Chest pain, acute STEMI, and EMS-witnessed VF arrest – Part 1

Here’s an interesting case I originally found on the UK Ambulance Forum.

It was submitted by Phil who is a citizen of the UK working in Australia as an Intensive Care Paramedic.

EMS is called to the residence of a 63 year old male with a chief complaint of chest pain.

The patient was found sitting on his front porch. He appears acutely ill.

Onset: Sudden but gradually increasing in intensity
Provoke: Nothing make the pain better or worse
Quality: “Tightness”
Radiate: The pain does not radiate
Severity: 8/10
Time: 45 minutes prior to EMS arrival

Skin is cool, pale and diaphoretic.

Patient admits to mild dyspnea. Breath sounds are clear bilaterally.

Abdomen soft and non-tender.

Past medical history: None

Medications: None

Vital signs are assessed (or a set of observations as they say in the UK).

  • HR: 64
  • RR: 20
  • NIBP: 200/90
  • Temp: 36.7 C (98 F)
  • SpO2: 98% on RA
  • BGL: 8.8 mmol (158 mg/dl)

A 12-lead ECG is captured.

An 18 ga IV is established in the left antecubital space.

The patient is given 324 mg of aspirin and SL NTG spray.

Vital signs are re-assessed.

  • HR: 62
  • RR: 20
  • NIBP: 130/70
  • SpO2: 98% on RA

The patient’s pain improves to 4/10.

A second 12-lead ECG is captured.

An additional NTG spray is administered.

Vital signs are re-assessed.

  • HR: 62
  • RR: 20
  • NIBP: 114/70
  • SpO2: 98% on RA

The patient’s pain improves to 2/10.

Otherwise, the patient does not appear to be doing well. There is a slight change in his demeanor and he states that he “feels funny”.

Suddenly the patient exhibits seizure-like activity.

As the paramedic applies the combo-pads he pushes the 12-LEAD button again.

How would you treat this patient?

See also:

Chest pain, acute STEMI, and EMS-witnessed VF arrest – Part 2


  • Bob says:

    I don’t always have a ventricular dysrhythmia… but when I do, I choose “Torsades de Pointes”.

    200J, CPR – ACLS.

    Magnesium Sulfate, if your protocol permits.

  • Tom B says:

    What if I were to tell you that it’s pulseless?

  • Clare Smith says:

    ECG shows ST elevation in leads II, III and aVF with reciprocal ST depression in septal leads.
    Is the final ECG Torsades de Pointes? In that case, VT ACS protocol

  • Colin Byerly says:

    I see anterior ischemia with elevation in V6. I would immediately presume a posterior wall MI and do a 15 lead ecg. I would avoid NTG.

  • Carl says:

    This is a super cool ECG and PT presentation. Initially we see signs of an inferior posterior & moving lateral infarct pattern. The interesting part is that it looks like we are seeing definitive U wave morphology which we could consider as an ‘early after repolarization’ sign which is probably put the PT into TdP. Does the PT have a pulse? If not immediate defibrillation followed by 2 min of CPR, and reassment. If they do, consider magnesium sulfate, amioderone

  • Jeff C says:

    I see ST elevation in Leads II III and AVF with ST depression in Leads V1-V4. I would think Inferior Posterior MI and suspect Right Side MI. 15 lead to confirm. The BP drop from 200/90 to 130/70 after NTG spray would definitely lead me think RVI. 02,ASA hold off on NTG. Bilat IV’s with fluid bolus. We currently do not have standing orders for fluid bolus so Medical Control would have to be notified first. Last Strip looks like Torsades. Defib at 200j since it is witnessed followed by CPR and ACLS. No Mag sulfate in our service.

  • Carl says:

    Whoops. Sorry for the spelling errors above, I am typing on an iPhone. In addition, the above should read early afterdepolarization, not repolarization.

  • Christopher says:

    Looks inferior/posterior potentially given the ST-E in II/III/aVF and ST-D in aVL/V1-V4. Got some taller R-waves than I would have expected in V1-V2 further pushing me towards some posterior involvement. With inferior changes I would always like a right sided before NTG, but an 18 w/ some fluids running would likely be sufficient to manage any fluid challenge required w/ RVI.

    Final 12L shows coarse VF (v rate >300) confirmed by 12 leads. Check pulses, CPR while charging, defibrillate. Update the STEMI facility that the patient went into cardiac arrest (its the holidays, give them the gift of an early notification).

    If you achieve ROSC, try for a post-arrest 12L.

    Good work by the UK crew!

  • Dave B says:

    IWMI, ST elevation in III > II suggests RVI, reciprocal depression in aVL, ST depressions in V1-V4…suggests posterior involvement and proximal RCA occlusion..Are we sure there is no hx of hypertension? With the elevated BP the ddx includes a Debakey I dissection, which causes proximal RCA occlusion..if this tore completely, it could explain plummeting bp with rapidly crashing pt..just something to consider in addition to what others posted.

  • sledogg says:

    Mag sulfate 1 g, Lidocaine 1mg/kg repeat in 5min at 0.5 mg /kg to 3 mg/ kg hang a mag drip or with this cardiovert biphasic at 100 j……..Nova Scotia Canada paramedic p@p

  • sledogg says:

    if it was pulseless cpr 2 min then 200 j biphasic

  • Matthew says:

    From the 1st 12lead, I notice elevation in leads: II,III & aVL, and a recip. change in aVF, which leads me to think a INFERIOR WALL MI. The 2nd 12lead I noticed elevation in leads V5 & V6 which leads me to a INFERIOR LATERAL WALL MI. Treatment plan for this: Obtained a V4R, 2-IV’s, withhold the NTG, High Flow Oxygen, Morphine for pain managment, transmit to a hospital that can handle a STEMI, 15 Lead and Etco2, Serial 12 leads and ressassess and reassess. When the patient voiced “I FEEL FUNNY” and has “Seizure” like activity, that is a clue for us to reassess this patient. the 3rd 12 lead showes what looks like “Torsades de Points” with the narrow to wide twisting shape. Now is there a pulse? or is this the “Seizure Activity”? I would like to know how long the “Seizure Like Activity” Lasted, maybe there is something in this patient’s history he forgot to mention? So I am going to go along that this is Torsades de Points: Treatment: With Pulses: Contact Medical Command: Magnesium 2mg, IV, O2. Without Pulses: Shock at 100j and follow ACLS and Regional Protocol.

  • NYCMedic says:

    I agree with other’s interpretation that initial 12 shows elevation in the inferior leads with possible lateral wall (elevation that changes in sequential 12’s) and posterior (significant depression in anterior leads) involvement. Personally, I would hold off on NTG for this patient at least until obtaining a right-sided and posterior ECG.

    What’s truly interesting about this case is the rhythm the patient unfortunately finds himself in after “feeling funny”. So far, commenters have described this as v-fib, v-tach, and torsades. Great, we’ve all determined it’s ventricular in origin, but cannot nail it down.

    One thing that is confusing to me, is that people seem to be ignoring the fact that this is a 12-lead, not a rhythm strip. Someone mentioned that it has a “with the narrow to wide twisting shape”. Well, I would say, of course it has a SOMEWHAT twisting shape, because as you move across the 12-lead, we are seeing many different vectors, which would naturally give the appearance of a changing axis if we forget that it isn’t a rhythm strip.

    I’m not sure I can agree with torsades for this patient. I personally don’t see a rotating axis on this 12, and I think we would need a rhythm strip to know for sure. The QTc is normal. The clinical presentation also doesn’t really fit, as I don’t see suspicion for hypomagnesemia/kalemia. However, we do know the patient is having chest pain with a clinically significant ECG for AMI. And, it is my understanding that VT or VF would be a more common dysrhythmia to enter secondary to AMI than torsades (which is a very rare rhythm to begin with).

    I guess I am tempted to call this VF like Chris. Regardless, treatment is the same, light him up 200J bi or 360J mono, CPR x 2minutes and go from there. Cool Case.

  • VinceD says:

    Infero-postero AMI in the first two. STE in V6 could be an extension of the posterior MI, or there could be lateral involvement in I/aVL,V5 masked by reciprocal changes from the inferior infarct, it doesn’t change treatment, and I’m leaning against lateral MI. The final ECG shows v-fib. If pulseless, immediate CPR with biphasic defib @ 200J as soon as possible and standard ACLS. I could see where some people might say polymorphic v-tach in the last strip, but to me it looks like v-fib with baseline sway. The QRS compelxes aren’t clearly defined, exceed 300bpm, and don’t follow any sort of morphological pattern across the leads .
    A note on semantics: the diagnosis of Torsades requires a prolonged QT interval leading to the arrhythmia, which this patient lacks, so “polymorphic v-tach” would probably be the correct term to use if this patient went into a wide complex tachycardia with changing QRS complexes. Of course, I claim it’s v-fib, so it doesn’t really matter, I’m just sayin’…

  • VinceD says:

    NYCMedic, you managed to post while I was typing, but it seems like we agree on every front, and you make a great point about the 12 different leads giving the illusion of “twisting.” Well stated!

  • Troy says:

    Well I would say a proximal RCA occlusion. Inferior MI (with RVI and posterior involvement I would guess). I dont like diagnosing posterior MI’s off of ST depression in the anterior leads because….well….sometimes ST depression is just that, DEPRESSION!

    The last rhythm I would have to know if a pulse was present or not. It looks like coarse v-fib but it could be polymorphic v-tach. Either way ACLS 2010 guidelines state the same thing, 200j biphasic defibrillation and i would run down the V-fib/V-tach tree.

    I wouldn’t call it Torsades because the baseline cardiac rhythm had no prolonged QT interval so if it would be polymorphic V-tach it would be in the absence of Torsades which is treated with amiodarone instead of magnesium

  • Emthun says:


    I cant understand after the second ecg and BP:130/70 why did he gave additional SL NTG? Is it in your protocol for ACS or STEMI?
    I think easing BP so fast like in this case cause global tissue hypoxaemia and polymorphic ventricular tachycardia or fibrillation was the expected effect.

    Benny (National Ambulance Service, Hungary)

  • M.D.Joo says:

    I think he had inferoposterior MI. sholu have avoid NTG. just do fluid resuscitation also prolmpt do ACLS algorithm.

  • Robin says:

    infero-lateral  located STEMI (ST depression in V1-V3 = ST Elevation V7-V9, looking for this), ST- Elevation decent in III, V6
    VFib : rapid DC Shock 200 J Biphasic, EKG Controll, check Pulse  ->CPR for 2 mins , ACLS Standards VFib
    -> Hospital ->  Coronarintervention

  • Frank says:

    I agree with NYC medic. I'm not at all convinced of torsade. I'd call VF (everyone agrees on the immediate treatment) complicated an infero-postero-lateral STEMI.
    Differential diagnosis, depending on the timing of the sudden deterioration would be be acute aortic dissection (dissecting in a dominant RCA). Long shot but must think about it with a 200 mmhg (very unusual to have such a drop in BP with nitro unless "adrenergism" is involved)

  • greg says:

    shock  ,   any  pulses   ,  treat  as  v  fib  cause  once  you  shock that  rhythym  its  going  downhill  this  ole  boy  going  to  the  cath  lab  for  an  n  stemi 

  • Paul says:

    I’m going John Wayne and giving NTG/GTN. There’s no reason to withhold it. He had a significant drop in systolic pressure after the first dose, but the second dose didn’t seem to do anything deleterious. I’m going to sit on my hands for at least 15 seconds and see if the patient self-converts. If not, Edison Medicine for the Torsades (although it might not work).

  • Pat says:

    Amioderone is contraindicated in Torsades

  • Shawn says:

    I would agree with the 12 Lead interpratetion of possible inferior MI, and I would have liked to get a 15lead prior to Nitro, especially the second dose.

    For the last rythem defiantly V-Fib with possible underling torsades (would have to see a strip). I would have a high suspicion of torsades, since my area has a high mag deficient population. Otherwise CCR, Fluids, Shock 200, vasopressin, Amiodrone (if refractory) and mag, epi, moving to ACLS if no conversion after 6 min.

    ROSC achieved move to active cooling and sedation.

    Neet case!

  • In Poland:

    Check Vital sings – especially breaths and pulse,
    If no pulse start CPR 30:2, next bring defibrillator, and shock 200J ASAP. Administer 2g of MgSO4 20% IV, CPR 2 min, check rythm, if still VF, Shock 300J, CPR for 2 min, check rythm, if VF shock 360J, after that administer 1 mg epinephrine (every 3 to 5 minutes) + 300 mg of amiodarone, next. Try to intubate, connect respiratore, call a ZRM S (medical rescue team with a doctor onboard in team)

  • pdquick says:

    He’s in TdP and he’s seizing—>apply electricity. Don’t overthink it.

  • Rosky1500 says:

    Inf STEMI with latersl extension. Downward sloping
    ST depression v1 to v3 = posterior involvement.
    Course VF = stacked shocks if pads already on. ACLS protocol.

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