All your videos so great and really appropriate the effort thank for doing all these videos .

Thank You very much for those videos. Liked it very much. Concise to the point.

Hysteresis is due to the property of surfactants. Their molecules are more apart during inspiration, leading to slight attractions between water molecules the surfactant is in between trying to reduce surface tension. In expiration, surfactant comes closer together and prevents that water-to-water attraction, reducing surface tension. So inspiration and expiration follow the different pressure-volume loops. This property of surfactants is the reason why the lungs don't collapse at the end of expiration. Without surfactants, your lungs collapse like in Neonatal respiratory distress syndrome or ARDS where surfactants are reduced/diluted.

It really has given intuitive idea....Good work..Thanks.

goooddd you're just beyond great! i watched all your videos! thanks a lottt :)))

Very useful presentation.... Regarding the hysteresis loop, I have a confusion. Sir, what is the cause of this different lung volume in inspiration and in expiration, at a certain point of pressure? That is what is the cause of Hysteresis?

There is something I'm really struggling to understand: why would the graph look so different on the way back (exhalation)? You stated what happens during Hysteresis, but really didn't give the logic behind it. You gave a good example with the balloon to describe the inflation phase, but this analogy is not valid for the exhalation phase (according to pascal law at constant temperature, V1*P1=V2*P2, regardless of the direction, inflation or deflation). Am I wrong? If so, where?

So in regards to Emphysema and PF patients. Due to different lung compliances would you expect one to be on a higher pressure than the other>I would expect a much greater volume assisted breath for the latter; or am I way off

You had it correct, the resting point is at FRC, not RV.

Wt about ASV mode

Thank you very much for providing a basis for the consequences of the positive pressure mechanics. Now that makes sense. So you need 3x more pressure for the same air volume with a ventilator than when breathing normally because of positive vs negative pressure. The lungs were built for the latter obviously. Like we know what high blood pressure does to blood vessels. 69% of over 65 year olds intubated die on the ventilator. The ones sent home have now twice the mortality rate than unintubated. It seems this procedure should be applied only to prevent impending death, forget sedation, and take them off the ventilator after a few hours if what caused the breathing issue can be stabilized enough. Why the hell don't they have iron lungs anymore (maybe a more sexy version), using negative pressure? That wouldn't cause any damage. The whole theory about recruiting bla bla seems to be not feasible anyway with the high pleural pressure. So if the patient can still mechanically move their lungs to effect negative pressure, then that would appear to be much better at oxygenating them than positive pressure ventilators. Why not focus on opening airways without ballooning the lungs? How are the collapsed alveoli supposed to heal if they are being stretched like balloons, just to overcome the surface tension (due to lacking surfectant? Figure out how to replace surfectant then. Or clear pathogens that can interfere with surfectants like candida. I just bought a dirt cheap 10g Ozone generator on Amazon. Works great. Ozone kills candida. As this is not doctor approved (though ozone therapy is very much a real thing, at the same time they say it's a pollutant and bad for the lungs..), I will test this out on myself for the next few days.

nice video

Can you not speak louder?

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