Quote from PeakRN
I agree with A-fib. Both the QT interval and the QTc are elongated. Depending on which beat you want to measure I would say that QTi is approaching 0.4 seconds which is the upper edge of normal, however because of his tachycardia his QTc is up to 0.9. ST segment length is normal however that also isn't the area of concern when Q on T is thought about and the primary concern for prolonged QTc.
So in terms of QTc his actual QTc based off the complexes i measured (the scary looking ones) is hanging out at roughly 520 ms.
The key here is to actually determine the slope of the terminal t with a straight object, and meticulously identify the isoelectric line with the same.
This ensures your measuring the true qt and not a q-p or q-u.
Careful account has to be taken for heart rate as well, as in a tachycardia like this, a single box of error means a potentially large change in heart rate.
Lastly try to measure qt on the same couple you're using for heart rate. This ensures in the case of a really irregular rhythm like afib, or an ectopic that youre correcting your qtc relative to the particular qt you measured.
That said you are correct, 523ms is still an issue. When it comes to qt its best to just scrap whatever they teach in the textbooks and just go with the magic number, 500. Over 500 Qtc or any patient whos symptomatic with a qt approaching that limit needs some more attention. Likewise symptoms such as syncope with no other explanation should carry a high index of suspicion for lqt.
Specifically for this patient a QTc of 520 effectively doubles their risk of a life threatening cardiac event (2.3x increase in risk to be precise). This is concerning, but compared to like... A run of VT.. It's not quite as worrisome.
I do like that others pointed out meds might be a factor this is definately a possibility to consider, and it makes sense given the condition of the patient.
Also a possibility is the fact that some patients with congenital lqts present with 'concealed' lqt. This lqt is typically unmasked during stress testing via treadmill or chenically through epinephrine; which is more effective than dobutamine stress for this purpose.
With this in mind it stands to reason that a patient experiencing a tachycardia due to a pathology such as tamponade may find his lqts exposed. For this patient Id venture to say this morphology would fit best with lqt1 or lqt3. Lqt1 being more common overall, more likely to be concealed in the first place, and more easily unmasked with increased demand and sympathetic stimulii. However the shape of the t wave itsself could also point to lqt3, which is much less likely, but also arguably less dangerous in this circumstance.
In any case I'm not entirely sold that correcting the qt should be the focus here. It is very likely that this patients qt will correct itsself if the heart rate goes down. Best way to do that of course would be to treat the underlying issue, if a restrictive tamponade or effusion type of situation is the primary suspect here, puncture.. If afib is suspected, cardiovert.. Hell do both if the situation really gives you the creeps.
Which brings me to the most important question; the rhythm itsself.
I know I'm sort of playing the devils advocate here, but theres not enough evidence to support this as afib based on the ekg provided.. In fact i would argue afib is inpossible throughout the entire period. There is at least 1 point in which the rhythm is absolutely reentrant, criteria for variability is not there during that run at the end of the reference strip.
Further v1 typically will show some sort of flutter circus. Not having one doesn't necesarily mean its not afib, in fact it means that it would be afib in its purest form.. Complete chaos without flutter substrate. Not a rare finding but an uncommon one.
Next id like to draw attention to the pattern here.. If you march out every larger/high voltage complex with the others its a pretty darn close match... Same can be said for the lower voltage complexes. Now granted afib variability is only 40 ms, and also granted that we have an absence of other criteria to truly base an afib diagnosis.
Now one can say 'but theres no p waves!".. But the tricky thing is.. There are p waves! Or so it seems! If you look closely at morphologies youll spot a few inconsistencies.. Theres 1 that pops up just before a qrs complex. When you march them out you can see a few places where the morphology fits and a few where it does not.. It is however very easy to find yourself marching on t waves, a very prophetic sign toward svt.. The few inconsistencies however is compelling toward afib.
Lets not also forget that in a coarse afib type of situation yoh can have fib deflections that resemble p waves. Which is the basis of an argument against the marching p's that makes perfect sense as well.
Im basing all of this on the assumption of course that the tamponade or effusion was confirmed by sonography.. If not theres the argument that this could be alternans or something else entirely. You gotta get that stat echo, or just get a fast exam for a parasternal long and see it to know..
Point being, i think theres evidence to point toward afib.. But its not slam dunk evidence.. Theres also not slam dunk evidence that any 1 particular etiology is implicated here.. This patient could have multiple things going on electrically speaking.
With this in mind we have to take what we know: its fast.. Its not ventricular... We are unsure of the precise origin(s) therefore we apply an umbrella term of SVT.