76 year old female CC: Diminished LOC

Here’s an interesting case study from a faithful reader named “Randy”.

EMS is called to evaluate a 76 year old female with a diminished level of consciousness.

On arrival the patient is found lying supine in bed moaning.

She is conscious but lethargic. She is oriented to person only.

She appears cyanotic around the mouth.

Past medical history: IDDM, CVA, MI
Meds: ASA, Baclofen, Atenolol

Breath sounds: diminished bilaterally

Vital signs are assessed.

RR: 24
Pulse: 48
NIBP: 99/33
SpO2: 78 on RA > 92 with O2 via NRB @ 15 LPM

Multiple ecchymotic areas are noted around the body. Discoloration is noted from the calf to the toes on the R side. No pedal pulse on R foot. L sided paralysis from previous CVA.

The cardiac monitor is attached.

A 12-lead ECG is captured.

What do you think is wrong?

See also:

76 year old female CC: Diminished LOC – Discussion

49 Comments

  • Troy says:

    I’m thinking possibly a beta-blocker overdose. 3mg Glucogon IV followed by another dose if needed. I would start pacing till then. Also I’m thinking he’s throwing clots with evidentally a DVT in the right leg

  • Hillbilly says:

    If anyone can see a P-wave let me know, otherwise this looks like poop! Go to hospital quickly! Pace? Looking like it!

  • Troy says:

    And possibly a PE

  • Hillbilly says:

    Only two ways to define EKG’s. 1. It looks alright – No life threat. 2. OH $HEETS! – I need more drugs than I have on my truck!

  • Mar says:

    Scary 12 lead!

    Hospital required ASAP

    DVT in R leg

    02, Cannulate and Diesel…. to hospital!

  • Dave B says:

    I am thinking… the 12 lead has a look of hyper-k… bizzare bradycardia, sine wave looking complexes, and some tallish T waves in the precordials…also, i think there is an inverted p wave in aVR, but in most leads i believe the p wave is flattened due to the hyper-K..because of the bruising and discoloration, i am wondering if the pt is suffering from Rhabdomyolysis, which has precipitated the hyper-K..

  • Mark says:

    I’m curious to what her blood glucose would be? Hyperkalemia could be caused by severe DKA.

  • Tom B says:

    Excellent point, Mark! I’ll see if I can find out for you.

  • randy says:

    mark, the bg was 195

  • Christopher says:

    Fat gnarly nasty QRS, my mind goes right to HyperK. However, given presentation I’m also keen for a PE. QRSd 210ms, QT 440ms, rhythm is tough to distinguish P-waves, 3AVB. 12L doesn’t really change my mind in terms of HyperK vs PE.

    BGL, some big lines, NPA w/ NRB, capnography.

    Orders for a trial of 1g calcium given presentation and ECG. I don’t believe this would be harmful should this end up being a PE. I’m also strongly considering intubation.

  • Christopher says:

    For rhythm I meant: idioventricular or ventricular escape w/ 3AVB (depending on presence of P-waves…).

  • David says:

    Wide complex brady, apparent DVT in R leg, border line hypotensive. I call block on the ECG which, explains the apparent ‘peaked Twaves’ and also pretty much makes it useless unless you have an old one to compare to. GCS is decreased, I bet if you administered fluids and paced her to an appropriate rate she’d improve in all aspects.

  • Troy says:

    I guess I stand alone on my beta blocker OD theory. Lol. But my thinking is with the bradycardia would it hurt to eliminate that factor??? Definitely has some clot. Thinking back over it what was the temp? Possible DIC? Definitely a ventricle escape. I don’t know about hyper K. Not a usual MO in my mind

  • Troy says:

    And don’t hold back in telling me I’m a failure Tom and Chris! Lol.

  • Dave O says:

    A little late in the game, but I’ll throw in another vote for the hyperK. Widened QRS, Hx of DM, maybe causing PVD?- compromised circulation in R lower extremity. Can’t get past the fact that this is screaming compartment syndrome.

  • Maunay says:

    It almost looks like she was worsening between the 3 lead and 12 lead. In the 3 lead, in lead II, there looks like P waves distinguishable starting on the fifth beat the best I can tell? But other then that I am not seeing any on the 12 lead or any other leads. I agree with Dave on the Hyper K and the Rabdo. Was she a non compliant IDDM? Did she live by herself? Does anyone know how long she has been like this? A BGL of 195 is not super high but could cause DKA. I am curious what her BS’s usually run… She is on Atenolol so as Troy said DD could possibly be a Beta Blocker OD. Did her LOC improve with the O2? If her LOC didn’t improve then obviously it was not the hypoxia causing it.
    I am thinking initially SB if those are truly P waves I am seeing on the 3 lead… It looks like Idoventricular on the 12 lead tho… Other then her HR, the other VS are not too bad, RR is a little high but she was hypoxic so that would be expected.. Calcium Chloride would be a good choice, that and lots of fluids. Depending on the
    Very interesting ECG! I am anxious to see the outcome! =)

  • Christopher says:

    Troy, I had to go look to see if widened QRSd was part of the B-blocker OD toxidrome. I found a few research articles, but atenolol didn’t appear to prolongate the QRSd beyond 150ish in any of the studies. Acebutolol evidently can prolong it to durations greater than 170ish. Definitely a strong differential though, given access to a B-blocker, bradycardia, and AMS are present!

  • Brandon O says:

    My main question is whether she improved, and if so to what extent, with the improved oxygenation.

  • Tracey says:

    Baclofen is a muscle relaxer..Combine that with a beta blocker and that can acount for low HR, low O2 SAT and low bp…I am going to treat conservatively. Continued 12 lead. large bore IV with option to titrate, O2 continued on non-rebreather. FUEL. Having a significant hx of both diabetes and DVT..I will go on a limb and say thrombi turned emboli or even possibly a bleed ( I would question an aneurysm..below the level of renals-or brain aneurysm) The discoloration can be due to chronic ASA use, or a DVT..Regardless, My treatment is as above.I am not pacing the patient..Interested in the answer.

  • Hungary Paramedic says:

    Pulmonary Embolisation

  • Alex says:

    This is difficult to determine due the small amount of information presented. There is also a lot to be said about you “general impression” of a patient. Hopefully that presentation will accurately bridge your way to a correct diagnosis.

    The route I would probably take is accelerated idioventricular rhythm possibly due to severe cardiomyopathy from her previous MI (would need more information to determine extent of damage from previous MI). I am unable to positively identify P waves in either images. This would lead me to rule out AV block. When strictly speaking about idoventricular / ventricular escape I would expect the heart rate to be lower than 40. Although the enhanced automaticity may be caused by the patient’s hypoxia and increase the rate to greater than 40. There is also nothing given to definitively rule out a PE. Also, what type of CVA did she have: Ischemic or Hemorrhagic? When? This could change possible treatment modalities. In any event, the patient seems hemodynamically unstable (or very close to being significantly unstable). . I would love ample time with some of you to determine a differential diagnosis that we all agree on.

    Treatment: Oxygen NRB, modified-trendelenburg (depending on patient’s tolerance), trending vitals every 3-5 minutes, two large bore IV’s, NS TKO, repeat 12-lead, atropine 0.5 mg IV (no absolute contraindications), depending on response to above interventions consider TCP (I would consider patient moderately symptomatic due to AMS, transport (and as always consider expert consultation..)

    Sorry for long winded response, I am new to this website.

  • Hendo says:

    I’m considering hyperkalaemia/rhabdomyalisis secondary to compartment syndrome in right lower limb after prolonged immobilisation. ? immobile due to new CVA or ? unable to get up due to decreased mobility from previous CVA.

    Aiming for high-flow o2, bi-lateral large bore cannulas with aim of fluid loading prior to movement & extrication and requesting ICP back-up for possible administration of 20mg nebulised salbutamol, 10ml 10% calcium gluconate or 100ml 8.4% sodium bicarbonate.

  • DJ M says:

    Rapid transport. too much atenolol give her .5mg atropine and be ready to push the other .5mg if her heart rate drops from a “tease” affect. That will bring her heart rate to a normal range which will give her increased blood flow and restore a pulse to her lower extremity and make the patient more alert. If her heart rate doesn’t improve pace her and if her pressure doesn’t come up consider dopamine. By this time you should be close to the hospital.

  • just another medic says:

    Dave-I like rhabdo/hyperk based on egk, but wont pretend I came up with rhabdo:)

    I would not expect a pedal pulse at that BP. Not that it rules out dvt.

    Excited for the conclusion on this one!

  • Mark says:

    Random protocol question for everyone…if this patient had a DNR, would your protocols allow you to pace? How about use atropine? Dopamine? (Just kind of curious. Mine says “no cardiotonic drugs or pacing”)

    Randy – thanks for the BGL…I guess it’s high but not super DKA high. (Though I always worry about high blood glucose readings not being accurate on glucometers.)

    I’ll also say to pace, also using caution to make sure there is actually capture (thinking about previous HyperK patient on the 12lead blog that didn’t capture even though it looked like it).

  • Maunay says:

    Oops ignore the uncompleted sentence on the previous post before the last paragraph. 🙂

  • Maunay says:

    Atropine would probably not be effective with the wide QRS and absent P waves, Since the actions of atropine are to block the binding of acetylcholine to muscarinic receptors, thereby reducing vagal input at the SA node, and increasing conduction velocity through the AV node and really has no effect on a vertricular rhythm. Just a thought… 🙂

  • Rose says:

    Maunay, thank you for the input above.

  • Maciek says:

    hyper K

  • Christopher says:

    Maunay, additionally in B-blocker ODs atropine is not effective.

  • randy says:

    Small update……. im attempting to get update on this patient. The pt has negative dvt in right leg. other drugs she was on were prilosec and lisinopril. Attempting to get lab work and ekg from ED.

  • Troy says:

    ACE inhibitor and Beta Blockers…..bad combination sometimes

  • Maunay says:

    Did she improve at all with O2? How did her pupils look? Lung Sounds? Need more input! As Johnny 5 would say. hahaha

  • Derek says:

    Hi guys, Randy informed me this was up here. I’m actually the person who took this call, captured the 12-lead, and attempted to treat this patient. Let me see if there’s anything I could add from memory (don’t have the run report in front of me)…

    -The Patient was a DNR. As we were leaving the ED, the ED physician was discussing this with the Pt’s husband.

    -Her BP upon leaving the ED was 50/20.

    -“SpO2: 78 on RA > 92 with O2 via NRB @ 15 LPM” Although her pulse ox increased, there were no signficant changes in her LOC or presentation.

    I should also point out that the ED was less than 5 from this patient’s location.

  • Derek says:

    P.S. I believe pupils were EARL, Randy you have the report if you want to look that up for sure, I can’t say for certain.

    Lung sounds were dim.

  • harrison says:

    12 lead shows IVR with hyperkalemia.
    P wave is not present, wide complex QRS at a bradycardic rate. IVR by definition, keep it simple.

    V1 and 2 show a questionable P, but I would not bet money on it.
    If this were my patient, Atropine is out the window. Not only do I not suspect increased vagal tone, but the patient is also unstable, rendering pharmacological treatment out the window.

    Patient needs immediate TCP, which would be my treatment until patient arrives at the hosptial, which is 5 miunutes out. TCP on scene, load and go. IV en route. IO per protocol if no IV access obtained, then an emergency transport to closest facility.

    If we had a longer transport this patient would probably buy a tube as well, if DNR permits.

    Provide immediate notification to the hospital as they need to be ready for this.

    I would be curious to know lab values as well to include chemistries and PT/INR.

  • Tracey says:

    Any updates on this patient by chance? I keep checking back for the final diagnosis? Very interested in such. Please keep this thread updated if you could..appreciate. 🙂 Thanks.

  • Tracey says:

    I am still thinking a bleed or embolus..( sorry, I forgot to add this oon last post.!)

  • Mike M. says:

    Junctional, left axis deviation, RBBB, PE (S1Q3T3)

  • Dave says:

    3rd degree heart block duh

  • CBEMT says:

    Random protocol question for everyone…if this patient had a DNR, would your protocols allow you to pace? How about use atropine? Dopamine? (Just kind of curious. Mine says “no cardiotonic drugs or pacing”)

    Mine says “Do not place the patient on a cardiac monitor,” so theoretically this is all moot for me…

  • ARSHAD HASAN says:

    1.Bradycardia’
    2.V4,5,6….Reciprocal Inhibition of ‘R’Wave&ST Elivation(Anterolateral STEMI)
    3.Notched ‘P’..Rt Atrial enlargment..
    4.Rt leg DVT..

    Dx..ANTEROLATERAL STEMI WITH BRADYARRHTHMIA

  • Francis says:

    While a I do suspect R leg DVT there were no physical signs noted about the R leg ie. swelling redness or pain. A field venous Doppler would be great in this case as well as an echo.  I believe it could also be Hyper K. Do what you can  and get her to the ED ASAP 

  • Paul says:

     
    Severely profound hyperkalemia classically produces the multiple EKG abnormalities seen here: 
     
    Sagging ST segment, LAD, LBBB-like appearance, QRSd WELL in excess of 400msec, Brugada-like ST-segment appearance in several leads, and profound hyperkalemia is known to cause stroke/stroke-like symptoms(hyperkalemic paralysis/severe muscular weakness; fitting this patient's presentation) that have resolved following correction of serum potassium. I have seen several EKG's with this appearance in patients with serum potassium levels >8.
     
    Electrical pacing can have severely deleterious effects because of the extremely irritable myocardium, and several pharmacological agents are known to exacerbate this problem even further by increasing serum potassium. One of these such drugs is succinylcholine.
     
    I would immediately give 2 grams of calcium and 2 amps of bicarb; both are really benign in this setting. I would follow this up with 40mg of furosemide/1mg bumetanide, and start albuterol at 20mg an hour. I would not do anything further about the bradycardia/relative hypotension, other than IV fluids and said pharmacological interventions.

  • MerlinMedic says:

    CBEMT has a good question:  what are the directions (if filled out @.@) on the DNR?  Also, why not go with the atropine followed by TCP if (and more than likely when) the atropine doens't work. IVs O2 etc w/o saying.

  • lotfi djilali bensekrane says:

    i think that giving calcium gluconate would be a test if it bring the rythm to sinus one then it's Hyperkaliemia however it would resolve the probleme temporarely.

  • Paul says:

    Paul for the win!!! Lol

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