I hope you all had happy holidays!
Here is the discussion for 90 year old male cc: chest pain. You may wish to go back and review the case.
So, let's get into the case! There are the usual questions we need to answer as we try to determine the rhythm. Is the rhythm wide or narrow? Regular or irregular? Is there atrial activity?
It is also important to note that there were a couple confounding factors. The data quality was not great, which is never helpful. The crew tried to get a better tracing, and this was the best they could get. As a side note, refer back to this post where Tom Bouthillet outlines his approach to achieving a high level of data quality in his tracings. Sometimes, there is nothing we can do to improve the data quality on a particular patient. But it is important to make excellent data quality a priority.
Another factor in this case was that a couple of leads, notably V2, looked unusual and narrow, and could throw off someone's interpretation.
So, back to our initial 12 lead:
It is a wide complex tachycardia, at a rate of about 150, which appears at first blush to be regular. Our differentials include:
- Sinus tach with aberrancy
- SVT with aberrancy
As far as the wide complexes go, there are no real signs of atrial activity, although as some pointed out, in lead V2, there appears to be something resembling an atrial wave preceding a narrow QRS. Let's talk about that piece, because many of you put a lot of stock in V2 looking narrow.
We should remember that when considering whether the rhythm is narrow or wide, we look at the widest complex we can find and use that for our measurement, not the narrowest. Why? Because from time to time, part of the QRS in a particular lead may be isolectric, and make the QRS appear narrow when in fact it is not. Consider the following:
If we draw a line connecting the beginning of the QRS complexes in these leads, we can see that what appears to be a narrow QRS and possible P wave in lead V2 is actually part of the wide QRS as measured against the other leads! If you use this method on lead III, you will also find that what appeared to some as an inverted P wave, is actually part of the QRS as well. This is precisely why we use the widest complex to determine QRS duration and not a narrow one.
What was also confounding was that the rhythm did not look regular, but regularly irregular. If you look closely at the 12 lead and the rhythm strip, you will see that there are two alternating cycle lengths, a short R-R followed by a longer R-R at 340 ms and 380 ms respectively. Thanks to Christopher Watford for the following graphic illustration:
While the default for a regular WCT is to assume VT unless proven otherwise, I have to admit that this ECG left me feeling uncertain, because of the irregularity. We have to be extremely concerned about an irregularly irregular WCT, such as A-Fib with WPW, but this rhythm is not irregularly irregular so that is off the table.
Because this ECG seemed somewhat unusual to me, I took the liberty of asking Stephen Smith, M.D., of Dr. Smith's ECG Blog to take a look at it. He also ran it by his associate, renowned ECG Master K. Wang, M.D. for analysis:
From Dr. Smith:
"I believe this to be VT. Much VT does not have concordance, and aVR has a wide, monophasic initial R-wave".
Although as yet unvalidated, Dr. Smith prefers Sasaki's criteria for VT, and you can find a great post on his blog that deals with Sasaki's criteria here. As to the alternating cycle lengths, he had this to say:
"If there were some consistent variation in the QRS morphology, I would say that there is something else going on. But there is no such consistent difference between QRSs after 340 ms vs 380 ms…So I would just have to say that it is VT with grouped beating, although I admit that is strange."
From Dr. K. Wang:
"I agree it is VT. As you know, if either of the initial or the last part of the QRS is isoelectric in a given lead, the QRS can be narrower than what it actually is in that lead (it can never be wider than what it actually is). Judging from the other leads taken simultaneously, that is what happened. Also look at lead III. There seems to be a negative P wave in front of each narrow QRS, but again, judging from other leads taken simultaneously, what appears to be a negative P wave is already within the wide QRS of other leads and it is part of the QRS, not a P wave. That is what i think."
My sincere thanks to these two ECG greats for their contributions to this case.
One more caveat with regards to using criteria for VT which you have heard early and often on this site: While it is ok to use the criteria to rule in VT, the failure of the criteria to rule in VT does not rule out VT!!! VT can look like almost anything, so don't fall into the trap thinking that if it doesn't meet "criteria", or a certain morphology, it can't be VT. It most certainly can.
Now that we have settled on VT, how do we treat this patient? Where will we transport him? Well, if you believe that the VT is the primary problem, and that the patient does not need PCI, it certainly seems reasonable to go to the closest facility ten minutes away rather than the PCI facility.
As for the patient, he is alert and oriented, has a pressure of 130/90, but has substernal "chest pressure". Is this patient stable? Do we treat with antiarrhythmics? Cardiovert? Or do nothing?
While you can say that under ACLS guidelines, the chest pressure makes this patient unstable, However, I do think there is a difference between "chest pressure" and "crushing chest pain." From the presentation the patient was ambulatory, in "no obvious distress", apparently tolerating the VT. I think it would be fair to say the patient is stable enough to not need immediate cardioversion in the field.
If we decide the patient does not need to be immediately cardioverted, antiarrhythmics become the other choice. His pressure is good, and the risk of giving amiodarone or another antiarrhythmic is that we cause the very hypotension and instability that we are trying to avoid. I think it is reasonable prepare for deterioration, but at the same time monitor closely and hold off on treatments that could be detrimental to the patient until ED arrival.
To me, this is another case that illustrates the difference between decisions we learn in class and decisions we have to make in real life. Patients do not read our text books or attend ACLS. They present in that grey-not-so-sure zone where their stability is delicately balanced against what we do and what we decide not to do.
In this case, the crew was unable to gain IV access. They applied the pads as a precautionary measure, and transported the patient to the ED without further incident. After arrival at the ED, IV access was secured. The patient was treated with a trial of antiarrhythmics, then successfully cardioverted.
Thoughts and comments?