49 Year Old Male: Chest Pain

 

This excellent case comes to us from our friends in the UK. The author wishes to remain anonymous, but we thank him for his contribution.

It is about 8am on a gorgeous Wednesday morning, when your Paramedic unit is dispatched to a 49 year old male, "chest pain".

You arrive at the bungalow of a summer resort and are greeted by an elderly couple.

"They don't look too bad", you think, but you are not that lucky.

"Our son has been complaining of chest pain and vomiting for a couple of days".

You are led back to a room where you find your 49 year old patient lying in bed.

His parents say they found him like this and called 911. They tell you he seemed ok when he went to bed last night.

Your patient is lying supine in bed, responds to verbal stimuli only, and it is difficult for you to make sense of his answers.

You note that he appears anxious and uncomfortable, with dried vomit on his shirt.

His airway seems clear, but his respirations seem quick and a bit shallow, although clear bilaterally. You put him on a non-rebreather.

The rest of the vitals are as follows:

  • Pulse: 85 and regular
  • RR: 27, shallow
  • BP: 86/62
  • Pupils: equal and reactive
  • Skin: cool and slightly diaphoretic

While he is not adequately answering your questions, you are able to determine from his parents that he is an insulin dependent diabetic. You are unable to determine any other past medical history, medications, or allergies.

You check his blood glucose while your partner puts him on the monitor. The BGL reads "High". 

Here is the 12 lead:

 

 

You are 15 minutes from the local community hospital, and 30 minutes to the PCI center by ground. Air transport to PCI is a possibility.

 

What's your differential diagnosis?

What does the ECG show?

What do you want to do about it?

 

 

 

 

26 Comments

  • niyas says:

    dka
     

  • Caleb Seavey says:

    1) Sinus Arrythmia with rate of 89 with slight QRS widening and Long QT
    2) Axis- Normal
    3) Enlargements- None
    4) Blocks- None
    5) Ischemia- ST elevation is present in the right precordials, however this is unlikely relating to Ischemia, Wide spread ST-depression however unlikely to be ischemia, No Q-waves
    6) Misc- Tall, Peaked, Tented, and Narrow T waves are present consistent with Hyperkalemia. In addition, the QRS is widened further confirming Hyperkalemia. V1, V2 morphology shows possible Brugada Syndrome morphology. 
    Diagnosis- Hyperkalemia with Acquired Brugada's Syndrome.
     
    Treatment-
    O2 NRB 15L, Position for Shock, IV 16-18 G with Fluids running Wide Open, Consult for Calcium Chloride 0.5-1.0 g given slow IVP over 5-10 min, Consider Sodium Bicarb 50 mEq Slow IVP, Consider Albuterol 20 mg High dose Nebulizer, Do not administer Zofran because the patient has Long QT, Transport to Local ED Priority 2.

  • Ben Dowdy says:

    Beautiful 12-lead of hyperK; widened QRS, peaked T-wave in V3, and pseudoinfarct pattern in V1-V2.  Almost looks like Brugada in V1!
    This seems to fit with a field dx of DKA, but I suppose you could also consider the other common causes of altered LOC like hypoxia/postictal/OD.  Given the vomit present, I'd be suspicious of aspiration and consider some airway management (if I had a paralytic other than sux, I'd think about some RSI).  You could also make an argument that the 12-lead is showing signs of a TCA OD; I think hyperK fits better, but it's still a possibility.
    Other treatments…IV access and some IV fluids if clinical signs of hypovolemic shock are present (I'd treat the hyperK first to see if it's somehow inhibiting reflex tachycardia).  For treating the hyperK, I'd think about calcium of course, but if TCAs are on the differential bicarb might be preferential since it would treat both conditions.  Then gather a refusal….just kidding :)  This patient has probably bought an ICU bed for a few days.

  • Ivan J. says:

    Hmm. My differential would be Hyperkalemia induced by Hyperglycemia. I see what appears to be a supraventricular of origin, most likely sinus rhythm, with IVCD. There are spread symmetric and tall T waves which are >2/3 of the R waves with a marked prolonged QTc. P waves are still visible but not as I would expect and frontal axis is still normal. You should always suspect ischemic  changes but based on the glucometer reading and ECG findings, I think this is a Potassium imbalance secondary to hyperglycemia. Stabilizing the cardiac cell membrane and potentials are a must, so Calcium Gluconate, Sodium Bicarb and even Albuterol which are the meds I carry in my county, would be useful here. Insulin also would help but we don't carry it here. I believe addressing the Hyperglycemia will fix alot of the secondary complications. The disrhythmia is cause by the electrical potential abnormalities so addressing the hyperkalemia/hyperglicemia should help, you can alway attempt antiarrhythmics like Amiodarone along with the hyperkalemic treatments if a ventricular dysrhythmia occurs.
     

  • FB says:

    DKA is up there. Hyperkalemia is up there. STEMI is also up there because of his history and EKG even though hyperkalemia can mimic ST elevation. Chest pain and nausea could have started from ACS and then the ACS triggered his hyperglycemia and subsequent DKA which led to hyperkalemia? Start with intravenous fluids and calcium chloride. As to which hospital, I don't think it matters. He needs his hyperkalemia and DKA treated first. If ACS did trigger this then it sounds like its been going on a few days maybe the cath lab isn't as important or might not provide the same benefit as someone having chest pain that started 30 minutes ago. Anyway, treat the hyperkalemia and then get another EKG.

  • Newbie says:

    DKA w/ hyper K. Almost looks brugada-ish too

  • FB says:

    I think that hyperkalemia, DKA and STEMI are all a possibility. I think its possible, if he's been having chest pain and vomitting for a few days then its possible this all could have started as ACS which then triggered hyperglycemia/DKA which then led to hyperkalemia. 1st treat his hyperkalemia with calcium chloride and start giving him IV fluids to help with his dehydration/hypotension. Its possible for hyperkalemia to mimic ST-elevation so after his K is lower you can do another EKG. Since he has possibly been having ACS for a few days I don't think that a cath lab will be as beneficial to him as it would be for someone having chest pain/STEMI for 30 minutes. He needs quick treatment of his hyperkalemia then focus on his DKA/ACS. 

  • Ryan says:

    Initial thoughts are DKA, however generally the skin is hot and flushed, not cool and diaphoretic. I would start with a fluid challenge and see if that increases the b/p. If the b/p does not improve then my suspicions would increase to the pt having a potential cardiac problem in addition to DKA. 

  • Eric says:

    DDx: DKA, HHNKA, Hyperkalemia, MI w/ Cardiogenic Shock
     
    EKG Shows ST-elevation in V1, V2, notable for electrolye imbalance, as well as aVR.  Absence of reciprocal depression or elevation in V3-6 also limits suspicion of MI; Cannot rule out without labs.
    Tx: 1L Bolus NS, if BP stabilizes consider transport to PCI facility by ground should angiography be needed; if fluids do not stabilize BP to SBP >100, transport to local facility.  If local protocol permits, 6 units regular insulin IVP w/ fluids.  

  • Alan Coombs says:

    What's your differential diagnosis?
    Hyperkalemia
    What does the ECG show?
    Tall peaked T-waves
    What do you want to do about it?
    PPV with in-line neb treatment
    IV-NS wide open
    NA Bicarb 1meq/kg

  • Brooks Walsh says:

    Great ECG!
    Kind of guessing here, but I suspect that either the RR was higher than reported, or the depth greater than shallow. The hypernea associated with metabolic acidosis is not quite as dramatic as the hyperventilation associated with CHF or COPD, and may be underappreciated.
    If the patient's breathing is indeed shallow, I'm concerned that there would be a superimposed respiratory acidosis on top of the metabolic. Bad news bears. And he sure wouldn't benefit from the dye load of an angiogram!

  • Brian says:

    Ste in alr, v1, v2 and depression all over. Possible high lmca lesion or high occlusion. Sugar is high but I’m guessing he was unable to take his insulin because he was too sick. He definutely needs insulin but I feel he needs a PCI facility fast, so I’d bypass local. On the way in, o2, fluid, zofran if he’s still vomiting

  • Hecmunozob says:

    Sinus Rythm. BrugadavType ECG due to Hyperkalemia. possible renal insufficiency 
    perhaps treat as if hyper kalemia with calcium 

  • Benjamin says:

    Given Hx and ECG I susspect strongly hyperkalemia due to metabolic acidosis caused by the hyperglycemia and secondary nutrient usuage creating ketones thus causing potassium swaping within from the cell to reduce serum acid levels.
    Most likely this case is caused by poor sick day management possibky he has stopped his insulin due to feeling nausious. I strongky susspect a cardiac issue duemto the several days of chest pain. Load and go with fluids and lots of them to a major hospital. For insulin infusion and GIK as well as tx of hyperkalemia. Early warning to hospital!!! 

  • Jess says:

    Presentation fits DKA with 3 [previously stated] exceptions: cool diaphoretic skin, "normal" heart rate in the presence of hypotension, and shallow resp – even though @ rate of 27/min.
    The 12 lead shows hyperkalemia.
    R-R between beats 2&3, then R-R  from 3 to 4 show irregularity, but that seems to be an exception to an otherwise regular strip. I would assume this is a sinus rhythm.
    PRI is on the long side, QRS wide – IVCD, and the obviously tall, peaked & symmetrical T waves all say Hyperkalemia. This also fits a pt in DKA.
    STE in V1-V2 & avR + a relatively low HR + cool diaphoretic skin – I would not rule out STEMI. I considered brugada's but thought it very unlikely – normally seen in post syncopal pt with no current complaints [so wouldn't explain the CP, or HR or skin.] So MI seems a better fit with the signs/symptoms. [even though I've never seen a STEMI with STE in so few leads]. R sided & posterior leads might be revealing.
    As for treatment, immediate Tx of hyperkalemia is priority #1 – calcium chloride or gluconate, sodium bicarb, high dose albuterol neb, insulin if you have it. 2 large bore IV's and a 20ml/kg fluid bolus [listening regularly for cough &/or wet lung sounds] would be next. I would provide enough O2 to keep pulse ox as close to 99% as I could, whatever the route. I am a little concerned about the depth of respirations and would also like to monitor ETCO2 with a cannula if possible. If it's high I would ventilate the pt as well. Another airway concern is depressed LOC + vomiting – easier to determine if I'm actually looking at the pt, but I would consider at least basic protective positioning and at most RSI  [NOT with succ!].
    I would ultimately like this pt to go to a PCI capable facility, but my prehospital tx for hyperkalemia seems pretty thin: I've never worked for a service that carries insulin, I can only give albuterol so fast when it comes 2.5 mg/3ml [the dose is what, 20mg?!], and I can't use lasix.
    So honestly not sure where I'd take him. If his EKG improved dramatically with hyper K tx and 2nd 12 lead still looked like possible STEMI I'd consider taking him the 30 miles. If he had to be intubated or I couldn't treat the hyperK I would take him to the closest. Honestly I'd probably take him to the closest. Thanks for the post!
     

  • Russ says:

    Looks almost like D winters t-waves. I'd be concerned with the presence of chest pain. Either way this is a sick pt.

  • Darren says:

    I would take this patient to a facility capable of PCI, but I'm not convinced he needs it.  I think it's DKA or HHNK with corresponding hyperK.  Judging by the ECG presentation and the shockiness of the patient, the potassium needs to get fixed right now.  Insulin if you have it would start the process well; also calcium.  With ground transport of 30 minutes, by the time you get the patient to the aeromedical crew, give report, transfer the patient to the chopper, and they begin transport, you would have already been to the PCI facility.  Manage B/P; you may have to use pressors to keep this guy alive.  If you have to maintain airway, DON'T USE SUCCINYLCHOLINE! I personally hate the drug altogether in the emergency environment, but this is a definite case in which it could be fatal.

  • FlyerRN says:

    Seems to me that we are dealing with a case of Hyper-K.
    Looking at this 12-Lead I see peaked T-Waves everywhere with flattening of P-waves in most leads.  My guess is that this EKG is a result of the pt being in DKA.  With the elevated GLU in the body, K+ isnt shifted into the cells.  He is presenting with pretty common S/S of DKA as well.  First, the most obvious elevated GLU.  Second, he has quick respirations, probably consistent with his metabolic acidosis that the body is trying to buffer out.  
    As far as Work-Up/Tx:
         - Serial 12-Leads/Cardiac Biomarkers to r/o MI (the Hyper-K could be the result of an MI with the elevated GLU as a stress response in the body). CMP to determine renal function as well as CK-MB to look for Rhabdo. (Even though thats a pretty large Zebra for this case given no trauma).
          – Fluid bolus (1-2 L)
          – CaCl 1g IVPB to stabilize the cardiac cell membrane
          – RHI 10 units to drive K+ back into cells.  D50 1 amp to off set hypoglycemic effect.  
           - NaHCO3 1 amp to drive K+ back into cells.  
    In the long term, Lasix 40mg IVP and consider the need for IHD to filter out excess K+.   Intubation may need to occur depending on respiratory status, however, I would avoid Succ's as a paralytic due to increased risk for Hyper-K+.  
    For a transport decision, if you have the capability to handle this pt by ground in your jurisdiction great if not I would fly the pt to the PCI capable hospital.  This is complex medical pt regardless of if they need cardiac intervention so a local community hospital may not be able to handle this depending on where you are.  

  • Soozey G. says:

    Hi everyone! First time poster, long time reader here. I am a very new medic (6 months as a medic, 2.5 years as an EMT prior), and I admit that my knowledge is limited but here's my take on this case:
    DDx: DKA (HHNK due to dehydration), hyperkalemia, rule-out MI. For lack of eloquence, the patient's electrolytes are going to be wacky with such metabolic abnormalities. The seemingly disproportionately low HR concerns me in the face of hypotension, so I would be concerned for myocardial injury, though perhaps the patient is on a BB?
    EKG: Sinus arrhythmia in the 80s without ectopy. Morphology suggests Brugada's Syndrome and hyperkalemia. I do not see any indication of acute ischemia or injury.
    Transport: I would plan to transport this patient by ground to the facility capable of PCI, although I don't believe he is having an MI. That facility will have the advanced cardiac care the patient will need to manage the suspected Brugada's and the hyperK. I would be concerned that transporting to a community hospital would only delay the inevitable transfer to a higher level of care.
    Treatment: Continue with high-flow O2, establish IV access with serial fluid boluses in 500cc increments as long as lung sounds remain clear to maintain  SBP of 100, keep the patient supine with suction ready, possibly 4mg Zofran if patient continues to complain of nausea and I can confirm that the patient does not have an allergy, serial EKGs. I would transmit the EKG and ask for orders for 1g CaCl (10mL of 10% solution). 
    Looking forward to the conclusion!

  • Anon says:

    Would like to gather a Nasal EtCO2 before treatment. If EtCOs is low, I'm going down the DKA induced hyperkalemia pathway. Solution to pollution is dilution, 16g preferred, nothing smaller than an 18g. Not giving Zofran due to QT/QTc. Transmit EKG prior to Community and PCI EDs. IF they are thinking there is an actual STEMI underneath the peaked T-Waves, they may not want Albuterol at all, same for the Calcium as they both would probably increase rate and cause tachycardia potentially. and increase myocardical oxygen demand, same reason we often do not give atropine in STEMI. However most likely going to say treat hyperglycemia per protocol. Would also request orders to start  the hyperkalemia protocol, Calcium IVP, NaBicarb IVP, Albuterol Neb and NaBicard in LR drip. Most likely not going to the PCI, going local.

  • Dominic says:

    Can it be a combination of hypomagnesemia and hyperkalemia? Because of the diuretic effects of hyperglycemia and the excessive vomiting  + DKA.  

  • Robert says:

    The 12 lead is indicative of hyper k, but should not be treated as such. DKA will present with false readings of hyperkalemia because of the shift of pottasium from innercellular to outer. This patient should be treated for DKA best treated in ICU. O2, heavy fluid resuscitation, insulin, and potassium. Possibly bicarb as well…

  • Jess says:

     
    "dialyzable current of injury" pseudoinfarct pattern that can be caused by hyperkalemia?
     

  • Daibheid says:

    Hyper-K secondary to DKA. Calcium, bicarb, fluids. RSI, insulin (if available). 

  • I’m amazed, I have to admit. Seldom do I come across a blog that’s both educative and engaging, and let
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