68 yo female – AMS
The patients family visiting from Louisiana during Hurricane Ida calls 911 due to the patient collapsing after quickly running downstairs when her sister was attempting to light a gas stove she was not familiar with.
EMS finds her lying on a carpeted floor alert to voice and diaphoretic. Airway is intact, the patient did not have the strength to hold herself upright in a sitting position, had weak bilateral radial pulses with cool clammy extremities and increased respiratory effort with clear lung sounds, pupils are normal. The family mentions she is diabetic, my partner takes her BGL and SPO2 while I try a manual blood pressure. SPO2 reads 71% but again, her hands are cold – we can assume by her presentation that she is most likely hypoxic but we don’t know to what extent. BGL- 104. A nasal cannula set to 4 lpm placed on her. Blood pressure had to be palpated due to no diastolic being heard = 78/P.
A quick look at the SPO2 (I had my partner also place a hot pack in her hand) and we had little to no improvement. My partner put her on a NRB at 15 lpm while I obtained a 12 lead.
It’s worth mentioning at this point that the patient is upstairs (as nearly all of our critical patients are), the stairway is very narrow, the room she is in has several sharp narrow turns and the residence is absolutely full of furniture making access, assessment, treatment and extrication ever so challenging.
The Fire department arrives on scene and I call over the radio to have them bring up our stair chair.
First 12 lead tracing:
Regular Sinus Rhythm at ~ 90 bpm.
QRS is 103 ms
QTc measured at 463 ms (just slightly over normal)
The axis is -13°
Deep Q waves noted in leads III and AVF with minimal ST elevation – AVL has reciprocal ST depression as does lead I.
The T waves in III and AVF have a bit of a biphasic appearance and lead II may actually have a slight amount of ST depression.
♦Of course the computer reads this as Inferior Infarct, age undetermined. Very helpful.
Lead I has a flat ST segment and AVL has a concave downward sloping ST segment
QS waves noted in V1 with upright T wave. ~ 0.5mm of ST elevation
T waves in V2 and V3 are a bit fatter than I would expect and nearly symmetrical
V4 has loss of R wave voltage with increased S wave
R Wave Progression not fully transitioning until V5
ST Depression in V4-V6 *maximal in V6* as well as depression in I/avl
♦ A Posterior MI would have STD maximal in V1-V4 whereas LVH would have maximal STD in the left laterals.
Now at this point, I have 2 prevailing thoughts:
1. The changes seen here are simply due to LVH.
-LVH presents with ST depression maximal in V5/V6 -seen here
-“Strain” pattern is highly suggestive of LVH – seen in AVL
◊ Cornell Criteria for LVH – The R wave in AVL + the S wave in V3. >28mm in men / >20mm in women = LVH
I believe we have that satisfied here Note – V3 S wave is “cutoff” by the computer.
2. New or old Inferior ischemia:
-We have 2 contiguous leads with minimal STE + 2 reciprocal leads with STD
◊ I do not mention STEMI / NSTEMI on purpose due to no traditional criteria being met. I do however favor the more accurate term OMI (Occlusion Myocardial Infarction)
– There are clear pathologic Q waves in both Leads III and AVF. These however do seem a bit deep for an acute occlusion – possibly subacute *there is a biphasic component to the T waves leaning towards reperfusion.
◊ Q waves can develop in little as 1 hour of the ischemic process starting
– STE in Lead III is greater than in lead II + STE present in V1 – very suspicious for a RV Infarct.
Actually a 3rd thought – a combination of the above findings.
The patient is able to speak clearly although she is very lethargic – She is FAST negative and as we start the process of moving her on the stair chair, through the obstacle course and into the ambulance – I inquire about chest pain.
She admits to having an episode of chest pain just prior to collapsing – I am unable to determine if she actually lost consciousness or this was “near” syncope.
She also admits to having several short episodes of chest pain over the past few days, each time while physically exerting herself. She did not seek medical care during any of these episodes. I took a look at her ankles – minimal edema she says has developed recently. New CHF? she had no history of it.
We get her loaded into the ambulance, obtain IV access with fluid bolus and a recheck of the SPO2 – we’re now up to 91% and her mentation is improving; states she has chest pain now 8/10 described as sharp, non radiating. 324 mg ASA administered and I repeated the 12 lead which was nearly identical. In our local EMS system, we have what we call a Cardiac Alert. We use this when we suspect an ACS event without STEMI criteria. I transmitted the ECG and transport emergently to a PCI capable hospital.
I decide to capture a right sided V4R:
Notice there is no St elevation noted in V4R making a RV Infarct less likely
The ST morphology of Lead III has changed to more a “strain” pattern as well as V5 and V6
PAC present in the augmented leads
The patient has ongoing, non radiating chest pain but this is making a strong case for LVH with some other underlying acute condition – possibly CHF and not an occlusion. After a fluid bolus, the BP improved to about 86/P.
A 3rd ECG captured (standard 12 lead) ~ 5 mins from the ED:
Not much change other than the STD in V4 increasing. Minimal STD now present in V3
The ED 12 lead:
Better quality but not much change
The jr doctor took a look at my ECG’s, compared them with the hospital tracing and clearly stated – “NO STEMI”.
How very astute.
By now, the BP had improved to 98/40 with SPO2 hovering at 92% on oxygen, she still complains of chest pain but now the pain increases with deep inspiration.
POCUS shows “a flat right ventricle” – his words, not mine. I took a peek over his shoulder, ultra sound is not my thing but I could clearly see there was little to no movement over the RV.
The Attending doc says – Massive acute or subacute PE. He starts rapidly ordering labs etc. as they wheel the most pleasant patient I had all day into the recesses of some unknown portion of the hospital.
I have to admit, I was a bit surprised by this. In my opinion, none of the ECGs were indicative of PE – there was the elevation in III > II with minimal STE in V1. I had a suspicion of a problem in the right ventricle but there were no episodes of Tachycardia, no dominant R in V1, no right axis deviation, no rightward strain pattern and no S1Q3T3.
In hindsight, I think this demonstrates how much LVH mimics an ACS event. There were even some dynamic changes over ~30 mins on the tracings – not all that uncommon for LVH.
The Q waves could have developed over the past few days but I have to assume the ST elevation and biphasic T waves were from the RV wall motion abnormality +/- the hypertrophy.
In an ironic way – Hurricane Ida probably saved her life since she normally lives alone.