This generated some great discussion. Now let's do a deep dive

The first odd thing here is the Paw waveform. Traditional teaching is that in VC with continuous flow, the initial ⬆️in Paw corresponds to the pressure required to overcome resistance (as lung filling is minimal)

1/

https://twitter.com/Thind888/status/1752432498041294871

Since flow is constant, this 'resistive pressure' remains constant throughout the breath as revealed by the post-inspiratory pause (image 1)

Hence, the height of the initial Paw spike should equal the height of PIP - Pplat. This is not the case in our patient!

2/

As promised, here's a summary (?X-torial) from my talk at @accpchest this year.

https://twitter.com/Thind888/status/1710769441741631974

The main objective was to do a primer on respiratory mechanics and understand how the information obtained from the esophageal balloon can be useful.

There are a lot of pressures in mechancial ventilation. It is important to understand their physiological meaning.

Paging ENTtwitter & AirwayTwitter. Had a patient with moderate subglottic stenosis s/p recent dilation Intubated twice post-dilation for episodic stridor. During the second episode, scope showed laryngospasm. How common is this in non-OR (ICU) setting? Any tips on prevention/Rx? @LarynxUK @AirwayMxAcademy @AndyHiggsGAA @ProfEllenO @otolaryngolofox @rammoorthyENT @jducanto @JohnCSakles @NicholasChrimes @doctimcook @DrEricLevi @jstgeorgemd @drlauraduggan @NaveenEipe @dr_imranahmad @TBayEDguy @PedsAnesNet @gaspasser @drlauraduggan @juniordocmicro1

**Volumetric capnography: data points & equipment**

🧵[1/20]

There are three major reasons for limited utilization of volumetric capnography (VCap):
(1) Lack of education/training
(2) Lack of understanding of the data
(3) (Perceived) lack of equipment

Lets try to address 2 & 3 Let's start with a TL;DR of what VCap is:

Conventional capnography is 'time-based': Time on the X-axis and pCO2 on the Y-axis.

VCap has volume on the Y-axis.

VCap requires simultanoues measurement of exhaled pCO2 and expiratory flow.

This brilliant thread has me get my proceduralist nerd on. Continuing the conversation -

(I) Although French and Gauge typically refer to outer diameters of needles/catheters, there are exceptions:

A. When describing luminal dimensions of a multilumen catheter...

https://twitter.com/rbarbosa91/status/1532622531558903808

..In this case, the 'gauge' refers to the luminal diameter (image 1),

B. By convention, the size label of a percutaneous sheath introducer (PSI) (e.g. Cordis) refers to its inner diameter. This is because the whole purpose of a PSI is to allow introduction of another catheter...

@cjosephy @icmteaching @vaszochios @msiuba @IM_Crit_ @emireles_c @MegriMohammed @HamiltonMedical @ecgoligher @drhaty Ah, it's too complicated for a twitter thread, Clay, but I'll give it a shot!

Nomenclature is key. Ptp = Airway pressure (Paw) - Pleural pressure (Ppl);

*not* alveolar pressure (Palv) - Ppl, as often misquoted.

Hence, Ptp = transairway pressure + transalveolar pressure. @cjosephy @icmteaching @vaszochios @msiuba @IM_Crit_ @emireles_c @MegriMohammed @HamiltonMedical @ecgoligher @drhaty When we're trying to assess lung stress, what we really want to determine is 'transalveolar pressure'.

Now here's the kicker -
In the absence of airflow, transairway pressure is zero. In this state, Ptp equals transalveolar pressure!

**Tachyarrhythmia case**
- Middle-aged patient admitted with septic shock on norepinephrine. Home meds include metoprolol 100 qday.
- Baseline rhythm: sinus at HR ~100.
- STAT call to bedside for HR in 170s-180s with escalating norepi requirements.

- The monitor screenshot:

1/ 2/
-Initial read: narrow-complex tachycardia.
-First therapy: Adenosine
-Result: rhythm not converted but adenosine confirms underlying P-waves with atrial rate of ~180
-Interpretation: SVT at rate of ~180 with 1:1 conduction
-Differentials considered: sinus tach vs atrial tach.

1/
I've heard this argument before that "an amp of sodium bicarb raises blood pressure as it is hyperosmolar". I thought it'd be a good idea to quantify its effects:

Let's consider an average 70kg adult with TBW = 42L, ICFV = 25L (60%), and ECFV = 17L (40%), osmolality = 280.

https://twitter.com/emily_fri/status/1327695873837502464

2/
1 amp of bicarb=50 meq of Na and 50 meq HCO3 --> a total of 100 mosm of solutes are added. A key point is that all new osmoles remain in ECF-->ECF osmoles increase to 4860 mosm

To predict changes after equilibration, we have to look at changes in total body solutes and water.

1/ **Septal kinetics in acute cor pulmonale (ACP)**

I'm glad @load_dependent brought this up. I think it's helpful to analyze the mechanistic reasoning behind why 'diastolic' flattening is seen in ACP

In general, septal position depends on the relative RV/LV pressures.

https://twitter.com/load_dependent/status/1307664574385205249

2/
Normally, LV pressures during the entire cardiac cycle are higher than RV pressures so the curvature of septum is towards the RV.

Now let's consider what happens in acute massive PE:
(i) Acute pressure overload results in prolongation of RV systole, compared to LV systole.

An excellent question that is unfortunately not asked enough. The major mechanism, of course, is low V/Q lung units as nicely explained by @MegriMohammed

Here's a follow up poll, however:

Which location of clots poses the highest risk for hypoxemia?

(Poll below):

https://twitter.com/MegriMohammed/status/1291051792155910145

Poll:

contd

Part 2B:
*Transmural and intramural pressures*
– More on tendencies for pulmonary congestion vs pulmonary edema

Part A recap: Changes in ITP affect pulmonary post-capillary (venous) pressures and PCWP equally --> do not affect the gradient for pulmonary venous return.

1/

https://twitter.com/Thind888/status/1279564399984799745

2/ Therefore, the best way to assess tendency for pulmonary congestion is to measure PCWP when ITP is close to zero (at end-expiration), or normalize PCWP for ITP (PCWP – Ppl).

Let’s try now to dig a bit deeper into ‘tendency for pulmonary edema’ using the example of obesity.

Part 2A:
*Unique effects of transmural(tm) pressure and intramural(im) pressures*
–Introduction and basic concepts

Some of these ideas are quite convoluted so I’m splitting them up for clarity.

(NB: Some interpretations are a bit personalized so I can’t guarantee accuracy!)

1/ 2/
Definitions:

Consider a hollow organ located in a pressurized compartment.
- The pressure inside the organ = intramural pressure.
- The pressure outside = extramural pressure. -
- The pressure across the wall of the organ is transmural pressure ('mural' = wall).

(See image)

Part 1:
*Defining ventricular preload*

The conceptual definition of preload is quite straightforward: end-diastolic myocardial load/stretch. At the microscopic level, it's the sarcomere length we are interested in, which would increase with higher end-diastolic load (preload)
1/ 2/
The importance of preload is in effecting the Frank-Starling mechanism: increase in ventricular performance with ⬆️ preload. The basis of F-S relationship is primarily the sarcomere Force-Length relation.

At sarcomere length of ~2.3 μm, actin-myosin interaction is optimized.

*** PCWP in Muller's maneuver || Poll ***

Muller's maneuver (forced inspiration with closed mouth) is an excellent way to study heart-lung interactions.

In the experiment below, compare PCWP before and a few seconds into the maneuver (2 blue boxes) and take the poll below 👇 Compared to baseline, estimated LV preload near the end of the maneuver is ...

(Feel free to comment!)

1/
**Doppler knobology microskills: Wall filter**

I realized I haven't done an ultrasonography post for a while now so here goes.

Spectral doppler knobology is often overlooked but the basic settings include (i) Doppler Gain (ii) Scale (PRF) (iii) Sweep speed, and (iv) Baseline 2/ Just like B-mode ultrasound, doppler settings should be optimized to get the best tracing.

Here I'll talk about the less recongnized setting of "wall filter" and give a clinical example of how it may be useful to adjust.

But first, let's briefly review doppler physics.

1/ **How does pleural pressure (Ppl) affect alveolar capillary transmural pressure?**

This was brought up recently-

https://twitter.com/ArgaizR/status/1254838818412335106

Although it's impossible to do justice to this topic in a #tweetorial, I'll give it a shot

This is important to understand for 2 reasons: 2/ (i). If the transmural capillary pressure (pressure distending the capillaries) is highly positive - it will favor pulmonary edema.

(ii). If the transmural capillary pressure is highly negative - it will favor capillary collapse --> West zone 1 condition --> increased PVR.

1/11
**Nuances of IVC assessment**

So I was asked by @msiuba and @NephroP to talk about about the various nuances of IVC assessment in mechanically ventilated patients. I thought I'd go over some basic concepts for both spontaneously breathing and vented patients

Thread/ 2/11
Concept 1:
The core mechanism of respirophasic alterations of IVC diameter is its relationship with (actual, not transmural) CVP.
⬇️CVP -->⬆️venous return -->⬇️pressure within the IVC --> tendency to collapse (& vice versa).

Concept 2:
The IVC pressure-diameter relationship

*Fine-tuning breath delivery to maximize CO2 elimination in ARDS*

1/
In these testing times, I've resorted to learning new concepts to distract myself. Sharing something I learned recently due to its current relevance.

(Discussion is limited to passive mechanical ventilation) 2/ Why does CO2 elimination matter in ARDS?

Enhanced CO2 elmination would allow reduction of delivered minute ventilation (and hence, VILI).

The question I had was, is there's something that can be done to maximize CO2 removal for a given tidal volume and RR. The answer is yes.

1/ Can't love this enough!💕 Sharing a few thoughts:

(i) Personally, I like IV bumetenide for pharmacodynamic reasons: mg-for-mg, bumetenide is 5x more ototoxic than furosemide but 40x more potent = resulting in an ototoxic potential of 1/8th that of furosemide. (PMID: 7338574)

https://twitter.com/PulmCrit/status/1215247550707617793

2/ This is perhaps why *conventional* maximum doses of bumetenide are twice as potent (e.g. 2mg/hour of bumetenide vs. 40mg/hour of lasix). So the loop diuretic dosage can be maximized with lower potential for ototoxicity.

(ii) The term "contraction alkalosis" is a troublesome.

1/ *Can we see Torsades coming?*

A few months ago, I had the chance to study the rhythm changes leading up to an episode of Torsades. Discussed here -

https://twitter.com/Thind888/status/1208928426301755392

This helped me pick up some "warning signs" that may help facilitate early recognition.

#tweetorial 2/There are 3 critical substrates for Torsades:
(i) Prolonged action potential (long QT)
(ii) Early afterdepolarizations (EAD)
(iii) Dispersion of repolarization (DR)

(i)A long QT is essential but not sufficient. E.g. Amiodarone prolongs QT but reduces DR - low risk of Torsades.

1/
*Case of the bizarre PVCs*

Switching gears to rhythm interpretation - a rather under-appreciated art in non-cardiac ICUs.

A 77 yo M admitted due to resp failure from CHF. Nurse calls to evaluate "bizarre" looking PVCs noted on telemetry.

A telemetry snapshot is attached - 2/ Scrolling back a few minutes, the following progression is noted (all images are timed).

The patient appears well and vital signs are normal.

- Thoughts?

@ArgaizR @load_dependent @EM_RESUS @smithECGBlog (Feel free to tag more ECG geeks)