Thread by @Thind888

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.

3/Example 1: Obesity
We first have to appreciate basic respiratory mechanics in obesity. Extra chest and abdominal weight pushes on the chest wall causing a positive ITP during expiration (say ~10 cmH20). Mechanically, this is actually quite similar to forceful expiration (image)

4/ The reason for expiratory flow limitation with forced expiration is collapse of airways proximally (see image). The same happens in obesity.

Importantly, Palv never drops < Ppl

This mechanism is helpful otherwise we would collapse our alveoli every time we forcefully exhale!

5/ We have established that increased Ppl in obesity does not affect tendency for pulmonary congestion (image).

What about tendency for pulmonary edema?

‘Pressure gradient’ for transudation is tmPc = imPc – Plav.

What happens to imPc and Palv when ITP is raised from 0 to 10?

6/
-Pc (intramural) increases by 10 (as both pre-capillary and post-capillary pressures increase by 10).
-Palv does not drop below 10 during expiration (see above).
Hence, at end-exp, both imPc and Palv are increased by 10 --> no change in tendency for pulmonary edema.

(Image)

7/ In other words, mass loading of chest wall with obesity raises end-exp ITP but does not change tendencies for pulmonary congestion or pulmonary edema. So at least in this case, tmPCWP provides an accurate estimate of tendency for both pulmonary congestion and pulmonary edema.

8/ Example 2: Mueller’s maneuver
A person performs Mueller’s maneuver at end-expiration.
-At end-exp: Ppl = 0 ; Palv = 0
-With Mueller’s: Ppl = – 20 ; Palv = – 20 (as insp effort is with a closed glottis, ΔPalv mirrors ΔPpl).

Tendencies for pulmonary congestion/edema: see image

9/ Note that these calculations are valid for the very first instant of Mueller’s but things change quickly! (later)

The discussion on ‘tendency for pulmonary edema’ is not complete without mentioning the effect of CVP. We know that tmPc (= imPc – Palv) drives fluid transudation

10/ However, pulmonary lymphatics continuously drain this into the RA. An increased imCVP, apart from causing systemic congestion, would also impede lymphatic clearance of pulmonary interstitial edema.

I learned this from my friend @FH_Verbrugge -

https://twitter.com/FH_Verbrugge/status/1255340691561099264

11/ Example 3: PEEP/PPV:
This can get tricky. Let’s start at FRC (end-exp) where Palv = 0; Ppl = 0.
A positive pressure of 20cmH20 is added that inflates the lungs enough to cause a Ppl of 10.

Q1. Tendency for pulmonary congestion?
Answer: Exactly same as the obesity example.

12/ Q2. Tendency for pulmonary edema.
Ans: Just like example 1 (obesity), imPc has increased by 10. But the big difference is in Palv. In example 1, ΔPalv mirrored ΔPpl. But here, ΔPalv is twice as ΔPpl. (PEEP went from zero to 20; Ppl went from zero to 10).
(Analysis in image)

13/ Starting from relaxation volume (~FRC), tendency for pulmonary edema decreases with lung inflation. Lung volume is proportional to transpulmonary pressure (Paw – Ppl).

For given transpulmonary pressure (PL), PPV vs NPV doesn’t matter. See image for NPV with same PL.

14/ Therefore, we can see that tmPc (tendency for pulmonary edema) is inversely proportional to lung inflation (and hence PL).

In fact with high lung inflation, tmPc becomes so low that we start worrying about West zone 1 or 2 conditions causing ⬆️PVR 👇

https://twitter.com/Thind888/status/1255329852112207874

15/
-Summary:
-Tendency for pulmonary congestion vs pulmonary edema are distinct concepts driven by unique pressure gradients.
-We discussed impact of heart-lung interactions on PCWP interpretation using 4 examples (i)⬆️ITP (obesity) (ii)⬇️ITP (Mueller’s) (iii) PPV/PEEP (iv) NPV

16/
- tmPCWP (not imPCWP) always (always!) accurately predicts tendency for pulmonary congestion.

- With lung inflation (doesn’t matter PPV or NPV for a given PL): imPCWP is (paradoxically) a more accurate reflection of tendency for pulmonary edema; tmPCWP overestimates it.

**Bonus question**
How can you correct the measured PCWP in a patient with PEEP?
Ans: There is an easy way to determine the end-exp Ppl caused by the PEEP:
1.Calculate the driving pressure (Plateau – PEEP): convert to mmHg
2.Calculate ΔPCWP (PCWPinspiration – PCWPexpiration)

3.‘Index of transmission’ (increase in Ppl per 1mmHg of Paw) = ΔPCWP/Driving pressure
4.End-exp Ppl = PEEP x ‘index of transmission’
5.Corrected PCWP = measured PCWP – end-exp Ppl

(Next part: Pericardial restraint and true assessment of LV preload!)

Link for original thread -

https://twitter.com/Thind888/status/1276954595298852867

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