46 year old male CC: Chest Pain

Here’s an interesting case from Associate Editor Christopher Watford.

As a reminder, Christopher has his own blog called My Variables Only Have 6 Letters.

46 year old male presents to EMS complaining of chest pain.

After sitting down on the gurney he states, “My heart is jumping out of my chest!”

  • Onset: Sudden while doing yard work.
  • Provoke: Nothing makes the pain better or worse.
  • Quality: Heaviness and “jumping” sensation.
  • Radiate: The pain does not radiate although his hands are numb and tingling.
  • Severity: Not reported.
  • Time: Denies previous episodes.

The patient is alert and oriented to person, place, time and event.

  • Skin: mottled, cool, diaphoretic. Vital signs were assessed.
  • Resp: 18
  • Pulse: Too rapid to count
  • BP: 120/60
  • SpO2: Not reported.
  • Breath sounds: Clear bilaterally.
  • Capillary refill: 5+ seconds
  • BGL: 140 mg/dL

The cardiac monitor is attached.


A 12-lead ECG is captured.


What is your differential diagnosis? What is your treatment plan?

*** UPDATE ***

The treating paramedics gave 1.5 mg/kg lidocaine. After administration of the drug the following rhythms were noted on the monitor.


Pay close attention to this rhythm change….


There is a critical clue here, and it has to do with the R-R interval. Now take a look at a 12-lead ECG of the irregular rhythm.


Was lidocaine the best possible choice? Is there a safe antiarrhythmic for a patient like this? Is this patient at-risk for sudden cardiac arrest? Why or why not?


  • Anonymous says:

    Wide and fast is VT until proven otherwise (even if the LP12 interpretation is atrial flutter with RBBB),so…….valsalva to see if I can slow it down enough to see the underlying rhythm. If not I'm giving Amiodarone 150 mg dripped in over 10 mins. O2 via NC. Get the defib. pads ready and call ahead for orders for Versed for sedation in case I need to cardiovert. High flow diesel !DaveO

  • Tom B says:

    I generally agree with that, DaveO! However, with a heart rate above 250 an accessory pathway is high up on my list!That's why I think it's helpful to think in terms of a differential diagnosis.In other words:I think it's W.It could be X.I don't think it's Y.It's definitely not Z.(Credit to Ray Fowler MD for this approach.)So in this case mine would look like this:I think it's WPW.It could be VT.I don't think it's reentrant SVT.It's definitely not sinus rhythm.Tom

  • john says:

    This is outside of my skill set, hence the reason I lurk here. I would have said SVT not knowing the diferential between that and WPW and also leant based on age and lack of cardiac history towards supra ventricular rather than VT. Considered the MAP of 80 as the reason for signs of shock, considered anxiety based hyperventilation as a cause of periferal numbness.My treatment is a call for ALS,O2, 1 valsalva,cannulation,pads for cardioversion incase he reaches my threshhold, reassurance and go. I would give ASA and consider morphine for pain. I am rural with 30 min transport.John

  • John Wright says:

    I've been studying wide complex tachycardia recently and haven't got it mastered yet, but here is my best guess. I am a fan of calling this WPW, (with a rate dependent bundle branch block?) but its too fast to really see the Delta waves clearly. I can also see where you might circle a few flutter waves, but those might be part of an rsR' pattern.I don't think its V-Tach, it does not meet any of the criteria that I have been looking at (ERAD with upright V1, right axis deviation with negative V1, QRS morphology in V1, ect.), and I didn't think V-Tach usually got ran at that high of a rate. Its definitely not A-fib with rapid ventricular response, its not irregular. (I really hate saying 'efinitely' in an online forum….that guarantees that someone will post a Captain Obvious remark to blow you out of the water)And here is what I would have done if this were my patient. He isn't symptomatic enough for me to cardiovert. I like his blood pressure and the fact that his only complaint was jumpiness. Cool diaphoretic skin…that is pretty much me when I mow the yard, so I'm not all that worried about that either. I would try the "bear down like you are having a bowel movement…….but please don't" and record a few seconds of the underlying rhythm. We stopped carrying Amiodarone so all I have to choose from is Lidocaine and Adenosine. I'd try the Adenosine, its got a short half life and a pretty good safety record, so why not? Worst case scenario, I'm pretty good at working asystole. And Hell yes on the bolus of diesel. I'm always a fan of that!

  • Anonymous says:

    Antidromic atrioventricular reciprocating tachycardia(AVRT). Commonly mistaken for ventricular tachycardia because of its morphology, antidromic conduction is still created in the atrium. In antidromic conduction the impulse travels down the bundle of kent and pre-excites the ventricles retrogradely. Since the AV node is bypassed atrial rhythms may be much faster than normal. Your 3:1 atrial flutters can now be 1:1! So if you have an abnormal pacemaker, or an atrium that wants to beat faster than normal, it can. This is pretty dangerous and may in fact lead to ventricular tachycardia or ventricular fibrillation. If the patient become dangerously symptomatic, electricity would be the safer route. If you were to slow down conduction of the AV node, you could expose the patient to all kind of arhythmias because the only coduction would now be through the accessory pathway. Electricity would hopefully reset the entire electrical system. Also, Past medical history would be a nice thing to get from the patient. I would wonder if he has had this before and how they treated it last time

  • Chris O'Connor says:

    I tend to agree with Tom B. Given the rate: Pre-excitation syndrome ought to be close to the top of the differential.Also, A-fib should not be ruled out (the rhythm appears to be a little irregular, although at this rate, it is difficult to be certain-my printer isn't working! !). Not that this really matters, the fact is: the patient is showing signs that they are becoming unstable, and therefore, the most prudent management would be: sedation, analgesia and DC cardioversion.

  • Geoff says:

    WCT around 270/minute, I'm thinking accessory pathway as well. For my treatment initially per our protocols for stable WCT, O2, IV, Monitor. His B/P seems fine for now, but his skins & CR are a bit worrisome to me with his heart rate. I would probably prep everything in case we needed to cardiovert.In regards to whether lidocaine was the right choice…it didn't seem to hurt, that is following the WCT algorithm. I seem to remember amiodarone slows AV conduction, so I wouldn't want to give it with an accessory pathway. We don't carry procainamide, so I'm not up on the particulars of that drug, but I believe it is still in ACLS correct?Oh, I agree with high flow diesel as well.

  • Billy says:

    Yes, there is one safe drug for AF+WPW patients, as well as all tachydysrhythmia patients: propofol, followed by DC cardioversion.

  • Duke Powell says:

    1. This rhythm does not appear to be V-tach. I would not give Lidocaine.2. It could be an a-fib. When rates get this fast it is difficult to determine if it is regular or not.3. In any event, you do have a symptomatic patient that needs treatment.4. I have doubts about the B/P. but, frankly, that wouldn't be mymain consideration when deciding how this patient should be treated.The post indicates that the patient looks bad – poor skin color and diaphoretic. He is having ischemic pain. His heart is working overtime and there is a danger of cardiac arrest due to inadequate oxygenation of the heart muscle.I would cardio-vert as soon as I could. Adenosine would be my second choice.

  • t says:

    just off the top of my head the delta waves in wpw are usually only seen in the baseline rhythm, but not in its associated tachycardia.

  • t or medic says:

    my thoughts:1. first 3 tracings do not look like VT, even in the 3-lead tracing. (can you remember trying to tell VT vs. others in the field before 12-leads? it seems very cowboyish now.)2. history can help guide rhythm interpretation.3. this rate favors WPW-related tachycardia.4. 4th rhythm is A-fib/flutter and may or may not mean his underlying baseline rhythm is A-fib. Without a definite timeline (<48 hrs) for this, cardioversion is contraindicated unless this pt is nearly dead.5. i don't think lidocaine is theoretically effective for this pt, assuming we're close in calling this some kind of A-fib WPW. but i don't know why the rhythm changed from regular to irregular.6. the only appropriate drug we carry for A-fib/flutter WPW is amiodarone.7. i have found that a fluid bolus works pretty well for fast a-fib too. (but not likely this one.)7. don't know about sudden death other than i'm told wpw-tachycardias are not terribly lethal.

  • VinceD says:

    There's a slurring of the QRS upstroke in some of the beats (after slight pauses) in strip D, making me think there may be an underlying accessory pathway. What I wanted to call retrograde p's at first are all upright inferiorly, making me think this is actually some sort of a-tach. I really want to say the initial 12-lead is AVRT to account for the regular rhythm, but I just can't get all the pieces in my mind to fit together.My stab at the big picture is: AVRT with WPW, a rate dependent RBBB, and I'm on the fence between a-fib/flutter.Flutter works better if underlying the initial rhythm, while fib fits with the irregularity of the final 12-lead.Very interesting case, glad I didn't have to be the one making decisions here, but I would have liked to avoid adenosine.

  • Anonymous says:

    I think is supraventricular tachycardia with aberrance in your conduction. The patient is instable for Skin: mottled, cool, diaphoretic.Capillary refill: 5+ seconds. Nothing makes the pain better or worse.He has pain!!and he need sedation, analgesia and DC cardioversion.ByeLuis A.

  • Anonymous says:

    Thanks a lot, very interesting case.Thank you Tom B – useful approach – agree with you I think it's WPW.
It could be VT.
I don't think it's reentrant SVT.
It's definitely not sinus rhythm -)1. We have 2 DD: WPW/VT2. WPW – adenosine, verapamil, digoxin – contraindicated (do not act on accessory pathways) can do even worse, would avoid completely in resuscitation if in dough weather I see narrow complex tachy or not. 3. Maintain BP and still conscious – maintain central circulation, reduced CRT – shut peripheral circulation – still compensate – does not need cardio version urgently, but still in pain4. Amiodarone would be my best choice: effective for VT/WPW/VF/AF, if not in stock lidocaine can be used.5. Management: -A/B: 100%O2, RR, SAT monitoring and anaesthetics on call to resus rom. – C: i/v accesses, bloods, HR, PS, BP, ECG – monitoring, apply pads for urgent cardio version in case …, long i/v line for amiodarone, urine output monitoring. Drugs: Morphine/diamorphine for pain control, heparine/clexanie , amiodarone 300 mg i/v over 1 hour, NSaline. 6.Additional history, PMH, FH, DR 7.Seniour review.

  • Anonymous says:

    In addition: I think this patient is at high risk of cardiac arrest, even if it is WPW first presentation, I do not think that he would compensate for a long time if left untreated. But if it is MI and VT as a possibility the chance of cardiac arrest even higher, unfortunately can not provide figures. In this case I would add aspirine 300mg and clopidogrel 300 mg. to C-management.

  • I as well agree with DaveO. Wide aberrant rhythms are Ventricular in origin until "proven" other wise. Also electrical activity is not always representative of mechanical activity as B/P and mentation appear to be intact. To answer your question about sudden cardiac arrest, "Yes" all cardiac events are in danger of sudden cardiac arrest. generic answer : ) Looks like the Lido worked on the rate which is in the order of treatment (rate, rhythm, and B/P). Note the change in QRS width on the tracings as well 0.172 to 0.092 normal being 0.08 to0.12 as we all know. I would like to have seen a set if vital signs status post Lido and conversion to atrial flutter w/ RVR.Treatment modality would have been basics, ALS, cardioversion preparation, Valsalva, antiarrhythmics, calcium channel blocker, sedation, and transportation to an appropriate facility. As we are a rural provider, this patient would have been air lifted.

  • Christopher says:

    Post conversion vitals BP 140/80, hands regained color, pt stated no chest pain.Pre-conversion pt stated he had no real medical problems, took no medication, had no allergies.Post conversion, he let us in on his Hx: ETOH abuse, MI w/ diagnosed CHF 3 yrs prior, non-compliant w/ meds for 2-3 months due to cost. Pt did not remember what his meds were.Pt was more concerned with not having insurance than anything else. Pt went AMA from hospital after his amiodarone drip completed. "Lost to follow-up," because he had no way to pay for the treatment.

  • Bren says:

    Hi all, Late to the party on this one….Just want to clear up a common misconception: Verapamil is actually NOT contraindicated for WPW patients.Wait, let me explain…..If you have an orthodromic AVRT/CMT (narrow complex re-entry tachycardia) you are generally happy to treat with Verapamil, but as soon as you see an antidromic (wide complex) CMT, people say that Verapamil is contraindicated….and picking the difference between AVRNT and AVRT can be very difficult at times!Technically, It would work to use verapamil, as slowing AV conduction will break the re-entry circuit, and thus terminate the SVT. The drama comes form the fact that if patients presenting with CMT then develop Atrial fibrillation or have that as an underlying arrhythmia, they will rapidly deteriorate as the bundles of Kent rapidly conduct all atrial impulses. If you do a literature review, this misconception is based around several articles published in the early eighties, where ONE patient given verapamil then developed/reverted to atrial fibrillation, and deteriorated. (Although this patient in the case study could potentially be another, or it could be a side effct of drugs/hypoxia…)So repeating.. no randomised controlled clinical trials…. only case report evidence….In a second study, people with AF accidentally treated with verapamil were able to be reverted with cardioversion.. there have been no reported deaths to my knowledge by administration of WPW and AF with Verapamil.Then came along adenosine and research into Verapamil pretty much ended….I'm not saying that verapamil is a great drug, because it has some really horrible cardiac side effects (hypotension and bradycardia) and a reasonably long duration of action, just wanted to clear up a common misconception.Now having said all that, if you have a wide complex tachycardia, and you are happy to certainly call that a SVT with aberation and willing to treat as such you are foolish! Always treat as VT, which is the worst case scenario. Your VT treatment drugs may infact work, and cardioversion is always an available fall back position.If anyone is interested in seeing the relevant journal articles, then please let me know via this forum or Tom.Cheers!Bren(PS: Tom did you get my email a while back?)

  • Christopher says:

    Bren,I'll have to disagree and say the literature is decidedly not in favor of CCB's in the treatment of WCT. While perhaps in these case reports most everybody "made it" (except for one), I would say that the patients did in fact die as they went into cardiac arrest secondary to CCB administration.As you pointed out, one is unable to find any controlled studies, however, given the sheer volume of case reports of Bad Things(tm) happening during CCB administration during WCTs coupled with the knowledge of a decrease in refractoriness of the AP using CCBs, it is obvious no controlled study would get off the ground due to failing a simple safety for patients review.So as you said, treat WCT as VT, safer choice!- Buxton AE, Marchlinski FE, Doherty JU, et al. Hazards of intravenous verapamil for sustained ventricular tachycardia. Am J Cardiol. 1957; 59:1107-1110.- Klein G J, Bashore TH, Sellers TD: Ventricular fibrillation in theWolff-Parkinson-White syndrome. New Engl J Med 301; 1979:1080-1085.- Gulamhusein S, Ko P, Carruthers G, et al: Acceleration of the ventricular response during atrial fibrillation in the Wolff-Parkinson-White syndrome after verapamil. Circulation 65; 1982:348-354.- Jacobs AS, Nielsen DH, Gianelly RE. Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation. Ann Emerg Med February 1985;14;159-160.- McGovern B, Garna H, Ruskin JN. Precipitation of cardiac arrest by Verapamil in patients with Wolff-Parkinson-White syndrome. Annals Int Med. 1986; 104:791-794.- C. Garratt, D. Ward, A. Antoniou and A.J. Camm, Misuse of verapamil in pre-excited atrial fibrillation, Lancet i (1989), pp. 367–369.- Strasberg B, Sagie A, Rechavia E, et al. Deleterious effects of intravenous verapamil in Wolff-Parkinson-White patients and atrial fibrillation. Cardiovascular Drugs and Therapy. 1989; 2: 801-806.- Kim RJ, Gerling BR, Kono AT, et al. Precipitation of Ventricular Fibrillation by Intravenous Diltiazem and Metoprolol in a Young Patient with Occult Wolff-Parkinson-White Syndrome. Pacing and Clinical Electrophysiology. 2008; 31: 776-779.

  • My training Captain has made an attempt to post his interpretation on here without success (computer trouble), so I will share his thoughts. 1:1 Atrial Flutter with possible accessory pathway [with orthodromic conduction], however there is no proof of a WPW like pathway other than the rate itself.

  • Tom B says:

    Bren -Yes! I did receive your email. I apologize for not responding.Things are a bit hectic for me at the moment.Thank you for being patient and bringing it to my attention again!I haven't had time to view the practice guidelines yet, but I'm definitely interested! I will contact you as soon as I have a chance to catch up! Thanks again!Tom

  • Anonymous says:

    Hi Christopher!Thanks for your comments, and I agree with what you're saying, and yes bad things ™ do happen which is why we need to play it safe. My point was from a purely electrophysiological point of view, that as long as you are sure that it is not AF, Af, or VT, calcium channel blockers do work, it is only when incorrect ECG interpretation is done that the bad things ™ seem to happen. My point was that misinterpretation and CCB's lead to bad things, not necessarily the CCB's themselves! That being said, Verapamil is a nasty drug and should only be used when you are 100% of your interpretation, which gets harder and harder as rates go up and fatigue sets in – and when you work without any form of medical control…. so play it safe!PS the 2008 article is a new one to me, i'll look at it at work tonight!Thanks again Christopher!

  • Terry says:

    I think they got lucky in giving this pt lidocaine. To say this is v-tach and to not treat it as v-tach is foolish is a foolish statement. The reasons this is not v-tach is there are pwaves before the qrs complexes the axis doesn't support v-tach and there is rwave progession in the v-leads. It is also to fast for v-tach. Looks more like WPW. Adenosine could make this pt go into a rate > 300bpm. Lidocaine if he has a BBB could cause asystole although it didn't this time. CCBs those are bad stuff to give in the field. Treatment of choice would be cardioversion. You would be supported by all the literature. Trouble is getting past the psychological barrier of shocking a pt that is still alive. We definitley live in the gray world of EMS try as we may with all the protocols and such.

  • Brad says:

    Well, My call is that of a WPW. You can see the Delta waves when the rate broke. He is young with a sudden onset of VT.

  • malcolm x says:

    atrial tachycardia with acute posterior wall M. the tachycardia is an overcompensating mechanism. treat the occlusion. PDA or LCx

  • malcolm x says:


  • Andrew B. says:

    My approach.
    All WCT = VT.
    This one is too fast for “regular” VT so strong suspicion for accessory pathway.
    Towards end of strip just before conversion there is irregularity.

    Procainamide or proposal with DCC.

  • B Baker says:

    Since there is a distinguishable QRS I would first treat as SVT since it seems that the pt is somewhat stable. Give Adenosine to find the underlying rhythm and treat accordingly. Probably would be looking for a cardiac center if there was one close by. Start small and work my way up to possible cardioversion if the pt becomes unstable.

  • mike says:

    This to me looks more likely to be an SVT with aberration. There are few features to support VT. The initial rhythm is not pre-excited AF and so adenosine is safe, this would help determine whether the rhythm is in fact:-
    i) flutter with 1:1 and RBBB – will reveal flutter waves
    ii) fascicular ventricular tachycardia – should terminate
    iii) antidromic AVRT in a patient with WPW
    If adenosine failed –> dc cardioversion

  • karim says:

    had a case like this recently with the first two ekg's … fast wct with a regular rr interval in a stable patient; 10 years ago we would have hung procainamide but this time we gave amiodarone 150mg ivpb over 30 min. the patient cardioverted to sinus. done. 

  • Paul says:

    First 12 lead clearly shows a supraventricular tachycardia, and I agree with atrial flutter 1:1. The paramedic gave lidocaine for a supraventricular rhythm, which accelerates conduction through the AV node(that’s how it abolishes VE!). This action which could have killed the patient, accelerated conduction through the AV node, and increased the rate from 260 to > 300. The patient then went into atrial fibrillation with obvious RVR, in my opinion as a cardioprotective mechanism to keep the ventricles from fibrillating.

    Adenosine would have been a MUCH better drug from the outset, followed by procainamide, which is great because it is safe for all SVT’s and VT’s, including those with WPW or some other bypass tract!

  • J Jones says:

    I think one needs to understand that there are two ways in which the accessory pathway can be used: first, as one limb (antegrade or retrograde) of a reentry circuit and second, as a simple conduit for entry (antegrade) from the atrium to the ventricle. In the first type, the accessory pathway is part of the cause of the reentry circuit. In the second type, there is no reentry circuit – the atrial flutter is the cause of the tachycardia and the accessory pathway is simply an "open door" into the ventricle.
    When the reentry circuit is what is actually propagating the tachycardia, blocking either the AV node or the accessory pathway will terminate the tachycardia. When the accessory pathway is not a limb of a circuit but rather just a conduit, you want to block the accessory pathway while leaving the AV node alone (and unblocked). The AV node has a decremental conduction which will protect the ventricle while accessory pathways that can conduct antegrade typically do not (and consequently can conduct impulses at dangerously high rates).
    I'm old school – I would just use procainamide in this situation.

  • Diana says:

    What are others thoughts, experience with cardizem vs. adenosine? I have found SIVP cardizem very effective and less stressful on patient than adenosine. My albeit limited experience, adenosine didn’t work more times than it did.

Leave a Reply

Your email address will not be published. Required fields are marked *