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/
Then your brain made your legs move.

Basal ganglia 👋🏼. Pre-frontal motor cortex⚡️thru internal capsule, brainstem 🔀, corticospinal tract.

Alpha-motor neuron⚡️thru spinal root and nerve to neuromuscular junction.

Acetylcholine+🥩=⚡️

Actin + myosin shorten. ATP releases.

3/
Your big muscles doing work led to two things.

First, locally released vasodilatory substances made a new path of least resistance for your cardiac output. More blood flowed there, less everywhere else.

..but only for a second.

4/
The pressure receptors in your aorta and carotids felt the drop. Less ⚡️up the vagal and glossopharyngeal nerves disinhibited sympathetic outflow from the brainstem.

Foot on the gas. The spike in norepinephrine made your heart squeeze harder and faster.

5/
Your cardiac output doubled, to make sure to still send the usual 5 L/min to the brain and kidneys and such on top of the extra 5 L/min your legs were suddenly siphoning.

Then when your legs stopped siphoning, you felt some extra pep go up your carotids.

6/
And all of this was to bring extra O2 and fuel to the muscles (without making you faint). But what happened to those?

O2 + glucose ➡️ CO2 + H2O.

A little electron transporting here, a little Kreb’s cycling there made this happen.

7/
And the Kreb’s cycle has a little byproduct that the body likes to keep in a very exact range: CO2.

8/
As the extra CO2 coursed through your🩸, peripheral receptors told your medulla that your pCO2 was now 42 and not 40. Two sec later, 44. Uh-oh.

Chemoreceptors in medulla itself sensed a pH of 7.33. Some of that was from the CO2... some from a little lactate in the mix.

9/
Nearby, the pontine respiratory groups got the message, and signaled your diaphragm and company to breathe deeper and faster. To blow off more CO2 and bring it (and the 🩸 pH) back to set point.

10/
One of the things that can make us feel aware of our breathing (or feel short of breath) is a mismatch between ventilatory demand and ventilatory reality. In this case, it was mild and transient, as your compensation caught up and the exertion soon ended.

11/
There’s a lot of other things that happened and changed on those stairs and in the hallway after (... and every second since).

Being aware of even a small fraction of it can bring wonder and aesthetic joy.

12/fin

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More from @sargsyanz

27 Nov
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
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
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
15 Sep
+1 for organization/structure as foundation of effective communication.

Learners often struggle with shifting expectations. And teachers sometimes associated highly structured presentations with wordy ones. So I want to emphasize:

Organized does not mean wordy.

1/6
Example: here is a organized and efficient yet thorough presentation. < 1 minute. < 3 tweets.

“Ms J is our lady with HF and DM here with pyelo.

This morning back pain is better, dysuria’s gone. Didn’t sleep well from noise.

Tmax 99.7, BP around 150s, other VS normal...”
“...Looks more comfy, oriented. JV 10cm, lungs clear. CVA less tender.

White count 10 from 16. Chem 7 totally normal. Sugars were 180, 203, 144, 130. Urine with E.coli, sensies pending.

Right now she’s on ceftriaxone, lisinopril, metop, Lantus + prandial, senna, prn APAP...”
Read 6 tweets
10 Sep
I agree; there’s a theme there to be explored.

We have a tendency to overcorrect, to gravitate to extremes.

And to get overemotional or snarky when advocating for what we think are best clinical practices.

I’m guilty too. But I think there are downsides.

1/8
First, our own practice & quality of care suffer when we think in extremes and absolutes.

Second, we can communicate oversimplified or wrong messages to learners who don’t have the same contextual knowledge.

Some examples of such misunderstandings...

2/
#NeverFOBT 😡, people say.

What about CRC screening?

What about this stool, which might be blood or food pigment? Or the self-evacuated black stool of a patient who’s on iron or pepto, and is tachy today?

I’d Guaiac that, and change management if overtly + vs -.

3/ Image
Read 8 tweets
3 Sep
Had a realization about quiet heart sounds that came about a decade late.

Short thread.

1/4
Ok.

S1 and S2 happen when pressure gradients snap them shut. Right-sided cardiac pressures and thus valve-closing pressure gradients are lower, this P2 is quieter than A2.

And if you get pulmonary hypertension, P2 gets louder.

A bit more from UpToDate:

2/4 Image
What about hypOtension? If you’re septic or bleeding or in cardiogenic shock, the lower pressure gradients should translate to quieter sounds.

Thus, quiet heart sounds in this setting are probably less discerning for pericardial fluid.

3/4
Read 4 tweets

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