64 yom CC: Chest Pain

Here’s another great case submitted by a faithful reader who wishes to remain anonymous.

The patient is a 64 year old male with a chief complaint of substernal chest pain.

Onset: Sudden onset at rest.
Provoke: Nothing makes the pain better or worse.
Quality: Patient describes the pain as “sharp”.
Radiate: Pain radiates to right arm.
Severity: Patient gives the pain a 15/10.
Time: 10 minutes prior to EMS activation.

Skin is cool, pale, and diaphoretic.

He denies shortness of breath. He admits to nausea but has not vomited.

Past medical history: CVA with right side deficit. IDDM with below knee amputation. Electric wheelchair bound.

Allergies: No known drug allergies

Medications: Vicodin

Vital signs:

Resp: 18
Pulse: very rapid, weak
BP: 103/81
SpO2: 99 on RA

BGL: 283

Breath sounds are clear bilaterally.

The cardiac monitor is attached.


A 12-lead ECG is captured.


And another.

What’s next? 
*** Update 02/12/2010 ***
A rhythm change is noted on the monitor.
An additional 12-lead ECG is captured.
And another.
Does this shed some light on the situation?


  • Christopher says:

    Wide, regular (minor variation), rapid: VT. Additionally, it looks like VT-RBBB criteria is met (monophasic R in V1, R/S ratio < 1.0 in V6).Synchronized cardioversion, with sedation if I have the time for a line. BP isn't where I'd want it for amiodarone. I'm considering my H's/T's, but strongly considering MI. O2, IV, monitor, repeat 12L. STEMI notification if anything is found. Safe and expeditious transport to a PCI capable facility based on presentation anyways.

  • TatonkaDTD says:

    I agree with what Christopher says, wide & fast is VT until proven otherwise, but I'd be interested to see if the pt has taken his Vikes and if so, how much… Vicodin is an opiate and I'd have thought that acute overdose would have been accompanied with bradycardia, but the rest of the symptoms (except for the CP) would be consistant with opiate overdose…I'd check his pupils and question his intake before cardioverting. Worst case scenario, maybe you don't need the sedation before you shock him cause he's already coked-up…

  • Anonymous says:

    Cardizem. Slow it down and see what's underneath. Granted he's showing signs of instability, but I think Cardizem is the way to go first.

  • Tom B says:

    Christopher – It does have all the hallmarks of VT! Right superior axis, monophasic R-wave in lead V1 with slurred upstroke. rS complex in lead V6. Very wide QRS duration."Wide and fast" should always be considered VT until proven otherwise, but this ECG in particular meets several "rule-in" criteria.Tom

  • Tom B says:

    Tatonka – According to the gentleman who contributed the case, the patient's run sheet indicated that he was "not compliant" with the Vicodin.I'm not sure what that means, since Vicodin is typically prescribed PRN for pain.Tom

  • Tom B says:

    Anonymous -Of all the intravenous medications I would never give as an experiment, it's a calcium channel blocker for a wide complex tachycardia.What if it turns out to be VT?Tom

  • Anonymous says:

    Okay, he's a diabetic and an amputee so you know he has no veins !Lets try a valsalva first and then…On the off chance that he does have a decent vein I'd do a fluid bolus and get his pressure up a bit and then try the 150 mg Amiodarone drip.I'm kinda suprised that his SaO2 is 99% on RA though.DaveO

  • I agree with Christopher. I think Edison medicine is the way to go one this one. Given his medical history I'm willing to bet that a line isn't going to be a simple thing. Synchronized cardioversion should work for VT or SVT. I'm calling it VT.I had VT once where in lead 2 it had narrower complexes than many SVT's. The give away, the rate was 270 (and he was still A&O;). I can try to dig up that strip if you're interested.

  • Nicky G says:

    I agree with conscious VT, just wondering why the LP12 states sinus tach?

  • Tom B says:

    Firefighter/Paramedic -I'd love to see that strip!As far as I'm concerned, a heart rate of 270 in an adult patient involves an accessory pathway until proven otherwise!Tom

  • Tom B says:

    Anonymous (DaveO) – If I were to give this patient an antiarrhythmic, it would be amiodarone!Tom

  • Tom B says:

    Nicky G. -The GE-Marquette 12SL interpretive algorithm should not be trusted when it comes to rhythm interpretation! It's just a tool like any other. Trust your own eyes! Tom

  • Hillis says:

    It seems that i've missed alot !! Thanke you as usual Tom for this interesting case.. Very difficult alot to think !!. I would say the rythm is SVT with extreme right axis deviation and complete right BBB. The 4th ECG shows SR with AV I degree, vestricular extrasystole , RBBB.. But the Question is, does the patient recieve some treatment or the ECG resolve sponteneously !! Does the patient have a histroy of RBBB or it's new pattern in the setting of acute MI or Acute pulmonary embolism ?? The patint is diabetic with history of CVA , with SVT, hypotensive with tachypnoe am thinking about embolisation to pulmonary artery.. O2, monitoring, the histroy of 10 min. histroy of pain would make the treatment with thrombolytic , anticoagulant and antiplatelet therapy very effective if not contraindicated. PCI is very helpful too in the setting of diff. dg. and treatment.

  • Tom B says:

    Dr. Hillis – Very interesting analysis! Thank you for your insight into the differential diagnosis.I believe this rhythm converted spontaneously.I thought it was very unusual for a supraventricular rhythm to show this morphology! I'm very concerned about the concordant ST-depression in lead V2. It looks bad! Tom

  • Christopher says:

    Woah, now with a normal ECG I can rule out VT and rule in SVT w/ aberrency! Would be nice to have those for viewing in the truck.I guess that's one of those that the rules let's slip through (one of the few).

  • Tom B says:

    Christopher -There was an interesting article in Circulation that discussed how pre-existing intraventricular conduction defect nullified the "rules" for differential diagnosis of wide complex tachycardias.It's available online somewhere. I'll see if I can find it.In my mind, the fallibility of the criteria is exactly why "wide and fast" is VT until proven otherwise.If you treat a heart rhythm like this as VT and it turns out to be SVT, what's the harm?On the other hand, if you classify a wide complex tachycardia as SVT and reach for a CCB, and it turns out to be VT, that could be a huge problem! It's just not worth it when you're gambling with the patient's life! Tom

  • Hillis says:

    "I'm very concerned about the concordant ST-depression in lead V2. It looks bad! "Is like saying think about the posterior MI !! Honestly i would not think about this diagnosis without your hint !!Not all the classical findings of posterior MI are present in this case like the left axis deviation and the prominent R wave in V1-3 becouse the patient has RBBB , but the ST depression in V2 and the pathological Q waves in the inferior ( II,III and aVF ) leads are helpful in the diagnosis.Confirm it by using the posterior leads V7 – V9.

  • Another case for watchful waiting, while I agree that Fast and wide in extremis is Vt till proven otherwise, and even if it isn't electricty is theraputic.As to interpolation I diasagree as to concordance I read it as discordant, but the extreme Right axis (no man's land) speaks to Ventricular. it's interesting that post spontaneous conversion morphology and axis reamins for all intent the same. What would I have done I'm a big adovocate of good old time methodlogy, number #1 establish a safety net prior to screwing with success ( get them on O2 establish an IV even an IO if you're that concerned) then try mildly invasive and therfeore less lethal approaches first, In this case vagal mnauvers for it can be either theraputic or at least daignostic.Slows with VM then speeds upt = sinus tach, slows and demonstrates fib or flutter waves, doesn't do anything VT, stops it cold PSVT of some sort. Just an older curmudgeon's view of the practice of "Primum non nocere"

  • Geoff says:

    From what I understand about the patient, the rhythm did convert spontaneously.

  • Tom B says:

    Jon Levine – With regard to "concordant vs. discordant" this can be confusing because there are two different occasions that we use the terms.The first is with regard to bundle branch blocks where we talk about the "rule of appropriate T-wave discordance." In other words, the T-wave should be deflected opposite the terminal deflection of the QRS complex.The second is positive or negative concordance of the QRS complexes in the precordial leads, which supposedly helps support the ECG diagnosis of VT.Positive concordance – all QRS complexes positively deflected in leads V1-V6.Negative concordance – all QRS complexes negatively deflected in leads V1-V6.In this case, I referred to the concordant ST-depression in lead V2. That means the ST-segment is shifted in the same direction as the terminal deflection of the QRS complex.That's bad.Are we on the same page now?Tom

  • Tom B says:

    Dr. Hillis -I don't know why I didn't notice this before, but how about the PVCs in lead V3? Very impressive concordant ST-depression!Tom

  • Hillis says:

    It's so much complicated..If you mean that this patient is having STEMI in the anterior leads.. Would you please explain how we can differentiate it from posterior MI ? esp. in the setting of RBBB.Is it according PVCs ?? I read an article posted by Dr. Smith in the prehospital 12- lead ECG that STEMI some times better recognized in PVCs, but couldn't find it once again to revise it !! Or maybe once again am just far away from the right diagnosis !!Dose the patient in this case was diagnosed with MI wherever the location was according to the ECG alone??

  • Tom B says:

    Dr. Hillis – I am still talking about a possible posterior STEMI.The ST-depression in lead V2 is visible in the underlying rhythm. However, the ST-segment is only slightly depressed in lead V3…Except during the PVC! Then we see obvious and ugly-looking concordant ST-depression in lead V3 (first complex in lead V3 in the last ECG).These findings make me wonder if this isn't a "new" bifascicular block (or even so-called trifascicular block since 1AVB is also present — I know this terminology is controversial).If memory serves, left posterior fascicular block rarely presents as a right superior axis.Regardless, I don't have any further information about the case, so this is just speculation.Tom

  • J Primrose says:

    This patient is a wheelchair-bound diabetic with a history of hemiplegia and a glucose of 283, or well into the DKA range. I am suspecting hyperkalemia secondary to acidosis as the underlying cause – even after the resolution we are seeing a wide QRS with high T waves. Cardiovert if necessary if the unstable wide complex returns, but otherwise treat the possible hyperkalemia and resolve DKA. Cardioversion tends to be less effective in hyperkalemic patients, so make sure you have a plan B. Since the lungs are clear still, bolus to dilute the potassium and glucose and reduce the acidosis. DO NOT give Ca channel blockers, if the patient is hyperkalemic you would utterly bugger your best way of protecting the heart from excess potassium (e.g. Calcium chloride 10ml 10% solution, or 3 x the mass dose gluconate). I am very leery of CA blockers in wide rhythms unless we are absolutely sure what we are messing with; SVT's rarely kill people but VT's do, and treating VT with a CA channel blocker is essentially lethal injection. Insulin draws K back into the cells, and has the benefit of being an inotrope in sick hearts according to recent data.

  • Tom B says:

    J.Primrose – Awesome comment! I hadn't even considered DKA-induced hyperkalemia! We're definitely of a like mind when it comes to CCBs for WCTs! Tom

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