65 year old male CC: Fall with injury – Conclusion

This is the conclusion to 65 year old male CC: Fall with injury. You may wish to review the history and clinical presentation.

When we left off the patient was in severe heart failure with the following 12-lead ECG.

As we have mentioned before on several occasions, the most important thing when treating a patient with a tachycardia is to decide whether or not the tachycardia is causing the symptoms or the symptoms are causing the tachycardia.

In other words, you should try to rule out the possibility that it's a compensatory tachycardia. As this case clearly demonstrates, this can be very difficult! 

The crew felt that the differential diagnosis for this wide complex tachycardia (from most likely to least likely) was VT, 2:1 atrial flutter with LBBB, sinus tachycardia with LBBB, or some other SVT with aberrancy.

Due to the patient's instability, the treating paramedic felt there was little to lose and much to gain by attempting synchronized cardioversion. If the rhythm was VT or 2:1 flutter the patient's condition might improve dramatically. If it turned out to be sinus tachycardia with LBBB he'd be in the exact same position.

Attempt #1

Attempt #2

There appeared to be no change in the heart rhythm.

A report was given to online medical control and the patient was transported emergently to the hospital.

On arrival the patient was placed on BiPAP and started on a NTG drip.

Here was the 12-lead ECG on arrival.

The patient was given lopressor 5 mg slow IV push.

The conversion rhythm shows sinus rhythm at 92 bpm with left bundle branch block.

So, we now know that the patient probably had LBBB at baseline. However, without a heart rate histogram it's difficult to say whether or not this was 2:1 flutter that converted sinus rhythm or sinus tachycardia that was slowed down with the lopressor.

This is often overlooked in the emergency setting but in the inhospital setting it's very important to document the onset or termination of an arrhythmia for this very reason.

The patient's SpO2 came up above 90% and the patient became more alert and was attempting to communicate by the time EMS was done writing their report. No further information is available.


  • There are what appear to be flutter waves on the initial ECG, best seen in lead II.  Adenosine would have been great for confirmation, safe no matter what the etiology (because this is clearly not WPW with atrial fib, the only time when adenosine is dangerous) and, if it was PSVT, convert.
    Given that the patient is in pulmonary edema, and it could be reflex sinus tach, beta blockers could be very dangerous.
    Of couse shocking is excellent, but leaves a small amount of doubt as to the diagnosis of atrial flutter.
    Steve Smith

  • VinceD says:

    Great case! The only thing I would have done different is to switch to lead I for syncing before cardioversion. Although the spikes are tracking properly, the T-waves and QRS complexes look similar enough in the first strip that I'd still be a bit worried about the machine syncing to a T-wave while I held down the shock button. Probably overkill, but I'd rather be safe than in V-fib.

  • VinceD says:

    As for the in-hospital management, I agree with Dr. Smith that after failed cardioversion would have been a great time for a trial of adenosine. I hate seeing it overused in a-flutter, but it definitely has a role in a case like this where there is a lot of uncertainty concerning the rhythm and you really want to confirm the diagnosis before attempting therapies that could cause serious harm.

  • Christopher says:

    My notes on this case were the possibility of fusion beats versus profound respiratory variation, best seen in lead III. The use of B-blockers surprised me given VT had not been "ruled out" sufficiently (for my own comfort).
    Perhaps most interesting is that there does appear to be an axis change at the least between the prehospital/inhospital ECG's. We have QS complexes in lead III, rS complexes in V4, and Rs complexes in V5/V6 in the prehospital ECG's. Yet when you look at the in-hospital ECG's we have Rs complexes in III, and monomorphic R-waves in V4-V6! Electrode variation perhaps?

  • arnel c says:

    To the crew who gave these strips, good job for the trip. I hope you will be the crew who will take care of me whe I will be realy sick and needs a trip to the ED.
    This is really an interesting strip. As to how the case was managed, it is difficult to argue since we do not have all the data and I believe that they handled it based on sound medical judgment. 
    As for the strip, I am really intrigued by the quadrigeminal occurence of of QRS variation (best seen on lead III prehopsital rhythm strip). It could not seem to be rate variation but the morphology is similar to sinus rhythm morphology (comared to lead III in sinus rhythm). So this seems to be SR (as Chiristopher pointed out). So a qardrigemineal fuion. 
    It gets even more exciting for me. That complex (prehospital rhythm strip lead III) would even inscribe seemingly negative P wave 140 ms from that QRS. Marching  200 mm(300 beats/min)  forward from these "retrograde" P wave and comparing with the simultaneous reacodring in elad II, we see a distorted/odd shaped T wave. Coulld this be the holy grail  we are looking for? Maybe or maybe not but seem logical to accept that those are f waves. 
    Another interesting thing (on the rate controlled SR strip). The QRS direction flipped (negative to positive) in lead III (compelx # 3) before lead change to avF. I often see thisflip-flopping event in patients with bilateral/ or embolic stroke and they have respiratroy variation (periodic breathing). Woudl be nice if we coild know if this patient was worked up for stroke (h/o of syncope/ fall on the scene).

  • Ken Grauer says:

    GREAT CASE. Excellent teaching points – and don't know that we'll ever know for sure. Initially I was concerned about VT (VT until proven otherwise…). QRS morphology was to me indecisive – consistent with LBBB with steep S-wave  downslope (as it is supposed to have) in V1 – but clearly can't rule out VT from this morphology. Agree with Steve that Adenosine would have been a good drug to try (may act as "chemical Valsalva" – thereby revealing atrial activity if flutter or sinus tach). Agree that acute cardioversion on the scene was appropriate.

    In the comfort of my room with the luxury of calipers and a moment of time to use them as well as think this out (luxuries probably not available to the team on the scene) – I think in the retrospectoscope this was probably Sinus Tach with underlying LBBB for several reasons: i) the rate changes (slightly but real when I measure and confirm machine read between 147 and 150/minute) – and flutter and PSVT tend to stay the same; ii) to me – the extra hump in lead II on initial tracing doesn't march out with calipers as it should for flutter – I don't see it in other leads – and I don't see it on all post shock tracings; iii) Hard to believe flutter wouldn't respond to 2 attempts at cardioversion …; iv) Hard to believe flutter would immediately convert to sinus rhythm (instead of slowing its conduction rate) in response to IV lopressor; v) this is not VT (in retrospect) – because QRS morphology post conversion to sinus rhythm is virtually the same as during the WCT (minor variations in a few leads that I think are due to placement – but basic morphology I think IS the same);  vi) This leaves us with Sinus Tach – which I think is that much more plausible given the long PR interval during sinus rhythm – that would fall about where the notch is seen during the WCT.

    P.S. The KEY rhythm strip is MISSING (that is – WHAT HAPPENED immediately after the Lopressor was given … ).

    @Christopher – I see the change QRS morphology you cite in several leads. To me that is within accepted variation (for lead placement vs patient movement) – and to me the Gestalt is that the underlying LBBB pattern is basically the same …  

    @Arnel – I looked long and hard for fusion also – with the main difficulty I believe is a patient in extremis who is not still … so I was attributing change in QRS to motion artifact … Most interesting to me (as you also noted) is the tracing after IV Lopressor – Look in lead III – Note how dramatically the QRS shape changes between the 2nd and 3rd beats! (this is BEFORE the lead change). I don't think this was a change in degree of BBB – but rather a patient in extremis with acute dyspnea …

    Again – We'll probably never know for sure. It was interesting discussing. Great comments from everyone.

  • This is a serious strip that requires attention.  I am impressed by the ST elevationin leads v1 through v4.  I would rule out VTacj=h becasue of the lack of concordance in the V leads.  Concordance is when the QRS complexes all point in the same direction, indicationg ventricular origin.   Nice case. 

  • Tyler says:

    Doesn't the lack of extreme right axis deviation rule out VT?

  • Christopher says:

    A lack of an extreme right axis does not rule out VT. In fact, ERAD is not even the most common axis deviation in VT.

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