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 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)!
Recent ICU shifts = newfound appreciation for this clinical dilemma.
The traditional breakdown of hypotension/shock is very classic: my schema aims to sub-divide this framework & cover some new buckets.
Read on! 🧵
First, recall BP is a product of Cardiac Output * Systemic Vascular Resistance.
When assessing hypotension, cardiogenic etiologies should come to mind first because a markedly abnormal Heart Rate derangement may provide an up-front answer.
Think extremes:
- HR < 30
- HR > 150
While the other cardiogenic etiologies cause ↓ MAP via Contractility/Preload issues, I find it more intuitive to group the leftover etiologies by:
- LV vs. RV failure
- Chronicity
If you group the DDx this way, you'll easily appreciate the common causes:
I loved creating this one-pager because my understanding of how to clinch this Dx shifted enormously throughout my intern year.
Turns out, "no diastolic dysfunction" on TTE doesn't = no HFpEF.
Let's go through the pathophys & see how this assists Dx.
The pathophys of HFpEF first involves diastolic dysfunction.
(This may or may not be visualized on TTE; more on this in a second.)
With an expected ↑ LV-EDP during exercise (+/- at rest), LA pressure then ↑.
This will, chronically, lead to LA enlargement.
Pulmonary venous pressure then ↑. In order for forward blood flow to be maintained in the face of this increased pressure, what can be called the "biventricular reflex" ensues, leading to PA vasoconstriction.
Of note, this process (initially) *prevents* pulmonary edema.