Differential for ST Elevation

The differential for ST elevation is broader than ACS (although it would be nice if medicine were that easy). In EM, the maxim is always to think about the worst first. After you have determined the patient is likely not experiencing an acute coronary occlusion aka ST-Elevation Myocardial Infarction, what else could lead to ST elevation? Outside of acute coronary occlusion, there are also a few causes that are not so benign. 

Hyperkalemia can be a cause of ST elevation, but distinguishing features include peaked T waves, widened QRS complexes, and decreased P wave amplitude. 

Another dangerous cause of ST elevation is Brugada syndrome, where ST elevation is most prominent in V1-V3 and is accompanied by T wave inversions. 

Chronic causes of ST elevation include Left Ventricular Hypertrophy, LBBB, & LV aneurysm. Of course, you could have an acute coronary occlusion leading to STEMI in patients who have baseline LVH, LBBB, or LV aneurysm. This is out of scope from this POTD, but modified Sgarbossa's criteria seeks to help identify STEMIs in patients who have underlying LBBB (or paced rhythms). 

LV aneurysm morphology often has deep Q waves with persistent ST elevation and T wave inversions and is accompanied by anatomical aneurysms that can be visualized on echocardiogram.

LBBB is characterized by a wide QRS with dominant S wave in V1 and a broad notched R wave in V6. 

There are many criterias for LVH, but morphology wise, ST elevations in LVH are usually confined to V1-V3. There can also be ST depressions in the lateral leads.

Two final causes of ST elevation include Benign Early Repolarization (BER) and pericarditis. These can often be tricky to distinguish from subtle STEMIs, especially subtle anterior STEMIs. 

Classically in pericarditis, there is PR depression, diffuse ST elevation (without ST depressions), and ST elevation in lead II > lead III. In BER, there is again diffuse ST elevation without ST depressions, elevations are often most prominent V2-V5, and there can be J point notching. 

Picture below showing some common causes of ST elevation

Sources:

https://litfl.com/left-ventricular-hypertrophy-lvh-ecg-library/

https://emergencymedicinecases.com/ecg-cases-st-elevations-mnemonic-occlusion-mi/

https://litfl.com/left-bundle-branch-block-lbbb-ecg-library/

http://hqmeded-ecg.blogspot.com/2020/07/subtle-ecg-findings-of-left-anterior.html

Wellens Syndrome & Pseudo-normalization

So Wellens syndrome is a STEMI equivalent right? That is part of it, but not the whole picture. When we say STEMI or STEMI-equivalent, the image of a fully occluded coronary artery that requires immediate PCI comes to mind. Wellens syndrome is not really a “STEMI” but more of a post-STEMI or a pre-STEMI (along with being a non-STEMI). I’ll explain why.

First we will review Wellens syndrome and then we’ll go into what it represents. Symptoms usually include resolved angina, either spontaneously or after treatment (nitro, aspirin). The troponin will be negative or minimally elevated & the EKG will not show signs of irreversible ischemia such as deep Q waves or poor R wave progressions. Lastly, you’ll see T-Wave Inversions in the anterior leads. There are two types of Wellens waves, pictured below and they occur when chest pain is resolved. Resolved chest pain means the artery has spontaneously reopened and the myocardium is being perfused. Thus Wellens waves are reperfusion waves, rather than waves that represent an acute coronary occlusion. 

However, if these patients do not receive PCI at some point, they are at high risk for large anterior MI due to near occlusion of the LAD. 

The phenomenon of pseudonormalization also occurs in Wellens syndrome, further making it easy to accidentally discharge these patients. In pseudonormalization, recurrence of chest pain results in normalization of T waves and elevation of ST segments. When the T waves are inverted, the artery is open (albeit barely) because the T waves represent reperfusion. When the patient develops chest pain (since the artery has fully closed), the T waves flip on their way to becoming hyperacute T waves. Catching an EKG at this unfortunate time could deceive you into thinking the patient has a “normal” EKG 

This nearly occluded lesion is classically associated with LAD and thus usually seen in the anterior leads. However, a 99% coronary lesion and thus occlusion/reperfusion phenomenon known as Wellens can occur in any coronary artery. For example, you'll see Wellens in the inferior leads for RCA lesions that spontaneously reopen. 

While resolved symptoms and EKG signs of reperfusion don’t require immediate cath lab activation, post-ischemic TWI require aggressive treatment while waiting for PCI. These are the highest risk NSTEMIs! Include these findings in your signouts. Be on the lookout for return of chest pain, which points towards acute reocclusion & do not be fooled by pseudonormalization. Also patients who have TWI and active CP are patients with typical ACS/NSTEMI, not necessarily Wellens/99% coronary artery occlusion. 

Wellens is a normal reassuring finding post cath lab since it means the interventionalist has successfully reperfused the coronary. It is scary in the ED because it was spontaneous reopening, which could mean an entire wall of the LV is only being supplied by an artery that is 1% open.

Right Heart Strain on EKG

EKG is neither sensitive nor specific for PE, but there are some clues that can be another data point in your decision making. Remember, EKG stands for electrocardiogram, not pulmonary-artery-gram. The absence of these findings should not decrease your suspicion of PE. 

As we all know, EKG can be completely normal in PE; sometimes, it can have the following changes. Changes in EKG occur due to acute cor pulmonale, resulting in acute dilatation and partial failure of the right side of the heart and the resultant abnormal electrical activity. 

Rate & Rhythm findings: Sinus tach, new onset atrial fibrillation

Axis findings: Right axis deviation, S wave in lead I. Remember lead I is looking at the left side of the heart, so a pronounced S wave and thus overall negative deflection of lead I means there is right axis deviation

Interval findings: QRS complex: New right bundle branch block. Remember, the RV contains the right bundle and poor blood flow to the RV due to dilatation and resultant ischemia to the right bundle results in the block.

Ischemia findings: 

• Delayed R wave progression due to dilatation of the RV and resultant shift in electrical activity towards the right side

• ST segment changes: 

  • (S1)Q3T3 

  • Anterior T wave inversions (almost mimicking Wellens - apparently in Steve Smith’s book, there is a way to tell the difference from T wave inversions in Wellens/ACS vs T wave inversions from PE/pseudo-wellens, but they look identical to me)

  • Anterior ischemia along with inferior (lead III) inversions is more specific than just anterior ischemia (which can be Wellens/ACS) 

  • V1 ST-Elevation due to RV ischemia 

  • Diffuse ST depression with reciprocal STE in aVR due diffuse subendocardial ischemia in obstructive shock from a PE 

Hypertrophy findings: A dominant R wave in V1 and other evidence of right ventricular hypertrophy on EKG (right atrial enlargement) speaks against an acute process such as PE. The patient likely has chronic cor pulmonale.  

Those with more hemodynamically significant PEs are more likely to have these changes. Conversely, having some of these findings below in a patient with known PE such as anterior T wave inversions, ST depressions with reciprocal aVR elevation, & sinus tachycardia makes the patient at high risk or in RV failure (so maybe don’t overload that RV with 3L of fluids or cardiovert the compensatory atrial fibrillation). Don’t forget the differential for T wave inversions/depressions also includes other pathologies such as ACS. 

https://litfl.com/right-ventricular-strain-ecg-library/

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

Vanni, Simone & Polidori, Gianluca & Daviddi, F. & Ponchietti, Stefano & Curcio, M. & Conti, Alberto & Vergara, Ruben & Grifoni, S.. (2007). Right Ventricular Strain Pattern at ECG Predicts Early Adverse Outcome in Patients With Acute Pulmonary Embolism and Normal Blood Pressure. Journal of Emergency Medicine - J EMERG MED. 33. 336-336. 10.1016/j.jemermed.2007.08.043. 

https://emergencymedicinecases.com/ecg-cases-26-pulmonary-embolism-and-acute-rv-strain/