Category Archives: electrocardiography

Subtle ECG Findings in ACS: Part III Benign Early Repolarization vs. Anterior STEMI

Author: Jamie Santistevan, MD (@jamie_rae_EMDoc, Senior EM Resident Physician, University of Wisconsin) // Edited by: Alex Koyfman, MD (EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital, @EMHighAK) & Justin Bright, MD (EM Attending, Henry Ford Hospital, @JBright2021)


Look at these two snakes: One is a deadly coral snake, the other a friendly harmless mimic. I learned to tell them apart in the 5th grade using this rhyme: “Red next to black, you’re alright Jack. Red next to yellow, you’re a dead fellow.”


You may be wondering what reptiles have to do with ECGs. Well, welcome to the third blog post in a series on subtle ECG findings in ACS. This post about mimics: benign early repolarization (BER) and the anterior STEMI. Each of these can mimic the other. The problem is that one of these diagnoses is deadly and the other is a normal variant. Today I am going to discuss the key differences between benign ST-segment elevation, also known as J-point elevation or benign early repolarization (BER), and the subtle ST-segment elevation seen occasionally in acute LAD occlusion.

In the previous post concerning hyperacute T-waves, I said that the STEMI criteria are poorly sensitive for diagnosing vessel occlusion.  This means that some patients with acute coronary occlusion may not meet criteria for STEMI.  In fact, about one quarter of NSTEMI patients have complete vessel occlusion on angiogram [1]. Wang and colleagues studied 1,957 NSTEMI patients and compared baseline characteristics, ECG findings, and long term outcomes, between patients with and without occluded arteries. The group of researchers found that 27% had an occluded culprit artery and those patients had larger infarcts and higher six-month mortality compared to NSTEMI patients without an occluded artery [1].

Remember, the STEMI criteria are arbitrary, based solely on the size (in millimeters) of ST-segment elevation and are only guidelines for reperfusion therapy. We typically use the term “STEMI” to mean complete coronary artery occlusion. “NSTEMI” traditionally means that the patient has had an MI (elevated troponin), but without complete coronary artery occlusion. However, as Wang and colleagues data shows us, some patients have an occluded vessel but do not develop diagnostic ST-segment elevation. These patients, therefore, have a “STEMI-equivalent”, or may be described as having a “subtle-STEMI”.

The subtle STEMI, as defined by 0.1-1mm of ST-segment elevation, occurs in about 18% of patients with an occluded coronary artery [2]. These patients have smaller infarcts compared to patients with obvious STEMI, however subtle STEMI patients are more likely to experience greater delays to reperfusion [2, 3]. Interestingly, subtle STEMI patients do not have better outcomes than those with obvious STEMI [2].  Marti and colleagues studied 504 patients who were taken to the cardiac cath lab for suspected coronary artery occlusion. Patients with subtle and obvious ST-elevation MI had similar rates of pre-interventional TIMI flow of 0/1 (86% of the patients in the subtle STE group and in 87% of the patients in the marked STE group).  Among patients with coronary artery occlusion, 18.3% did not have any lead with at least 1 full millimeter of ST-segment elevation. Subtle STEMI patients were more likely to have multi-vessel disease and experienced greater delays to reperfusion.  Comparing the subtle-STEMI patients to those with obvious STEMI, the authors found that the rate of reinfarction or death were similar between the two groups (10.0% vs 12.6%, P = .467) [2].

Therefore, recognizing the subtle findings of coronary artery occlusion and taking the next steps to rapidly evaluate for ACS may allow us to recognize these subtle-STEMI patients early and provide timely revascularization. Anterior MI carries the worst prognosis compared to other anatomic areas; it has the highest mortality and rates of complications [4,5]. Early anterior MI can have less than 1mm of ST-segment elevation and can mimic benign early repolarization. So today I will discuss the findings that differentiate BER and LAD occlusion by exploring 5 different ECG features.

Benign early repolarization

The ST segment represents the period between ventricular depolarization and repolarization. In a normal ECG the ST-segment is isoelectric, meaning neither elevated nor depressed relative to the TP-segment [6]. Benign early repolarization is the most common normal ECG variant. It has been reported in both men and women of all age groups and various ethnicities [6] and occurs in about 1% of the population [7] with higher occurrence in black males 20-40 years old [8].

ECG characteristics that are more likely to be seen in BER include:

  1. ST elevation at the J-point with upward concavity
  2. Notching of the J-point
  3. Diffuse ST elevation (typically highest in V3-4)
  4. Concordant, prominent T-waves with large amplitudes
  5. Normal R-wave progression
  6. Relative stability from one ECG to the next

Here is a classic example of benign early repolarization:


The ST-segment elevation is most pronounced in V2-4. There is upsloping ST elevation. The T-waves are asymmetric: they have a concave upslope and a steep downslope. There is good R-wave progression across the precordium with a very tall R-wave in V4. Also, notice the absence of certain features: there is no ST-segment depression and there are no anterior Q-waves.

Acute LAD occlusion will also manifest as anterior ST-segment elevation, often maximal in V2-3. So how does anterior MI differ from BER? To answer this question we are going to discuss 5 ECG features:

  1. ST-segment morphology
  2. Reciprocal changes
  3. Poor R-wave progression
  4. Anterior Q-waves
  5. Terminal QRS distortion

ST segment morphology

It is often taught that up-sloping ST segments are benign. However, you should not rely on ST-segment morphology alone to rule out ACS. While convex (“tombstone”) ST-segment elevation is highly specific for AMI [9], it is less common than either straight or upsloping (concave) elevation in acute anterior MI [2, 10]. Straight ST-segment elevation is the most common ST morphology in anterior MI [11]. However, in one retrospective review of patients with LAD occlusion on angiogram, 43% (16/37) had concave morphology [9].

Reciprocal changes

Reciprocal change is ST-segment depression in the leads opposite of the ST-elevation. Occasionally reciprocal ST-segment depression is the first (and rarely, the only) ECG findings in AMI. It is important to look specifically for ST-segment depression because it may be subtle. The absence of ST depression does not rule out AMI, but its presence does make the ST-elevation more specific for coronary artery occlusion [4, 12].  And, the presence of ST depression correlates with a larger infarct area at risk and higher mortality, independent of ST elevation [13].

Reciprocal ST depression can occur in either anterior or lateral MI. An anterior MI will manifest ST-segment depression in the inferior leads when there is a more proximal LAD occlusion (the first diagonal branch is occluded) [4, 14]. If you see ST-depression leads II, III, or aVF, you should carefully scrutinize the ECG for subtle anterior (V1-4) or high lateral (I, aVL) ST-segment elevation or hyperacute T-waves. The bottom line is that in the presence of reciprocal ST-segment depression in the inferior leads, you should be very cautious about diagnosing benign early repolarization.

Poor R-wave progression

Normally, the height of the R-wave increases gradually across the precordial leads to the point where the R-wave is bigger than the S-wave at V3 or V4 and eventually there is only a very small S-wave remaining in V6. One commonly accepted definition of poor R-wave progression is R-wave height ≤ 3 mm in V3. Causes of poor R-wave progression include left ventricular hypertrophy (LVH), inaccurate lead placement, old anterior infarct and acute anterior MI. Remember that BER should always have good R-wave progression.

Here is normal R-wave progression in BER:



Here is a patient who has poor R-wave progression secondary to old anterior infarct:


Notice there are QS-waves in V1-3 and only a very small R-wave in V4.


Pathologic Q-waves result from the absence of electrical myocardial activity secondary to ischemic cell death. The infarcted area of myocardium does not conduct electricity, so the deflection on the ECG paper is negative (downward). Q-waves are classically taught to develop in MI after several hours to days [10]. However, Q-waves can form early in acute MI, as early as less than 1 hour [4, 15].

Pathologic Q-waves in the anterior leads are defined as Q-waves in leads V2–V3 ≥ 20ms [16]. A general rule of thumb is that in acute MI the most common type of Q-wave is a QR-wave. QS-waves may develop later in anterior MI, so they may be suggestive of a subacute presentation, or they can be there from a previous MI. However, when anterior QS-wave are paired with very large, wide and towering T-wave (hyperacute T-waves), this may be a sign of acute LAD occlusion [17].

Here are QR-waves accompanied by ST-segment elevation:


Contrast that to these QS-waves paired with a hyperacute T-wave:

This image originally appeared at:

In summary, in the presence of anterior Q-waves, anterior ST-segment elevation cannot be considered benign early repolarization. The ST segment elevation may be due to:

  • Acute anterior MI
  • Subacute anterior MI
  • Old anterior infarct with persistent ST-segment elevation (possibly due to LV aneurysm formation)

This is an example of a patient with LAD occlusion who’s ECG demonstrates all 4 ECG criteria discussed here:

This ECG originally appeared at:

This ECG shows upsloping anterior ST-segment elevation. Although this may be confused for normal variant ST-elevation, there are four concerning features make this ECG diagnostic for LAD occlusion. There is a QS-wave in V1-V2 paired with hyperacute anterior T-waves. There is reciprocal ST-segment depression in lead III and poor R wave progression across the precordium.

Dr. Smith’s ECG formula

I would like to make special mention of a mathematical formula developed specifically to differentiate BER and acute LAD occlusion [18]. Smith and colleagues conducted a retrospective study comparing patients with subtle anterior STEMI to those with proven early repolarization. They found that several ECG measurements were independently predictive of STEMI versus BER:

  • Greater height of ST-segment elevation (measured at 60ms after the J point)
  • Longer QTc interval
  • Lower R-wave amplitude
  • Higher T-wave/R-wave amplitude ratio in leads V2-V4

Using logistic regression, they derived and validated an ECG-based formula using the first three measurements as follows:

[1.196 x ST-segment elevation 60 ms after the J point in lead V3 in mm]+[0.059 x QTc in ms]-[0.326 x R-wave amplitude in lead V4 in mm]

A value of >23.4 was found to predict STEMI, and </= 23.4 predicted early repolarization with an overall sensitivity and specificity of 86%, 91% respectively [18]. A calculator for this formula and further explanation can be found at

Before applying the formula there are some things you must consider:

The equation only applies when trying to distinguish between subtle LAD occlusion and early repolarization. The rule does not apply if there is left ventricular hypertrophy (LVH). Most importantly, if there are other findings on the ECG that support the diagnosis of LAD occlusion such as inferior ST depression, ST-segment convexity, terminal QRS distortion, or Q-waves, then the equation does NOT apply because these kinds of cases were excluded from the study as representing an obvious STEMI.

Terminal QRS distortion

Terminal QRS distortion is defined as emergence of the J point ≥50% of the R wave in leads with QR-wave, or disappearance of the S wave in leads with an RS-wave. [19] In acute MI, terminal QRS distortion predicts greater size of infarct and higher mortality [20].

Here are two examples of terminal QRS distortion:


This is the more obvious, with emergence of the J point ≥50% of the R wave in leads with QR-wave

This ECG first appeared at: LITFL

This is more subtle terminal QRS distortion. Notice how the S-wave does not extend below the isoelectric line.


As always, it is important to correlate the ECG findings with the clinical picture. You should be incredibly cautious diagnosing BER in a patient over 55 years old, or anyone with concerning symptoms or history. If the ECG is subtle and you are concerned about ACS, get serial ECGs (every 15 minutes) and use adjunctive information such as comparison to an old ECG or obtain echocardiogram. Remember that ACS is a dynamic process and can present subtly. The ECG is a cheap, noninvasive and fast tool, which can provide valuable diagnostic and prognostic information. Missing subtle presentation of ACS can have dire consequences for our patients who may be inappropriately discharged or experience significant delays to reperfusion. As emergency physicians, it is our job to own the ECG and we should strive for mastery to recognize even the subtlest cases.


  • Anterior STEMI can be subtle and present with less than 1mm ST-segment elevation anteriorly and can mimic benign early repolarization.
  • Do not rely on ST-segment morphology alone to rule out AMI because about 40% of patients with anterior MI have upsloping (concave) ST-segment elevation.
  • Be very cautious about diagnosing BER when there is poor R-wave progression, anterior Q-waves, inferior ST depression, or terminal QRS-distortion.
  • Be cautious diagnosing BER in patients older than 55 years old or anyone with concerning symptoms.
  • When concerned for subtle STEMI, use adjunctive information such as serial ECGs, comparison to prior ECGs, and/or echocardiogram.


References / Further Reading

  1. Wang TY et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. Apr 2009;157(4):716-23.
  2. Martí D et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction. Am Heart J. Dec 2014;168(6):884-90.
  3. Sharkey SW et al. Impact of the electrocardiogram on the delivery of thrombolytic therapy for acute myocardial infarction. Am J Cardiol. Mar 1994;15;73(8):550-3.
  4. Smith SW. The ECG in Acute MI: An evidence-based manual of reperfusion therapy. Lippincott Williams & Wilkins 2002.
  5. Lee KL et al. Predictors of 30-day mortality in the era of reperfusion for acute myocardial infarction. Results from an international trial of 41,021 patients. GUSTO-I Investigators. Circulation. 1995 Mar;91(6):1659-68.
  6. Somers, MP et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002 May;20(3):243-51.
  7. Mehta MC, Jain AC: Early repolarization on scalar electrocardiogram. Am J Med Sci 1995;309:305-311
  8. Thomas J, Harris E, Lassiter G: Observations on the T wave and S-T segment changes in the precordial electrocardiogram of 320 young Negro adults. Am J Cardiol 1960;5:368-374
  9. Smith SW. Upwardly concave ST segment morphology is common in acute left anterior descending coronary occlusion. J Emerg Med. Jul 2006;31(1):69-77
  10. Nable, JV and Brady, W. The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction. Am J Emerg Med. 2009 Jul;27(6):734-46.
  11. Kosuge et al. Value of ST-segment elevation pattern in predicting infarct size and left ventricular function at discharge in patients with reperfused acute anterior myocardial infarction. Am Heart J. 1999 Mar;137(3):522-7.
  12. Brady WJ et al. Reciprocal ST segment depression: impact on the electrocardiographic diagnosis of ST segment elevation acute myocardial infarction. Am J Emerg Med. 2002 Jan;20(1):35-8.
  13. Willems JL et al. Circulation. Significance of initial ST segment elevation and depression for the management of thrombolytic therapy in acute myocardial infarction. European Cooperative Study Group for Recombinant Tissue-Type Plasminogen Activator. 1990 Oct;82(4):1147-58.
  14. Engelen DJ et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999 Aug;34(2):389-95.
  15. Raitt, MH, et al. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol. 1995 Apr;25(5):1084-8.
  16. Pathologic Q waves. ECGPedia. Web. 12 Dec 2015.
  17. Left ventricular Aneurysm Morphology Distorted by Right Bundle Branch Block, Mimicking Acute STEMI with RBBB.
  18. Smith S et al. Electrocardiographic differentiation of early repolarization from subtle anterior ST-segment elevation myocardial infarction. Ann Emerg Med. Jul 2012;60(1):45-56
  19. Birnbaum Y, et al. Distortion of the terminal portion of the QRS on the admission electrocardiogram in acute myocardial infarction and correlation with infarct size and long-term prognosis (Thrombolysis in Myocardial Infarction 4 Trial).Am J Cardiol. 1996 Aug 15;78(4):396-403.
  20. Mulay DV, Mukhedkar SM. Prognostic significance of the distortion of terminal portion of QRS complex on admission electrocardiogram in ST segment elevation myocardial infarction. Indian Heart J. 2013 Dec;65(6):671-7.
  21. Flickr photo. Web. 12. Dec 2015.
  22. “Anterior Myocardial Infarction”. Life in the Fast Lane Medical Blog. Web. 12 Dec 2015.
  23. ”Conclusin to snapshot case: 44 year old male-chest tightness”. EMS 12 Lead Blog, 2014. Web. 12 Dec 2015.

Subtle ECG findings in ACS: Part II Hyperacute T-Waves

Author: Jamie Santistevan MD (@jamie_rae_EMDoc, EM Resident Physician, University of Wisconsin) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) & Justin Bright, MD (EM Attending Physician, Henry Ford Hospital, @JBright2021)


What if you could identify a patient with complete coronary vessel occlusion almost immediately after it occurs, before the ST segments begin to elevate? What if you could pick up the very subtle, early MI? We know that early recognition and intervention improves outcomes in patients with coronary artery occlusion. Sometimes patients presenting with ACS are obvious. Sometimes it seems that the patient has read the textbook. However, more often than not, patients are not obvious, especially in the early stages of ACS. That is why we are concerning ourselves with subtlety.

Welcome to Part II of a three-part series on subtle ECG findings in ACS. Last time we reviewed the ECG findings associated with left main coronary artery disease, where we discussed the meaning of ST elevation in lead aVR. Now we are going to turn our attention to the T-waves.

The T-wave represents the period of ventricular repolarization on the ECG. The normal T-wave appearance varies based on lead placement, age, and sex. In general, T-waves are tallest in leads II and V4 and will decrease in size with age. A normal T-wave usually has amplitude of less than 5mm in the precordial leads and less than 10mm in the limb leads [1]. The normal shape of a T-wave is asymmetric, with a slow upstroke and a rapid down stroke. Normal T-waves are always upright except in leads aVR and V1 and have a normal QT interval (QTc of 350-440ms in men or 350-460ms in women). Additionally, the R-wave amplitude should progress normally across the precordial leads.

In this post, we are going to review 4 causes of abnormal T-waves:

  1. Hyperacute T-waves in AMI
  2. The de Winter T-wave pattern
  3. Pseudonormalization of T-waves
  4. Hyperkalemia

Hyperacute T-waves

Immediately after coronary artery occlusion, the ECG undergoes predictable temporal changes. Classically, coronary vessel occlusion leads to elevation of the ST-segments (producing STEMI). However, the earliest findings on an ECG are subtle changes in the T-wave shape and size. When a coronary artery is occluded, within the first 30 minutes, the T-wave amplitude increases [2]. The next changes are ST-segment elevation and loss of the R-wave amplitude.  If the vessel remains occluded, Q-waves develop. Without intervention, the ECG will then begin to exhibit T-wave inversions and eventually, the ST-segments will normalize [3]. Persistent ST-segment elevation suggests aneurysm formation.

This image originally appeared at


Early in the course of AMI, biochemical markers may not be elevated, although this may be changing in the era of highly sensitive troponin assays. Regardless, the development of T-wave changes is the first sign that we can see on the ECG and the ECG is fast, cheap, noninvasive, and readily available in the ED. In the early stages of MI, prior to the development of necrosis, the myocardium is suffering from ischemia. Timely revascularization may actually prevent complete infarction and death of the affected portion of the myocardium. Therefore, recognizing ACS early is beneficial because patients have improved outcome the timelier revascularization occurs [3], and delay to reperfusion causes larger infarction size and worse functional outcomes [4].

It is well known that new ST-segment elevation represents complete vessel occlusion and transmural infarct. However, the STEMI criteria have limited sensitivity in diagnosing coronary artery occlusion [5, 6, 7]. This means that some patients ultimately diagnosed with NSTEMI will also have complete coronary artery occlusion.

Below are the AHA criteria that define STEMI [7]:


Of course, it is important to recognize an obvious STEMI, but patients may present initially with only subtle ECG changes and minimal ST-segment elevation they may not meet the official criteria. These “subtle STEMI” patients have higher rates of inappropriate ED discharge and significant delays to reperfusion [8, 9, 10]. It is true that more ST elevation indicates a larger area of infarcted myocardium, however patients with subtle ST elevation MI experience similar functional outcomes and mortality rates as those with obvious STEMI [10]. Furthermore, approximately 25% of patients who do not meet the STEMI criteria, and are diagnosed with NSTEMI, have a completely occluded artery on angiography [11]. Some experts would argue that patients with subtle findings of coronary vessel occlusion should be treated as expeditiously as patients with obvious STEMI [10].

 The T-wave is often the first deflection on the ECG to change in acute vessel occlusion. Initial changes to the T-wave are straightening of the ST-segment and enlargement of the T-wave height and width.  The T-wave becomes disproportionately large when compared to the QRS. The prominent T-waves seen early in coronary vessel occlusion are called hyperacute T-waves. They were first described in 1947 as an early marker of coronary artery occlusion [2].

Hyperacute T-waves are often bulky, and wide at the base and are localized to an anatomic area of infarct. The widening of the T-wave may also lengthen the QT interval. It must be emphasized that hyperacute T-waves are not necessarily always tall, they may only be relatively large when compared to the R-wave. This means that even a small T-wave can still be hyperacute if paired with a low-voltage QRS. It is important to note that there is no acceptable universal definition of hyperacute T-waves, but there can be other clues on the ECG. During the development of hyperacute T-waves, there can be associated ST-segment depression in the reciprocal leads.

Here is an example of an ECG with hyperacute T-waves localized to the anterior region:

This ECG originally appeared at

Do not be distracted by the first-degree AV block or by the PVCs. This ECG shows very prominent, broad-based T-waves in the anterior leads (V2-6). Notice also the loss of R-wave height throughout the precordium and the how the T-waves are massive in comparison to the QRS complexes. This ECG is concerning for LAD occlusion.

 The patient underwent repeat ECG 40 minutes later, which showed obvious anterior ST elevation:

This ECG originally appeared at

Now there is obvious ST elevation in the anterior leads (V2 and V3), as well as ST elevation in the lateral leads (I, aVL, V5 and V6) with reciprocal depression in lead III. Also, the Q-waves are deepening in the leads V2 and V3.

Here is another example of hyperacute T-waves, this time in the inferior leads. This is the ECG of a 75 year-old woman presenting with chest pain:


Notice the large T waves in the inferior leads. The total height of the T-waves is not all that impressive, but when compared to the QRS complexes, especially in aVF, the T-wave is massive. The ST-segments are straighter than normal and there is subtle ST elevation in lead III, aVF, V5-V6. Notice the subtle reciprocal ST depression and T-wave inversion in aVL. The machine read this ECG as Early Repolarization. Her Troponin I came back slightly elevated (0.07 ng/mL). She was found to have complete occlusion of the RCA on angiogram and was diagnosed with “NSTEMI”.

De Winter T-waves

An interesting variant of hyperacute T-waves are those paired with J-point depression. This causes a T-wave takeoff point that is below the isoelectric line. This “depressed T-wave takeoff” pattern was first described in 2009 by Verouden and colleagues and was found to represent complete LAD occlusion (a STEMI-equivalent) [15]. This pattern of up sloping ST-segment depression paired with a tall, prominent T-wave is present in about 2% of patients with LAD occlusion [15]. It was initially postulated that these findings are not dynamic, but rather that they remain static throughout coronary vessel occlusion until the time of reperfusion [15, 16]. However, some experts have documented de Winter T-waves developing during anterior STEMI and would argue that these findings may represent subtotal occlusion of the LAD. Regardless, these patients require immediate reperfusion.

This ECG initially appeared at:

Notice the up sloping ST depression seen in leads V2-V6 followed by very tall and symmetric T-waves. Notice also the subtle reciprocal depression in the inferior leads (II, III, and aVF).

For an interesting case of the de Winter T-wave pattern occurring in a patient who initially presented with an obvious anterior STEMI, read this case on Dr. Smith’s ECG blog:


Another interesting phenomenon of the T-waves is the pseudonormalization in AMI. This occurs when a patient with baseline T-wave inversions presents with acute coronary occlusion. Hyperacute T-waves in these patients manifest as upright T-waves, which may be confused for a normal ECG. This finding highlights the fact that it is not solely the height, but rather the increase in positive amplitude, that signifies a hyperacute T-wave [2]. The other scenario for pseudonormalization is a patient who presents with re-occlusion of a recently reperfused artery, also known as Wellens’ Syndrome.

Here is the classic appearance of Wellens’ syndrome, type A (left) and type B (right):


These images originally appeared at:

It is important to note that this pattern appears when the patient is asymptomatic because this represents a reperfusion pattern on ECG. Type A, the biphasic T-waves, are seen immediately upon reperfusion. As the artery remains open, the T-waves evolve to be more deeply inverted, a Type B pattern. When the patient becomes symptomatic it is because the vessel re-occludes. When that happens the T-waves become upright (pseudonormalization) and if it remains occluded, ST-segment elevation will appear. These lesions are unstable because the vessel can re-occlude at any time and the patient requires revascularization.


Perhaps the most well known cause of prominent T-waves is the peaked T-waves seen with hyperkalemia, and they can be confused with the hyperacute T-waves of ACS. There is no exact correlation between serum potassium and onset of ECG changes but about 80% of patients begin to exhibit ECG changes at 6.8-7.0mEq/L. The typical progression of ECG changes in hyperkalemia is first the development of peaked T-waves, followed by decreased P-wave amplitude, widening of the QRS complex and finally development of a sine wave. But, as we know, hyperkalemia can cause a myriad of ECG changes including AV and bundle branch blocks, bradycardias, and even a STEMI mimic. Here are the typical changes with hyperkalemia.

This image originally appeared at

Although the T-waves of early hyperkalemia are very tall and prominent, the key differentiator from hyperacute T-waves is the shape of the T-wave.  Hyperacute T-waves are fat and wide with a more blunted peak. The T-waves of hyperkalemia are very pointy, peaked or “tented” with a narrow base, they have sharp apex and tend to be extraordinarily symmetric [1].

Here is the ECG of a patient with a history of type I diabetes who presented with nausea and vomiting. EMS reported that the patient was in sinus tachycardia with a rate of 300.

ECG Courtesy of Dr. Morgan Wilbanks, University of Wisconsin.

Notice the very tall, pointy T waves, which have a narrow base and are extremely symmetric. This patient was found to be in severe DKA, with a pH of 7.17 and a potassium of 7.1 mmol/L. The tall T-waves were likely being mistaken for QRS complexes and cardiac monitor misread the rate to be 300, when in fact it is about 150.


The earliest changes on an ECG after acute vessel occlusion are hyperacute T-waves and patients with coronary vessel occlusion can present with only subtle ECG changes. The ECG is an important tool, but should not always be used in isolation (unless clearly diagnostic). The clinical picture and adjunctive information should always be considered. If suspicious for vessel occlusion by the appearance of the ECG, it is important to look carefully for reciprocal changes and get serial ECGs every 15 minutes (not in an hour or two) and look for evolving changes because ACS is a dynamic process. Other adjuncts that may help diagnose ACS in patients with subtle ECG changes include continuous ST-segment monitoring, echocardiogram to evaluate for wall motion abnormality, and cardiac biomarkers.


  • Hyperacute T-waves are often the first manifestation of complete vessel occlusion; they are wide, bulky and prominent.
  • Hyperacute T-waves are not necessarily tall, and small T-waves can still be hyperacute when paired with a low-amplitude QRS complex.
  • De Winter T-waves represent LAD occlusion (a STEMI equivalent) requiring immediate revascularization.
  • Previously inverted T-waves can appear normal and upright in the setting of acute vessel occlusion. This is known as pseudonormalization.
  • The tall T-waves associated with hyperkalemia are sharp, pointy, symmetric, and have a narrow base.
  • When in doubt, get serial ECGs (every 15 minutes) and use adjunctive information.

Well, that concludes this post on hyperacute T-waves and other T-wave abnormalities. Please stay tuned for the third installment on subtle ECG findings: the subtle anterior STEMI mimicking benign early repolarization!


References / Further Reading

  1. Somers, MP et al. The prominent T wave: electrocardiographic differential diagnosis. Am J Emerg Med. 2002 May;20(3):243-51.
  2. Dressler, W and Roesler, H. High T waves in the earliest stage of myocardial infarction. Am Heart J. 1947 Nov;34(5):627-45.
  3. Nable, JV and Brady, W. The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction. Am J Emerg Med. 2009 Jul;27(6):734-46.
  4. Keeley, EC et al. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003 Jan 4;361(9351):13-20.
  5. Zarling, EJ et al. Failure to diagnose acute myocardial infarction: The clinicopathologic experience at a large community hospital. JAMA. Sep 1983;250(9):1177-81.
  6. Scott, PJ et al. Optimization of the precordial leads of the 12-lead electrocardiogram may improve detection of ST-segment elevation myocardial infarction. J Electrocardiol. Jul-Aug 2011;44(4):425-31.
  7. Thygesen, K et al; Third universal definition of myocardial infarction.  Circulation. Oct 2012;126(16):2020-2035.
  8. Pope, JH et al. Missed diagnoses of acute cardiac ischemia in the emergency department. N Engl J Med. Apr 2000;20;342(16):1163-70.
  9. Sharkey, SW et al. Impact of the electrocardiogram on the delivery of thrombolytic therapy for acute myocardial infarction. Am J Cardiol. Mar 1994;15;73(8):550-3.
  10. Martí, D et al. Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction. Am Heart J. Dec 2014;168(6):884-90.
  11. Wang, TY et al. Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non-ST-elevation acute coronary syndromes undergoing diagnostic angiography. Am Heart J. Apr 2009;157(4):716-23.
  12. “ECG changes in acute MI”. Doctors Gates Blog. 22 Oct 2015. Web.
  13. “Anterior Myocardial Infarction” Life in the Fast Lane Medical Blog. 22 Nov. 2015. Web.
  14. “Is the LAD really completely occluded when there are de Winter’s waves? Dr. Smith’s ECG Blog. 22 Nov. 2015. Web.
  15. Verouden, NJ et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart. 2009 Oct;95(20):1701-6.
  16. de Winter, RW et al. Precordial junctional ST-segment depression with tall symmetric T-waves signifying proximal LAD occlusion, case reports of STEMI equivalence. J Electrocardiol. 2015 Oct 13.
  17. “Hyperkalemia” Life in the Fast Lane Medical Blog. 02 Dec 2015. Web.
  18. “De Winter’s T-waves”. Life in the Fast Lane Medical Blog. 02 Dec 2015. Web.
  19. “Wellens’ Syndrome”. Life in the Fast Lane Medical Blog. 02. Dec 2015. Web.

EKG Practice #4

Ray Fowler, MD is Professor of EM/EMS at UTSW/Parkland.
Edited by Alex Koyfman, MD


A 67 year old woman with metastatic squamous cell cancer presents to the emergency department having been found on the floor by a family member. She lived alone and cared for herself and was apparently given to heavily imbibing in solutions containing two carbon fragments.

She was clearly quite ill, hypothermic, and confused. She was very weak and had difficulty moving her extremities. Her blood pressure was 95/55, and her temperature was 34 degrees centigrade. Her 12 lead ECG revealed this:

A closer look at leads V1 through V3 is found here:


What is your interpretation, and what do you think that this patient’s electrolyte panel would show?

EKG Practice #3

By Ray Fowler, MD
Professor of EM / EMS
UTSW / Parkland

Edited by Alex Koyfman, MD

Case #1

This 77 female presents with chest discomfort of several hours duration. She has a hx of stable angina, and she has not had any coronary intervention. On this evening, her discomfort worsened, and she called 911 and EMS responded.

En route you are contacted through BioTel that they would like for you to come and look at the transmitted ECG. They are worried that the patient may need cardioversion (see V1) or to at least go onto an antiarrhythmic drip. The following 12-lead is handed to you as you walk into the radio room. Look at V1. You have to make a decision NOW. Make your decision as to what to do.


Case #2

An 80 year-old male presents in acute distress with the worsening of chest tightness over the last few hours of the afternoon. He has had this before, he has stable angina, he has had a previous stent placed in the LAD, and he is compliant with his daily Plavix use. The ED is packed, the triage nurse has brought him back in a wheelchair, and he speaks only Burmese. What would you do?


EKG Practice #2

By Ray Fowler, MD
Professor of EM / EMS
UTSW / Parkland

Edited by Alex Koyfman, MD

Case #1

A 38 year-old female presents about a month after having had epigastric and chest pain that was quite severe for an entire day about a month ago. She took some Zantac and Maalox, felt better, and went to bed. The next day she was weakened, but she gradually felt better and went about her business.

In the last 24 hours she has noticed that she has had episodes of lightheadedness and occasional palpitations, so she comes to the ED. Your nurse hands you her ECG. What is your interpretation?


Case #2

A 36 year old male calls EMS due to chest pain and palpitations. Medics come and pick him up, and find him to be having severe chest pain with a systolic of 90. The medics call into BioTel (the online medical control) requesting instructions. They tell me that the man has a history of SVT. I asked them to transmit the ECG, and they sent this:


They are still on-scene, and their ETA will be about 10 minutes once en route. What would YOU do??

EKG Practice

By Ray Fowler, MD
Professor of EM / EMS
UTSW / Parkland

Edited by Alex Koyfman, MD

45 male with intense epigastric pain radiating to his left arm with associated NV and diaphoresis.


55 female with crushing anterior chest pain and diaphoresis.



A sinus tachycardia is present in this 54 year old man with severe chest pain radiating to the left arm.


This is a narrow complex tachycardia in a 31 year-old female that is perfectly clock regular. There is no obvious atrial activity seen. The QRS is narrow.

This 65 year-old woman presents with lightheadedness and worsening dyspnea on exertion.

This 81 year old man had a syncopal episode. He presents a little confused, GCS 14 (lies with his eyes closed), and is “not right” per his wife. His BP is 110/76, and he has the cardiogram below.


This is an odd 12 lead ECG to have done in this 54 year old man. The rate is profoundly slow, in the 20’s or so. The rhythm is regular. There is no evident atrial activity. The QRS is very widened.