Compendium of ECG findings concerning for ☠️♥️occlusive MI ♥️☠️ (1/11)
First, back to basics & traditional STEMI criteria! Here's a nice figure of Lead Anatomy. I saved this forever ago, so not exactly sure of the source ¯\_(ツ)_/¯
(2/11)
STEMI criteria is met if: STE at least 1mm in 2 contiguous leads, but with higher cut-offs in V2-V3, & with addition of new LBBB in setting of compatible clinical picture. You can localize the coronary lesion using the leads affected! Localization chart by @DrEricStrong (3/11)
Before going into "STEMI equivalents" (better phrasing: "occlusive MI amenable to revascularization"), here's a figure from @LITFLblog on the J-point, which will be referenced later in the thread!
Next, ♥️Wellens' Syndrome♥️, a clinical syndrome characterized by biphasic or deeply inverted T waves plus a history of recent chest pain now resolved. The progressive T wave changes can be understood as follows: litfl.com/wellens-syndro…
(6/11)
Speaking of anterior MIs, a higher level concept that should be more widespread involves ☠️Terminal QRS Distortion☠️, defined as the absence of S-wave & J-wave in either V2/V3. Such distortion suggests Subtle Anterior MIs! @smithECGBlog
♥️ First Diagonal Occlusion ♥️ presents with a fun pattern called the South African Flag Sign! An easy way to remember this is the upper leads (on ECG strip, not anatomical leads) have upward changes (STE & upright T waves), while lower leads have downward changes.
♥️ Posterior MI ♥️: horizontal STD in V1-V3 & upright T waves in V1-V3.
However, STD maximum in V1-V4 can also be due to subendocardial ischemia (not occlusive MI) when there is tachycardia, especially if due to AFib with RVR.
What? → Fluid-filled skin lesions occurring by 1 of 3 mechanisms:
1. Acantholysis
2. Spongiosis
3. Epidermal-dermal Dissociation
The key pivot of this schema emphasizes a search for exogenous culprits of life-threatening disease, as these culprits must either be treated or avoided in the future.
🚨 This classification is very imperfect (e.g. numerous SJS/TEN cases are idiopathic) 🚨
EXOGENOUS culprits of life-threatening disease include medications & infections.
Recall from my prior thread on Paraprotein testing that one path to sending these tests is based on suspicion for a Paraprotein-mediated disorder; namely, the Plasma cell dyscrasias & MGCS diseases.
Today, @Gurleen_Kaur96, @Mark_Heslin, & I bring you our diagnostic approach to myocarditis.
First we'll give a lay of the HFrEF land; then, we'll cover presenting features & Endpoint DDx.
Onward!
The "diagnostic arc" of HFrEF 🏔️
Lots of ways to break down the assessment of new HFrEF... Here's how we do it:
☠️ 1st Pass = Base Rate/Sick
- Ischemic cardiomyopathy reigns in the elderly & at-risk: ECGs should be scrutinized for signs of occlusive MI & pathologic Q waves👇
Additionally, in critically ill patients, stress-induced cardiomyopathy (i.e. Takotsubo) should be considered.
📚 Note: while stress-induced CM is often suspected by clinical picture, left heart catheterization +/- cardiac MRI is needed to exclude OMI & other diseases.
What do these abbreviations mean & how does one arrive to the land of paraproteinemias?
Here is a tweetorial for the internist diagnostician, in collaboration with @cullen_lilley!
🗻 The path to paraprotein evaluation may or may not begin with the observation of a "protein gap," meaning a (roughly) 4 g/dL difference between the serum Total protein & Albumin.
A gap may therefore be due to:
⚪ ↑ immunoglobulins (antibodies)
⚪ ↓ albumin
Since albumin is literally half of the equation, this tweet is just a reminder to not chase a 🦓 paraprotein disorder if ↓ albumin, unless there is other suspicion (e.g. nephrotic syndrome)!