This was an MI of the RV + inferior LV, with complete heart block, caused by a thrombotic occlusion of the proximal RCA.

Thanks all for commenting. 🧵 below has some basic stuff + nerdy stuff, hopefully something helpful for everyone.

1/
Most people quickly noticed the marked ST elevations and jumbo T-waves in the inferior leads. Some inferior STEMIs can be very subtle. This one isn’t.

You're right to want to page the interventional cardiologist the minute you see this.

2/
But several folks also pointed out that this ECG exemplifies the importance of a systematic approach.

My system is Rhythm-QI-ACS.

Rhythm and rate
QRS
Intervals
Axis
Chambers
ST/TW/Q aka ischemia

3/

The rate is 50s, but the rhythm is complete heart block. Sinus-looking P-waves (+ in II) march out at a rate of ~150 (quite the hypersympathetic state), but have no relation with the QRSs. It may look like some precede the QRS, but others are buried in the T-waves, QRSs, etc.

4/
This is a critical finding, because the escape rhythm may not last forever, and the bradyarrhythmia may quickly become an additional life-threatening problem you may need to manage before (and less likely after) reperfusion.

5/
Moving on. The QRSs are variable. Beats 1 & 6 are narrow (proximal His bundle escape beats), but others' morphology is LBBB or incomplete RBBB / delayed RV. This is important, because ischemic changes are best assessed with normal depolarization (narrow QRSs).

6/
The axis is normal. QT is normal. Chambers - there may be LVH based on precordial voltage in non-LBBB pattern beats. Meh.

Finally, let’s take a closer look at those ischemic changes that jumped out…

7/
We'll avoid complexes #2 and 3, since LBBB distorts things (but doesn't hide STEMI here).

Based on the other complexes, we see an inferior MI:

~5mm STE in III and F
~2mm STE in II

The STD in I, L, V4-V6 are likely of this injury current (reciprocal changes).

V1-V3 later.

8/
The inferior LV wall is usually fed by the PDA.

The PDA usually comes off the RCA, less commonly LCx.

As such, the most clinically relevant question with IMI is whether it’s caused by a PROXIMAL RCA lesion.

9/
If the occlusion is in the RCA proximal to the acute marginal branch, then the RV is involved meaning different prognosis and considerations in management (e.g. not dropping preload).

There could be hints of this on exam. But how do you mediate this suspicion on ECG?

10/
The quickest screen is to look at the relative magnitude of STE in lead III vs. II.

STE in III > II is a sensitive finding for RVMI (see table from PMID 11179532).

If present, PPV is high enough (and sensitivity of STE in V4R low enough), that you can act on it.

11/
BTW, mechanistically, this makes sense – an additional injury current involving the RV will contribute to more STE In III (a right-and-downward pointing lead) than II (a left-and-downward pointing lead).

12/
Finally, let’s talk about V1-V2. In most IMIs, V1-V2 have ST depressions, reciprocal to the inferoposterior STE.

But V1-V2, esp V1, also overlie the RV - the anterior ventricle.

V1 STE > 0.5mm in setting of IMI is predictive of RV involvement.

13/

pubmed.ncbi.nlm.nih.gov/30497759/
One nerdy thing:

The above study by @SmithECGBlog and co also found that the sensitivity of STE in V1 for RVMI was only 35% if there WAS STD in V2, but higher at 69% if there was NO STD in V2.

14/
Basically, the injury currents from the inferior LV and the RV are competing in V1/V2, and can cancel each other out.

If there’s less inferioposterior wall current, it allows the RV injury current to be seen better.

15/
Another nerdy thing:

I think V2 and V3 may have been reversed in this ECG based on the QRS and ST segment progression/continuity.

16/
Take-home points:

- Always be systematic even if an overt abnormality jumps out at you
- In IMI, STE in III > II is a sensitive screen for RVMI
- Its PPV is enough too, but STE in V1 or STE in V4R are even more specific
- If RVMI, don't drop preload, watch for brady rhythms

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More from @sargsyanz

23 Apr
When an adverse health event happens shortly after a covid vaccine, it's hard not to try to make a connection.

"I got the shot Monday and had a heart attack Wednesday... is it really a coincidence?"

Let's do some quick math:

1/12
Let's round the US population to about 300 million.

Around 3 million people per day are getting a vaccine dose.

Now let's look at heart attack rates in the US (we'll abbreviate them MI for myocardial infarction):

2/
There are 1.5 million MIs in US per year

That's 1/200 ppl per year (1.5 M / 300 M)

That's 1/73,000 ppl per day (1/200 / 365 d)

That means that every single day, out of every 3 million people, ~40 have an MI.

3/
Read 12 tweets
8 Mar
Interesting experience at the dentist, with #zentensivist and #healthpolicy lessons.

Had a cleaning a couple weeks ago, she said I had a small cavity worth filling. I went back today to do that.

1/5
She pokes around, makes eyebrows, says let me go look at that X-ray again.

Pokes around some more, pauses for a moment.

“Let’s just leave it alone and watch it.”

2/
I’m de facto happy but also curious about the reasoning. She explains. It makes sense (but not quite enough for me to relate it here).

On my way out I ask her if there’s a billing code for her careful consideration.

Nope. You only get paid if you do stuff.

3/
Read 5 tweets
7 Dec 20
As you turned the corner on the second flight of stairs, you felt your breath pull a little deeper, the next one come a little earlier. Your heart said 👋🏼, bounding softly in your neck.

Ten seconds down the hall, all that faded. You were back to mulling some thought.

1/
But hold on. Let’s pause for a minute and retrace the steps.

A lot happened before the extra breath and the tug in your neck caught your attention.

And it’s all so damn cool.

2/
At the foot of the stairs, anticipation of exertion 🔔 and the stretch of muscle fibers 🦵🏽sent a signal to the sympathetic nervous system: start the car.

3/
Read 13 tweets
27 Nov 20
I’m fascinated by the question raised in this great blog post (read first).

“Always address the abnormal vital signs first”

I’m gonna think through some physiologic uncertainties and hope that @smithECGBlog @JSawallaGusehMD @MKIttlesonMD @BCMHeart can help me.

Thread 1/
I’ve always thought of severe hypertension as a cause of increased myocardial oxygen demand. Which makes sense for the SBP (afterload, wall stress)... it’s what the LV is contracting against.

2/
But what role does the DBP play?

Not much of one as far as the LV’s workload far as I can think...

But diastole is when coronary perfusion happens. Applying Ohm’s law in that vascular bed,

DBP - LVEDP = coronary blood flow (CBF) x coronary vascular resistance (CVR).

3/
Read 7 tweets
11 Nov 20
Folks always confuse 1:1,000 vs. 1:10,000 epinephrine, when you're supposed to use which, what the dosing is, etc

Here's what helps me remember/teach.

Thread 1/9 Image
There's two main indications for epi - code blue and anaphylaxis.

1. Code blue is a 1mg IV dose of 1:10,000 epi

2. Anaphylaxis is 0.3mg IM dose of 1:1,000 epi

Shouldn't be that hard to remember... but it is.

2/
There's the route, the dose, and the concentration.

The route is easiest. Think of epi being pushed IV during a code. Think of the epipen people jab into their thigh muscle for anaphylaxis.

1. Code – IV

2. Anaphylaxis - IM

Great, moving on.

3/
Read 9 tweets
1 Oct 20
Descriptive terms are great.

Take “calcific uremic arteriopathy.”

Arteriopathy. There’s a problem with arteries, so you might guess manifestations may be ischemic/necrotic.

1/6
Calcific...

Calcium deposits in the arteriolar walls, usually of the skin, causing fibrosis, thrombosis, obstruction.

Uremic...

This usually happens in the setting of kidney disease and a high calcium-phosphate product, though it’s complicated.

PMID 29719190

2/
Ischemic skin hurts, and necrotic tissues get infected. It’s a very bad disease.

The original (and still most commonly used) name, calciphylaxis, doesn’t tell as much of a story. Where did it come from?

3/
Read 6 tweets

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