58 year old female CC: Chest pain

EMS is called to the residence of a 58 year old female complaining of chest pain.

On arrival the patient is found walking around the kitchen. She is anxious and hyperventilating.

Past medical history: Hypertension (controlled with diet and exercise)
HTN Medications: Xanax

The patient is asked to sit down in a kitchen chair and to control her breathing.

Onset: Sudden after coming home from the gym
Provoke: Nothing makes the pain better or worse
Quality: Unable to describe
Radiate: The pain does not radiate
Severity: 8/10
Time: No previous episodes

The patient appears to be in excellent physical condition and states that she works out several times a week.

Skin is warm, pink and moist.

Breath sounds are clear bilaterally.

Vital signs are assessed.

RR: 36
Pulse: 104
NIBP: 155/93
SpO2: 99 on RA

The cardiac monitor is attached.

Paramedics press the PRINT button to obtain a cleaner tracing.

A 12-lead ECG is captured.

What is your impression of this 12-lead ECG?

How would you treat this patient and why?

See also:

58 year old female CC: Chest pain – Conclusion

25 Comments

  • mike says:

    I had a similar case to this about 3 weeks ago… only difference was it was a 75 yo male with anxiety history, hypertension and renal problems. I aired on the side of caution when I witnessed ST elevation appear in II III & AVF 4 hours later and a nice generous dose of ativan he was sent home.. this is interesting!

  • Brian C. says:

    Good thing they ran a 12-lead, I know a few of Medics that would have said its just anxiety and not ran a 12lead….as my preceptor once told me, no one is ever going to get mad at you for doing too many 12-leads.

  • Jordan says:

    So this 58 YOF has an interesting EKG with an interesting HPI. She has multiple risk factors (female/HTN), and her story is fitting to an acute pathology.  It sounds like she also has a PMHx of Anxiety (HTN Meds:Xanax?). She has anxiety induced HTN? Either way, bravo the paramedic who decided not to turf this as a BLS anxiety attack.  Her 12L is interesting. She is tachycardic just over 100 (Monitor:104). Her PRI, QRSd, and axis are all WNL.  She does has a few findings that are worrysome.  Most notably, she has STE in V1-V5 (extensive anterior/proximal LAD lesion) and also; associating the tachycardia, tachypnea, and acute onset, I wouldn't mark off PE from my DDx.  She has S1,Q3,T3 signs in this EKG which can hint towards a pulmonary embolus. She is not hypoxic at this time but still worrysome.  Hopefully she was treated with O's, IV lock, serial 12L (with and without change in s/sx), 325mg ASA, and even some therapeutic/diagnostic NTG SL, and of course transport L+S to a PCI capable facility.  Great EKG with a classic story and findings. I would love to know the final Dx and findings of this patient.

  • Chris T says:

    Brugada syndrom? there is no axis deviation so im curious, never dealt with it before but no axis deviation makes me look for other reasons for the elevation in someone additionally with no risk factors
    Prolly way off but thats how i learn, it would be easy to just call it an anterioseptal STEMI

  • It just so happens that I know the final dx and findings for this patient, Jordan! 

  • Jordan says:

    well…..? was i close with either one of my two suspects?

  • jmorrison349 says:

    It would seem recless to not follow MONA/CP protocols. Healthy/ anxious people have MIs. Maybe the CP is causing anxiety????? Anterior Septal elevation. I would follow CP protocol and do my best to calm and reassure. If possible I would transmit. If not, STEMI activation would be appropriate

  • I'll post the conclusion on Monday.

  • Chris T says:

    Id treat as anteriolateral MI, calm the patient. Possibly contact med control consider ativan instead of morphine and discuss STEMI activation, i want his name with mine on this one? No 02 at this time, meditation slowing breathing best we can verbally. Continue 12 leads. Skin non diaphoretic. Comfort care, reevaluate, addition Hx so on so on I was just throwing it out there for fun. Thats what I do, think outside the box and work my way in. Just doing my best never to have tunnel vision
     

  • Chris T says:

    additionally i would expect with LAD MI anterioseptal the recip depresession should be notable in II, III, avF wouldnt it?
     

  • Chris T says:

    I didnt see any depression. Also I have to ask because it will bother me. In v5 and v6 most notably the first complex the second, then the third largest in aplitude. Doesnt look like artifact from the respiratory rate. Maybe her electrolytes are jacked up, diet what kind of diet, exercise what she taking to enhance her performance. I have seen the most "healthy" patients make themselves very sick with that stuff. but when her breathing slows or she passes out whatever comes first, take a new 12 lead see if there are any changes?
     

  • Rob M says:

    Start with the basics.  You won't kill her with high-flow O2 & calming her down, then dropping her back to 2-6L on a NC after that.  The limb leads are showing some artifact, possible due to her anxiety & movement.  Consider the narrower picture of placing the limb leads on her body vs. getting her calm & still for a good tracing.  Its difficult to see an ST-Depression & other reciporcal changes in the reciporcal leads when there's artifact.  But remember that reciporcal changes are highly confirmatory of STEMI.  My protocols don't spell out the need for reciporcal changes to call a STEMI in the field.  That said, with the fuzzy picture the limb leads paint, there does appear to be reciporcal changes.  At this juncture, hopefully we've been on scene for 5-7 minutes or less & are moving the patient to the unit.  We'll continue to get her HPI en route to the recieving facility.  Once we have her loaded, "slow emergency transport," allowing me to work, keeping her calm.  Serial 12-leads en route, IV, continued O2 therapy, 324/325mg ASA, SL NTG, & consult w/ my cardiac cath center, advise them what I have (be it a STEMI or not depending on the repeat 12s) & consider requesting MS (dosage in accordance to weight) titrate to effect.  This of course is subject to my findings on the repeat 12s.

  • I've got 2 working diagnoses, extensive anterior MI vs Tako-Tsubo (stress cardiomyopathy). Does it matter? Nah, both get a cath. Even if I had history of some stressor event, I'm leaning to AMI.

  • Stephen says:

    I would go with STEMI activation and treatment.  
    Also in regards to High Flow oxygen.  Her SPO2 is 99 on RA.  I would not be giving her much if any supplemental.  There is some data to suggest that more oxygen increases the likely hood of oxygen radical formation.  So oxygen is not as begin as thought and may be harmful in this circumstance.  In the UK they have taken the approach of just giving enough to keep the SPO2 above 92%.

  • R.Noone says:

    I would like to know how this woman is describing her pain. Whatever the answer; you are probably obligated to take her to ER.

  • her (lack of) R wave progression is troubling

  • Troy says:

    I would say either septoanterior MI or “broken heart” syndrome. IV, O2 (as needed), vitals and serial 12’s, ASA, nitro, fentanyl or MS (I’m becoming a fentanyl fan with all the research) and cath lab activation! Can’t wait till Monday to find out!

  • MJ Vuk says:

    Hmmm. She use alprazolam, maybe she's psychiatric disease. She worked out and she probaly was sweating much. The sweat can cause dysionic status (eg. hyperpotassaemia, hyponatraemia (!), hypocalcemia).
    The dysionia can cause chest pain and abnormal T wave on ECG. The chest pain could induce the hyperventilation syndrome (HVS) or panic syndrome. The panic syndrome/HVS could induce low-CO2 level and the low-CO2 level could induce vasocontriction and the vasocontriction could aggravate the chest pain and the worse chest pain could aggravate the HVS…. Circulus vitiosus.
    But she has HVS the high flow oxygen do aggravate her status. If we look the sign of hyperpotassaemia on ECG we could give Ca-gluconat iv. to the patient. To the restore respiratory buffer system we could try the auto-inhalation of CO2 (eg. from the bag) for a few minutes.
    If her breathing will be normal we need a new ECG. If the new ECG is nearly normal and her subjective symptoms are better, she likely hasn't MI (ACS). If she's has not too old ECG, compare the new with the old one. As the chest pain is the first in her life and she isn't too young, she need a cardiac examination.
    If the new ECG isn't nearly normal, she probaly has an anterolateral MI.
    The pre-hospital threatment is (in my country): IV line, ASA (300mg), MO (induvidual dosage), heparin 5000 IU, NGL (in some cases), O2, HR controll (e.g. metoprolol iv, if needed).
    Sorry for my poor English.

  • Shalom says:

    I'd play it safe and call it Anterior Stemi
    This whole scenario+ecg does smell like tako tsubo…
     I'm waiting for the angio with a little balloon in it 😉
     

  • Rose says:

    It appears that Print 2 is showing 1degree block that appears to have resolved in the 12 lead. Did the medics put the patient on O2 prior to taking the 12 lead?  I am seeing elevation in the anterior leads with no reciprocal changes.  I would try to get more hx and give ASA, O2, start IV.

  • Dave B says:

    agree with the observations already stated… STE in V1=V5… poor R wave progression, and lack of reciprocal changes… just to add a piece, the QTc is concerningly long at 481ms…

  • chris T says:

    Stephen Smith, M.D. (Dr. Smith’s ECG Blog) has a decision rule that states:
    If the mean R-wave amplitude from V2-V4 is less than 5 mm, then it is almost certainly MI. If greater than 5 mm, it is probably BER. A cutoff of 5 mm gives a sensitivity for MI of about 70%, but a specificity of greater than 95%  
    I also see that he stated in one of his decision rules for distinguishing anterior MI includes that the finding of the QTc of 481ms being also very conclusive to acute MI
    help me out anyone. I guessed of course but why is this ekg not brugada? a lot of the history and somewhat the ekg fit. Just curious

  • VinceD says:

    It seems I agree with the interperetations of everyone else, and I'd feel very comfortable calling this a STEMI with the clear ST-elevation and poor R-wave progression. The only note I'd make is that it's very easy to miss the ST-depression in II, III, and aVF on this 12-lead because the PR segment is depressed and downsloping. If you compare the J-point to the TP-segment, which is the true baseline, it is evident that there is at least 1 mm of depression in each of the inferior leads (and maybe 0.5 mm in I as well). This is a tough call to make since the P-waves arrive so near the end of the T-waves, but after comparison between leads I'd say there's at least 40, maybe 80ms of useful TP-segment baseline.

  • chris T says:

    thank you Vince!
     

  • darren says:

    I would be inclined to ignore QTC as rate is above 100 and unreliable to interpret less than 50 or more than 80.
    ST segments are interesting as is the history.
    PE was my first impression
    AnterioSeptal MI second impression but I’m inclined to consider LV Aneurysm as third Impression as no reciprocal changes?

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