Rate Related VS. Primary ST-T Changes:

A 56 year old black male presents to the Emergency Department via EMS, complaining of Chest Pressure, 10/10 pain scale. Pain started suddenly following sudden onset of palpitations, while mowing his lawn. All approximately 5 minutes prior calling EMS. Keep in mind, it was a hot and sunny day with temperature in the 90’s. He advised of prior episodes of chest pressure but never as severe as today’s episode. The pressure is generalized throughout his chest, and nothing seems to make it better.

PRIMARY ASSESSMENT:

  • Patent airway
  • Adequate ventilation with regular and equal chest expansion
  • Strong, irregular radial pulses with skin pink, warm and diaphoretic

INITIAL VITAL SIGNS:

  • Heart Rate: 206 beats/min
  • Respiratory Rate: 22 breaths/min
  • Non-invasive Arterial Blood Pressure: 141/102
  • SpO2: 98% on 3 lpm
  • Blood Glucose: 102 mg/dL

MEDICAL HISTORY:

  • Hypertension (complaint)
  • Non-smoker, occasional alcohol consumption

NO KNOWN ALLERGIES

EMS obtains the following 12 Lead ECG and transmitted to the ED:

 

Upon arrival to the ED, the following 12 Lead ECG was obtained:

Scan_20140918 (2)

What is your detailed 12 Lead ECG interpretation?

What is your course of treatment?

Do you think this patient requires Cath Lab activation?

 

11 Comments

  • Dayne says:

    LMCA/3-vessel disease

  • Dayne says:

    AF with RVR @167, LVH and prolonged QT.
    ST depression to I,II and V3-6 and reciprocal elevation to aVR equal to or >1mm highly suggestive of LMCA or 3-vessel disease. High specificity for proximal occlusion.
    Aspirin, GTN, IV access, Spo2 >95%, Transport to nearest PCI/Cath Lab facility ASAP

  • Michael Schiavone says:

    Isolated ST elevation in AVR with ST
    depression in several leads. Rapid, irregular rate suggests AFIB with RVR. I would provide entry
    note with this exact description and leave it to hospital whether or not to activate cath lab. My EMS treatment: IV access, 324 mg. ASA, NTG, Cardizem .25 mg/kg over 2 minutes, consider 1mcg/kg Fentanyl if pain persists at 10/10 level. Monitor BP every 5 minutes and treat potential
    hypotension with NS fluid bolus.

  • Brian says:

    Afib. There is widespread depression in most leads and aVR has some elevation…but I am skeptical about this ecg.

    If a quick fluid challenge of 500-1000cc did not slow down the HR I would give him some diltiazem (5mg increments is our protocol or 0.25mg/kg) and slow the rate down a bit and see if it is rate related ischemia.

    Some fentanyl would be nice
    I would give ASA just in case, but no nitro for this patient as it is relatively contraindicated in tachyarrythmias.

  • Sean V says:

    Atrial Fibrillation w/ Rapid Ventricular Response.
    There appears to be possible Delta Waves, the most prominent being in aVL, also leads I, II, and V6.
    In the EMS 12-Lead there appears to be a fusion beat, 3rd in V2, slurred R-wave appears quite consistent with a Delta wave.
    I would consider WPW as the primary cause of the A-Fib w/ RVR.
    The STE & STD is likely rate related, and I would expect to resolve post treatment.

    I would be interested in what his Temp is, as well what the circumstances are behind the other episodes of chest pressure.

    I would treat as per ACLS Unstable Tachycardia algorithm; the 10/10 chest pressure meets the inclusion criteria for unstable despite no hypotension.

    Move to airconditioned ambulance (AC on max)
    ASA 160mg PO
    Large bore IV access w/ 500ml NS bolus (preferably not warm).
    Obtain 2nd 12-Lead prior to cardioversion, if moving to cooled environment resolves the A-fib w/ RVR then transport w/o further Tx.
    If 12-Lead is the same:
    Sedation w/ Ketamine 0.5mg/kg
    Cardioversion @200J, repeat PRN & increase energy up to 360J (I have a biphasic LP15).
    Repeat 12-Lead ECG post cardioversion.

    If there is STE indicative of AMI post cardioversion I would follow our STEMI protocols (Xmit, plavix or ticagrelor, enoxaparin, TNK or PCI)

    I however wouldn’t activate the cath lab based off the above 12-Leads, rate control first.

    • Sean V says:

      Also forgot to mention decrease the FiO2, 3LPM is getting us a SpO2 of 98%, titrate down so we staying at or above 94%. No need to hyperoxygenate & create all those fun free radicals.

      I would also include using an EtCO2 nasal cannula, lets get another measure of our cardiac output.

  • John says:

    ECG is a rapid atrial fibrilation with ventricular rates approaching 300 beats per minute suggestive of WPW. Widespread ST segment depression is most likely rate related ischemia; elevation in aVR is not a reliable finding with a rapid heart rate point away from LMCA occlusion. Slow the rate before looking for ischemia, injury, or infract. After correcting the rate I doubt this patient will need a cath lab.

    Procanimide will be the drug of choice for this patient as it preferentially targets the accessory pathway causing the acclerated rate. Procanimide is not available in my system so syncronized cardioversion is my treatment option. Given this patient has a stable blood pressure and is conscious, alert, and oriented sedation with Versed would be appropriate before attempting cardioversion.

  • Michael says:

    I just don’t see adequate evidence for WPW. I would be confident administering this PT Cardizem at .25mg/kg based on his hemodynamic stability. I’d also like to know more about PT history, like does he have AFIB at baseline and, if so, what does he take for it. I would also ask about a history of WPW before I administer a calcium channel blocker. I also would administer ASA and Nitro as long as he remains
    hemodynamically stable. Obviously, I’d have 2 IVs established (ideally) with NS ready to go if needed. The 10/10 pain concerns me and Id be ready with
    1mcg/kg Fentanyl if it persists at that level. 02 via NC to maintain 94% Sat. I would notify hospital when I was 10 minutes out with PT’s latest condition and let them determine PT’s needs based on my updates report. It should be noted my service does not provide procainamide in the event of WPW.

  • Jeff says:

    He’s complaining of 10/10 chest pain that coincided with palpitations with a HR of 206 that is probably A-Fib. I am guessing that if you correct his rate you will allow his myocardium to become perfused again and his chest pain will subside. I would pre-sedate him with Midazolam 2mg and electrically cardiovert starting @ 120j biphasic. After he converts, re-assess, take another set of VS and an ECG to look or signs of ischemia or infarct.

  • Billy Bob says:

    I think I will have to agree with Michael; I just don’t see all that much evidence of WPW; typically with WPW & AF the complexes vary in width and morphology due to the combination of the accessory pathway and normal pathways which I just don’t see here. The rate doesn’t seem to match what we’d expect for WPW also where you would expect to see “pseudo Q’s” they are not there. I will say it’s simply AF RVR; thinking back to A&P the heart receives blood/perfusion during diastole which the high rate does not allow therefore this is more likely to be rate related. I think you could argue treatment either way. He is symptomatic yet stable (although the BP suggests compensation) so you could go with the IV’s ASA and cardizem and whatever you have for pain management. The other token is he is complaining of ischemic type CP so you could theoretically justify cardioversion if so IV’s ASA and whatever you have for sedation (personally I’d go with Fentanyl & Versed) then 120 j increasing if necessary. This pt doesn’t have a hx of AF that we know of so again theoretically you don’t have to worry about him throwing a clot and another perk is if you are worried about WPW in this case and are weary of giving him an AV nodal blocker then just to be safe and cover both possibilities electricity it is!

  • Justin says:

    I’m not sold on true A-Fib, as there is a fusion beat/PAC visible in lead V1, additionally I think that the “U” waves are possibly atrial activity. This pt could be having a fib/ flutter pattern; but its hard to say without slowing down the rate and getting expert consultation from a cardiologist. I Would treat him as symptomatic/ stable according to protocols here which includes IV/ O2 per pt assesment/ monitor and pharmacological therapy. He is well compensated and not at risk of imminent detorioariation. I would start with ASA 324 mg PO, morphine 2-4 mg IVP and adenosine 6 mg then 12 mg if needed to slow the rate and get a better handle on the underlying rhythm. I would then proceed to the diltiazem 0.2 mg slow IVP repeated at 0.35 mg SIVP in 10-15 minutes if rate remains above 140. I wouldn’t call a cath lab activation on him but I would divert him to a cath capable facility that has onsite cardiology. There is no evidence of WPW in the ECG and no history of it so we can reliably rule it out.

    Also as a side note, there is a possibility that severe electrolyte imbalance (related to dehydration) could have precipitated this event so I would also give a 10 ml/kg fluid bolus (0.9% NS) repeated X1 concurrent with the other treatments.

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