STEMI Equivalents

by David Shang

Each EKG this week comes from a patient with chest pain. Answer the following questions for each EKG:

1) What are the concerning features?

2) Where’s the lesion?

3) Does this patient require cath lab?

EKG #1

EKG #2

EKG #3

EKG #4

EKG OF THE WEEK #6 Answers

This week was recognizing STEMI equivalents.

·      While almost everyone can recognize STEMI on EKG (revisit Duncan’s examples of benign vs. scary STE), there are unfortunately many EKG patterns that are associated with coronary vessel occlusion.

While not an all-encompassing list, hopefully here are a few more patterns you can add (especially for my co-interns).

Besides possibly Wellen’s Syndrome (EKG #1), the other 3 EKG’s all demonstrate coronary artery stenosis that requires cardiac catheterization and reperfusion.

EKG #1: Wellen’s Syndrome Type A– Look at T-waves in V1-V4

-       Associated with proximal high-grade LAD occlusion. According to REBELEM, Wellen’s waves + history of chest pain + normal/minimally elevated troponin = 86% PPV for LAD lesion

-       Important to recognize that this pattern persists even if chest pain resolves. Refer to last week’s EKG for Duncan’s full explanation of the pathophys but…

o   Believed to be a pattern of sudden occlusion + reperfusion. The T wave morphology is very similar to patients who reperfuse following successful PCI.

o   Despite resolution of chest pain, patients remain at high risk of re-occlusion

-       Two Types – both involve T-waves in the precordial leads (usually V2-V3)

-       Requires cardiology consult but may not require immediate cardiac catheterization. However, if they do not go for cath requires antiplatelet and antithrombotic therapy as well as continuous 12-lead ST segment monitoring to detect any re-occlusions

Finally, an example demonstrating the pattern of LAD occlusion, reperfusion, and re-occlusion. From LITFL, EKGs in chronological order over a 45 min period.

 (a) Patient experiencing chest pain and diaphoresis

·       The ECG shows a clear anterolateral STEMI, with inferior reciprocal change.

·       The artery is occluded at this point.

(b) Resolution of pain

·       The ECG now shows a typical Wellens pattern of biphasic T waves in V2-3, plus improvement in the anterolateral ST elevation.

·       This indicates spontaneous reperfusion of the LAD — i.e. the artery has re-opened.

(c) Recurrence of chest pain and diaphoresis

·       With recurrence of pain there is pseudo-normalisation of the precordial T waves: the previously biphasic T waves have become prominently upright (= “hyperacute” T waves).

·       This apparent normalisation of the T waves indicates re-occlusion of the LAD artery.

Further reading: https://litfl.com/wellens-syndrome-ecg-library/

EKG #2: De Winter’s T Waves – Look at V1-V6, aVR +/- aVL

-        Also associated with proximal LAD occlusion (pattern found in 2% of acute LAD occlusions)

-        Anterior STEMI equivalent without obvious ST segment elevation

-        Findings

o   Leads V1-V4: Up-sloping ST depressions at J point

o   Leads V1-V4: Tall, symmetric T-waves

o   aVR +/- aVL: ST elevation

-       This has features of both De Winter’s T waves and anterior STEMI

o   ST elevations in V1-2, I, aVL with inferior reciprocal changes

o   Upsloping ST depression and peaked T waves in V3-6

Further Reading: https://litfl.com/de-winter-t-wave-ecg-library/

EKG #3: Posterior MI – look at leads V1-V3

-        Accompanies 15-20% of STEMIs, usually occurring with inferior or lateral infarction. Posterior involvement implies a much larger area of myocardial damage

-        Isolated posterior MI is less common (3-11% of infarcts). The lack of obvious ST elevation makes this more difficult to diagnose.

-        Typical next step is to get posterior EKG with leads V7-V9

-        Signs:

o   Horizontal ST depression in V1-V3

o   Tall, broad R waves (>30 ms)

o   Upright T waves

From LITFL: The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:

·       ST elevation becomes ST depression

·       Q waves become R waves

·       Terminal T-wave inversion becomes an upright T wave

I see it as viewing the reciprocal change of a posterior STEMI through the anterior leads. I use the PAILS mnemonic (P-posterior A-anterior I-inferior L-lateral S-septal): ST elevations in one set of leads has reciprocal changes in the leads of the next letter.

-       A posterior STEMI will have reciprocal changes in the anterior leads

Further Reading: https://litfl.com/posterior-myocardial-infarction-ecg-library/

EKG #4: Left Main Coronary Stenosis – Look at aVR in particular

-        No fancy name here - usually due to stenosis of Left Main Coronary Artery

o   Semantic, but some argue that it be called “stenosis” because complete occlusion would result in STEMI, cardiogenic shock, and death

-        Findings:

o   Widespread ST depression, most prominent in leads I, II, V4-6

o   ST elevation in aVR > 1mm

o   ST elevation aVR > V1

ST Elevation in aVR also found in:

-        Proximal LAD occlusion (remember it was also found in De Winter’s!)

-        Severe triple-vessel disease

-        Diffuse subendocardial ischemia

-        Mechanism: LMCA stenosis causes subendocardial ischemia to the left side of the heart, resulting in diffuse ST depressions (especially in leads I, II, V4-6)

o   aVR (representing the right side of the heart) is electrically opposite to the left sided leads à resulting in ST elevation in aVR

·       STE in aVR ≥ 1mm indicates proximal LAD / LMCA occlusion or severe 3VD

·       STE in aVR ≥ 1mm predicts the need for CABG

·       STE in aVR ≥ V1 differentiates LMCA from proximal LAD occlusion

·       Absence of ST elevation in aVR almost entirely excludes a significant LMCA lesion

· Marked ST elevation in aVR >> V1

· ST depression in mulitple leads (V2-6, I, II, aVL, aVF)

· This patient presented to ED in cardiogenic shock

NOT LMCA Stenosis!

· A septal STEMI, with ST elevation and Q wave formation in V1-2

· ST elevation in aVR = ST elevation in V1

· Widespread ST depression, most prominent in leads I, II and V5-6

Given the signs of septal STEMI, this ECG most likely represents a proximal LAD occlusion.

Further Reading: https://litfl.com/lmca-occlusion-st-elevation-in-avr/

More Resources: https://rebelem.com/five-ecg-patterns-you-must-know/

https://www.emra.org/emresident/article/stemi-equivalents/

https://emcrit.org/emcrit/who-needs-acute-pci/

https://rebelem.com/rebellion-in-em-2018-stemi-equivalents-by-tarlan-hedayati-md/

T Wave Inversions

EKG#1

2yoF with fever. There was a miscommunication and someone accidentally got this EKG – even no one asked for it. Many emails have been sent as a result, swaths of staff fired and ridiculed… but even still, you’re stuck with this EKG.

1. Is this 2yo having an MI? Spontaneous coronary artery dissection? Coronary aneurysm from Kawasaki?

EKG#2

48yoM with exertional chest pain. He’s wearing a fedora and sunglasses indoors. Is this clinically relevant? You decide.

1. Iunno, what do you think? Good? Bad?

EKG#3

88yoF found unresponsive in the bathroom. No cardiac history.

1. Which came first, the EKG or the fall?

EKG#4

33yoM, exertional SOB

1. Do you agree with the computer interpretation?

2. What test will your order next?

PRECORDIAL T-WAVE INVERSIONS (TWI) EDITION

What’s the differential?

Wow, look at this snazzy graphic you can reference!

Before we start…

…let’s review normal T waves.

T waves should be…

1.   Upright in all leads except aVR and V1 (sometimes V2)

2.   Asymmetric, with a gradual upslope and a steep return to baseline

3.   Smaller than the QRS

Lots of things can invert your T waves

·      We will focus today on the differential on the first page

·      In addition to these dangerous pathologies, consider…

o  Ventricular strain

o  HCM

o  Lead placement:  https://litfl.com/ecg-limb-lead-reversal-ecg-library/

ANSWERS 

EKG#1

2yoF with fever – Juvenile T Waves

·      Remember, TWI is a normal finding in children.

·      Note that these TWI’s are asymmetric, as opposed to the next pathologic example.

o   They have a gradual upslope, steep downslope

·      They may become upright as early as age 8, or they may “persist” into adulthood.

·      Persistent Juvenile T Waves (PJTW) typically present African American women <30yo

but…

·      As Dr. Richard Wang said, PJTW is a diagnosis of exclusion. It’s reasonable to interpret this TWI pattern as normal in a child, but consider this pathologic on the adult side until proven otherwise.

From Richard:

·      Remember right axis deviation is normal in pediatrics – remember that the R side of the heart does most of the work in-utero, so it’s normal to expect it to be [relatively] bulkier

·      This EKG shows “early transition,” meaning R > S in V1/2, suggestive of increased work in the R side of the heart

Additional Reading: https://pedemmorsels.com/pediatric-ecg/

EKG#2

48yoM with exertional chest pain – Wellens, Type B

·      Deep, symmetric TWI in the precordial leads = Wellens, Type B

·      There are two types of Wellens patterns, A and B.

·      Both indicate critical stenosis of the LAD and these patients should be treated as impending STEMI’s, though their ST segments may appear normal.

Here is a fantastic explanation of Wellen’s physiology from Life in the Fast Lane:

·       A sudden occlusion of the LAD, causing a transient anterior STEMI. The patient has chest pain & diaphoresis. This stage may not be successfully captured on an ECG recording.

·       Re-perfusion of the LAD. The chest pain resolves. ST elevation improves and T waves become biphasic or inverted. The T wave morphology is identical to patients who reperfuse after a successful PCI.

·       If the artery remains open, the T waves evolve over time from biphasic to deeply inverted.

·       The coronary perfusion is unstable, however, and the LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves — so-called “pseudo-normalisation”. The T waves switch from biphasic/inverted to upright and prominent. This is a sign of hyperacute STEMI and is usually accompanied by recurrence of chest pain, although the ECG changes can precede the symptoms.

·       If the artery remains occluded, the patient now develops an evolving anterior STEMI.

·       Alternatively, a “stuttering” pattern may develop, with intermittent reperfusion and re-occlusion. This would manifest as alternating ECGs demonstrating Wellens and pseudonormalisation/STEMI patterns.

Additional Reading: https://litfl.com/wellens-syndrome-ecg-library/

EKG#3

88yoF found unresponsive in the bathroom – Cerebral T Waves

·      Deep, SYMMETRIC TWI… are we sensing a pattern here?

·      This is a pretty rare phenomenon that occurs with stroke or increased ICP (think bleed).

·      This particular EKG is from a patient with a subarachnoid hemorrhage.

·      The pathophysiology is currently not known.

·      One study (https://www.ajconline.org/article/S0002-9149(17)31597-7/fulltext) found 2% of stroke patients had inverted T waves, and 18% of those had transient wall-motion abnormalities, suggesting that this finding may actually reflect true cardiac dysfunction.

·      It is common for stroke patients to spill troponin, so add ‘em on! 

Additional Reading: http://www.emdocs.net/ecg-pointers-intracranial-hemorrhage/

EKG#4

33yoM, exertional SOB – Pulmonary Embolism

·      TWI is more prevalent in PE than S1Q3T3, but still not totes specific
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5306533/

·      Remember that EKG in PE may be:

o   STONE COLD NORMAL

o   Sinus Tach

o   RBBB

o   New Right Axis Deviation 

·      Great EMCRIT article on how to differentiate AMI from PE:
https://emcrit.org/pulmcrit/two-ekg-patterns-of-pulmonary-embolism-which-mimic-mi/

References

https://litfl.com/ecg-changes-in-pulmonary-embolism/

http://ems12lead.com/2014/11/18/anterior-t-wave-inversions-and-pe/#gref

https://litfl.com/paediatric-ecg-interpretation-ecg-library/

https://litfl.com/t-wave-ecg-library/

EKG in Tox

EKG#1

80 year old demented female, unresponsive, BP 55/20, blood glucose 24

1. What’s the rhythm?

2. What’s the differential for bradycardia?

3. Think tox – now narrow your differential. What do the vitals suggest?

4. How do you want to treat this patient?

EKG#2

21 year old male, suicidal, intentional overdose

1. Rate, rhythm, axis, intervals – you can glean a lot of information from these pieces alone

2. What’s the suspected overdose?

3. Treatment?

EKG#3

41 year old female, sent from methadone clinic for nausea. Given Zofran at the clinic. Was acting belligerent at triage and required Haldol. Records show she is currently on azithromycin outpt for recent pneumonia.

You get this EKG right before she goes into cardiac arrest.

1. What the hell happened?

2. How you gonna treat?

EKG#4

92 year old demented man, wife found him unresponsive near an open medicine cabinet

1. This is a classic dysrhythmia secondary to which toxicity?

2. What is a classic, more subtle finding you can see when the patient in normal sinus rhythm?

ANSWERS

EKGotW #4 – Tox Edition

Brown and University of Cincinnati have amazing reference websites for this topic!

Here are some reference tables from their sites with links that you should totes check out!

http://brownemblog.com/blog-1/2018/6/20/the-poor-mans-tox-screen

http://www.tamingthesru.com/blog/diagnostics/ekg-toxicology, Table by Dr. James Li

EKG#1

Beta Blocker Overdose

1.     What’s the rhythm?

a. Junctional bradycardia.

These are QRS complexes without P waves – no P waves means the ventricles are either being triggered from the AV node or more distally (in the actual ventricles).

The complexes are narrow, which means the AV node is likely triggering the impulses, conducting electricity down the bundle of his through the normal conduction pathway.

If the complexes were wide, these might be ventricular escape rhythms – not only do the SA and AV node have their own automaticity, but the actual myocytes themselves may trigger impulses as well.

1.     What’s the differential for bradycardia?

a.     H.I.D.E.

                                               i.     Hypothyroid/Hypothermia

                                             ii.     Ischemia/Increased ICP

                                           iii.     Drugs

                                            iv.     Electrolytes (K, Ca, Mag)

2.     Think tox – now narrow your differential. What do the vitals suggest?

a.     Several toxidromes may cause severe bradycardia. Commonly we talk about calcium channel blockers and beta blockers. (Don’t forget digoxin from David Elkin’s M&M a few weeks ago!)

Classically, hypoglycemia + bradycardia = beta blocker overdose.

Beware of bronchospasm as a clue as well.

3.     How do you want to treat this patient?

a. Glucagon – increases intracellular cAMP and calcium

                      i.   Give with Zofran!

b. Calcium – increase inotropy

c. Epi Drip – for cardiogenic shock

d. High Dose Insulin – 1u/kg/hr, 30-60 min to take effect

e. Lipid Emulsion Therapy – uncertain mechanism

f. Atropine / Pacing can be considered – atropine often ineffective. (Remember, atropine counteracts excessive vagal stimulation, but this is not the etiology of bradycardia in BB OD patients!)
My fave article on this:
https://emcrit.org/pulmcrit/epinephrine-atropine-bradycardia/

EKG#2

TCA Overdose

1.     Rate, rhythm, axis, intervals

a.      Rate = QRS x 6 = 21 x 6 = 126

b.     Rhythm – You can see P waves hiding in I, V5/V6, and maybe small irregularities in the T waves of V3/V4 that hint at presence of P waves. This is sinus.

c.      Axis - Downward deflection in I, upward in aVF = RIGHT AXIS

d.     Intervals

                                               i.     PR < 200msec

                                              ii.     QRS > 120msec

                                            iii.     QTc = QT/Ö(RàR’) = 0.312 / Ö0.48 = 450msec

^^^(I used V2 for this)

Sinus tachycardia with RIGHT AXIS deviation and WIDE QRS complex

2.     What’s the suspected overdose?

a. Hallmarks of TCA Overdose EKG

                 i.  Widened QRS

                ii.  Big-ass R wave in aVR

              iii.  New right axis

iv. Deep slurred S waves, I & aVL

3.     Treatment?

a. Sodium Bicarb pushes

                      i.   Until the QRS narrows

b. Lidocaine for refractory arrythmia

Read about TCA -- http://www.emdocs.net/ecg-pointers-tca-overdose/

Video about TCA -- https://emin5.com/2015/12/22/tca-toxicity/

EKG#3

Long QT

1.     What the hell happened?

a. Haldol, azithromycin, methadone are all QT prolonging agents, which predispose to Torsades de Pointes, or Polymorphic Ventricular Tachycardia

b.     Using V5…
QTc = QT / (Square root of R->R’) = 0.74 / (SqRt(1.08) = 711msec

2.     How you gonna treat?

a. Defibrillate if in arrest

b. 2g Mag Sulfate slow IV push

c. Isoproterenol +/- pacer if super brady

This case: http://hqmeded-ecg.blogspot.com/2014/06/acquired-long-qt-do-not-trust.html

Torsades overview: https://wikem.org/wiki/Torsades_de_pointes

EKG#4

Digoxin Toxicity

1.     Classic Findings

a. This is Bidirectional V-Tach, classic for digoxin toxicity

b. Like David Elkin talked about a few weeks ago in M&M, lots of different arrhythmias possible with digoxin

c. Beware of atrial arrythmias and dangerous bradycardias

d. Classic EKG finding of scooped, down-sloping, Salvador Dali moustache ST segment

Remember the theoretical phenomenon of stone heart – dig tox may give you hyperK. When you treat with calcium, the theory is that it may cause tetany of the myocardium and precipitate cardiac arrest. Digifab (antidote) will treat hyperK, so consider your options.

Dig Toxicity EKG - https://litfl.com/digoxin-toxicity-ecg-library/

Treatment - https://www.wikem.org/wiki/Digoxin_toxicity

References

https://litfl.com/tricyclic-overdose-sodium-channel-blocker-toxicity/

http://brownemblog.com/blog-1/2018/6/20/the-poor-mans-tox-screen

http://www.tamingthesru.com/blog/diagnostics/ekg-toxicology

http://hqmeded-ecg.blogspot.com/2014/06/acquired-long-qt-do-not-trust.html