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Hypoxemia in COVID-19 pneumonia: Role of vasodilatation vs lung stiffness: MedPage Today

EM SARS-COV-2 emerging from apoptotic cells: NIAID

We already know that COVID-19 pneumonia results in acute respiratory distress syndrome (ARDS)– this is severe hypoxemia resulting in a requirement for oxygen supplementation, or possibly intubation followed by mechanical ventilation. Using a ventilator brings with it a host of additional problems because air containing high concentrations of oxygen is forced into stiff lungs– oxygen is toxic at higher levels, and stiff lungs don’t appreciate being forced open.

A new finding in COVID-19 pneumonia has been revealed by studies of potential brain damage caused by strokes– blockage of blood flow to the brain due to clotting. Severe COVID-19 also can result in enhanced blood clotting, causing blockages in arteries and veins throughout the body.

Researchers were looking at blood flow in the brain with ultrasound (high-frequency sound) scans that showed blockages– or not. The patients in these studies didn’t have strokes (others did, but that’s another story.) Not finding strokes, the researchers tried a different technique that demonstrated blood flow in the lungs actually increasing despite the low oxygen levels.

This technique, using tiny air bubbles introduced into the veins, found that the bubbles weren’t being filtered out during passage through the lungs (as they normally would have been) and demonstrated that the capillaries in the lungs had enlarged so much that the tiny bubbles passed right through.

These enlarged capillaries– vasodilatation– were hard to explain. The researchers had thought that the blood passing through the lungs didn’t take up oxygen because the thin membranes of the alveoli (the tiniest air cavities in the lungs) had been thickened by inflammation or fluid accumulation.

This is the phenomenon of “stiff lungs” that prevents air from inflating the alveoli. This always occurs in ARDS from other causes, and must occur, at least to some extent, in COVID-19. It appears, however, that even before the lungs become stiff from inflammation, the capillaries must be dilating dramatically enough to allow the blood to pass through so fast that it doesn’t take up sufficient oxygen.

The question is: why do the lung’s capillaries enlarge so much early in COVID-19 pneumonia? One hypothesis is that some substance produced early in the disease may be causing the enlargement. Bradykinin, a hormone that normally dilates veins to balance out the effects of angiotensin, (this is an oversimplification) may be increased due to the damage that the virus does to the blood vessels’ lining cells (endothelium.)

This is an area of active research that has not yet produced answers, but it may result in dramatic improvements to treatment of COVID-19 pneumonia.

(This post is an simplified summary of an already simplified story on Medpage Today dated September 1, 2020, which you can read here. The story is based on a letter in the American Journal of Respiratory & Critical Care Medicine.)

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