HOWDY, Y'ALL!
My name is Sam! I'm an ER RN at a level II trauma and comprehensive stroke center. I have been in the background, assisting with ParaMed but today, I'd like to introduce a case study of an interesting patient that I've cared for in the ED setting. While not explicitly exciting (no gnarly blood or limb loss here), this case study illustrates the importance of focusing on the fine details and reassessing your patient! Without further ado...
PRESENTATION
A 41-year-old male presents to the ED via triage with a chief complaint of chest pain with an acute onset while walking his dog shortly before arriving at the ED that did not subside upon cessation of activity. He has a relevant history of prior MI with multiple stents placed, hyperlipidemia, hypertension, and admits to still smoking daily. His presentation of chest pain is classic: 8/10 left-sided pressure ("feels like someone is sitting on my chest") that radiates to the jaw bilaterally and down his left arm. If all of that wasn't enough of a red flag, the patient reports "this feels exactly like my last heart attack."
Immediately, vital signs are collected and an EKG is completed. Vitals are stable (132/91; 56; 17; 99% RA) and the EKG is shown below.
TIMELINE
pain onset 0830
arrived at facility 0915
initial EKG 0918
[Initial EKG upon arrival @ 0918.]
EKG 1 INTERPRETATION
Quite readily, we can determine this EKG doesn't meet STEMI criteria. However, it's not perfect. With the patient's history, we may expect a pathologic q wave indicative of a prior MI (not present, in fact). But we shouldn't ignore other ominous signs. There is minor depression in V2 through V6 and lead I and aVL. With this finding we should immediately look for reciprocal changes (elevation) in our inferior leads (II, III, and aVF). Nothing currently. Another good practice, especially those within the in-hospital setting, is to compare prior asymptomatic EKGs if possible. When doing this, we see new t wave inversion in V5 and V6.
With this information, what area of the heart are we concerned about? Right or inferior or posterior!
IMPORTANCE OF REASSESSING
The first 20-or-so minutes of the patient's arrival included the above in addition to basic blood work (CBC, BMP, troponin, CK, BNP), 324mg baby aspirin, and 0.4mg SL nitro.
The patient reported subtle pain relief (8/10 to 7/10) with the nitro and BP was not adversely affected. Nitro paste was applied at this time with no effect on pain or pressure (which I personally have not had much success with paste over SL or gtt, if anyone has any input one way or the other, please let me know in the comments!).
Fentanyl and ondansetron were administered as the pt began to feel nauseated. After giving the medications adequate time to onset, the patient remained adamant the only relief was from SL nitro, not fentanyl or nitro paste. This is important to note and definitely something I emphasized to the ED docs and cardiology (who has since been consulted); your patient will not typically refuse a narcotic in lieu of SL nitro unless it's The Real Deal (read: MI)
In the meantime, the patient is due for another EKG which is shown below.
NITRO
Anyone think "hold up, nitro with potential inferior/right MI??" Good thought. But we need to recall:
NITRO GOALS:
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coronary dilation > increase coronary perfusion
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systemic dilation > decrease afterload/cardiac workload
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reduce pain (helpful indicator with the "is this cardiac or is this upper gastric pain" question)
NITRO CONSIDERATIONS:
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reduce BP > reduce preload > reduce cardiac output > reduce coronary perfusion
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ensure pt is adequately fluid resus'd prior to nitro
TAKE-AWAYS
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NEVER give nitro (even SL) without PIV already in place so if you inadvertently dropped BP too low, you can temporarily salvage with fluid or pressors
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check a pressure RIGHT BEFORE nitro administration (not even the pressure you got 15min ago)
[Second EKG @ 1009.]
EKG 2 INTERPRETATION
We can see a worsening, or deepening, of the ST depression in the precordials in addition to leads I and aVL. Once again, we look to our reciprocal leads: the inferiors (I, II, and aVF). And what do we have here? ~1mm ST elevation in III and <1mm ST elevation in aVF.
Does this meet STEMI criteria? No...
So, was this patient rushed to cath lab? No...
Why, you ask? This day we had multiple STEMI-positive EKGs arrive via triage and EMS that were expedited to the cath lab over our guy here.
But, what about labs? If labs are suggestive of MI, surely that'll solidify a ticket to the cath lab at some point today, right?
LABS & MEDS
Around this time, a heparin gtt and nitro gtt are started per cardiology.
Our initial troponin has come back negative (<0.01 ng/mL). If you can conveniently pull out that chart demonstrating the elevation of troponin within the blood in an ACS event, then we'd have our answer on why we're not surprised. If you don't have this readily memorized, see right.
Initial labs were drawn ~1 hour after pain onset which would place the trop value of <0.01 in the expected range for both non-ACS individuals and those in an early ACS event. Thus, we're still have no definitive diagnostic tool resulting in favor or acute MI.
A third EKG is conducted due to the patient's persistent pain despite medication (yes, even including that nitro gtt) and the ED team's desire to hopefully pull a STEMI-positive EKG so the patient will be expedited to cath lab. This third EKG still did not pull official STEMI criteria yet displayed further deepening ST depression in lateral leads. The elevation in lead II is >1mm yet there is no contiguous elevation >1mm thus the patient is still not definably having a "STEMI."
Repeat labs, the cardiac enzymes (including troponin), were drawn per protocol three hours after the first draw which places these numbers just past 4 hours after onset of pain. This troponin is 0.02 ng/mL. When the initial and current trop are compared, we can start to appreciate the curve of the graph to the right.
TIMELINE
pain onset 0830
arrived at facility 0915
initial EKG 0918
ASA, SL nitro 0927
initial labs 0937
second EKG 1009
heparin gtt 1045
nitro gtt 1050
third EKG 1053
repeat (3h) labs 1236
cath lab 1615
Figure below: evolution of troponin in ACS setting by the AHA with V. Mahajan and P. Jarolim.
CATH LAB
At 1615, the patient arrived at the cath lab suite.
The left image below shows the culprit of the pain our patient is experiencing. The entirety of the previously stented RCA (stented multiple times, might I add) has re-occluded completely. So, how did this patient not die or at least exhibit a gnarly tomb-stone-esque STEMI? Collateral circulation. In that same image, the purple line represents the patient's native collateral circulation. In essence, this is a patient-grown bypass that effectively saved his life. What's interesting is that this collateral circulation was not observed during his cath years prior during his last MI.
Now, looking at the right image shows the post-cath stenosis. This was achieved by PCI that included manual thrombus aspiration followed by balloon angioplasty with two different diameter balloons. 0% occlusion. Beautiful.
PATIENT OUTCOME
After successful PCI, the patient was discharged ~36h later to home.
THOUGHTS
Looking back, I believe this patient could have benefited from a shorter door-to-balloon time. A reduction in door-to-balloon time would not only have reduced cardiac death, it would have reduced the time on nitro and heparin. Yes, the nitro gtt for this patient was beneficial. However, it is NOT a treatment for MIs. Patients with MIs are at risk of cardiogenic shock and that diagnosis could have been delayed due to assuming the initial shocky symptoms were attributable to the nitro gtt as opposed to the patient's worsening of condition. As far as reducing the time on heparin, just like with any medication, there are always adverse reactions of which the chances of having increase the longer the medication is given. So, in short, getting our guy to cath lab faster would have been preferable.
But, how could we have made this happen?
I believe the only real push to expedite our guy's case higher on the cath-lab-priority list would have been to achieve that beautiful, textbook STEMI* EKG.
Theoretically this could have been accomplished via a right sided EKG. A right sided EKG (shown to the right) or an easier version of just moving V4 to the patient's right (V4R) would provide an improved view of the right ventricle, thus the RCA.
Further, after more research, I was able to identify striking indicators of RCA occlusion that are oddly specific (isoelectric ST in VI with V2 depression; ST elevation in III > II, etc.) that LITFL describes but overseen in STEMI criteria.
FEEDBACK
Thank you for taking the time to read through this case study! I hope it was as educational for you as it was for myself.
What are some tokens you learned or recalled while going through this case study?
What would you have done differently or advocated for?
*I want to make note here that the concept of "STEMI" is very exclusive, not specific for its actual goal, overall not great and hopefully will fade out in the next decade. Why? Read from someone much more knowledgeable on the subject and eloquent than myself via The OMI Manifesto.
[Right sided EKG illustration by LITFL.]
REFERENCES
E. Burns and R. Buttner. (2021). Right Ventricular Infarction. Life In the Fastlane.
V. Mahajan and P. Jarolim. (2011). How to Interpret Elevated Cardiac Troponin Levels. AHA Circulation. PMID: 22105197.
P. Meyers, S. Weingart, and S. Smith. (2018). The OMI Manifesto. Dr. Smith's ECG Blog.
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