STEMI equivalents have become a finding that many providers have either heard of or are familiar with, but how many can identify STEMI equivalents on the 12 lead ECG in your patients experiencing ACS-like symptoms? If you encountered bulky, tall, and disproportionate T waves with no ST-segment elevation seen anywhere on the ECG, would you assume the patient needed treatment in the cath lab, or would you expect the T waves are from hyperkalemia?
What if there was precordial ST-segment depression at the J point associated with symmetric, tall, and peaked T waves? What if the patient was 15 minutes without chest pain with biphasic T waves in lead V2 and V3? Would the receiving facility identify the “high risk” patterns associated with the presenting patient? I ask these questions because STEMI equivalents consist of important 12 lead ECG patterns that are important for a clinician to understand. This understanding, along with the ability to identify these rhythm patterns, can significantly benefit our patients.
The gentleman at FOAMfrat gave me an opportunity to take a stab at popularizing STEMI equivalents even though they are, “So 2016.” So here goes!
To start, STEMI equivalents are not ECG rhythms themselves, but findings/patterns on the 12 lead ECG that can give, you as a clinician, the ability to identify a "high risk" ECG. These rhythms/patterns are considerations for cath lab intervention, or at the very least, require attention regarding progression into an unstable condition. These interpretations represent coronary artery occlusion or pathology that warrants the same treatment as ST-segment elevation myocardial infarction but doesn't meet traditional STEMI criteria.
As a pre-hospital provider, you will transport STEMI equivalent patients with persistent chest pain, hemodynamic instability, and dynamic ECG changes to hospitals with varying capabilities. Not all receiving facilities will be familiar with STEMI equivalent ECGs; you will need to be a patient advocate consulting with the ER physician, or cardiology, expressing your concern for the patient’s situation.
Any new ST-elevation at the J point in 2 contiguous leads that is:
Men < 40 years of age: 2.5 mm in V2-V3, or 1 mm in all other lead
Men > 40 years of age: 2 mm in V2-V3, or 1 mm in all other leads
Women: 1.5 mm in V2-V3, or 1 mm in all other leads
What are the STEMI Equivalents?
Well, if you use the mnemonic I created just for this blog, it may be easier to remember this collective group of ECG patterns. Just ask yourself, "Where is WaLDO, and where is his SHIP?"
**This list is not all-inclusive and only serves to remind clinicians of the most common STEMI equivalent findings/patterns identified on the 12-lead ECG. The patient presentation along with signs and symptoms associated with ACS should be taken into consideration while diving into STEMI equivalent recognition and determination for cardiac alert**
I understand that I wrote a pretty darn long blog. For those who get bored reading long posts (which is me too, sometimes), here are the cliff notes:
Wellen’s Syndrome
The term Wellen’s Syndrome describes a pattern of biphasic or profoundly inverted T waves, particularly in leads V2-V3 (some resources branch it out further to lead V6), that is highly specific for critical, proximal stenosis of the left anterior descending (LAD) coronary artery. Wellen’s syndrome represents a pre-infarction state of coronary artery disease acting almost as the delivery boy of bad news of impending, and possibly sizeable, anterior wall MI.
Typically, patients with Wellen’s syndrome present to EMS or the emergency department following ACS-like anginal chest pain, pain-free, and with normal or only slightly elevated cardiac enzymes. They are found to have:
Deeply inverted or biphasic T-waves in V2 – V3, sometimes extending as far as V6
Recent history of angina, but pain-free at the time of ECG
Isoelectric or minimally elevated ST-segment; less than 1 mm
Preservation of precordial R-wave progression AND no precordial Q waves
Normal or slightly elevated cardiac markers
There are two abnormal T-wave appearances seen in Wellen’s syndrome; Type A and Type B. Findings with Type A are found in approximately 25% of cases, while Type B findings are present around 75% of the time.
Both Type A and Type B T-waves found in Wellen’s Syndrome are said to exist on a spectrum. With Type A T-waves evolving into Type B T-waves. Type A T-waves are said to occur following reperfusion of the coronary vessel, later developing into Type B T-waves. So, if the coronary vessel re-occludes, it’s thought to continue through the acute coronary occlusion/reperfusion cycle you see below.
Example Below:
aVR ST-Segment Elevation
Ah, aVR, the lead in paramedic school that "didn't mean anything" or is best ignored – You know, the red-headed stepchild of the 12-lead ECG… When I think of aVR, I think of it as a diagnostic tool in differentiating VT from SVT with aberrant conduction. But aVR, in conjunction with ST-Segment elevation and diffuse ST-Segment depression, is consistent with left main coronary artery insufficiency, proximal LAD obstruction, or three-vessel disease; all three of which may be an indication for cath lab activation. ST-Segment elevation in lead aVR can occur due to many different etiologies. Cath lab activation should only be implemented when the reason for the ECG changes can justifiably be from ACS. For the non-ACS etiologies, the underlying illness should be treated.
Criteria:
ST-segment elevation in aVR ≥ 1 mm
ST-segment elevation in aVR ≥ lead V1
ST-segment elevation in lead V1 > aVR suggests proximal LAD obstruction
Diffuse ST-segment depression
Typically the inferior leads (II, III, aVF) and low lateral leads (V5, V6)
Can be seen in the precordial leads as well
Example Here:
Left Bundle Branch Block
Is the left bundle branch new? What if the patient doesn’t know? What if they do have a history of left bundle branch block, but they present with heavy ACS-like symptoms? Should we activate the cath lab?! Many are likely familiar with the fact that a left bundle branch block is a STEMI mimic, but…
If a left bundle branch block is new or presumably new, it has a very low likelihood of ACS in need of cardiac center intervention. What we should instead use to identify whether a patient with a left bundle branch block should be considered for PCI is:
The presence of a left bundle branch block and one of these 3 situations:
Unstable patient (acute pulmonary edema, hypotension; signs of shock)
Sgarbossa Criteria is met
Modified Smith Sgarbossa Criteria is met
Sgabossa Criteria:
This criterion is based on a point system. A score of ≥ 3 is “positive” for MI diagnosis and should be transported for PCI.
Concordant ST-segment elevation ≥ 1mm in leads with a positive QRS complex (5 Points)
Concordant ST-segment depression ≥ 1 mm in V1 – V3 (3 Points)
Excessively discordant ST-segment elevation ≥ 5 mm (2 Points)
Modified Smith Sgarbossa Criteria:
A modification of Sgarbossa Criteria was created to improve diagnostic criteria – specifically to the rule of excessive discordance while leaving the other two as is. The use of 5 mm for the cut-off for excessive concordance was non-specific and considered arbitrary. The modified rule is positive if there is discordant ST elevation or depression that is > 25% of the preceding QRS complex.
Concordant ST-segment elevation ≥ 1 mm in leads with a positive QRS complex
Concordant ST-segment depression ≥ 1 mm in V1 - V3
One or more lead(s) anywhere with ST-segment depression OR elevation discordant with the QRS complex and with a magnitude of at least 25% of the preceding QRS
Useful algorithm for triaging the LBBB with Sgarbossa Criteria Here:
de Winter's T Waves
De Winters T Waves describes a static, often non-progressing, pattern on the ECG seen in LAD occlusions that doesn’t cause your typical STEMI appearance in the precordial leads; considered an anterior STEMI equivalent. This ECG pattern is seen in approximately 2% of LAD occlusion and is said to be under-recognized by clinicians. Although this pattern is only seen in approximately 2% of LAD occlusions, it warrants some attention as it may need immediate revascularization when associated with ACS-like symptoms.
Criteria:
Tall, prominent, symmetric T waves in the precordial leads
Upsloping ST-segment depression > 1 mm at the J-point in the precordial leads
Absence of ST-segment elevation in the precordial leads
ST-segmenet elevation (0.5 to 1 mm) in lead aVR
“Normal” STEMI morphology before or after the recognition of de Winter pattern
Example Here:
Out of Hospital ROSC
Out of hospital cardiac arrest with ROSC isn’t a rhythm pattern, if you haven’t already guessed. I won’t be pounding a rhythm pattern into your brain on this one… But, I am going to give you an algorithm to determine if your ROSC patient is a candidate for coronary angiography and PCI regardless of whether a STEMI pattern is seen or not. The AHA reports that coronary angiography is reasonable for select adult patients who are comatose after out of hospital cardiac arrest, when the reason for the arrest is suspected to be cardiac in origin, without ST elevation on the ECG. Meaning that the rhythm is treated like a “STEMI,” or “STEMI equivalent,” and will be evaluated in a cath lab. In July of 2015, the ACC/AHA published an algorithm to determine which cardiac arrest patients, who are comatose on presentation, may benefit from activation for coronary angiography and possible PCI.
Subtle Lateral and Inferior Wall MI
Subtle changes to the ST-segment of the inferior or high lateral wall can be so minimal, that the ECG appears “normal” and shows no signs of a STEMI. These rhythms are considered STEMI equivalents because they don’t fit the standard ACC/AHA guidelines for STEMI. The ST-segment changes are relative to the QRS complex, as well. So, if you have a tiny/low amplitude QRS voltage, any ST-segment elevation (even < 1 mm) may be diagnostic. Also, the presence of ST-segment depression in reciprocal leads makes minimal ST-segment elevation that much more significant. As we reference the inferior and high lateral wall, lead III and aVL are the leads most reciprocal to each other. Special attention to those two leads is essential for the identification of the subtle lateral or inferior wall MI.
Inferior Wall MI:
ST-segment elevation in two of the inferior leads
Elevation may be ≥ 0.5 mm in the presence of low amplitude/voltage QRS complex if accompanied by ST-segment depression in the reciprocal leads, typically aVL
Also, beware of isolated T-wave inversion in aVL. This also may be a soft sign of acute inferior MI, before ST elevation.
If there are QS-waves, there is a possibility that the ST-segment elevation is from an old MI. Also, keep in mind that if that repolarization abnormalities that produce depression in aVL include LV aneurysm, LVH, WPW, and LBBB – their presence decreases the likelihood of inferior wall MI.
To paraphrase Dr. Steve Smith, “If there is no ST-segment depression in aVL, then any ST-segment elevation in lead III is unlikely to be from an inferior MI.”
Subtle Inferior Example Below:
High Lateral Wall MI:
Essentially the opposite of the inferior wall MI
ANY degree of ST-segment elevation in lead aVL (yes, only one lead) with reciprocal depression in lead III
Subtle High Lateral Example Below:
Hyperacute T-Waves
When occlusion in a coronary artery occurs, the ECG begins to change predictably. The earliest changes were seen after occlusion is in the T-wave shape and size, becoming bulky and wide, often disproportionate to the QRS amplitude/voltage. This can be seen as early as two minutes following during the hyperacute phase of occlusion. If hyperacute T-waves are seen, serial ECGs should be obtained as they may morph quickly into a classic STEMI pattern.
Criteria:
Large; disproportional to the QRS
Bulky; wide with subsequent increase in the QT interval
Often asymmetric
Localized to the anatomic region of infarct
Causes a decrease in QRS amplitude
Not typically peak/tented as seen in hyperkalemia (If in doubt, measure K+)
Example Below:
Isolated Posterior Wall MI
Due to the absence of ST-segment elevation, an isolated posterior MI is often missed and under-treated. An “isolated” posterior MI is referenced as a STEMI equivalent because a generalized posterior wall MI usually has inferior and lateral involvement as well, causing ST-segment changes in those regions.
Criteria:
Changes in V1 – V3
Depression, often 2 mm or greater; may only be 1 mm
Tall, broad R waves (may be seen later in its progression)
Upright T waves may be seen
ST-segment elevation of 0.5 mm in the posterior leads V7, V8, and V9
Doing the posterior sided 12 lead adds specificity
Example Below:
- Jared Patterson, CCP-C, One Rad Dude
Reference(s):
O’Gara, P. T., O’Gara, P. T., Kushner, F. G., Kushner, F. G., Ascheim, D. D., Ascheim, D. D., … American College of Emergency Physicians and Society for Cardiovascular Angiography. (2012, December 17). 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. Retrieved from https://ahajournals.org/doi/full/10.1161/cir.0b013e3182742cf6.
Smith, S. W. (2002). The Ecg in acute Mi: an evidence-based manual of reperfusion therapy. Philadelphia: Lippincott Williams & Wilkins.
Scott Weingart. EMCrit Podcast 146 – Who Needs an Acute PCI with Steve Smith (Part I). EMCrit Blog. Published on March 29, 2015. Accessed on October 29th 2019. Available at [https://emcrit.org/emcrit/who-needs-acute-pci/ ]
Brady, & J., W. (2017, January 1). Pitfalls in Electrocardiographic Diagnosis of Acute Coronary Syndrome in Low-Risk Chest Pain. Retrieved from https://escholarship.org/uc/item/8nq6n3dk.
Chenniappan, M., Sankar, R. U., Saravanan, K., & Karthikeyan. (2013, September). Lead aVR--the neglected lead. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24772703.
STEMI equivalents. (n.d.). Retrieved from https://wikem.org/wiki/STEMI_equivalents#cite_ref-3.
Miner, B. (2019, March 9). Wellens Syndrome. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK482490/.
Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens syndrome. Am J Emerg Med. 2002;20(7):638-643.
Nahvi, F. (2016, August 24). Validation of the Modified Sgarbossa Criteria. Retrieved from https://coreem.net/journal-reviews/modified-sgarbossa-criteria/.
Cadogan, M. (2019, May 22). Sgarbossa Criteria • LITFL • ECG Library Diagnosis. Retrieved from https://litfl.com/sgarbossa-criteria-ecg-library/.
Burns, E. (2019, September 24). De Winter T Wave • LITFL • ECG Library Diagnosis. Retrieved from https://litfl.com/de-winter-t-wave-ecg-library/.
Hassen, G. W., Costea, A., Smith, T., Carrazco, C., Hussein, H., Soroori-Rad, B., … Fernaine, G. (2014, February). The neglected lead on electrocardiogram: T wave inversion in lead aVL, nonspecific finding or a sign for left anterior descending artery lesion? Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/24286713.
Birnbaum, Y., Sclarovsky, S., Mager, A., Strasberg, B., & Rechavia, E. (1993, January). ST segment depression in a VL: a sensitive marker for acute inferior myocardial infarction. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/8432289.
Birnbaum, Y., Sclarovsky, S., Mager, A., Strasberg, B., & Rechavia, E. (1993, January). ST segment depression in a VL: a sensitive marker for acute inferior myocardial infarction. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/8432289.
Van Gorselen E, Verheugt F, Meursing B, Oude Ophuis A. Posterior myocardial infarction: The dark side of the moon. Neth Heart J. 2007;15(1):16-21.
Levis JT. ECG Diagnosis: Isolated Posterior Wall Myocardial Infarction. Perm J. 2015;19(4):e143-e144.
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