pulmonary alveolus

Mm-hmm.

And so what they discovered at Cambridge is that at the alveoli interface, when we inspire or breathe in, we're generating O2 and N2 nanobubbles.

And as we expire or exhale, we're generating CO2 nanobubbles.

And these line the entire lowest layer of the endothelium and the endothelial glycocalyx, and the CO2 becomes fixed through interstitial cellular foams and proteins.

Key terms, make sure you guys highlight this or put a star next to it, whatever, but these key terms you absolutely need to know.

Alveoli, remember that's where oxygen, gas, carbon dioxide takes place, exchange.

Asthma.

adlectasis, COPD, cystic fibrosis, I put a star next to it, NCLEX, NCLEX does ask about cystic fibrosis, larynx, pneumonia, infection in the lung, you need to know that, pneumothorax, seasonal rhinitis, sinusitis surfactant i put a star next to it and clicks and you're going to see this again when you get to maternity back from the page all right Page 930, upper respiratory tract.

The upper respiratory tract, that includes the nose, pharynx, larynx, and trachea.

The lower respiratory tract includes the bronchial tree and alveoli.

Gas exchange occurs where? Alveoli.

Very good.

What are the little k- Uh, they look like broccoli, don't they? The, uh-

Alveoli.

Alveoli, yeah.

He's a good act.

Not areola.

And then maybe set them in dead space.

Yeah, I think PE is more likely like a dead space where the alveoli is getting air, but it can't actually provide, well, there's no exchange going to the blood because the blood isn't reaching the alveoli circulation.

Yeah, nice.

So dead space is ventilation reaching the alveoli, but the thrombus prevents the perfusion, which leads to reduced oxygenation of the blood.

Yeah, so those are the three things.

You get function and then inflammation of the lungs and the pleura.

They're hard to inflate, right? You've pushed air through the airways.

That air has now gotten to the alveoli, and those alveoli are trying to expand, right? But the compliance is the difficulty in expanding Those alveoli.

And again, we're gonna get more into this.

And this problem increases both the peak pressure and another pressure called the plateau pressure.

There's no movement of gas.

There's no flow.

So it takes airway resistance out of the equation, and what's left is just the pressure those alveoli are kind of exerting on the gas that is present, and that's lung compliance, right? Those alveoli get stretched when they expand, and then you pause that breath.

You don't let any air out, and those alveoli are pushing down on the air that expanded them, and that's representative of lung compliance.

And basically, what this means is that sodium chloride seems to change the way that the water, mucin, phospholipids, and pulmonary surfactant is interacting in the surface of the airways.

So as we know, the pulmonary surfactant, it has a very important role in reducing the surface tension and keeping the alveoli stable.

So this basically is raising the possibility that normal saline could also have some effects through this pathway and affect the airway mechanics and airway dynamics.

Another interesting possibility is that the chloride that we find in normal saline may also play a role in immunity, as while neutrophils, they can use this chloride through the enzyme that is the myeloperoxidase to produce hypochlorous acid that we know it is a potent antimicrobial molecule.

Jessica, that was extremely helpful.

I have a couple of questions I want to ask about that.

First, when you talked about pulmonary surfactant and the nebulized normal saline helping to decrease surface tension and keeping the alveoli stable, The first thing I thought was that'd be helpful for a ventilated patient or a patient in any type of respiratory distress because the more alveoli open, the better gas exchange will occur.

Is that a fair statement to make?