Friday, March 17, 2017

A 20-something with DKA and a regular wide complex tachycardia

Medics were called to see a 20-something type 1 diabetic with h/o DKA who had altered mental status.

He was found to have "Kussmaul" respirations and respiratory distress.

He was not in shock, his blood pressure was adequate, and pulses were strong.

He was put on the cardiac monitor:
Regular wide complex tachycardia.

A 12-lead ECG was recorded:
Regular Wide complex tachycardia at a rate of 200.
What do you think?
If you're the medic, what would you do?

Whenever there is a wide complex, especially in a patient with DKA, one should think of hyperkalemia (sinus rhythm, often with "invisible P-waves").

However, this rate is too fast for sinus tach and the morphology is not right for hyperkalemia.  Still, calcium is harmless and it is harmless to give 3 grams of calcium gluconate.

He arrived in the ED in the same condition.  He was hemodynamically stable but with altered mental status and respiratory distress.  Cardiac echo showed hyperdynamic performance.   Blood gas showed severe acidosis, with pH 7.00, pCO2 25 and HCO3 of 6.   K retured at 4.5 mEq/L.

He was treated with calcium, bicarbonate, and magnesium.  He was intubated.

He had this ECG recorded:
What do you think?
What do you want to do?
Suppose the patient did not have altered mental status from DKA and was not intubated?

Analysis: VT vs. SVT with aberrancy vs. sinus tachycardia with hidden P-waves.  (With a rate this fast, and no inkling of P-waves, sinus is very unlikely but if you were not sure, you could record Lewis Leads.)

This ECG is almost certainly supraventricular tachycardia with aberrancy.  Why?

First: pretest probability
The patient is young and without heart disease
Good LV function makes VT less likely (except for fascicular VT)

Second: the ECG itself:
1. There is an inferior axis.  The impulse originates cranially and propagates caudally.  In contrast, VT, because it originates in the ventricle, which is lower left, generally propagates toward the upper right.
2. More importantly, there is a typical right bundle branch block (RBBB) morphology:
    a. There is RR' in V1 and the R' is larger than the R.
    b. There is a rapid, narrow R-wave in V5 and V6, with a wide S-wave.

This latter makes SVT with RBBB aberrancy almost certain.

Thus, it is very likely that it will convert with adenosine.  The medics could have given adenosine and converted.  Since the patient was hemodynamically stable, there was no rush to convert and therefore it is OK that they left it alone.

If you're wrong and give adenosine to a patient with VT, don't worry.  Adenosine has been shown to be safe in Ventricular Tachycardia and is even recommended now in ACLS.

Of course, electrical cardioversion will work very well but generally requires sedation unless the patient is already obtunded.  This patient was intubated and sedated, so electricity is easy to use.

However, if this patient were not so sick with DKA that he needed to be intubated, adenosine would be the treatment of choice.

The patient was diagnosed with VT and electrically cardioverted.

Here is the post-cardioversion ECG:
Sinus Tachycardia with normal QRS and axis and nonspecific ST-T abnormalities

There is no baseline RBBB.  The right bundle generally has a longer refractory period than the left bundle, so that when there is a fast rate, it can result in RBBB aberrancy.  

The patient did well and was later diagnosed with SVT with aberrancy.

Learning Points:

1.  Adenosine is safe in regular wide complex tachycardia.  (But NOT in irregular polymorphic wide complex tachycardia, as this could be WPW with atrial fib)

2. If there is typical RBBB morphology, it is almost certainly SVT with aberrancy.  There are also fairly rare fascicular ventricular tachycardias which can mimic SVT with aberrancy.  However, you won't hurt them with adenosine.


  1. What does this mean "inferior axis" There is an inferior axis. The impulse originates cranially and propagates caudally. In contrast, VT, because it originates in the ventricle, which is lower left, generally propagates toward the upper right.

    1. The QRS impulse is directed inferiorly. Does this question mean you don't know what "axis" is? If not, then you should consult some more basic EKG sources to learn about it.

  2. Dr Smith

    Is there a concern with administration of calcium for such a rapid rate if hyperkalemia is not the case? And is there a danger in giving bicarb and albuterol without knowing potassium levels prehospital?

    1. Calcium is safe. Bicarb and albuterol could potentially be harmful. Neither are necessary in this case prior to lab evaluation.

  3. GREAT case. I’ll make a few comments that express a slightly different perspective (with similar bottom line). The reasons why I’d suspect SVT with aberration for the 2nd and 3rd ECGs shown here (in addition to young age) are: i) most leads (other than V1,2,3) look supraventricular, in that the initial deflection is sharp and rapid; ii) Lateral leads I and V6 in particular manifest an initial narrow QRS deflection with a terminal wide S wave that is extremely characteristic of RBBB; iii) QRS morphology is consistent with RBBB/LPHB (short r with deep S in lead I; predominantly upright QRS with early peak in II,III; wide terminal S waves in leads I,V6; and an upright R in lead V1 consistent with RBBB); and iv) The most common “fascicular VT” is left posterior fascicular VT — where morphology here would be more suggestive of anterior fascicular VT (given rbbb/lphb morphology for the QRS complexes we see). Where I differ — is that while QRS morphology in lead V1 is perfectly consistent with RBBB (since the QRS is wide and upright) — it is not in my opinion “typical” for RBBB, because we lack a clear distinct S wave in V1 that descends below the baseline before rising again to a taller R’ wave. When you see this typical rSR’ (with S wave descending below the baseline in V1 before sharply rising again) in association with wide terminal S waves in lateral leads I and V6 — then you can be over 90-95% certain the rhythm is supraventricular. In contrast, a monophasic R (or RR’ as we see here) in lead V1 is far less specific for a supraventricular rhythm. However, the other factors (i, ii, iii and iv) taken together ARE highly suggestive of SVT with aberration. Of interest — the 4th (last) ECG after conversion to sinus rhythm shows virtually identical direction and slope for the initial QRS deflection in ALL leads except V1,V2,V3 (where the RBBB was most manifest) — and this identical initial QRS direction and slope during and after tachycardia confirms that the tachycardia was indeed supraventricular. THANKS for posting!

    1. A very informative interpretation, Sir Ken Grauer. The 4th( last) ECG no longer shows RBBB, So can we call this case ( 3 first ECGs ) SVT with rate- related RBBB aberracy, sir? Thank you.

    2. Ken,
      there are 2 peaks the R-wave in V1: an R and and R'. The first one is not as tall as the second, and this favors SVT with RBBB over VT with RBBB morphology, as it indicates that the septum depolarizes first and the rest of the ventricle only after some impulse toward the right ventricle.
      Wouldn't you agree?

    3. Steve — The criteria I use for assessing QRS morphology were primarily derived from a paper by Wellens that I saw many years ago (unfortunately, I don’t think I still have that reference … ) — but those criteria were thoroughly reviewed and supported by Marriott at MANY of the conferences by him that I went to during the 1980-1990s. My understanding of those EP findings that Marriott extolled for so many years were exactly as I described them above — namely, for definition of a “typical” RBBB pattern that is highly predictive of a supraventricular etiology — you need a “clean” rSR’ (or rsR’) pattern in which there are not only 2 peaks with taller right rabbit ear, but ALSO an S wave that descends below the baseline. I illustrate some examples in Figure 2 from my ECG Blog #42, in which I give “my Take” on distinction between VT vs Aberrancy in a wide tachycardia by morphology and other criteria (Scroll down in the blog post until you get to Figure 2 near the bottom of my post — ). I realize that there are many different “perspectives” on how to distinguish between VT vs Aberrant conduction by many of the most esteemed voices in cardiology. All I can say, is that I have applied the criteria I describe in my Blog #42 (which are the same ones I’ve included in all of the ECG/Arrhythmia books I have authored) — and over the past 30+ years, I have found them to work amazingly well. There still are times (as you know from discussions you & I have had) when I don’t think it is possible to be 100% certain about the etiology of a WCT (Wide-Complex Tachycardia) — but in the vast majority of cases, my approach yields a high likelihood answer in no more than 5 seconds. To me, QRS morphology only helps if it yields a highly specific answer that is easy to apply at the bedside of a crashing patient. From all I have seen in the literature, the specificity of an RR’ complex in lead V1 (even if the R’ is taller than the R) is unsatisfactory as a discriminating factor. It becomes HIGHLY specific only if you truly have a typical rSR’ pattern.

      That said, as per our discussion in your blog post — the rest of the ECG and the clinical circumstances for this 20yo with DKA highly favor a supraventricular etiology.

      I fully acknowledge that the above merely reflect “my approach” based on my experience and my interpretation of the literature. I realize others may view this differently.

      Keep up the WONDERFUL WORK with your ECG Blogs!

  4. Interesting case and nice explanation of Dr. Smith. Thanks you.


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