Monday, July 3, 2017

A 50-something woman with chest pain and dyspeoa (an Aussie)

This case comes from Max Nelson, a paramedic in Australia.

See also this post:

40-something with severe CP. True + vs. False + high lateral MI. ST depression does not localize.


Case

I was dispatched to a middle age woman (~50YO) with chest pain and nausea.

Exam: pt is huddled around toilet bowel, naked and shivering. Pt appears “well” but with pallor.

Hx: pt was woken from sleep after midnight with chest aching, dyspnoea and significant nausea. Pt moved to the toilet and had one bilious vomit. The ambulance was called and arrived approx 20 minutes later.

Signs and symptoms: nausea, dyspneoa, cold, pallor.

Now states chest pain/tightness has resolved (gone).

Hx of pain:
D- aching
O- tonight roughly 30 minutes before assessment. First experienced 2 days ago while “rushing at work” with several intermittent pains since then.
L- central chest
O- nausea, dyspnoea. Unchanged on inspiration, palpation, movement.
R- nil radiation, relieved tonight with vomit, relieved past two days with rest, rated 7/10 (not current).

Risks: postmenopausal woman, paternal CABG. Non smoker.

Allergy: penicillin

Medication: anti-depressant

Past medical history: depression

VSS: GCS 15, PERRLA, 140/80, 96BPM, 22RPM, 98% ORA, 35.5*C, 6mmol/L.

Here is the ECG, after patient's pain has resolved:
Click here to enlarge
Automated interpretation: NSR, Normal
What do you think?
















Smith comment: I see significant ST depression in inferior leads.    Remember that when there is inferior ST depression, it is NOT "inferior ischemia," as subendocardial ischemia does not localize.  When you see this, it is nearly always reciprocal to ST elevation in aVL that may be very difficult to appreciate, often because of very low voltage in aVL.  Indeed, if you look at aVL, the QRS voltage is not even 0.2 mV (2 mm) and so the ST elevation (less than 0.5 mm) then is proportionally significant.

Also, the T-waves are down-up, which is particularly indicative of ischemia (or of hypokalemia, if QT interval is very long -- really a QU-interval).

See these posts about down-up T-waves.

Case continued

Patient is moved to ambulance with wheelchair, develops pain and second ECG is recorded roughly 7 minutes later (with pain):
Click here to enlarge 
Automated interpretation: NSR, ST depressionWhat do you think?



Smith comment:

The "inferior ST depression" is more pronounced.  There is now higher T-wave voltage in V2-V4.  It is beginning to look like an LAD occlusion, proximal to the first diagonal.


Mobile Intensive Care Ambulance (MICA) requested for worsening depression.

Two further ECGs are recorded roughly 8 minutes apart en route to RV:



Click here to enlarge
Automated interpretation: "NSR, ST depression, consider subendocardial ischaemia"


Smith interpretation: ST depression is deeper.  STE in aVL is higher.  There is new ST elevation in V1 and V2, and a bit in aVR.  T-waves are now hyperacute in V1-V5.  There is ST depression now in V5 and V6.
This is a proximal LAD occlusion and may in fact be proximal to the septal perforator.  This results in ST elevation in V1 and aVR, and can also result in reciprocal ST depression in V5 and V6, which are opposite the septum.


4th ECG:
Click here to enlarge
Not much different than the 3rd


Further ECGs (not shown) displayed developing elevation in anterior leads leads with runs of ventricular bigeminy.


Outcome
This woman had thrombotic occlusion of the LAD

Smith: It was reportedly of the mid-LAD, though I am skeptical, and suspect that the report was miscommunicated because the ECG clearly shows high lateral involvement.

Her clinical course was aspirin, GTN, opioid analgesia, anti-emetic, heparin bolus pre-hospital with uncomplicated angiogram and stent at cath lab. Discharged home two days later with full recovery.

Some thoughts on the ECG from Max:

  • ECG 1: bad tracing on limb leads but inferior ST depression is the most obvious abnormality here. Both the poor tracing and ischaemic pattern should prompt serial ECGs. aVL is concerning: there is very slight ST elevation that, when interpreted in the context of the QRS amplitude, is not so slight.
  • ECG 2: there is obviously a better trace and there is progression of the inferior depression (most notable in aVF). There is also progression of the elevation in aVL, which, at this point, is diagnostic of MI. Also note the changes in anterior T-wave morphology and the gradual straightening of the ST segment in the anterior leads.
  • ECG 3, 4: obvious progression in above findings. Now with some elevation in precordial leads and notably in aVR. Low lateral depression (V5, V6)

There is very little to say about this except to highlight the importance of serial ECGs. This woman is obviously very unwell but it is feasible that, with early morning night shift brain, her symptoms may have been interpreted incorrectly and the history of the pain brushed over.

In addition to that, the computer did not interpret these as “****STEMI****, acute infarct, etc.” Don’t trust the computer! It’s generally pretty good but it cannot see your patient. You do not need to be able to pick which vessel or to able to intimately explain the changes of the ECG. Simply recognising something that is abnormal/changing is better than relying on a computer. Do not take these people to a non-PCI capable hospital!

I want to commend Max on a great job.

Learning Points:
1. Recognize that "inferior ST depression" is reciprocal to high lateral MI (aVL)
2. Do serial ECGs
3. Don’t trust the computer interpretation.

2 comments:

  1. Great case and nice serial ECGs. It's crazy how the depressions in II, III, & aVF with down-up T-waves are really what shine through on the initial ECGs. I agree this occlusion appears to be proximal to D1. We know how difficult LAD occlusion can be to pick up on ECG and that high lateral involvement is notoriously "silent" (or at least relatively silent). This highlights the importance of really seeing the inferior changes for what they are. Nice job Max! Thank you guys for sharing.
    Sam

    ReplyDelete

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