Tuesday, November 26, 2019

Global ST depression with ST elevation in aVR - what is the cause?

Written by Pendell Meyers



An elderly patient with cardiac history presented with shortness of breath. This ECG was brought to me with concern for diffuse ST depression and STE elevation in aVR.

What is your response?
















Flutter waves are simulating diffuse ST depression, and therefore there must be the reciprocal finding of apparent STE in aVR.

The ventricular rate is slightly greater than 100 bpm, with 2:1 block. This means an atrial flutter rate of 200 bpm, which is somewhat unusual unless the patient has a very large, dilated left atrium and/or antidysrhythmic medications which slow the speed of action potential conduction (typically class 1, Na channel blocking agents).

AV nodal blocking agents were given and the rhythm changed to atrial flutter with slower, variable block (strip not available unfortunately).

The patient did not have ACS. Three troponins were negative. The patient was treated for atrial flutter and did well.



Learning Point:

Atrial flutter can mimic diffuse ST depression, which always must cause reciprocal ST elevation in lead aVR. It can also mimic ST elevation, or conceal true underlying ST deviations. See these other cases for examples:

Is this inferor STEMI?









===================================
MY Comment by KEN GRAUER, MD (11/26/2019):
===================================
I will add to the Learning Points on this important Teaching Case presented by Dr. Meyers.
  • For clarity — I’ve reproduced and labeled the ECG in this case in Figure-1 (See text).
Figure-1: The 1st ECG shown in this case (See text).



POINT #1: The clinicians who initially interpreted this tracing, and voiced concern about “diffuse ST depression with ST elevation in aVR” — were not systematic in their interpretation. Instead, they jumped to assessment of ST-T waves. The 1st STEP in the systematic approach for interpreting any ECG — is to start with assessment of the rhythm — which was clearly not done.
  • In my experience, the biggest mistake (by far! ) that I see even experienced interpreters make — is the failure to LOOK FIRST at the long lead II rhythm strip at the bottom of the 12-lead tracing. It literally should take NO more than 2-3 seconds for your “educated eye” to scan this long lead II. If you do not see an upright P wave preceding each QRS complex with constant PR interval in this long lead II — then you do not have sinus rhythm.
  • The only exceptions to this rule (when the rhythm could still be sinus despite lack of an upright P wave in lead 2) — are if you have: i) lead misplacement (most commonly, mixing up the left and right arm electrodes)orii) dextrocardia. Therefore, the rhythm in Figure-1 is clearly not sinus rhythm — because the P wave in lead II is not upright (RED arrow in lead 2).
  • Bottom Line: IF you don’t begin your assessment of each and every ECG you interpret with a 2-3 second “educated look” at the long lead II rhythm strip — then you are GUARANTEED to miss a lot of non-sinus rhythms.


POINT #2: Once you have ensured that the patient is hemodynamically stable — there are 5 Parameters to assess in the Systematic Interpretation of any cardiac rhythm. These 5 parameters are easily remembered by the saying, "Watch your Ps, Qs and the 3Rs". (CLICK HERE for detailed discussion on how I apply this systematic approach to rhythm interpretation).
  • NOTE  It does not matter in what sequence you assess these 5 parameters, as long as you always assess each one. I often change the sequence I use, depending on the arrhythmia I’m looking at (ie, Start with those parameters that are easiest to identify for the particular rhythm in front of you! ).
Applying this Systematic Approach to the rhythm in Figure-1:
  • P waves (or if definite P waves are not seen ... Is there evidence of atrial activity?) — As already stated, the RED arrow in lead II shows there is no upright P wave in lead II. That said, the consistent negative deflection that precedes each QRS complex in lead II (as well as in other leads) — suggests that there is atrial activity.
  • Is the QRS complex wide or narrow? It should be apparent in Figure-1 that the QRS complex is narrow in all 12 leads. Therefore — the rhythm is supraventricular!
The Rs: iRate of the rhythm; ii) Is the rhythm Regular?andiii) If P waves (or atrial activity) is present — is this atrial activity Related to neighboring QRS complexes?
  • In Figure-1 — the ventricular Rate of the rhythm is ~110/minute (ie, as shown in lead II — the R-R interval is just under 3 large boxes in duration — so the ventricular rate is a bit faster than 300/3 ~110/minute).
  • Unfortunately — there is some curving and distortion of Figure-1. That said, the ventricular rhythm appears to be Regular.
  • Atrial activity (in the form of the negative deflection that precedes each QRS complex in each of the inferior leads) — does appear to be Related by a constant PR interval with the QRS complex that immediately follows it.

POINT #3: As I have often emphasized — the fastest and easiest way to instantly become MUCH “smarter” in rhythm interpretation — is to regularly use CALIPERS.
  • In Figure-1 — it should be easy to see IF you are using calipers, that there are 2 negative deflections for each QRS complex — and that these negative deflections are precisely regular (BLUE arrows in the long lead II rhythm strip). Thus, there is 2:1 AV conduction.
  • Further confirmation of precise 2:1 atrial activity can be seen by the regular positive deflections in leads aVR and V1 (PURPLE arrows in these leads).

POINT #4: When the ventricular rhythm is regular, and there is 2:1 AV conduction — the best way to calculate the atrial rate is to double the ventricular rate. In this case — 110/minute ( = the ventricular rateX ~220/minute for the atrial rate.
  • Therefore — By the Ps, Qs, 3R Approach, the rhythm in Figure-1 is a regular SVT (SupraVentricular Tachycardia) at ~110/minute, with 2:1 AV conduction (atrial rate ~220/minute).


POINT #5: To remember that there is a Differential Diagnosis for any regular SVT rhythm, as well as for a regular SVT rhythm with 2:1 AV conduction (CLICK HERE for My Review of a similar case on the November 12, 2019 post in Dr. Smith’s ECG Blog).
  • Since in this case, there is 2:1 AV conduction in Figure-1 — we can for practical purposes, rule out sinus tachycardia and a reentry SVT (such as AVNRT or AVRT). This essentially leaves us with distinguishing between AFlutter vs ATach (Atrial Tachycardia).
  • Untreated AFlutter in adults is most often associated with an atrial rate of ~300/minute (250-350/minute range). Since the most common conduction ratio for new AFlutter is 2:1 — the ventricular rate of untreated AFlutter is most often close to ~150/minute (ie, 300/2 ~150/min.). The KEY to these generalities regarding the rates with AFlutter, is the word “untreated”. IF this elderly patient is on any antiarrhythmic (or antihypertensive) medication that might slow the rate — then AFlutter might present with a ventricular rate that is significantly slower than 150/minute. Missing from the history of this patient is mention of what drugs this elderly patient is taking!
  • It is not always possible by ECG to distinguish between ATach vs AFlutter, especially if the rate of AFlutter is slower-than-usual (See HERE). That said — the presence of typical sawtooth” atrial activity (slanted RED lines in the latter portion of the long lead II rhythm strip) — strongly suggests that despite the slower-than-usual atrial rate, the rhythm in Figure-1 is AFlutter and not ATach.

POINT #6: A semantic point that I feel is important to make — is that the rhythm in Figure-1 is AFlutter with 2:Aconduction (and not 2:1 AV “block”).
  • Use of the term, “block” implies pathology. Instead, it is physiologic that in the presence of the very rapid atrial rates seen with flutter, that only 1 out of every 2 impulses arriving at the AV node is conducted to the ventricles.

POINT #7: Finally — I doubt there would be significant ST deviation (elevation or depresson) if the AFlutter in this case resolved. With practice — one gets pretty good at “mentally subtracting” flutter waves from the ST segments — and to my eye, doing so would result in ST-T waves suggesting no acute changes in this patient.


Our THANKS to Dr. Meyers for presenting this instructive case!




2 comments:

  1. Regularly occurring peak to peak or valley to valley of the flutter waves are easily appreciated in lead V1 and lead II respectively. Or, the "sloping up, sloping down" of the flutter waves are obvious in lead III. Or, lead aVF will allow me to say "dome, dome, dome... of flutter waves".
    K. Wang.

    ReplyDelete
    Replies
    1. Thank you for your comment K — and I KNOW that you and I both INSTANTLY recognized AFlutter on this tracing for the reasons you state (and that I discuss and illustrate above in my Figure-1). But somehow, AFlutter remains the most commonly overlooked diagnosis. Using a systematic approach (ie, always beginning assessment by looking to see if there is an upright P wave in lead II) could go a long way toward improving recognition. THANKS again for your comment! — :)

      Delete

Recommended Resources