41 Year Old Female: Chest Pain

Here's an interesting case sent in by faithful reader Carl R. Christiansen, Paramedic, from Norway. As usual, changes have been made to protect patient confidentiality.

It's an early Sunday morning when you are dispatched to a hotel for a 41 year old female with chest pain. 

You and your partner enter the hotel room and find the woman lying in bed.  As she sits up to greet you, you notice the color of her face is pink, but she seems to be slightly uncomfortable and restless.  She tells you that she woke up at about 8 am with chest pain in the center of her chest, which does not move anywhere.  She isn't short of breath or lightheaded…no nausea or vomiting, or anything else out of the ordinary other than the chest pain.  The pain doesn't change with breathing, movement, or palpation.  She adds that she's had some similar pain come and go over the last three or four days, but never as bad as this.  You ask her to rate her discomfort, and she tells you 9/10.

As you assess her appearance, you don't see anything abnormal… no JVD, no edema.  Her pulse feels rapid but regular, and her lung sounds are clear bilaterally.  Inspection and palpation of her chest and back are normal.  You do a FAST screening, which shows nothing abnormal.  All she can tell you is that she had a couple of glasses of wine with dinner the night before, and slept through the night until the pain woke her up this morning..  She has no relevant medical history, and takes no medications.

While you are getting the history, your partner takes a set of vitals:

  • Pulse:   104 and regular
  • BP:        210/155
  • RR:       18 and regular
  • CTC:     Pink, warm and dry
  • SpO2:   99%

You acquire the following 12 Lead ECG:

What do you think? What would you do next?

The treating paramedic gave the following treatments:

  • One SL NTG
  • 300 mg ASA
  • IV established
  • 2.5 mg of Morphine IV
  • 600 mg Plavix orally

As the above are being done, a second 12 Lead is acquired:

After the treatments were given, the patient's blood pressure dropped to 129/84, and her heart rate dropped to and remained at about 80. The Paramedic called a Code STEMI and transported the patient to a PCI center.  Upon arrival there, this last 12 Lead was acquired by the crew:

What do you see on these 12 Leads?

Would you have called a Code STEMI?

What would your treatment have been for this patient?

 

 

 

37 Comments

  • *** Akutt hjerteinfark mistenkes ***

    You can say that again!

  • Mike M. says:

    Ahh hah! The printout in Norway is a bit different than here in the US, took me a second to see that, I'm so used to just looking at the section of the printout instead of the "I, II, III, etc" before seeing the tracing for that particular lead.
    1. Anyway, I see Anteroseptal injury (ST elevation V1-V4) with reciprocal ischemic changes in the inferior leads. And, due to the significant drop in BP after the dose of NTG and MS as well as the inferior wall involvement, I suspect there may be some RV involvement as well and I'd like to see a printout with some right-sided precordials. To top it all off, there might be a PE mixed in there as well as there (S1Q3T3).
    2. Call the STEMI.
    3. My treatment, would have been the same plus O2 and a right sided 12-lead. And after I see the drop in BP I'd start another IV line because we may be giving fluids.

  • Would love to know if this met the precordial lead LVH criteria prior to the onset of acute STEMI.

  • Billy says:

    Some st segment change in the second 12-lead with a lot of st segment depression also. Maybe some st elevation in v-2 through v-4 didnt see much in the first one to activate our STEMI here but if pain is unchange after ntg n ms04 then tx to cardiac center is deemed appropate. Would have to fly our pt from where im from due to 2hrs either way to the closest STEMI center. Cant wait for conclusion n please any.advise on what anyone saw diff in first 12-lead as im only a 2 year paramedic and just got 12-leads on our trucks. Billyscott25@gmail.com thanks

  • Mendez says:

    Yes, I would have called the STEMI , but did the pain subsided with the meds ?
    I think this is an anterior septal MI. But I would have done a r side lead. II, III, and avf look low on all 3 EKGs.

  • David Baumrind says:

    @Tom… i noticed as well the voltage seemed high in V5 and V6… i'd love to know if it met it as well, it would give credence to the theory that anterior MI attenuates the voltage in the right chest leads… if that's what you are referring to lol!

     

  • David Baumrind says:

    @Mike.. good comments! are  you saying that changes in the inferior wall represent inferior wall involvement? or are you saying they are reciprocal changes to the anterior involvement? @Billy…your transport decision is tough  with the closest STEMI center 2 hours away! Do you need certain criteria met to activate cath?

  • Lance says:

    There is PR segment depression found in the precordial leads.  The T waves are hyperacute with concave morpholgy and signs of global ischemia with ST depression and T wave changes.  
     
    I'm leaning towards pericarditis.

  • Bonnie says:

    Did they bother to ask the Question if she thought she might be pregnanat? After all, it seems we hear more and more females are becomming mothers in ther 30's and 40's..From what i read, i didnt see that question asked..From my training, u are to ask any female that if they are under the age of 55.

  • Josh says:

    LVH is definitely met here. The sum of V1 and V2 S waves clearly meet the criteria.

  • Aaron says:

    Obvious ekg changes between the first and second ekg, That alone with a symptamatic pt would warrant a cardiologist in a cath lab,  I would have felt comfortable activating a Stemi protcol on this pt,

  • ZTM says:

    Why is the QRS in AVR up?

  • DW says:

    Both ECG's show indication of LVH, and the second one showing the Anteriorseptal involvement with the ST elevation, I would call a STEMI.

  • Christopher says:

    ZTM,
    You're actually looking at -aVR, i.e. the electrical inverse of aVR. Confused me at first as well!

  • Mike M. says:

    @David B. – I'm confused as to what you're referring to regarding the term "involvement". Is it incorrect to say that the inferior wall is involved in this particular case just because it is showing signs of ischemia? Is the Anterior wall "involved" and the inferior wall is just getting the outside edges of the ischemic "circle" as the injury becomes more acute? 
    Thanks for keeping me on my toes! I'm a brand new paramedic (just passed internship and my NR written exam, have my skills practical this Sunday) so I'd love some clarification so I can talk the talk.
    What I think that I'm saying is that the changes we see in the Inferior leads are reciprocal ischemic changes. However, due to the significant drop in BP post treatment as well as the signs of Inferior ischemia, a right-sided look is more than warranted while en route to closest STEMI center.
     

  • Christopher says:

    Mike M,
    To perhaps clarify what David was pointing out, reciprocal changes are not ischemia but rather the injury being seen as an "electrically inverted" picture (hence the term "reciprocal"). Dr. Smith notes on his blog that ischemic changes do not localize and are diffuse instead.
     
    Consider the example of ST-depression localized to V1-V3: if you flip the ECG to its reverse side look at it upside down, you can "see" the ST-elevation from the posterior wall. Likewise, if you took V4-V6 and moved them around to be V7-V9 you would see the elevation without a paper trick.
     
    Does this help?

  • David Baumrind says:

    Christopher, thank you for clarifying!  @Mike M… just to add… if you see ST depression in one anatomic area, you should think if they are reciprocal changes to ST elevation elsewhere, even subtle elevation.

  • Troy says:

    The 12 lead confused me a little bit. Even the positive aVR. Lol. As far as the 12…..not good. I must say I absolutely love the aggressive treatment including plavix! Good job on the serial 12′s.

  • Mike M. says:

    Christopher and David, thanks very much for the help. Makes all kinds of sense now. 

  • Nick Adams says:

    12 Lead:  Sinus in orgin.  LAE, Boarderline LVH (V1 & V6 = 34.5mm) = Prolonged uncontrolled HTN.  Limb lead reversal in the frontal leads causing a positive deflection in aVR.  Also, LVH should cause a physiological LAD of 0 degrees to -40 degrees.  A negative aVR is showing that the impulse is going towards the positive lead in aVR, which is @ 210 degrees.  Unless this is ventricular in nature, aVR should never be positive.  There is ST segment elevation in V1 – V4 indicating an anteroseptal AMI.  I'm not sure what limblead reversal will do to the ST segments in the inferior leads, but maybe, there is actually ST segment elevation in II, III, and aFV indicating an inferior wall MI and the drop in B/P is due to a RVMI.  I would guess that a pt with a RVMI would not initially present so hypertensive, but I would do a 15 lead EKG anyway because it doesn't take much time, and the information you get from it is critical.  I would treat this patient as if it were a STEMI and activate the cathlab team….. as they did  (good job).  Nice job with the serial ECG's too.

  • Christopher says:

    Nick,
    The ECG is showing -aVR (i.e. aVR electrically inverted) rather than normal aVR found on most of the LifePak print outs on this site! Otherwise spot on sir.

  • Nick Adams says:

    Oh….I see.  It says -aVR and not aVR.  That's different (and confusing)….lol
    Thanks Chris for the eye opening.
     

  • AW says:

    Wow, interesting their 12 leads print like that, what a great eye opener for us here on this side of the pond.  I was fooled too by the -aVR printout, but the rest of the layout I could learn to like, the arrangment in many ways makes sense.
    I'd be interested to hear the gal's street drug history, and what their FAST screening involves.  Here that includes ultrasound, which we don't carry on car so it's not done till the ER.
    I agree with the ECG comments so far and would have activated.  It is a bit odd this 12 lead and the voltage discussion is interesting, can't wait to hear the outcome.

  • Carius says:

    So my question goes: Would any acitvate cath lab on the first EKG alone? Or is it the second EKG which is the determinant for Code STEMI?
     
    @AW: FAST-negative would mean no obvious stroke symptoms. FAST is the acronym for Face Arm Spech Test (and not a ulatrasound abdomen FAST, lol). 
    Quck info: http://en.wikipedia.org/wiki/FAST_(stroke)
    Article: http://stroke.ahajournals.org/cgi/content/full/34/1/71
    The ad: http://www.nhs.uk/actfast/pages/stroke.aspx

  • Carius,

    In the first one I see 1mm in V1, but V2/V3 are isolectric at the J-point with the TP-segment. I'd have held off for another 12-Lead. Given the ST-D in I/II/-aVR I'd have watched it with the anticipation of eventual elevation, which we find only 7 minutes later in #2.

  • Da Bomb says:

    Anyone see the ST elevation in the first 12 lead V1-V3? It's like 3mm already.
    Or am I mistaken…

  • Chris T says:

    First 12 lead im suspicious of paricarditis as well. But the follow up 12 leads I cannot ignore. Cath lab if i had one available.
     

  • Dave B says:

    Question for discussion, because it has been raised by several of you:
    How would you characterize the FIRST 12 Lead that was acquired?

  • Jimbo says:

    Possible PE (S1Q3T3).  Call the STEMI to CYA, but my money is on the PE.  Global ST elevation.

  • Erik W says:

    Hi,
    Being a newbie here and the presenter's collegue and hence having English as second language, please bear with me:
    I do miss some information about risc factors I generally find useful in cases like this, including:
    - Cardiac history in near family.
    - Patient's weight.
    - Any disposing other factors, like diabetic disorder (type II, which many patients tend to regard as a non-medical problem, just a diet issue), hyper cholesterolism, neurologic dysfunctions, etc.
    Anyway:
    I would call STEMI based on the first ECG alone, or at least have a cardiologist have a peek. Not specifically based on the ECG alone, but because history taught me that younger and younger people get ACD, and I always try to force myself to regard any patient as in the worst possible condition to avoid overlooking something serious. And the clinical findings here support suspecting cardiac issue, in addition to an ECG with elevations in V1-V3 (in my view, so I agree with you, Da Bomb).
    The treatment given is to my liking, however I wouldn't give Plavix until a cardiologist had prescribed it, as per protocol. If he did, I'd administer 5000IE Heparing aswell, also per protocol.
    I would however administer ASA (first!), Nitro, Morphine before conferring, also per protocol. I must confess that I had an acute MI on a patient aged 37 years only a few weeks before the  presenter had his case, which to me was a wake up call. MI is not  only "older people's problem" anymore, and we better keep that in mind, in my opinion.
    Kindest regards,

  • Christopher says:

    Jimbo,
    The dynamic changes in the ST elevation virtually guarantee this is a STEMI. I'm not saying this patient isn't also having a PE, but given how insensitive the ECG is for PE's, I wouldn't bet the farm on it..
    Elevation is not a common finding in PE at all, but rather inverted T-waves in the precordium. Global elevation is a hallmark of pericarditis, but in this case there is reciprocal ST-depression present, which rules out pericarditis (especially given the dynamic ST changes).

  • Patrick S says:

    I would definately consider this a STEMI due to the EKG changes between the two seperate 12-Lead reports.  Personally with the drop in heartrate and blood pressure after the treatment, I would not be overly concerned.  The drops could be contributed to the effects of anti-coagulation and vasodilation of the Nitroglycerin, Aspirin, and Morphine.  The depression in the reciprocal leads is just that recprocal changes that are to be excepted with a STEMI.  My only additional medications would be Oxygen and Lopressor, and if pain persists additional nitroglycerin up to total of 3 and then 1 ich of Nitropaste; as long as systolic BP remain >= 100 mmHg.

  • Igor PT says:

    Hi everyone. I'm newbie in this discussion's. I agree with the diagnosis of STEMI, and cath lab should be activated. Pericarditis doesn't seem at all for many reasons allready (well) pointed, and also agree of what was said about PE. the FIRST ecg seems STEMI with no doubt. And it gets ( a lot) better with medication, and the BP drop to good levels.

    So now, let me introduce opics for discussion… 

    what about a STEMI, caused by prinzmetal angina? (which could be caused by the high BP!)  it could explain the effect of NTG  ( altough its action being primarly in veins..) and the morphine ( which slows down the nervous system..), and the fact that the ST elevation got better substancially..  =) 

    last question: what was the BP on arrival? still was good, around 130/85, or high again?

    And even a more deep case: what about miocarditis caused by pheocromocytome ?  ( or just miocardial injury, as seen pos-mortem in pheo, cocaine addicters and sub-anarac hemorrage)

    Hope I didn't bring anarchy to the discussion! ;)

  • Scott says:

    Is the patient on digitalis?

  • Carius says:

    @Scott: No relevant previous medical history, uses no medicines.

  • Linda says:

    Yes Stemi.  Possible Anterioseptal MI.  V1-V4 ST elevation.  I & aVL S-wave deflections uneven, possible slight intermittent RAD with slow conduction toward RV.  Are those U-waves in V2-V3?  Significant Q-wave in III and aVF.  Prolonged QT?   My oppinion MI in progress, ischemia and infarction happening.  LAD.  Nitro, Plavix, Lovenox, oxygen, Aspirin and a good doctor.  At least that's what they gave me.

  • Baker says:

    As wild as this theroy may seem I believe that the very reason the initial 12-Lead showed only minimal possibility of a STEMI was due to the Pt.s B/P. Being extremely high therefore forcing blood past the LAD occlusion and letting oxygenation take place. I believe that after the pt. Received the first NTG the drop in B/P caused the LAD occlusion to become complete even with the vasodilation, and I believe this is why the second 12-Lead showed the prominent signs of a STEMI, great treatment this pt needed the cath lab without a doubt.

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