A 75 yo M presents to the ED for chest discomfort. 

Fig 1

Our pt is hemodynamically stable therefore we have at least a few moments to inspect the tracing closely. 
-In our consideration of “Big Sick vs Little Sick” – I would at least place the pt somewhere in the middle simply due to the obvious tachycardia. 

Unfortunately, we do not have a simultaneously recorded long rhythm lead across the bottom – this format is using the conventional ordering of the Hexaxial leads (from top to bottom: I, II, III, aVR, aVL and aVF). This tracing also has a fold in the paper which does distort some of our measurements, however, I believe we have enough clear tracing to offer a reasonable interpretation.

When we have a stable pt, I favor determining the underlying rhythm first then looking for ischemic / aberrant findings.

Here, I don’t think Lead II is the best lead to determine the rhythm – I used a combination of several leads including Leads V1 and V5 to begin with. See Fig. 2

Fig. 2

Since Lead II has no obvious P waves, I focused on V1, then V5 looking for atrial activity. As denoted by the red arrows – I believe these show clear indication of MOSTLY regular atrial activity. There is obviously a longer “R to R” (actually a QS in V1) between beats 5 and 6, then shorter between 6 and 7. There is no clear “P” wave preceding beat #7. 
           – Could this be Ashman Phenomenon? This is typically seen in A Fib, the rhythm is irregular yet clearly not AF.
To quote Ashman Phenomenon (my-ekg.com):

Ashman phenomenon is an aberrant ventricular conduction that follows a short R-R interval preceded by a long R-R interval.

It is a physiological aberrancy and is typically seen in atrial fibrillation, but it can also be seen in atrial tachycardia or in premature supraventricular beats.

Gouaux and Ashman reported that in atrial fibrillation, when a relatively long cycle was followed by a relatively short cycle, the beat with a short cycle often has right bundle branch block pattern 1.

This phenomenon may cause diagnostic confusion with premature ventricular complexes because it is seen on the EKG as a single wide QRS complex during atrial fibrillation with narrow QRS complexes.

Single, wide QRS aberrant complexes are caused almost exclusively by the Ashman phenomenon 2.

I do NOT think what we are seeing in beat #7 of V1 is Ashman Phenomenon. Instead – I think we are seeing a change in Ventricular response of variable Atrial Flutter with 2:1 conduction to 1:1 conduction. The QRS of beat #7 is too similar to nearly all of the other QRS complexes.

I sent this tracing to my friend and mentor Dr. Ken Grauer; his response: 
  “The fact that the relative (short) pauses are probably of the same duration with usually similar PR intervals before the pauses — suggests Wenckebach-like conduction at 2 levels through the AV node (which is common with AFlutter, and NOT necessarily a pathologic “block”, but rather physiologic of the fast atrial rate)”.

See his phenomenal ECG blogs on Atrial Flutter including audio: 

I feel another clue to this being AFlutter is in the “PR Interval” (This isn’t really a PRI due to Flutter waves). With a ventricular rate this fast *varying from ~140-160 bpm* – we would expect the “PRI” to shorten, what we are seeing here is a “PRI” that is measured at the upper limits of normal – not shortened.


The typical Atrial Flutter we are taught is the “sawtooth” pattern. However, with any tachycardic rate over ~150 bpm, we should always consider Atrial Flutter as this is probably the most misdiagnosed tachycardic rhythm! 

The QRS:  All QRS measure approximately 120 ms. V1 has no R wave and is predominantly negative followed by what appears to be a terminal positive deflection. I admit – this terminal portion is difficult to be 100% confident on due to superimposed flutter waves. Normally, I would call this an atypical RBBB – however, with Leads I AND V6 BOTH not producing an S Wave (therefore no “slurring” of an S Wave), we cannot say for sure if this would then qualify as a LBBB with superimposed flutter wave OR an Intra Ventricular Conduction Delay (IVCD). 
Both Leads I and V6 show an all-upright complex that is widened. In addition: All 4 Lateral Leads *I, aVL, V5 and V6* have no “expected” Septal q wave preceding any of the QRS’. These findings would lead us to “typical LBBB”, however with a Terminal Positive R’ wave in V1 – I would call this an IVCD.

ST Deviations:
Clearly Leads I and aVL both have ST Depression of ~1-2mm depending on where you measure from (V5 and V6 have none as would be expected being “contiguous leads”. 
The reciprocal of aVL is Lead III which reveals not only a clear pathologic Q wave but ST Elevation of ~ 1mm – again – depending on where you measure from. Normally – I would say this is definitive for acute ischemia, however – the ST deviations could be explained by “Rate demand ischemia”. Even though the Troponin level returned positive – the priority here is we MUST control the rate first then repeat the tracing.
*Infarct with this rate of tachycardia is rare with an underlying cardiogenic shock. It is true that there can be concomitant infarct with A Fib with RVR and/or variable Flutter but one must get the rate into normal ranges prior to PCI. There have been innumerable false cath lab activations simply due to rate related ST changes. 
– The amount of ST Elevation seen throughout V1-V4 are what’s referred to as “Appropriate Discordance”. Note how large the voltage is with V3 and V4 overlapping. There could be Chamber Enlargement present – Echo would confirm.

*Additional quote from Dr. Ken Grauer: “1st Priority — Treat the rhythm. Personally, I doubt an acute MI (despite the appearance of leads III and aVF) — because: i) the sawtooth pattern of flutter here is probably exaggerating what we are seeing; and ii) I have seen on occasion ST “elevation” that mimics infarction — but which is simply (amazingly) just rate-related and GOES AWAY when the tachycardia is controlled. And clinically — it does NOT matter if we suspect ST elevation of ischemia/infarction — because even in that case, our 1st priority is to slow the rate — and THEN we can repeat the ECG and see what’s left!”.

Additional notes:
Lead II – On the upstroke of the R waves, there is a noticeable “notching”. I do not believe this is QRS Fragmentation since it is not seen in the other 2 Inferior Leads but rather superimposed Flutter waves. I cannot be 100% certain of this especially with the pt’s age of 75 and not having a full medical history or known prior cardiac issues however, it’s simply what this looks like to me 🙂
– Also, did you notice the inverted T waves in all 3 Inferior leads? These are inverted Flutter waves – not uncommon in AFlutter. 

T Waves: Upright in V1 and negative in V6 – This is expected when there is LVH, LBBB and in the young. 

Axis – Normal – Predominantly positive QRS’ in both Leads I and aVF

R Wave Progression – Slightly delayed with full transition by V5.

Interpretation: Variable Atrial Flutter with 2:1 and occasionally 1:1 conduction with IVCD and ST-T changes consistent with Rate Related Demand Ischemia. 

Learning Points:
– Atrial Flutter is one of the most commonly missed rhythms
– Atrial Flutter can and will mimic acute ischemia
– Even if there is acute ischemia – control the rate first, then repeat the ECG. You may be surprised at the resolved findings.
– All WCT should be considered VT first then work backwards for any other findings

– If Adenosine was considered and given – what would have happened? The slowing of the Ventricular response would most likely have revealed a more obvious Atrial Flutter. Although not recommended, it is worth noting that many times the use of Adenosine inadvertently helps diagnose AFlutter. 
– Since the pt was stable, the modified Lewis Lead configuration could have been captured which many times reveals obvious A Fib / A Flutter. I’ll write a detailed explanation on Lewis Leads at a later time.
– I was asked if this could be WPW. That would require a short PR Interval. As stated earlier, with tachycardia, we would also expect a short PRI not normal to upper limits. 

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