Slide 1: 57-year-old male with cardiomyopathy (ejection fraction 15-20%) reports 1 week fatigue and weakness, abdominal swelling, 10 pound weight gain. What are the emergent findings?

Slide 2: 2 mm STE in V3/V4. What’s on the differential for ST elevations?

Slide 3: Approach to ST elevations. What is the ST segment morphology? Concave ST elevations. Up-sloping ST elevations (concave) in asymptomatic patients are not typically due to coronary causes. A “smiley face” is reassuring!

Convex ST elevations. Down-sloping ST elevations (convex) are more likely to be acute myocardial injury. A “frowny face” is worrisome!

Remember that history is the more important factor for your ddx! Note that the STE distribution in our patient is limited to leads II and V3-4 (not consistent with a specific coronary distribution). What is your ddx now for our patient with STEs?

Slide 4: Approach to ST-Elevation. Presence of acute, subacute or acute on chronic symptoms? Yes. Coronary Causes: Plaque rupture/ACS, coronary, SCAD (spontaneous coronary artery dissection). Non-coronary causes: aortic dissection, electrolyte abnormalities, acquired prolonged QT, pulmonary embolism, myocardial aneurysm, pericarditis, acute intracranial event, Takotsubo cardiomyopathy.

Slide 5: Approach to ST-Elevation. Presence of acute, subacute or acute on chronic symptoms? No. Conduction abnormalities including chronic LBBB or IVCD, Brugada syndrome, RV pacing, congenital prolonged QT-syndrome, ventricular pre-excitation (WPW pattern). “Normal Variants” including early repolarization and young athletes (typically male). Myocardial changes including LVH, RVH, chronic myocardial aneurysm (past ACS event)

Slide 6: Returning to our case, the presence of peaked T-waves, widened QRS, and STEs suggested hyperkalemia as the differential. Labs are notable for potassium 8.6 and creatinine 2.6, consistent with AKI and hyperkalemia