Thursday, July 5, 2012

ECG Interpretation Review #47 (Normal Variants - Early Repolarization - Benign - ST Elevation - Pericarditis - ERP - STEMI)

The 12-lead ECG shown in Figure 1 was obtained from 50-year-old man with chest discomfort.
  • Is this ECG likely to reflect acute anterior STEMI?acute pericarditis? – or ERP (Early Repolarization Pattern) without acute process?

Figure 1 – 12-lead ECG from a 50-year-old man with chest discomfort.

INTERPRETATION: Using our systematic sequential approach (rate-rhythm-intervals-axis-hypertrophy-QRST changes) – We interpret the 12-lead ECG in Figure 1 as follows:
  • The QRS complex is narrow.
  • There is slight but definite variability in the R-R interval throughout the tracing. The rhythm is sinus arrhythmia.
  • All intervals (PR,QRS,QT) are normal; the axis is normal (approximately +70 degrees).
  • There is voltage for LVH (deepest S in V1,2 + tallest R in V5,6 35). No other sign of chamber enlargement.
  • Q-R-S-T Changes: There are small q waves in the inferior and lateral precordial leads.  R wave progression is normal (ie, transition occurs between leads V3-to-V4 ).  T waves are peaked.  There is some J-point ST segment elevation (with upward concavity = "smiley" configuration) in multiple leads - and there is shallow symmetric T wave inversion in lead aVL.
IMPRESSION: There is some baseline artifact (seen most in leads I, II, III, aVL . . . - albeit not enough to impede our interpretation). Sinus arrhythmia. Voltage for LVH. Shallow T wave inversion in lead aVL – plus – 1-2mm of J-point ST segment elevation with upward concavity in a number of leads … STOP! ...
  • Interpretation of the ECG in Figure 1 beyond the “STOP” depends greatly on the clinical setting.
  • IF this ECG was obtained from an otherwise healthy young adult without cardiac symptoms – we would interpret the isolated shallow T inversion in lead aVL as normal given the relatively vertical QRS axis and predominantly negative QRS complex in this lead (See Figure 2 below).
  • Similarly – We would interpret the slight (but real) upward concavity (“smiley”) precordial ST elevation as consistent with ERP (See Figure 3 below).

HOWEVER – The situation in this case is different – because the patient whose ECG is shown in Figure 1 is 50 years old and IS having chest discomfort ...
  • Consideration therefore HAS to be given to the possibility that the precordial lead ST elevation seen could represent an early stage of acute anterior STEMI (ST Elevation Myocardial Infarction) – especially given the T wave inversion in lead aVL.
NOTE: We complete our interpretation of this case (and the ECG in Figure 1) at the bottom of this Blog post. Before doing so – we address a number of key concepts relating to clinical assessment of anterior lead ST elevation.

Normal T Wave Inversion:
Five leads (III,aVF,aVL,aVR,V1) – may normally display moderate-to-large Q waves and/or T wave inversion in otherwise healthy adults. Thinking of a “reverse Z” (à la Zorro) may help recall which leads these are (Figure 2):
  • While we cannot rule out the possibility that the shallow T wave inversion in lead aVL of Figure 1 reflects ischemia – this T inversion is much more likely to be normal in this patient because: i) T wave inversion is isolated (it is only seen in lead aVL); ii) T inversion is shallow; iii) the QRS complex in aVL is predominantly negative in this patient with a relatively vertical QRS axis (conditions that predispose to the normal finding of some T inversion in aVL); and iv) no acute change is seen in other limb leads.

Figure 2 – Schematic tracing showing those leads that may normally manifest even large Q waves or deep T wave inversion (leads III,aVF,aVL,aVR,V1). Thinking of a “reverse Z” may facilitate recall.

ST Segment SHAPE:
The shape of ST elevation is more important than the amount of elevation (Figure 3). Acute MI may occur with only minimal ST elevation:
  • ST elevation with an upward concavity (ie, smiley configuration) is usually benign – especially when seen in an otherwise healthy, asymptomatic individual (especially when seen with notching or slurring of the J point in one or more leads). This ST segment variant is known as ERP (Early Repolarization Pattern).
  • In contrast – ST elevation with coving or a downward convexity (frowny ) – is much more likely to be due to acute injury (from ischemia/MI).
  • KEY POINT: History is ever important. Although ST elevation with a “smiley” configuration and J-point notching often reflects a normal variant – this is only true IF the patient is asymptomatic. An identical ST-T wave pattern from a patient with chest pain must be assumed acute until proven otherwise.
  • IF in doubt – Admit the patient! Look at old tracings to compare. Repeat the ECG.

Figure 3 – Schematic showing upward concavity (smiley ) ST elevation that is usually benign – especially when J-point notching is seen in one or more leads. In contrast – ST segment coving (frowny ) – is much more likely to be due to acute injury/infarction.

Are ST Segments Truly Elevated in Figure 1? 
ST segment elevation in Figure 1 is subtle but real (Figure 4):
  • We judge ST segment deviations with respect to the PR segment baseline. In Figure 4 – the blowup of leads V1,V2 shows the J-point to be clearly elevated above the PR segment baseline. We estimate 1-2mm of upward concavity ST elevation in lead V2 (although we admit that subtle rounding of the J-point area in this lead makes precise determination of the amount of ST elevation difficult).

Figure 4 – Second look at the ECG shown in Figure 1 from this 50 year-old man with chest discomfort. Blowup of leads V1,V2 illustrates subtle but real upward concavity ST elevation above the PR segment baseline (See text).

Putting It All Together:
As stated earlier – the ECG in Figure 1 shows sinus arrhythmia; voltage for LVH; shallow T wave inversion in lead aVLplus – 1-2mm of J-point ST segment elevation with upward concavity in a number of leads … Our impression is probable ERP (and not anterior STEMI or pericarditis) because:
  • ST elevation manifests and upward concavity (“smiley” ) configuration (albeit no J-point notching is seen).
  • ST elevation is seen (at least in small amount) in all precordial leads. IF acute anterior STEMI was evolving – one would expect additional ST-T wave abnormality elsewhere on this tracing given the extent of ST elevation.
  • The shallow T wave inversion in lead aVL is isolated and probably normal given the patient’s relatively vertical QRS axis and predominantly negative QRS in lead aVL.
  • The q waves seen on this tracing are small and narrow. They most probably are normal septal q waves (which are typically seen in lateral leads and sometimes also in inferior leads in patients with a vertical axis).
  • The ECG picture in Figure 1 is not suggestive of acute pericarditis (it lacks sinus tachycardia; ST elevation is absent in the limb leads; there is no PR depression).

We conclude our interpretation of the ECG in Figure 1 with the statement: Urge clinical correlation. The point to emphasize is that although we would be relatively comfortable that the ECG shown in Figure 1 is unlikely to represent early acute anterior STEMI – We can not rule out this possibility on the basis of this single tracing! How to proceed with only a ~90% comfort level that the ECG in Figure 1 is benign would depend:
  • IF this patient presented to the office with a history of chest discomfort that was relatively unconvincing for ischemic pain – we would probably manage the case on an ambulatory basis. We would be that much more inclined to do so IF history and physical exam suggested a non-cardiac cause (peptic ulcer disease; musculoskeletal chest pain, etc.).
  • Access to a prior ECG on this patient might prove invaluable (especially if it confirmed baseline anterior ST elevation and T wave inversion in aVL of similar nature to that seen in Figure 1).
  • On the other hand – IF this 50-year-old man presented to the ED (Emergency Department) with new-onset chest discomfort (and no prior tracing available) – he would almost certainly be admitted to the hospital. One simply can’t rule out the possibility of early anterior STEMI on the basis of this single tracing… (In our experience – such patients with new-onset chest discomfort are not sent home from the ED).

Should the Cath Lab Be Activated?
Taking the 2nd scenario presented above (ie, that this 50-year-old man presented to the ED with the ECG in Figure 1 and a history of new-onset chest discomfort) – the question arises as to whether the cath lab should be activated for possible acute reperfusion on the basis of this tracing? IF Figure 1 in fact represents an early stage of anterior STEMI – then prompt reperfusion becomes a critical determinant of optimal prognosis.
  • At what point to activate the cath lab is difficult to say from the comfort of our home computer as we view this tracing …. Sometimes – “Ya just gotta be there …”. That said – We most probably would not activate the cath lab on the basis of what we see in Figure 1.
  • Access to a prior ECG on this patient might be revealing (if a prior tracing can be found…).
  • Repeating the ECG in short order may establish the diagnosis. With acute evolving infarction – significant change may be evident on ECG in as little as 20-to-30 minutes.
  • Obtaining an Echo at the bedside in the ED while the patient is having chest discomfort may provide invaluable assistance in determining the likelihood of an acute event. If an anterior wall motion abnormality is seen during symptoms — this becomes highly suggestive of an acute event. On the other hand, if during chest discomfort the Echo is entirely normal — this makes an acute event much less likely. (NOTE: We emphasize 2 points regarding ED use of Echo for this purpose: i) these Echos may be challenging to read, so expertise is needed to KNOW whether wall motion abnormality is or is not present; and ii) an Echo is only helpful IF obtained during chest discomfort. If chest discomfort has resolved and the Echo is normal — unfortunately nothing can be ruled out!)
  • STAT troponin values may confirm acute infarction (though even high-sensitivity troponins would not rule this possibility out if they were normal).
  • IF still in doubt after reexamining the patient and the above series of steps – Consider consulting the Cardiologist-On-Call to assist in the decision-making process. There are times when acute cath may be performed even without definitive diagnosis – although in this case, careful observation with close serial follow-up will almost certainly tell the tale over the next few hours. But at least the cardiologist is aware in the event a surprise occurs and the ECG evolves ...

FINAL Thoughts: Is there Help in the Literature?
Smith et al have developed a multivariate equation to assist in acute evaluation of the patient with anterior ST elevation (Ann Emerg Med 60:45, 2012). Findings from their retrospective analysis of a large data set are insightful in this case – and further support our suspicion that the ECG in Figure 1 is most probably benign. These include relatively taller R wave amplitude and a QT interval that is not prolonged in Figure 1. That said – overlap exists in the parameters used in the calculated Smith equation, such that we are still left with being unable to exclude an acute process on the basis of the number score reported.  – END OF CASE 

Please click on the icon below for a pdf Link to Section 09.0 (from our ECG-2014-ePub) on assessment of ST-T waves. The part on Early Repolarization begins in Section 09.14 in this pdf:



  1. Always admire those putting their teachings selflessly on the web in the name of education. Great article great lessons for me about aVL

    1. Thanks so much Patrick for your kind words — My pleasure!

  2. Your blog is a valuable source of learning. Your passion for sharing and teaching is much appreciated. Thank you.

    The Smith et al 2012 paper your referenced is a wonderful addition to the ECG literature, but it should be noted that the rule should not be applied in the setting of LVH (as evident in this case). The author specifically advises and warns against using the rule in this patient population with large anterior voltages because of the incidence of false positives.

    Of note, Smith and colleagues published this year ( a derivation (not validated yet) of a 4 factor rule to help differentiate Normal Variant STE from subtle Anterior STEMI that has slightly improved accuracy.

    1. @ Dr. K. Theakston = PART 1 (Answer) — THANK YOU for your comment. I will address it in some detail. I’ll begin by noting that I posted this ECG Blog over 5 years ago! (in 2012)! Next, I’ll emphasize that I have the highest respect and admiration for the superb work of Dr. Stephen Smith — who I feel is the BEST Emergency Medicine ECG Researcher anywhere! The cases he continually posts on his ECG Blog are amazing and highly insightful with the most wonderful clinical correlation. That said, my approach, opinion and interpretations are not always identical to his. I believe this is a GOOD thing — since over the course of the past 7 years, Dr. Smith and I have corresponded a few hundred times — and I believe we each continue to learn from each other. I have participated in a large ECG interpretation study with Dr. Smith (he was chief investigator) — and I’ll emphasize that having the computer automatically generate a score on Dr. Smith’s scale WAS indeed helpful to me in reassuring (and expediting) my ECG interpretations of patients with questionable anterior lead ST-T wave findings in association with chest pain. That said, I do have concerns about his 3 and 4-factor rules. I feel they CAN be helpful as a guide, especially for clinicians who have interpreted many fewer tracings than I have over the past 45+ years since I began reading ECGs. But my concern is about an overdependence on numerically derived scales, that by definition are retrospectively derived (even though they have been “validated”). Many clinicians forget the details (ie, that the scales have not been validated when there is LVH — or that they don’t hold true when an obvious acute stemi is present). My other concern is that I’ve observed far too many clinicians who become “fixed” on a number, and as a result fail to assess the actual 12-lead ECG as carefully as they should. I’m concerned about the patient who starts with early repolarization, and develops an acute stemi on top of that … At what point during the process do the scales change from a “normal value” to a value of concern? And I’m concerned about the fact that the scales are less than 100% sensitive and 100% specific — which means that they are not infallible.

    2. PART 2 (Answer): — I just think ( = MY Opinion) — that while the scales most definitely CAN be helpful if used appropriately in the right setting (!) — that nothing substitutes for “Being There” and exercising good clinical judgement and close clinical correlation. So, if you go back to my FINAL Thought in the above Blog post — I was not advocating calculation of a number score in this case — but rather extrapolating 2 clinical findings that I have found VERY HELPFUL in my qualitative (rather than “quantitative number score”) assessment of these problematic acute tracings, namely: i) The finding of preserved R wave progression (especially when R waves tend to be relatively tall in V3,V4) — IS helpful at times in reducing (not eliminating) the likelihood of acute anterior stemi; and ii) The finding of a normal, if not tending toward shorter-than-usual QTc — IS also helpful at times in reducing the likelihood of acute anterior stemi. BOTH of these factors are present here (ie, R wave amplitude is already 10 mm in lead V2 — and I estimate the QTc at under 400msec in Figure-1 above)! Again, NO signal factor is by itself “diagnostic” — but by taking the complete clinical picture into account and “being there” — I believe the right clinical decisions can almost always be made. And, in those cases when doubt still exists — Call the Cardiologist who is On Call. Sometimes, a cath may need to be done in order to attain the required amount of certainty in diagnosis. P.S. As I indicated in my write-up above — there is “voltage” for LVH in Figure-1 — but in the absence of strain, this finding in a 50yo man lacks specificity. In fact, if one took all comers — more such patients (with only voltage criteria) would not have true chamber enlargement than would, given the lack of ST-T wave repolarization abnormalities of “strain”. So, are the 3- and 4-factor formulas truly invalid in such cases? The answer to me personally is less important in this particular 50yo man — because I believe other factors AND the entire clinical picture are far more important in the decision-making process here. THANKS again for your astute question! I hope I have addressed your concerns — :)