it was the first STEMI! Because STEMI is defined by mm of ST Elevation!)  All previous ECGs were OMI without STEMI [STEMI (-) OMI].

On this ECG, you see what appears to be evidence of inferior injury as well.  However, as Dr. Balasubramian pointed out, this is due to lead misplacement. 

Immediately after this ECG, the patient was transported to the cath lab.

Angiogram--Culprit for the acute anterior ST elevation MI is ruptured plaque/thrombotic occlusion of the proximal and mid LAD.  A stent was placed with subsequent TIMI III flow and with "good runoff" after wards (a very good sign that there is good microvascular reperfusion).

Formal Echocardiogram--Normal left ventricular size, normal wall thickness and moderate systolic dysfunction.  The estimated left ventricular ejection fraction is 38%.

Regional wall motion abnormality

--mid and apical segment of the septum, anterior, anterolateral and apex akinetic and large.

--Regional wall motion abnormality-apical inferior wall, dyskinetic.  This confirms the inferior OMI.

Here is a 36 hour ECG

Evidence of significant amount of infarction (barely any R-wave left in V2 and V3)

Reperfusion T-waves (look exactly the same as Wellens' waves because Wellens waves ARE reperfusion T-waves.

Learning Points:

1. Normal ST Elevation can be exaggerated by tachycardia.

2. Stabilize vital signs and record another ECG if the diagnosis is unclear

3. STE from OMI can be mistaken as Normal ST Elevation 

4. Recognize hyperacute T-waves

5.  Use the 4-variable formula if needed