17 year old male CC: Chest pain and palpitations

Here's a great case submitted by a faithful reader who wishes to remain anonymous.  Some details have been changed to ensure patient confidentiality.

You are called to the local ER to transfer a 17 year old male to a large metro hospital for evaluation. Your patient  presented to the local ER with chest pain and palpitations following mild exertion. He was alert and oriented, and other than his elevated heart rate, his vitals were within normal limits.  Upon presentation to the ER:

  • O:   Discomfort began during exertion
  • P:   Exertion makes it worse
  • Q:   Dull pain, substernal
  • R:   non-radiating
  • S:   3/10
  • T:   about 20 minutes prior to ER arrival


  • S:   Chest pain/palpitations
  • A:   NKDA
  • M:   N/A
  • P:   No previous medical hx
  • L:   Unknown
  • E:   Mild exercise

As far as vitals go, all i can tell you is that they were within "normal limits" with the exception of heart rate. The patient is given trials of adenosine, lidocaine, digoxin, and cardizem, without successful conversion. In fact staff noted that the rhythm seemed to "speed up a bit" after the adenosine. He is put on an Amiodarone drip, which slows the rhythm a bit.  They then elected to cardiovert, and after three attempts he converted to a sinus rhythm.  Here is one of the rhythm strips and a 12 lead they acquired:

At the time you make contact, the patient has no complaints and is still in sinus rhythm. You apply your cardiac monitor and acquire your own rhythm strip and 12 lead:


Your trip to the metro hospital is uneventful, and he remained stable in your care.


What do you think is going on with this patient?

What is your interpretation of the ECGs?

Is there anything further you want to do for this patient?




  • renegade medic says:

    Uhh II, III, and aVF look pretty bad on the second 12-lead with reciprocal T-wave inversion. The T-wave abnormality is to be expected as the O2 demand is likely through the roof, but II, III, and aVF look pretty elevated to me.

  • Tom says:

    mmm, short P-R interval, Delta wave visible on the QRS.  ? WPW

  • Joe says:

    Looks like wpw for me.. Although I am not a medic and I am looking at this on my phone… But looks like delta waves and a short pr interval…. The ischemia and or elevation may be due to the ischemia from the fast hr… But like I said I am not a medic so any help would be nice ..

  • waleed ibrahim says:

    AF with WPW , RBBB + LAD , delta wave is evident 
    Ablation therapy is a golden option 
    Procainamide , Amiodarone are OK
    digoxin , beta blockers and CCB are disastrous
    do EPS for definitive diagnosis  

  • Brugada…? I see elevation and t wave inversion… not quite sure. It would explain the tach with lack of conversion initially. No known hx? I would inquire about family history, we could be dealing with a congenital issue…

  • Oooooh! Go figure I don’t pay attention to the delta wave. No afib, I see pwaves. But delta, I’ll agree and opt toward wpw.

  • mohammed albesh says:

    AF with WPW 

  • SNunes says:

    p waves, regular rhythm. Not AF

  • Tj says:

    WPW definitely. On the hospitals rhythm strip, it looks like a fib, but not on their 12 lead, so I’m not completely sold on the a fib. Actually, this makes me think that there could be more than one extra pacemaker causing this problem. Either way, I think an ablation is the answer.
    As far as the elevation and depression go, they were probably caused by some rate induced ischemia, mixed with the half dozen antiarhythmics and 3 shocks he received at the hospital. Also, being a young man, small amounts of elevation are expected. In my opinion, only the elevation in lead III is significant.
    As for patient care, I think the most important thing is to keep him from getting worked up. If he exerts himself too much again, all that hard work put in by the hospital might have to be repeated.

    I’m curious to see the followup to this case!

  • sara says:

    it could be vt secondary to silent  inferior myocardial infarction as after converting to sinus there s acute st elevation.. though he s the young man with no previous history there is d possibility of acute MI which cant be ruled out .. another dd for me stunned myocardium / t s cardiomyopathy..  

  • Night Heart Watch says:

    For me this is an interesting ecg case. Based on the timelines on the ecgs, the 12L (1835) revealed an initially  narorw complex tachycardia (prob long RP)with RBBB morphology and extreme RAD. From then on it became a wide QRS tachycardia (RBBB morphology) and LAD. Did it convert to SVT with aberrancy or VT with RBBB morphology. On the wide QRS part, we have qR in V1 and rS in V6 (rS ratio <1) and ? hump on the R of V1 (difficult to say due to strip given). So based on the V1 and V6 morphology this could be VT. Probably they followed the new ACLS algorithm and game adenosine which on the rhtyhm strip (1929) showed an irregular rhythm (narrow) which could be AF. An interesting note is the "speed up a bit" comment after adenosine. So most likely this is the reason why they gave cardizem (no control) then digoxin (still no control) then cardiovert (sinus rhythm).
    The 12L post-cardioversion (2126) is sinus tach, short PR,delta waves, LAD, RBBB, inverted T waves V1 to V3, upsilon in V1(?). So could this patient also had an ARVC on top of a WPW?
    The adenosine speed up the rate because is suppressed the AV node so conduction is favored in the accessory pathway. Also in WPW shy away from drugs that supresses the AV node (dig and betablockers).
    An EP is the answer to this problem.

  • VinceD says:

    Hindsight's always 20/20, and it's easy to make the call when I'm not the one caring for the patient, but I think that some poor decisions were made here. I don't mind that the physician failed to administer the correct med, but the fact that he or she gave incorrect ones because they did't know what else to do with the rhythm is, well, just plain wrong. There's some merit to the phrase "shock it till you know it," and if the heart's doing someting crazy and fast that you can't pin down, indescriminate trials of multiple pro-arrhythmic medications are not the answer! Ugh. With that out of the way, it's pretty clear the patient has WPW, confirmed by the prehosital 12-lead. What's more debatable is the actual rhythm causing all the trouble. Of initial interest is the apparent regularity of the hospital 12-lead. The first two narrow-complex beats are about 400ms apart and lead III exhibits what appears to be a biphasic T-wave, however given the rate and sawtooth-like morphology of that T-wave, underlying flutter must be strongly considered. Then a very early beat arrives and is followed by a fairly regular, but not perfectly regular, tachycardia at ~200 bpm. That early beat could be be a PVC triggering V-Tach, or the patient could be in a-fib and first two beats were just flukes travelling down the normal pathway before preferential accessory conduction took over for the rest of the strip. Fast a-fib can look mighty regular. Of passing interest is the ability of this tracing to mimic sodium channel blocker overdose, with tachycardia, a large terminal R-wave in aVR and a wide, slurred QRS. After looking at the first set of hospital rhythm strips, however, it becomes clear the patient is in a-fib. The top one could easily be confused with artifact, and even with the diagnosis made there's a chance it could be, but the second strip leaves no doubt as to what's going on. Several different morphologies, in an irregularly irregular rhythm, with beats closer than 200ms apart, means it's a-fib with WPW. Usually I'd advocate for a trial of procainamide, but with all the drugs he's got on board already, electrical cardioversion would be the way to go.

  • Jim Hendey says:

    av reentry tachycardia d/t wolf parkinson white. I think it was treated appropriately initially but ablation is the best choice.

  • Brian Terzian says:

    Nice case. I agree with the AF with preexcition dx….lucky he didn't go into complete CV colapse after the nodal blockers! I would expect avrt in someone with WPW, but AF warrants searching for another cause….wonder if he had a few too many cocktails the night before….

  • Prehospital RN says:

    Afib + WPW  … any hx of substance abuse that could have contributed? Cardiovert, or if you prefer to give meds, procainamide … NO calcium channel blockers or adenosine.

  • n0ss says:

    this is the WPW syndrome, accessory pathway in the posterior septal wall probably in the left part b/c of the RBBB, LAHB morphology. Positive delta wave  in leads I, aVL and V6, q wave in lead III and isoelectric delta wave in aVF, and Rs in V2 and V3 all indicate this location of the Kent bundle.Afib in the first rhythm strip, then orthodromic AVRT in the first ECG.
    Any R-R interval less than  270ms is high risk and less than 240ms onfers a very high risk of VF. Septal acessory pathway is also more riskfull than other accessory pathways. DOC for this patient when in a-fib would be procainamide, according to norwegian guidelines, dunno know if this is the same in the US. Amiodarone can also be used.

  • n0ss says:

    edit, second ecg also a-fib, too irregular for AVRT.

  • Yakub says:

    Do Echo, ECG, Chest xray then check those results very quickly then if the artery veins are blocked the urgently proceed angiogram to unblock the valves arteries and veins. If angiogram not necassery then may be proceed a boipsy from the jugular (neck) if thats not needed then give pain killers from serline (drips) because blood pressure need to be monitered every 5- 10 mins then ECG every half an hour while the patient will have a bed rest nurses should check on patients regularly…

  • Shahid says:

    very nice case……
    In my opinion it is A-Fib with WPW syndrome
    So Procainamide should be considered on first contact with physician.
    If it failed, then ELECTRIC CARDIOVERSION…….

  • Troy says:

    WPW of course and I am calling it type A. Procainamide and ablation therapy

  • Whit says:

    I agree WPW hence why adenosine did nt work

  • Brian Terzian says:

    Anyone notice how the rhythm is initiated (the left edge of the tachy 12 lead)? Looks like a sinus beat, then maybe a junctional, or premature juntional beat followed by the initiation of the tachyarrythmia. Looks like the rhythm might be initiated by an r-on-t complex, although maybe just coincidental (since an r-on-t intiated tachyarrythmia would probably be ventricular). Thanks to my prized paramedic student GR for this observation.

  • Dr.Walaa says:

    WPW,Ablation(i know it since "speed up a bit" ) 

  • brando says:

    ep study should be considered… 

  • Dr. mohammed says:

    it seems to me that there is a Delta wave so it is most likely to be WPW syndrome

  • Device geek says:

    WPW. Cardiovert then EPS with ablation.

  • Christopher says:

    Brian Terzian,
    Good question about the possibility of this being R-on-T. My question to you would be: is the resulting tachycardia regular or irregular? And does that even matter for R-on-T?

  • Brian Terzian says:

    The resulting tachycardia definitely looks irregular to me….I'm calling it AF. I've never heard of AF resulting from r-on-t (I've only heard of VT). So, I'm not sure if this is just coincidental or if there is something more going on….

  • Christopher says:

    Brian Terzian,
    You're correct that the resulting rhythm is AF, although VT can be somewhat irregular just not this irregular. When you looked at the R-R interval you noticed it was dangerously short, upping the possibility of an R-on-T problem causing VT or VF. So while in this case the resulting rhythm wasn't because of R-on-T, it certainly came close to causing it!

  • Billy Bob says:

    Well the first ekg could be MAT but I'm gunna call it A-Fib with RVR. I agree with the drugs, they didn't work on to electricity which seemed to do the job. 2nd ekg is WPW and concerning; all of that could be secondary to the WPW but can you rule out STEMI just because he is 17? Someone mentioned the possibility of substance abuse perhaps a stimulant (would tie all of this together). I see LAD, RBBB, Inferior STE with lateral recip changes, STE 3 > 2 suggestive for possible RVI. Agree with the ablasion; I'll agree that more than likely all the changes are from the previous rates, WPW, drugs and all the other crap this kid went through. However my question now is why the most dramatic changes in those leads (2,3, AVF V1,2,3) I would think that I would see the most dramatic ischemia changes in the left chest leads being that part is more muscular and more sensitive to O2 changes? Feel free to throw some input in on how off i am lol 🙂

  • Newer EMT-I says:

    Looks to me like WPW…however with the slight elevation in II, III, AVF along with the reciprical changes and the downsloping in AVL…I can't rule out STEMI.  I certainly wouldn't give Adenosine.  Since he has been converted…I would treat as a stemi and note the WPW.  O2, IV, MONA, Monitor.

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