Thursday, September 12, 2019

Chest pain, pelvic and abdominal pain, hypotension, and severe ischemia on the ECG

An elderly male was lethargic at the nursing home and complained of some pelvic pain, but then also chest pain and abdominal pain.  He was hypotensive.  His medications include beta blockers.

BP on arrival was 66/31, pulse 80, saturations 90% room air.  The patient was lethargic and shocky.

An ECG was recorded:
There is severe diffuse ST depression of subendocardial ischemia, with the obligatory reciprocal ST Elevation in aVR.
One might also think there are hyperacute T-waves in inferior leads, with reciprocal STD and T inversion in aVL.  

A bedside echo showed good LV function, no pericardial effusion, and normal right ventricle.  There were no B lines and the inferior vena cava looked somewhat flat.

Is this Acute Coronary Syndrome?  What do you think?

The cath lab had been activated by the time I walked into the critical care area and saw this.

However, I was skeptical that this was ACS.  Not all severe ischemia is due to ACS.  Shock/Hypotension can be the cause of ischemia or the result of ischemia.

How do we differentiate?

If ACS is the cause, then shock/hypotension is cardiogenic shock.  Cardiogenic shock has 3 etiologies:
1. pump failure
2. dysrhythmia (too fast or too slow)
3. valve dysfunction

The rhythm is sinus.  The bedside echo showed good pump function.  There was no evidence of valve dysfunction on our bedside echo.

Because of the above considerations, I thought ACS was very unlikely.  I suspected some other catastrophe as an etiology of hypotension which then caused a decrease in coronary flow and consequent ischemia.

The patient responded to fluids, but also developed pulmonary edema.  Although ACS with valve dysfunction must be considered, this was not the etiology.   (Among the investigations was an aortic CT which was negative.)

Without going into detail, sepsis was discovered as the etiology of hypotension, which in turn resulted in ischemia.  Beta blockers prevented any compensating tachycardia.

In spite of adequate BP, his ECG did not improve by the next AM, but peak troponin I was only 0.200 ng/mL, confirming that acute ACS was not the initiating factor.

Learning Points:

1. When the ECG shows ischemia, it does NOT show the initiating event of the ischemia.
2. If there is good LV function and no dysrhythmia, and no valve dysfunction, then shock is not cardiogenic, and ACS cannot be blamed as the instigating factor.
3.  Thus, you need to look elsewhere for the many etiologies of shock.  Do not fixate on ACS just because there is severe ischemia.
4. ST Elevation in aVR does NOT mean left main occlusion.  Usually it does not even represent ACS.(1)

(1) Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

How does acute left main occlusion present on the ECG?

Comment by KEN GRAUER, MD (9/12/2019):
Interesting case! — with the important clinical point “brought home” that not all ischemia on ECG is due to ACS. It is worth memorizing Dr. Smith’s deductive reasoning for why the cause of this elderly man’s marked hypotension — was unlikely to be ACS.
  • Apparently the cath lab was initially activated — but we are not told if cardiac catheterization was done … or if the order for cath activation was cancelled. While not needed for effective management of this patient (whose hypotension was found to result from septicemia) — I’d be curious to know what cath would have shown … (See below).

MTHOUGHTS on this ECG: I found the ECG in this case especially interesting — since in my opinion a few of the findings did not “fit”. None of these alter the astute decision-making deductions by Dr. Smith — but in the interest of ECG discussion, I feel the following points worthy of mention:
  • There is generalized low voltage. That is, QRS amplitude in none of the limb leads exceeds 5mm — and relative QRS amplitude is small in all 6 chest leads. This is a nonspecific finding — which in this case appears not to be due to pericardial or pulmonary effusion, nor to acute infarction. No mention is made of the patient’s body habitus (obesity is a common cause of low voltage) — and, we know nothing about whether the patient has hypothyroidism or emphysema. Perhaps voltage increased after treatment of septicemia, and after an increase in this patient’s blood pressure … ? (MY POINT is to recognize low voltage — and to at least contemplate potential causes.)
  • There could be lead misplacement in the chest leads — since lead V2 looks “out of place”. Wouldn’t the sequence of both R wave and ST-T wave progression look more natural IF lead V2 was lead V3; and lead V3 was lead V2? (Repeat ECG after verifying electrode lead placement might help explain some of the questions I raise below.)
For all of the reasons mentioned by Dr. Smith (especially good pump function with lack of wall motion abnormality on Echo — no evidence of valvular dysfunction — no more than minimally elevated peak troponin) — this ECG should be interpreted not as ACS — but rather as consistent with subendocardial ischemia. However — the typical ECG presentation of diffuse subendocardial ischemia should show significant ST depression (sometimes with T wave inversion) in virtually all leads, with the exception of leads aVR (and sometimes lead V1) that show ST elevation. The ECG in this case does not quite fit with this picture:
  • As already noted — there is no more than modest ST depression in lead V3 (Lead V3 looks “out of place”…).
  • The waves in each of the inferior leads look hyperacute! This is most marked in leads III and aVF — in which compared to the QRS complex in these leads, T waves are HUGE, being disproportionately “fat” at their peak and wide at their base. In addition, the ST segment in lead aVF is flat before the onset of the T wave — and, the ST segment “takeoff” in lead III looks like it is about to be elevated.

WHY Might This Be? To answer this question — I’d love to see this patient’s baseline ECG — and if cath was done, I’d love to learn the results ...
  • I initially considered that the ST-T wave appearance in the inferior leads (with the mirror-image opposite ST-T wave picture of lead III being seen in lead aVL) — was the harbinger of acute coronary occlusion. But, as per Dr. Smith — results of bedside Echo, troponin and serial ECGs (which apparently did not evolve) — along with clinical confirmation of acute septicemia as the etiology for this patient’s hypotension all negated a theory of acute infarction.
  • My GUESS — is that this elderly patient may have had underlying multi-vessel coronary disease — in which hyperacute inferior lead changes might reflect a “cancelling out effect” with what otherwise might have been frank inferior lead ST depression. Could there have been spontaneous reperfusion ...?

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