77 year old female CC: Abdominal Pain

It's a quiet Sunday afternoon when you're dispatched to a residence for a 77 year old female complaining of abdominal pain. Your dispatch notes indicates she was at the ED the day prior. Upon your arrival, you're met on the porch by the patient's son who directs you inside.

Your patient is sitting in a recliner, with mild respiratory distress, clutching her abdomen. Her skin appears a bit moist, and is warm when you touch her arm to feel for a radial pulse. When you ask her what is going on, she simply replies, "my belly won't stop hurting."

Your partner makes quick work of her vitals while you get the run down on her history.

  • Signs/symptoms: 7 of 10 abdominal pain going to her back, belching, intermittent vomiting
  • Alergies: Codeine
  • Medications: lisinopril, metoprolol, furosemide, potassium chloride, magnesium oxide, lipitor, albuterol, vitamin supplements, metformin, iron
  • PMHx: renal failure with dialysis (shunt Rt arm), hypertension, hypercholesterolemia, type II diabetes, pacemaker, asthma
  • Last ins/outs: vomiting x 3 today, did not do dialysis on Friday due to nausea/vomiting
  • Events: progressive worsening of pain and nausea

Your general impression of the patient is she just looks unwell. Your partner relays her vitals.

  • Pulse: 80 bpm, irregular
  • BP: 210/100
  • RR: 24, wheezes
  • SpO2: 94% on room air
  • T: 99.1 F (37.3 C)
  • BGL: 194 mg/dL (10.7 mmol/L)

Her son asks that you take her to the smaller, local hospital so, "she does not have to wait as long as she did at the ED yesterday." When you ask for her discharge instructions, he can only find the sheet which says Chest Pain and very generic information.

When you ask about her pain earlier, she denied any chest pain, however, to be prudent you obtain a 12-Lead:

Up and Down We Go - 12-Lead

You assist her to your stretcher, securing her with seat belts, and begin moving her to the truck.

  • What does this patient's 12-Lead ECG show?
  • What is this patient's rhythm?
  • What are your treatment priorities?
  • Can you still take this patient to a community hospital?



  • emcd says:

    SR at a rate of 78 with borderline 1st degree AV block, normal axis, and diffuse and deep, asymmetrical T wave inversion in inferior, anterior and lateral leads.

    Pt has Hx of renal failure this concerns me to electrolyte imbalance, along with 3/7 vomiting I would be concerened about hypokalaemia (GI losses of K+) this could explain T wave inversion (although this is very pronounced!). Pt also has prolonged QTc and prominent U waves in several leads perhaps lending argument to this.

    Otherwise ECG may represent diffuse subendocardial ischaemia. 
    Other causes of large T wave inversions include CNS injury, massive PE or apical hypertrophic cardiomyopathy but I don't think these are applicable here.

    Treat for the worst (ischaemia first) but I'm going to take a wild stab and guess marked hypokalaemia. 

  • Spencer Oliver says:

    This 12 lead shows Sinus rhythm with upright p waves noted in several leads with a steady PR interval. The concerning part of this 12 lead is the ST depression with deep flipped t waves throughout this 12 lead. Even worse is the ST elevation in lead aVL that is greater than the ST elevation in V1 which leads me to believe that we are dealing with a possible occlusion of a left main. Though a triple A is possible, it seems unlikely the aneurysm had spread up and is occluding the blood vessels feeding the heart without the tearing chest and back pain to go with it. I will suspect atypical chest pain with the patient being female and diabetic. I would of course palpate the abdomen to ensure there are no pulsatile masses and look for other signs of AAA including unexplained lower limb weakness or discoloration. But without having those pop up my treatment consists of ASA, IV's and NTG with fentanyl or morphine (depending on your protocols). With an Spo2 of 94 I would withhold O2 per my protocols. I would explain to the son that the preferred hospital would be one with PCI capabilities and transport code 3. This isn't technically a STEMI but that doesn't stop me from consulting with a MD en route to inform them of my findings. If I worked in a system that had transmitting capabilities I would transmit the ECG. Serial ECGs would be prudent to take as well.

  • Jason says:

    Ok, so I'm only an EMT-B, but I thought I'd take a stab at it. Based on the SAMPLE history, and vitals, and ignoring the 12-lead since I can't read one anyway, I would be worried about a couple of possibilities:
    Primary concern for me would be PT not having dialysis for several days. Depending on her diet, I would be worried about an abundance of K+, leading to an MI. The increased vomiting and abdomen pain would also lead me to think this was due to increased urea in the blood, or hyperkalemia causing cramping.
    Since she is on iron and dialysis, I would also suggest that a portion of the wheezing and low Sp02 is due to fluid buildup in the lungs.
    Could also be a PE, but I really think this is mostly due to not having had dialysis for a few days. Blood chemistry will probably show a marked increase in K+, which would give an increased risk of MI.
    Treatment priorities for me would be O2 and transport. If breathing becomes more difficult, administer patients MDI or albuterol treatment enroute. Pt can choose to go to community hospital, but due to increased risk of MI, I would counsel going to facility with cardiac facilities. If she's not already having an MI, the hyperkalemia could very easily become an MI.

  • Spencer Oliver says:

    Correction on my last. I mistakenly said aVL elevation is greater than V1. That was a typo. I meant to say aVR elevation is greater than v1

  • Hugh Smith says:

    I see a sinus rhythm at a rate of roughly 80 and regular. This 12 lead is notable for LVH (V2+V5>35 mm) as well wide spread T wave inversions and U waves ( II, III, aVF, V3-V6) and associated ST depression in aVF and V5/6 and elevation in aVR. Also, I notice that t waves are upright in V1 which I do not think is pathological but I normally see inverted T waves there and the context of so many other T-wave inversions I wonder if that isn’t another one? Also note that almost all of the T waves are broad based and symmetric indicating some kind of pathology underlying the presentation.

    Based on her HPI and pmhx I am more inclined to think that this is an electrolyte issue, and the U waves make me think GI loss hypokalemia (as others have suggested) however in the context of such wide spread st depressions and T-wave inversions I’m not comfortable ruling out atypical ACS altogether in her case and would prefer to take her to a facility with a Cath lab aand the deep mid precordial t wave inversions could also indicate wellens syndrome especially following an episode of chest pain. Another support to going to the hospital that the pt visited previously is the ability to compare EKG changes to her previous EKG as well as lab values.

    Also as a point of information that I don’t know, in hyperkalemic patients is it possible for T wave tenting to be inverted or would the increase in serum potassium force a positive deflection of the T wave?

  • Spencer Oliver says:

    After some further reading and listening to the thoughts that Hugh and emcd shared about hypokalemia I have to agree that that makes a lot of sense in this case. After reading up  and learning about ECG changes that happen with hypokalemia I can see their points. But this is where someone smarter than me would have to explain the process here; my thought is that if she's on dialysis and missed her last appointment it seems likely that there would be a build up,of potassium? Especially if she's taking her potassium supplements as she's directed to? When I first read through for some reason I read epigastric pain radiating to the back which lead me to dig into my atypical chest pain process especially with that 12 lead and those deep inverted T waves. After reading through again I saw just abdominal pain with no specifics of location or type or onset. I there any more information on her abdominal pain? Not all pain is equal. Diffuse cramping pain versus sharp pain versus burning pain take me down different avenues of thought for possible causes. Please provide some feedback! I want to learn more. 🙂

  • Paramedic student says:

    Just learned cardiology and ECG reading last semester so I could be completely wrong here…but there are upright p and t waves in lead avr suggesting limb lead reversal.  ECG is unreadable. 

  • Christopher says:

    Paramedic student,
    Astute findings, but the ECG was acquired properly. Either way, still interpretable!
    So what does that mean?

  • jason says:

    Wellen’s syndrome. Comes in two forms. Deep symmetrical T waves or biphasic up then down T waves. Differential to include intracranial bleed due to Pt’s vomiting, high BP and can also cause deep t wave inversion ekg changes. Don’t think it’s hypo K which produces biphasic down then up t waves as well as flattening of the t wave and the presence of u waves. Also pt missed dialysis which lends to hyper K and can present as just about anything on an EKG.

  • jason says:

    Also, the pt does have LVH and this does resemble a strain pattern. No PE as room air sat is 94.

  • Scaley Old Man Fish says:

    Wellens syndrome. I would go into more detail but I'm bouncing around in the bolance

  • Alex Kroeze says:

    Bear in mind that I am looking at this on my phone so my "squint" factor is high on this one, combined with not the best tracing I'd say.
    -Atrial Tachycardia with a 2nd degree AVB with 3:1 Conduction (or is it 3:1 block?  I always forget how to properly say ratios like this) at an atrial rate of 260 and a ventricular rate of 80ish
    -Borderline LVH
    -ST in aVR > V1
    -Diffuse ST-T changes
    As hyperkalemia is the syphillis of electrocardiography, I think it would be reasonable that given the patient's history we should consider at list an attempt at correction of any hyperkalemia.  Given her history she is certainly at high risk for it.
    As this patient's rhythm is most commonly caused by digoxin toxicity I would be concerned that she hasn't shown you all the medications she is on.  Double check… but hyperkalemia could be the cause too.
    Are the ST/T-wave changes a strain pattern from LVH?  Possibly.
    Is this an LMCA/MVD type patient?  Possibly.
    -Hyperkalmeia (first suspicion, easiest to rule out)
    -Digoxin toxicity (doesn't seem super likely in this case)
    -Aortic Dissection through to coronaries (not likely given the widespread changes)
    How totally off base am I?

  • Alex Kroeze says:

    Re: Wellens Syndrome

    It is my understanding (I'm no expert and am only passingly familiar) that you don't see the changes in the limb leads.  I could be totally off though.

  • Brian behn says:

    Near global T wave inversion, all leads except the lateral leads and aVR. The differentails include      CVA, PE, MI/ ischemia, pheochromcytoma/ catecholamine excess, cocaine, maybe electrolytes ?  Maybe wellens? Post pacemaker syndrome, hypertrophic cardiomyopathy…
    We can cross CVA off the list as she seems to be neurologically okay.
    cocaine is pretty doubtful.
    I suspect that her electrolytes were checked at the ER in the past 24 hours and it is unlikely that things changed that much in the past 24 hours to do this. 
    Could this be a pheochromocytoma? Her blood pressure is pretty darn high..but probably not any zebras here.
    I want to make a case for hypertrophic cardiomyopathy, aka yamaguchi, but without an echo I am struggling by criteria alone. 
    PE is unlikely as she is 94% on room air, however a bit tachypneic….so maybe a slight possibility here but unlikely it is large enough to cause ecg changes, but to allow an  sPO2 of 94%. Any calf tenderness/ redness/swelling?  Still, keep it in the differential. And remeber you dont need s1q3t3 to dx a PE
    Wellens type A,  I am thinking with v2 having a " normal " T wave you will have an uphill battle getting that dx to stick.
    Aortic dissection seems like a possibility here. If her pain was higher up, chest/back it would correlate better with the ecg findings suggestive of  a LMCA problem. A aortic dissection in her abdomen doesnt explain the ecg findings
    Looking at lead aVR there is some elevation. Combining that with the near global T wave inversion, the most likely culprit here is LMCA stenosis/occlusion. The systolic hypertension probably isnt helping things here. I would transport to somewhere that has a cath lab

  • Jim says:

    In research, I found this great abstract on T wave inversion: http://www.medschool.lsuhsc.edu/internal_medicine/residency/docs/ST-T%20depression%20Hanna.pdf
    I offer it as it hits on all points discussed here. May be helpful to some.
    My interpretation, without of course lab values and an echo… is that when unusually deep inversion of the T waves is the most salient feature of global T-wave inversion, it is my understanding that the most common cause is myocardial ischemia. T  waves are inverted, in most leads symmetrically here, in all leads except aVR and V1, and the QT interval (604 ms with a QTc of 643 ms) was markedly prolonged. Others have used the term diffuse T-wave inversion for this widespread T-wave inversion which always shows a reciprocal upright T wave in lead aVR and may also spare leads V1, III, and/or aVL.  With already concerns of "suggested" CHF revealed by prescribed Furosemide, florid pulmonary edema and MI may be in my prehospital treatment plan. 

  • zel says:

    Sounds like an Acute Pulmonary Edema. Remember this is a dialysis patient who's gone about 5 days without dialysis (fluid overload), tachypneic with wheezes, low RA sat, marked HTN, heartrate is beta-blocked, also from her meds/hx it seems she has CHF as well. 
    EKG is NSR with a normal axis and diffuse T-wave inversions. EKG is suggestive of ischemia. 
    Skip the community hospital as she's probably going to require emergent dialysis and the community hospital won't be able to do it. 

  • HereAndNow says:

    My first thought was atrial flutter instead of atrial tach, but I could easily be wrong. My train of thought is that Flutter is a more common arrhythmia to live with than Atach, and that might explain the (currently not firing) pacemaker placement and perhaps the beta blocker, too. I can't really zoom in or map out though, so I'm stuck with an eyeball diagnosis too.
    I agree with HyperK+, given the hx and Twave morphology.
    Although I still can't put my thumb on the cause of inversion.
    I thought long and hard about Wellens, and the only thing for it is that we could argue she had CP yesterday but not today. That doesn't even touch her current presentation though, and you would have to have some seriously uncommon circumflex distribution to feed the anterior, isolated low lateral, and full inferior myocardium (which I think would technically make it Wellens-like versus true Wellens, as it's not a high LAD/LMCA thrombus).
    QUERY: How many Renal Failure pt's have you seen on Dig? I can't think of any off the top of my head, and given it's already narrow therapeutic window, I can only imagine the havoc of having to correlate it with dialysis treatments. Not to mention the fear of what happens if you miss one.
    The only other thing I've seen look like that is severe brain injury, but that seems even more unlikely than the rest.
    I keep wanting to lean toward is dissection, but that's like 90% because of the presentation, 10% T waves. And its still quite a stretch.
    In the end, I would have to default to LMCA occlusion, if only to trump the son's hospital request. Even if she doesn't need the cath lab, if the underlying rhythm is Atach (or a new Aflutter) then she would need an EP consult or mapping/tx anyway, and around here most places with cath labs have ep labs too.
    PS-Amazing post, Chris. Everytime I start to think I've got this stuff down pat, you guys pull something like this out of the woodwork!

  • lino mori says:

    a)atrial tachycardia with complete AV block,3 QRS complexes induced by pacemaker.Inferolateral ischemia
    b)treatment of abdomianl pain
    c)tranfer the patient to a comunity hospital to exclude myocardial inferction or aortic dissection.

  • Pelagic says:

    LMCA with ACPO – lots of GTN, ACS trimmings and a Cath Lab super quick if she makes it
    QRS looks too tight for HyperK to me

  • erik says:

    Just my two cents on this, why is everyone looking for ZEBRAS, treat your patient… This patient is clearly in heart failure with most likely a cardiac wheeze I'm not suggesting CPAP at this time, but definately high flow oxygen nitrates, loop diuretics no renal failure who knows if they even produce urine. definately fluid overload pulmonary edema look at the blood pressure, as far as the 12-lead is concerned likely myocardial ischemia which is probbably putting this patient in failure, other wise NORMAL SINUS RHYTHM. most likely will be hyper K+ opposed to HYPO they have nt been dialyzed in how many days? why would it be hypo OK theres no evidence on the 12-lead i.e peaked T waves and WIDE QRS, treat your patient the abdominal pain is most likely a symptom from what the big picture is!

  • Sean says:

    LVH with strain pattern. I think she's heading down the pulmonary edema road, no crackles yet, but wheezes are likely cardiac wheezes, and the fluid is soon to follow. I would like to see an EtCO2 waveform to see if we're looking at a shark-fin morphology, but my gut feeling is that we probably are not. 
    We could call the ABD pain an anginal equivelant and treat with ASA & NTG. I would hold off on any additional O2 at this moment as her sats are >92% (depending on the literature you read 92 is good, some says 94). 
    I would consider having CPAP available, but I wouldn't look at applying it just yet, as I think she'll respond to the NTG. 
    If I had my Trop & BNP meter I would draw labs as well. 
    I would transport to a hospital with dialysis & PCI capability because she'll likely need dialysis, and if she ends up being an NSTEMI then PCI. 

  • Jess says:

    Atrial tach [slow flutter?] with complete AV dissociation [see lead V1] Vent rate 80-ish.
    QRS appears wide – v leads, I & aVL looked narrow initially with buried "p"s somewhat obscuring J pt, but II, aVF & aVR made me take another look and I'm calling this wide. I guess I would say this is closest to a RBBB pattern but not much of an r' [or maybe it's just the P] so might call it an IVCD [1 pt for Hyper K] and would expect discordant T waves. 
    QT interval is also long. I do not see prominent U waves. 
    Lead I meets ECG criteria for LVH but this does NOT look like LVH strain.
    Now the T waves: In addition to being wide, symmetrical & deeply inverted, they are inappropriately concordant in II,III,aVF, aVR, v3-v6 [and possibly v1].  T waves in I are flat, and in aVL are smaller & discordant [good] but symmetrical [bad]. Since I think v1 has a terminal r wave I would call it concordant as well. v1&v2's morphology is altered b/c buried P wave, but they both look symmetrical as well. 
    Now ST seg: STE 1mm in v2, <1mm STE v1 if any. In all other leads the ST segement appears to touch baseline before plunging – including aVR. 
    Symmetrical T waves appear to be the only "global" finding, the most disturbing T wave inversions seem to be inferolateral [+ aVR?].  
    Wellens? inversions look late to me, and I don't remember them extending to limb leads. Though I certainly don't know enough to say "definitely not". 
    RV strain [acute or chronic] is in my list of Ddx for precordial T inversions, but I'd expect a more rightward axis, a more positive v1 & inverted T's to start earlier. 
    LMCA occlusion seems like a reasonable differential, but I just can't call the ST seg in aVR elevated. [though what I'm calling the terminal portion of the QRS could look like STE if you thought it was narrow.] Again, don't know enough to say definitely not.
    This took forever and it got really long. =) I have to go but will post my treatment later. 

  • Jess says:

    to continue:
    Atrial tach with block makes me think Dig tox, Resp disease & Hyper K, the last 2 fit better in this case. I don't see the T/U wave if it's here, so don't think hypo K. 
    Because I assume she is fluid overloaded b/c missed dialysis + HTN + wheezing I would treat for CHF – NTG, Lasix [didn't think it worked with renal failure? maybe her distal loop still works? I see she has it Rx'd] and see if wheezes improved or she felt better. I could also do Albuterol [which would be marginally helpful if hyperK] but I would go the CHF route first. Also I would consider that she's been unable to take some/all meds x 3 days due to emesis? And oxygen N/C if needed to keep sats 94+. 
    I would take her to hospital that has cath lab & dialysis. Could be she has a virus [abdo pain + vomiting + low grade temp] which lead to missed dialysis & med doses and CHF exacerbation, and inferolateral ischemia. 
    Sorry this ran so long! Thanks for posting it – such great practice and always an opportunity to learn something new!

  • New to the game says:

    Can someone please explain to me why everyone is saying a Sinus Rhythm, when it cleary states in the vitals as her pulse being irregular.  Where I come from a Sinus Rhythm is not irregular 

  • Paul Catum says:

    Nice case!  One of our EM residents recommended a nice site to help me learn ECG interpretation.  The focus is EM, but it has a bunch of nice markups of common emergency rhythms and a useful quiz tool. 


  • Spencer says:

    @ New to the Game: It is sinus rhythm because there are upright P waves preceding the QRS complexes in the 12 lead. They are very evident in V1. This means the sinus node is firing and appears to be the pacemaker for the heart thus making it a sinus rhythm. You are correct in that it cannot be a Normal Sinus Rhythm if it irregular but sinus rhythms are allowed to have ectopic beats caused by PACs, PJCs, and PVCs which could make the best irregular. I was taught you phrase those as sinus rhythms with (insert ectopic beat). Hopefully this made sense.

  • FLMedic311 says:

    So I am going to answer these questions a little out of order..
    -Rhythm- NSR, note P wave per QRS, QRS Narrow with normal R to R intervals, PR interval < 0.2sec, Check pulse to monitor to confirm each QRS is producing a pulse.
    -12 lead- My best guess given the following is takotsubo cardiomyopathy.  @77y/o she is most likely post menopausal and the stress may simply due to illness and no dialysis.  Vast inverted T waves with slightly longated QT interval  With that being said I understand that this cannot be diagnosed with out first ruling out CAD.  So I will treat as such and relay that information to the pt and family and "HIGHLY!!" recommend that we are allowed to transport to an ACS capable facility.  Either way the end result needs to be a cath.
    –  I would treat as and ACS pt IV O2 as needed, which @ current O2 sat I would say 1LPM at most, Nitro and aspirin, and Zofran for NV.  Beyond that care would support of stable vitals

  • Darren says:

    I'm having a hard time telling if there is A/V dissociation or not.  I honestly wouldn't mind seeing a Lewis lead here to see what the atria are actually doing.  As it is, I'm guessing possibly sinus in origin.  Far more concerning to me are the global T wave abnormalities and the history combined with the present exam.  History of hypertension, current profound hypertension, and abdominal pain radiating into the back scream dissection or aneurysm until proven otherwise.  Goals should be cautious reduction of blood pressure, pain, and anxiety.  Nitro given cautiously might be a good option, as would morphine.  Depending on the patient, a low dose benzo might be in order too.  This patient needs to be at a hospital with bypass capabilities.  I might be wrong on the diagnosis, but it's what I would rule out first.

  • FLMedic311 says:

    Additional thought.. Possibly 3 vessel disease…?

  • I think the rhythm is a clear atrial flutter. The flutter waves are relatively slow, but they're clearly visible marching along underneath the other waves, and she has a sometimes irregular pulse.
    I would guess that she has some chronic congestive heart failure going on. Maybe a mild ACS/NSTEMI is happening and I can't rule it out, but this has been developing for three days and she's already been to the hospital. If they gave her discharge instructions for chest pain, presumably they drew cardiac enzymes and found that they came back negative. Given her cardiac history (i.e, that she has a pacemaker and a bunch of beta blockers) I wouldn't be at all surprised if this is her normal rhythm. Despite the consensus above and even though this is a 12-lead blog I don't think her primary issue is cardiac in nature.
    I think it's quite possible that the missed dialysis appointment is in play here, and I would want to question her about her recent medication compliance. I also think that sepsis is a possibility which must be strongly considered: the mildly elevated blood glucose and temperature both point to it, as could the elevated blood pressure and even the abdominal pain. There are alternative explainations for each of these findings given her history, but as a dialysis patient she's in an at-risk population, and with all of these things taken together it seems like a distinct possibility to me.
    If I have point-of-care lactate testing available, I'm going to use it and find out for sure. If I don't, my major differentials at this point are either sepsis, ACS, acute abdomen, or plain old sequalae of having some sort of GI bug that made her miss her dialysis appointment. None of those things can be dealt with particularly well within my scope. Depending on my anticipated transport time I may consult with medical control, not to look for a specific order but just to recognize the limitations of my own practice and seek the advice of a higher-level practitioner on a complex, acute patient. Given her blood pressure and renal history, I can't give even sambutamol/albuterol for her wheezes.
    This patient would not be going to a community hospital. Ultimately, this patient seems to need some lab work for a definitive diagnosis, and while most facilities should be capable of providing thrombolytics or EGDT if her condition proves to be a result of either ACS or sepsis, I'm taking her where she was yesterday so that she will be where yesterday's workup is documented and available for comparison.  

  • Mario says:

    Diphamic changes or MI needs echo

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