63 year old female CC: Chest Pressure

Here's a case from a faithful reader who wishes to remain anonymous.  As usual, some information has been changed to protect patient confidentiality.

You are called to transfer a 63 year old female from a community hospital to a large medical center.

Upon arrival at the local hospital, you are confronted with chaotic scene. You see your patient, now resting, and are told she presented with chest pressure and palpitations a couple of hours ago, was also becoming obtunded, and her family had stated she had not had any any similar episodes in the past. Her vitals are as follows:

  • Pulse:   200 and irregular
  • BP:   132/76
  • RR:   22 regular
  • Eyes:   Pearl
  • Skin is cool and dry

They hand you an ECG and tell you she presented in the following rhythm:

And with the following history:

  • She had sudden onset of chest pressure and palpitations, which began while she was doing some work around the house.
  • Nothing changed the discomfort
  • felt like "pressure" and "palpitations"
  • No radiation
  • she rated the pressure as a 7/10
  • began one hour prior to presentation
  • No allergies to medications
  • She takes a "pill for blood pressure", name unknown
  • Past medical history significant only for hypertension
  • had a normal breakfast and lunch
  • She can not recall any specific trigger for the episode

In the ED prior to your arrival, she had received the following treatments:  Lopressor, Amiodarone, Magnesium Sulfate, Heparin, Lidocaine, Morphine and Versed.

None of these treatments changed the patient's rhythm:

The patient's mentation continued to decline, and her BP started to crash. After three attempts, she was successfully cardioverted. Here is the post-conversion 12 Lead:

You transport your patient, now stable, to the medical center without incident.

So, now the key questions:

  • What was the presenting rhythm and why?
  • What is the post-conversion rhythm and why?
  • What are the best treatment options for this rhythm?

See also:

Conclusion to 63 year old female CC: Chest pressure

28 Comments

  • Brooks Walsh says:

    Let me try that again…
    An iiregular wide-complex tachycardia that responds to cardioversion. I'm guessing that was WPW.

    On the other hand, the post-conversion doesn't show any sign of preexcitation. Interestingly, though, there is a small "blip" at the end f the… QRS complxe in V1. Could this be an episolon wave? http://hqmeded-ecg.blogspot.com/2011/08/young-man-with-syncope-while-riding.html

  • Brad J. says:

    Kind of strapped for time right now, but I’ll write a short response for now. I think the initial strip is abberrant Afib w/ RVR. I think all of the antidysrhytmics were over kill and made the QRS wider and the BP drop. It looks like they didn’t know what to call it since they gave mag, amio, lopressor, and lido…. I think Cardizem would have been the drug of choice.

  • Brad J. says:

    Oh and post rhythm is NSR…. That Q wave in III and AVF caught my eye too. Old/new?

  • Ben says:

    there looks to be extreme Right Axis deviation, wide complexes especially in the right precordials. The rate is >200. Going on one of the previous cases discussed here we should consider the width of the QRS of the widest complex, therefore I would call this VT – until proven otherwise. The largely upright complexes in aVR support this I feel. The morphology appears to be RBBB. There does look to be some inferior pattern ST elevation with reciprocal changes in the early ECG as well. I wouldn't be surprised if it turns out to be AF with fast ventricular response with RBBB, but I would be treating as VT unless I was 100% sure.
    The post conversion ECG appears to be a sinus rhythm, with a normal axis. There is significant Q waves in III and aVF, and what looks to be ST elevation in III, aVF with possible ST depression in aVL. Considering the proportion of the QRS to the T, I would say it was an inferior MI and the pt needs to go to a PCI centre for an angiogram.

  • Simon M says:

    Hmm.. tough call.
    Irregular rate about 200, absence of P-waves (as I see it), axis close to -150, wide QRS, inital R in aVR. The post-conversion ECG doesn not reveal any signs of wide QT, brugada or WPW.
     
    On the post-conversion ECG there is subtle STE in leads III, aVF and maybe in lead II. "wide" Q-wave in III, and very subtle STD in lead aVL.
     
    My guess would be that the presenting ECG shows irregular VT, and the post-conversion ECG points towards inferior STEMI -> ASA, nitro, heparin, morphine, oxygen and PCI.

  • Ahmed says:

    I think the patient has WPW with AF which cause wide complex Tachy ( irregular) 
    When patient cardioverted WPW appear 
    ttt is Radiofrequency ablation of accessory pathway

  • Great ECG set.
    On the first ECG I see mainly a wide complex monomorphic irregular tachycardia. Then on the rhythm strip just under V6 the rhythm narrows, and now we see a rapid, possibly regular rhythm (difficult without calipers) without identifable p waves and with a very long QTc.
    The second ECG is entirely the monomorphic irregular wide complex tachycardia, probably with even wider QRS.
    The third ECG is sinus, now normal QTc and possibly some very subtle inferior ischemia.
    I don't think it is incorrect to look at either of the first 2 ECGs and think 'V-TACH!', but I think there are some clues that this is not what is going on:
    First, on the first ECG there is revision to a narrow complex rhythm that has the same rate and (ir)regularity as the previous wide complex rhythm.
    Second, I do not see any fusion beats.
    Third, I do not see any retrograde p waves.
    Fourth, the rhythm is markedly irregular which would be surprising for a fast ventricular tachycardia.
    Next is the question of an abberent conduction pathway, ie. is this afib with WPW. Again on the first strip we see the conversion of wide to narrow without any significant slowing of the rate. If this conversion was due to alternating conduction down an accessory pathway and the sinus pathway I would expect to see the rate slow a bit as the conversion occurs. We do not see this.
    Finally, the complete lack of response to a cornucopia of antidysrhythmic medications. This always makes me think about a-flutter, a rhythm refractory to many of our medical machinations. It is possible that what we are seeing in ECG 1 and 2 is actually a-flutter with variable block causing the irregularity. A set of calipers and calculating the intervals is really the best way to differentiate this from a-fib.
    Overall I think this is a-flutter with variable block (vs a-fib) and a rate related bundle branch block. The post conversion ECG possible shows some subtle new inferior changes but I would probably do another ECG 10 minutes later and see if these resolved (ie. if they were due to rate related ischemia).

  • Arnel C says:

    1. VT  – positive concordance
    2. short QTc
    3. Acquired vs congenital. Probable acquired short QTc. Thinking of hypercalcemia.

  • Brad J. says:

    @ Aaron, very good explanation to your thoughts. As you can see above I’m also leaning towards an atrial rhythm, but I’m thinking more afib than anything. I also considered A-flutter, but don’t see any flutter waves at all (I know it’s too fast to see flutter waves). I’m honestly not seeing any signs of WPW though even with post conversion…. One thing I noticed now that I didn’t originally notice is that there are flat T waves in AVL and V1. Also in the limb leads I notice longer gradual building T waves which would also indicate hypokalemia. Just a thought….

  • Brad J says:

    @ Arnel, short QTc? Can you explain your reasoning on this bc if anything they appear to be elongated.

  • Atrial flutter with variable block should be REGULARLY irregular and this is not.  The only way I can explain this rhythm is to invoke 2 problems: a slightly irregular monomorphic VT AND atrial fib with RVR and narrow complex (seen at the end of the first 12-lead).  It is not irregular enough for atrial fib and not bizarre enough for WPW with atrial fib.  That's my two cents.

  • Chris says:

    I think it’s WPW.
    First and second ECG are FBI: Fast, Broad and Irregulair.
    Positive concordance precodiaal. Only responding on cardioversion.
    So this must be an a.p. conduction.
    For a-flutter i think there are no signs.
    Post cardioversion ECG i see in V1- V3 a slighty slurred upstroke of R-wave
    and still positive concordance. Compare with old ECG if recorded.
    Consider an a.p. located left posterior septal

  • @ Dr. Smith
    That's an interesting thought, that we are seeing V-tach followed by a-fib with RVR as a seperate rhythm. Maybe I am trying too hard for a single diagnosis in my analysis.
    Any comment on the treatment here? I am always very nervous to engage in an extended series of medications when cardioversion is on the table..
    Aaron

  • Brad J. says:

    Afib is irregularly irregular, but how well can you really see the pattern with a rate of 200+? Honest question and not saying anyone is wrong.

  • I asked K. Wang to look at this and he agreed with me, except he called it polymorphic VT: "polymorphic VT converting to atrial fib during V4, 5, 6.  The second one is polymorphic VT."
    I think he is right.  He always is when it comes to rhythm.

  • Aaron, I agree.  Use electricity when in any doubt.  Much safer IF you can handle the sedation and its potential complications, which any ED should be able to do.
    Brad, I think you can tell atrial fib's irregularity even at rates > 200.  It still should be very irregular.  If it is only a bit irregular, it is not likely to be atrial fib.

  • Ric Stafford says:

    I would have been leaning towards a rapid a-fib, poss wpw. i would have looked at 6 mg of adenosine to slow the rate down to get a better look at what the underlying rythm really was. once the rate was slowed down and we had a better understanding of what the rythm was we could treat the conditon better.

  • DrJohnM says:

    I purposely did not look at the comments. I will look after hitting "post comment."
    Here's my best guess:
    The initial rhythm is AF. The wide complex beats have a RBBB/left axis, but are still irreg-irreg. I think it is AF with intermittent conduction over a left infer-post accessory pathway.
    Why the lack of prexcitation post cardioversion? Two reasons: the pathway is clearly left sided and away from the septum; in other words, it is geographically distant from the av node. Second, this patient has a really good av node–as evidenced by a short pr interval despite an onslught of av node blocking drugs (amio and lopressor.)
    In AF, an AP is immersed in a barrage of impulses. The fib waves are constantly hitting the AP, from close proximity. In SR, however, the wave of depolariztion coming from the northern RA (sinus node) traverses the av node before it reaches the left-sided AP. What's more, in this case, the AV node is fast and AP is made slower by amio and age of patient (APs slow with age.) After CV, she is conducting down a good av node, before the impulse gets to and down the left-sided AP.
    I like to imagine heart conduction to vectors and geography. Sinus node is Seattle, AV node, Iowa, vetricle is the Southern states and AP here is located in Maryland. Thus, the Sinus impulse gets to Iowa and down to Texas before it reaches Maryland and can traverse to Florida, wheras in AF, the northern (atrial) impulses originate from everywhere in the Northern states, not Seattle.
    A picture here would be better than words.
    The best treatment in this case is amio, as the drug slows conduction in both the AV node and AP. On the less than 2% chance that this is an irreg-irreg VT occuring simultaneously in a patient with AF and no structural heart disease (a rarity), amio would also be a good choice.

    The reason why it is not RBBB aberration is that the RBBB morphology here is not typical.  The wide QRS is too wide, and broad, and ventricular, to be an aberrantly-conducted supra-ventricular rhythm. Remember, the initial QRS in bundle-branch aberration is sharp and narrow, the delay comes later in the QRS. When the inital portion of the QRS is broad, the activation must be originating in ventricular muscle.
    Anothr note, it's not uncommon for accessory pathways to conduct intermittantly when injured (from ablation) or aged, or suppresed with meds (amio). For instance,I have had cases where an injured (partially-ablated) retrograde-conducting left-sided pathway stopped conducting with right-ventricular pacing. In these cases, placing a LV catheter and then pacing from close to the pathway showed the manifest conduction and allowed mapping.
    This case presents an interesting and important dilemma for EP docs. Some would rec AF ablation. I would, on the other hand, rec an EP study and ablation of the AP, as a single ablation lesion, rather than the many needed for AF ablation, may be enough.
    Great case. Thanks for alerting me.
     

  • Ken Grauer says:

    Bless you DrJohnM – Your explanation is highly insightful and makes the most sense!  I got in on this one "after the action was over" (numerous fascinating comments) – but "played" for a good while trying to find P waves (fusion beats) and some rhyme or reason to the happenings. My 2 cents about the 3 things that helped me most are:

    i) The irregular irregularity in Tracing 1 continues throughout the entire tracing without alteration at all in the last part of the tracing (V4,V5,V6) when the QRS narrows following a slight pause at the lead change;

    ii) Use of the Lead II rhythm strip at the bottom is INVALUABLE – esp. drawing simultaneous vertical time lines which provides insight as to where the QRS begins and ends (and which reveals given part of the QRS on the baseline how the very wide QRS persists through until resumption of normal conduction in V4,V5,V6); and

    iii) Seeing normal conduction on the 3rd tracing (which confirms that normal conduction did in fact resume in V4,V5,V6 of the 1st tracing since the QRS in these leads is identical in the 1st and 3rd tracings).

    The underlying rhythm in Tracings 1 and 2 is AFib (too persistently irregular without any fusion, capture beats or patterned beating that may occur with some forms of VT). This is not aberrant conduction (morphology clearly ventricular). The rate of AFib is slower than usual with WPW – but the patient is a bit older and has already received many meds (including amiodarone). THANK YOU DrJohnM for your insight that: i) APs may conduct intermittently when injured, aged or suppressed with meds (amio) as we see in V4,V5,V6 of Tracing 1 – and ii) for your insight on left-sided AP location accounting for no delta post-conversion.

    MORALE – You cannot always tell what a WCT is at the time you are seeing the patient – in which case electricity usually works (and is what was needed in this case when meds didn't work and the patient was deteriorating …). GREAT CASE!

  • Ken Grauer says:

    P.S. The post-conversion tracing shows sinus rhythm with a Q in III, a tiny q in aVF – and a hint of ST elevation in these leads and perhaps also lead II – with a hint of ST depression in aVL – plus tall R waves in V1,V2,V3 – suggestive of infero-postero MI. The question is WHEN this may have occurred … One clearly would expect much more in the way of acute changes if the sudden onset of chest pressure in this 63yo woman was due to acute mi …  Troponins and follow-up 12-lead tracings will tell – but perhaps her acute symptoms were all new-onset of AFib with rapid rate/WPW …

  • Christopher says:

    Dr. Grauer,
    The tall R in V1 and the Q in III could be due to transmission down an AP.

  • Stephen says:

    What would you do if the patient had persisted in the wide rhythm despite cardioversion?  

  • Stephen,

    Step 1 would be to increase the energy. Step 2 would be to evaluate your pad placement, if you're Apical-Anteriolateral switch to Apical-Posterior. Step 3 would be to add an antiarrhythmic, namely procainamide. Step 4 would be add a second defibrillator. Step 5 may be to consider the patient has some sort of electrolyte issue and add mag. Hopefully you've arrived or nearly arrived at the ED by this point and they've got somebody from the EP lab meeting you there!

  • Stephen says:

    Lets say the patient above had not been able to cardiovert.  They had Amio and Mag.  Would you add the second defibrillator and try at increasing levels of energy until 720 joules.  I guess what I am asking at what point do you decide that cardioversion is futile and what is the next option?

  • Todd says:

    Does anyone else see a few delta waves in there?

  • ROY JOHNSON says:

    Looking back at Bob Pages’ lectures, it’s polymorphic V-Tach. Extreme right axis with a positive V1. Second ECG in V1 is notched and kinda looks like the fireman’s helmet. You have concordance (+) in all V-leads. I would cardiovert and ask questions later. Shocks go away, drugs don’t.

  • Chris says:

    The positive concordance is also present in the sinus rhythm, so that's not confiming it's a V-tach the first and second ecg

  • Dan says:

    I believe we are looking at Vtach. Cardiovert now, ask questions later.

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