Diffuse ST depression, and ST elevation in aVR. Left main, right?

This ECG was recorded on a middle-aged male with sickle cell disease and diffuse pain.

Sinus rhythm
Left ventricular hypertrophy (LVH)
Diffuse significant ST depression with ST Elevation in aVR
Computerized QT = 494 ms, QTc = 538 ms
What else?
What do you think?

Here is a Previous ECG for comparison:

Baseline LVH
Only minimal ST depression

Diffuse ST depression with ST Elevation in aVR

Knotts et al. found that such ECG findings only represented left main ACS in 14% of such ECGs: 
Only 23% of patients with the aVR STE pattern had any LM disease (fewer if defined as ≥ 50% stenosis). Only 28% of patients had ACS of any vessel, and, of those patients, the LM was the culprit in just 49% (14% of all cases).  It was a baseline finding in 62% of patients, usually due to LVH. 

Reference: Knotts RJ, Wilson JM, Kim E, Huang HD, Birnbaum Y. Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? J Electrocardiol 2013;46:240-8.

Hypokalemia is frequently forgotten as a cause of ST depression.

The ST depression is accompanied by what appear to be down-up T-waves diffusely.  The "up" portion is really a U-wave.  Whenever there are down-up T-waves and what appears to be an extremely long QT, you must suspect that the "Up" wave is a U-wave and that this is hypokalemia. 

When there is ST depression, one must:

1.  Assess the QRS.  It the abnormal repolarization (ST depression) secondary to abnormal depolarization (an abnormal QRS), such as LVH, LBBB, RVH, RBBB, IVCD, WPW.

2.  If the QRS is normal, or does not explain the abnormal depolarization (in this case, the ST depression is increased over the baseline, so we cannot blame it on the LVH), then there are 4 basic etiologies that I know of:
   a. Ischemia
   b. Hypokalemia
   c. Digoxin
   d. Baseline, uncertain, non-pathologic (sorry, not really an etiology)

3. When there is a down-up T-wave, which is really a U-wave, and especially when diffuse as here, then it is pathognomonic for hypokalemia.

Diagnosis: Hypokalemia and LVH

Lab value: K = 2.6 mEq/L

When is hypokalemia dangerous?

This is uncertain.  To my knowledge, there is no data on this, but we are attempting to study it.  Opinions vary widely on the K level at which a patient must be admitted on a monitor because of the risk of ventricular dysrhythmias.  

Until some real data is available, my opinion is this:

1. K less than 2.8.
2. Any hypokalemia that results in clear ECG abnormalities, such as here.  My rationale is that if the K is affecting the ECG, then it is affecting the electrical milieu and can result in serious dysrhythmias.  I have no data to support this except for face validity!


 More cases: 

Here are down-up T-waves of posterior MI: 

Series of Prehospital ECGs Showing Reperfusion

Here is down-up "T-waves" of hypokalemia: 

Biphasic T-waves in a Middle-Aged Male with Vomiting

Many other cases:

Several Cases with the Classic "Wavy" Pattern of Hypokalemia

A middle-aged man with severe syncope, diffuse weakness

A woman in her 50s with reproducible chest pain (seems to be chest wall pain)

STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes

Patient with severe DKA, look at the ECG

Pre-existing Left Bundle Branch Block and Atrial Fib: what is alarming on this routine pre-procedure ECG?

Palpitations in a Young Healthy Male

A pathognomonic ECG you should recognize instantly

A middle-aged man with severe syncope, diffuse weakness

Chest pain and Diffuse ST depression, with STE in aVR. You probably think it is left main.....

Are These Wellens' Waves??

Biphasic T-waves in a Middle-Aged Male with Vomiting

Diabetic Ketoacidosis: is there hypokalemia?

ST depression: is it ischemia? No, hypokalemia.

And more cases, if you want, at this link.

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Comment by KEN GRAUER, MD (3/2/2019):

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The importance of this case lies in recognition of a number of findings, and the differential diagnoses that these findings should evoke. For ease of comparison — I’ve put the 2 tracings in this case together (Figure-1):

Figure-1: The 2 ECGs in this case (See text).

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As per Dr. Smith — the principal findings in ECG #1 are the following:

• Rate & Rhythm: Sinus rhythm at ~80-85/minute.
• Intervals: Normal PR and QRS interval duration — but a prolonged QTc.
• Axis: Slight left axis deviation of about -10 degrees (the QRS is slightly more negative than positive in lead aVF).
• Chamber Enlargement: Obvious LVH.
• Q-R-S-T Changes: Small Q waves (small considering respective QRS amplitude) in leads I, aVL and V6 — Early Transition in the chest leads (the R wave becomes taller than the S wave is deep already by lead V2) — and, diffuse ST-T wave depression.

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COMMENTS: My thoughts reinforce the important concepts emphasized by Dr. Smith — albeit with an approach from a slightly different perspective:

• Common things are common! This patient presented with what sounds like a typical sickle cell crisis for him. By dint of demographics and the natural history of patients suffering from sickle cell disease — LVH is exceedingly common. The increase in QRS amplitude that we see throughout ECG #1 is among the greatest voltage you’ll see in many weeks of work in a busy ED practice. QRS amplitude in most leads is either off the page, or overlaps with neighboring leads. For example — R wave amplitude in lead I is >25mm — >22mm in aVL (whereas ≥12mm qualifies as LVH) — and well over 25mm in each of leads V3, V4, V5 and V6. S wave depth in lead V1 is ~25mm.

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• For those wanting a user-friendly primer on ECG Diagnosis of LVH — Please CLICK HERE.

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• This tracing provides an excellent teaching example of how to assess R wave and S wave amplitudes when waveforms overlap in neighboring leads. For example — Focus on S wave depth in lead V1 of ECG #1. Then focus on R wave amplitude in lead V2. Note the COLOR within the area of amplitude overlap becomes DARKER. This allows us to appreciate that S wave depth in lead V1 is 5 large boxes ( = 25mm) — and R wave amplitude in lead V2 is over 4 large boxes ( ~22mm).
• The reason I advocate a Systematic Approach to ECG Interpretation (which I detail HERE) — is that unless one is systematic, it is all too easy to overlook the early transition in ECG #1 (The “R” in “Q-R-S-T Changes” serves to remind us to assess where transition occurs in the chest leads).
• The reason it IS relevant to assess the area of Transition in ECG #1 — is that transition occurred much later (ie, between leads V4-to-V5) in ECG #2. This suggests that there probably was a difference in lead placement between the 2 tracings — which is essential to appreciate when comparing one ECG with another (more on this below).
• In general — Sensitivity of the ECG for detecting LVH in adults is poor (typically no more than 55%, even by the most skillful of electrocardiographers). That said — Specificity of the ECG for detecting true chamber enlargement of LVH may exceed 95% when: i) the clinical situation is suggestive (ie, a middle-aged African American man with longstanding sickle cell disease); ii) when voltage criteria for LVH are met (almost impossible to do this more emphatically than in ECG #1); and, iii) when typical ST-T wave abnormalities suggestive of LV “Strain” are present in one or more lateral leads (the classic slow downslope-more rapid upslope ST-T wave appearance of LV “strain” is evident in all lateral leads here = I,aVL; V4,5,6).
• As per Dr. Smith — the finding of ST-T Wave Depression in the absence of QRS widening should prompt recall of a number of diagnostic entities. My LIST includes the following: i) LVH with “strain”; ii) Ischemia; iii) Digoxin use; iv) HypoKalemia and/or HypoMagnesemia; v) Tachycardia; and, vi) Any combination of i-thru-v. Often more than one entity is operative — as is likely in this case. Clinical correlation helps to sort this out.
• As per Dr. Smith — the QTc was clearly prolonged in ECG #1. I have found it helpful to consider another brief LIST of entities whenever you see QTc Prolongation: i) Drugs (many drugs and combinations of drugs may prolong the QT interval); ii) Electrolyte Disturbance (low K+/low Mg++/low Ca++); and/or, iii) any CNS Catastrophe (ie, stroke, seizure, coma, CNS bleed, trauma, tumor, etc. — may all cause profound QTc prolongation). Clinical correlation again helps greatly to sort this out.

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What are the Differences between ECG #1 and ECG #2?

As per Dr. Smith — the obvious difference between these 2 tracings is the marked increase in ST-T wave depression in ECG #1. What are the other differences?

• The heart rate was somewhat FASTER in the baseline tracing. This is important to note — because increased heart rate is a potential independent cause of increased ST depression. That said, the fact that the rate was slightly faster in the Baseline ECG (ie, ECG #2) means that this factor was not operative in this case.
• There was slightly more left axis deviation in ECG #2 (the S in lead aVF is relatively more negative in ECG #2 compared to ECG #1). Clinically, the slight axis shift in this case does not affect our overall impression. NOTE: Sometimes — a significant shift in axis between the 2 tracings you are comparing may make a huge difference in assessing whether or not there has been real interval change in ST-T wave deviations.
• The area of Transition occurred much later in the Baseline ECG ( = ECG #2) — in which the R wave does not become predominant until between leads V4-to-V5 (Transition occurred between leads V1-to-V2 in ECG #1).
• While definite criteria for LVH were clearly met in the Baseline ECG on this patient ( = ECG #2) — overall QRS amplitude was MUCH LESS on this baseline tracing!
• The QTc was not as prolonged in the Baseline ECG — and, terminal positivity of the ST-T wave is much less (just barely seen in leads V5, V6 of ECG #2).

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THOUGHTS Regarding Comparison of ECGs #1 and #2:

• At least from comparison of these 2 tracings — there has been marked increase in QRS amplitude since the Baseline tracing was done!
• NOTE: We do not know how long ago this baseline tracing was done! Clinically — it would be important to find out WHAT HAS HAPPENED in the interim between the time that ECG #2 and ECG #1 were done. Does this patient have hypertension and/or heart failure that has worsened? (This might be a common scenario given this patient’s demographics and his underlying disease).
• Increase in severity of LVH since the Baseline ECG may account for some of the increased ST-T wave depression that we now see in ECG #1. That said — the shape and amount of the ST-T wave changes in ECG #1 made me think it unlikely that this more severe LVH was the entire reason for the increased ST-T wave depression!
• Despite the likely difference in chest lead placement (which we surmised from the change in the zone of Transition between the 2 tracings) — lead placement also seemed unlikely to fully account for the marked increase in ST depression that we see in ECG #1.
• BOTTOM LINE: I was not certain about the diagnosis of electrolyte disturbance (low K+ and/or low Mg++) when I saw ECG #1. In my experience, I’ve seen U waves not only with low K+/low Mg++ — but also in patients with bradycardia, LVH, and sometimes in normal subjects. But what IS apparent, is that ECG #1 shows marked LVH + lots of ST-T wave depression + a long QTc in this acutely ill patient with sickle cell crisis — and, that evaluation for common causes of ST-T wave depression and QTc prolongation (as suggested on our LISTs in the commentary above) was in order. It was therefore no surprise that serum K+ came back at a low level.
• Finally — While impossible to rule out acute ischemia as a factor accounting for the increased ST-T wave depression in ECG #1 — an acute cardiac event would seem less likely given the clinical scenario of an acute sickle cell crisis in this patient with marked LVH and lab confirmation of hypokalemia. In any case — there is NO indication from ECG #1 for activation of the cath lab at this time. Instead, treatment of this patient’s acute condition (ie, with hydration, electrolyte replacement, pain control measures) takes 1st priority — after which the patient can be clinically reassessed, and the ECG repeated.

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FOR MORE:

• For “My Take” on use of the Systematic Approach to ECG Interpretation — CLICK HERE.
• For “My Take” on ECG Diagnosis of LVH — CLICK HERE.
• For “My Take” the LISTS for ST Depression & QT Prolongation — CLICK HERE.