Monday, January 25, 2016

Atrial Fib with RVR. What treatment? Then SVT. Is it sinus? Use ultrasound and Lewis leads!

An elderly man with a history of diabetes and HTN presented with lethargy and weakness.  He had no CP or SOB, and it was unknown if there was a previous history of atrial fib.  He was on atenolol, but it was not known if this was simply for hypertension, or for atrial fib.  He was not anticoagulated.  He also had decreased urine output.  There was no history of any GI bleeding or other hemorrhage.  There was no fever.  He had an ECG recorded upon arrival:
There is atrial fibrillation with a rapid ventricular response (rate of approximately 120).  There are aberrantly conducted beats (Ashmann's phenomenon), which are easily confused with runs of VT.
There is ST depression in V2-V6 that is clearly ischemic.
The ischemia on the ECG could be of several possible etiologies: 
1) New atrial fib with RVR causing demand ischemia (but the rate is not terribly fast).
2) Old atrial fib with poor rate control causing demand ischemia.
3) ACS with possible additional ischemia from atrial fib with RVR
4) Hemorrhage/dehydration/sepsis/etc., with new or old atrial fib, resulting in reflexive tachycardia and demand ischemia.

To find the answer, it is wise to assess volume status, which can be done with ultrasound:

A bedside ultrasound was done from the subcostal view, concentrating on the IVC.  If this is due to etiologies 1-3, one would expect a full IVC.  If etiology 4, then one expects a flat and/or collapsing IVC:

This shows a collapsing inferior vena cava (IVC), consistent with volume depletion

Another with a better view of the heart.  RV is on upper part of the view, next the liver:

RV is quite small.  LV is also small and has good contractility.  This supports volume depletion.

The appropriate therapy would be fluids and further workup for hemorrhage/dehydration/sepsis/etc.

However, BOTH an esmolol bolus and drip, and IV fluids were started.

But beta blockade should NOT be given, at least not yet.  In a volume depleted state, this patient needs the reflexive tachycardia for cardiac output.

By the time I arrived and was involved, the esmolol had not been at a high enough dose to do any harm.

In the meantime, the first troponin I returned at 0.562 ng/mL.  I was fairly certain that this was a type II (demand ischemia) MI and that this patient was not having ACS.

I stopped the esmolol and gave the patient 2 liters of fluid.  After fluids, the IVC was less collapsing:

But the patient monitor then showed a regular tachycardia without any P-waves.  The rate was very constant at 140 and so I wondered if this was SVT or sinus tach.  Another ECG was recorded:
Now there is a regular supraventricular rhythm.  There are probable P-waves, but I wasn't entirely certain.
What to do?
Lewis Leads!!

I went into the patient's room, and, according to the interview with Christopher Watford on EMCrit, I changed the monitor leads around (this is not a 12-lead!)

  1. Place the Right Arm electrode on the patient’s manubrium.
  2. Place the Left Arm electrode on the 5th intercostal space, right sternal border.
  3. Place the Left Leg electrode on the right lower costal margin.
  4. Monitor Lead I.
I printed it out.  This is what I recorded:
Now the P-waves are obvious

So the patient now has sinus tachycardia.

The next troponin returned at 5.0 ng/mL.

I gave more fluids and the heart rate came down.  Here is the next ECG:

He developed a fever and urine showed WBC's.  He was treated for urosepsis and did well.  He did not have ACS.

Learning Points:

1. Not all myocardial infarction is due to ACS
2. Atrial fibrillation with RVR may be a consequence, not a cause of, illness
3. Volume status is critical in the management of Atrial fibrillation with RVR
4. If you are not certain of a source of SVT, do Lewis leads


  1. When doing Lewis leads, where exactly to put LL electrode?
    Thx! This is very cool tip! Will try it as soon as i can!

  2. The solution, Anonymous, as always is wiki knowledge

  3. Dr. Smith,

    thanks for sharing another interesting case.

    Congrats on your excellent blog which I discovered only very recently. I have learned a lot of things in a couple of week (modified Sgarbossa criteria, subtle STE and its formula and last but not least Lewis leads).
    Regarding the present case, I have a question: I suppose the patient has been recovered but in which ward? Cardiology (given MI type-2) or Medicine (given urosepsis)?
    Many thanks in advance.

    Mario Parrinello

    1. Mario,
      The patient was admitted to general medicine. Good question.

    2. Steve...

      Great case with a lot of practical information discussed. I just wanted to point out that the very long pause followed by three aberrantly conducted beats has resulted in only one aberrant beat due to the Ashman phenomenon and that would be the beat that ends the short interval. Actually, it's not very aberrant but the two beats that follow it are. However, they cannot be due to the Ashman phenomenon because neither one ends a long-short interval combination. They are aberrant due to concealed transseptal conduction.

      In my classes, I find a lot of participants who think the Ashman phenomenon consists of a long interval, a short interval and THEN an aberrant beat, which would require a 4th beat. In the Ashman phenomenon, it's the 3rd beat - the beat that ends the short interval - that is aberrant. Any aberrancy after that (without an intervening long interval) is due to something else.

    3. Jerry,
      You are right, except that the successive beats are also due to a prolonged refractory period after the first complex of Ashmann's. So, strictly speaking, it is not Ashmann's, but it is a result of Ashmann's. The main point is that these are not PVC's.


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