I believe we do NOT understand PE pathophysiology. Therefore, we do NOT understand COVID19.

Serotonin rules PE cardiovascular changes.
Serotonin rules COVID19 pathology.

1967 paper:
https://www.sciencedirect.com/science/article/abs/pii/000291496790104X

@iceman_ex @Acute_Pulmo_Med @ThinkingCC @srrezaie @cameronks @gattinon

The absolute most indisputable piece of evidence in COVID19 that implicates serotonin-induced DIFFUSE pulmonary microvascular spasm is provided by @jwmdebacker - there is DIFFUSE spasm of entire microvascular bed of the lung, not just in areas of GGOs. https://twitter.com/i/status/1313139869292662785

Now can serotonin infusion / release in pulm vascular bed lead to "silent" hypoxia? YES!

To hyperpnea (via carotid sinus)? YES!

Why hyperpnea? To compensate for dead-space physiology, to reduce high V/Q mismatch developed due to pulm vasoconstriction

https://pubmed.ncbi.nlm.nih.gov/13435356/ 

Further evidence of such changes due to serotonin
- hypoxia
- reduced compliance
- hyperpnea
- large intrathoracic pressure swings (even after succ) --> "P-SILI" @gattinon?

https://www.sciencedirect.com/science/article/abs/pii/0002870357901898

P-SILI anyone?
Pneumothorax in absence of positive pressure??

Serotonin hyperpnea demonstrated

What happens when you remove platelets in experimental micro-PE (e.g. akin to COVID19)?

Same thing that happens when you treat with heparin.
Same thing that happens when you antagonize serotonin.

Hypoxia resolves.
PVR rise diminishes.

http://pdfs.semanticscholar.org/2c1f/4d08df25ac4083a33a8621f4d04eede4b465.pdf

Now can SEROTONIN freed up from PLTs in micro-PE induce a SEVERE intrapulmon VENOUS hypertension, with no increase in large extrapulm veins?

Pulm edema of PE?
GGO of COVID19?

Acute alveolar filling due to hydrostatic P? All due to PLT serotonin?

https://bit.ly/3qVjCHa