A discussion of surface tension, with emphasis on the role surfactant has in reducing surface tension within the lungs, and the consequence this has for respiratory mechanics.
It may not be obvious from the video, but the role of surface tension and surfactant in the lungs is much more complicated than presented. This was just to give a basic introduction to the principle and one place it's applicable in medicine. However, not all physiologists are a fan of this simplistic view of the alveoli. In the spirit of open dialogue, here's a counterargument from someone who doesn't mince words ("It is time we understood that the Y-tube model of the alveolar inflation ... deserve a place, not in our minds and textbooks, but in the museum of wrong ideas."): www.physiology.org/doi/full/10.1152/advan.00024.2002
I appreciate this video. Surfactant and its effects do not come easily to me, even after reading my text, but you really cleared it up for me. Thank you.
Thank you so much. This has made my understanding of surfactants in the lungs as clear as day. I'm a student in an Anatomy and Physiology class and this is exactly what I needed.
Absolutely fantastic video. I really enjoy the format of this video, with the relevant demonstrations of the concept and the familiar parallels drawn. Awesome stuff. Subscribing now, hope to see more videos like this. Thank you!
Great video, very helpful. I just started school in Respiratory so i can use videos like this to help me learn. Thank you for this and I plan to keep watching your channel and learn more.
Thank you so much for this video!! I have been struggling for a long time to understand the concept of surface tension and lung mechanics in general, and this video has been extremely helpful and delivered exactly what I needed.
I'm looking for a video on the mechanism by which surfactant reduces surface tension. Is it by increasing entropy? Cathrage cages? or some other mechanism?
Excellent video. I'm a Physiology instructor, and I'm going to teach Respiratory Physiology to medical students in Venezuela, your lecture has been really helpful. Thanks!
I'm studying physics, but your medical perspective in these things was still very interesting and helpful! Thank you! May I suggest next topic: quantum mechanics in medicine. :)
Good stuff man, you made it much simpler to understand surface tension in the alveoli and the role surfactant plays than this long and dubious text book on ventilation. Sometimes I wonder if the authors just want to trip you up or they really want recognition of their wits.
I still don't understand what exactly water does to the internal surface of the alveoli, in the case no surfactant is present. This fluid (containing water) is only coated on the internal surface of the alveoli. It "contracts" in the alveoli, and this somehow reduces the radius of the whole alveoli? How? Why?
(Sorry for the delay in response - just saw your comment now!) Water molecules attract one another, and adhere to the inner surface of the alveolus. Think of it like this: As each water molecule attracts the molecules immediately adjacent to it, they get pulled together and the distance between them decreases. But if the distance between every possible pair of water molecules decreases, they must be moving closer to one another. As they are also attracted and adherent to the inner surface of the alveolus, this necessary must pull the alveolus inward. That is, until the inward pull of alveolus (quantified as the alveolar wall tension) is balanced by the air pressure inside.
@@harishguna4191 Here's a link to some videos from my buddies Corporis and Up and Atom who talk about quantum biology: ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-Zc9Xk99gCr4.html
Why is the surface tension of the mixture of h20 and surfactant proportional to the surface area?? And not so with the water alone? Is this answered y the article you cite in the description of the video? Thanks
@Utkarsh balani (sorry, unable to directly reply to your comment), I am unaware of any clinically relevant, direct effect by which surfactant helps to prevent pulm edema. Indirectly, as surfactant prevents atelectasis (i.e. alveolar collapse), it theoretically helps to prevent the development of pneumonia, which would result in focal pulm edema. Pulmonary edema, on the other hand, directly reduces surfactant content, most likely due to proteolytic enzymes in the edema fluid breaking down the surfactant, but a mechanical "washing out" of the surfactant by the edema fluid may also play a role.
Increased pressure of inflation will draw water from the capillaries into the alveoli. Therefore, by decreasing pressure (increasing compliance) surfactant will prevent pulmonary edema, and even possibly reduce the edema in some cases. The edema is simply water moving along pressure gradients. Reduce the gradient and reduce the edema.
Mike Birkhead Mike, thanks for the response, but I'm not sure that higher intraalveolar pressures necessarily pull water into the alveoli per se. I think what probably happens in situations of surfactant depletion, collapse of alveoli from the increased surface tension then results in a reduction in the pulmonary interstitial pressure as adjacent alveoli tug at the interstitum from opposite directions as they collapse. It's this reduction in interstitial pressure that creates a pressure gradient favorable for fluid loss out of the capillaries. The net result is that there is more fluid in the interstitium, not necessarily in the alveoli - though this is still referred to as pulmonary edema, and would essentially have all of the same effects of fluid in the alveoli (e.g. hypoxemia with elevated A-a gradient, lower lung compliance, etc...) See: www.ncbi.nlm.nih.gov/pubmed/1399997 In 15 years, I've never once heard this come up on the wards; I would imagine that the clinical relevance of this specific issue (i.e. surfactant loss leading directly to pulmonary edema) is probably quite low. Please feel free to reply again if you still have different thoughts. This is me hypothesizing, not me stating known physiology facts.
Eric's Medical Lectures I don't have any time in the "Wards", I'm a first year medical student. The basis of my statement came from reading what we call a "SuperObjective" Which is a compilation of several students study guides (usually four or five students will put together several superobjectives over the period of each block). With that said, they tend to get a lot of information from research papers as well as UpToDate. I am not sure of the exact source used in this as the individual study guides will cite sources, but the superobjectives usually do not. However, I decided to clarify this for myself. A precursory look on UpToDate states that pulmonary edema is associated with surfactant deficiency (especially in RDS) due to the following: 1. Sodium channels that remove fluid tend to develop in a linear fashion with surfactant production (ie. preterm births tend to have both complications) 2. Inflammation due to lung injury 3. RDS patients tend to have low urinary output that exacerbates edema. "Pathophysiology and clinical manifestations of respiratory distress syndrome in the newborn" Firas Saker, MD A look through some of the study guides that mentioned similar phenomenon as I originally stated (in the first reply) cited a book that I do not have: Respiratory physiology-- the essentials (by John B. West). If I remember to do so, I will check for the book in the health science library and validate the source. Suffice it to say, I also like your posting on interstitial edema and it makes since. Thanks for the response! - on another note, in what situations would surfactant be deficient other than in RDS? If I remember correctly, it is related to NO somehow (foggy speculation)
Great lecture. I saw that water is coating the inner surface of the alveolus. You mentioned that the surface tension of water coated is independent of the volume of the alveolus because surface tension is intrinsic. But I think if the alveolus has bigger volume, it might have wider inner surface and therefore more water molecules are able to stick which makes higher surface tension because there are more water molecules...? I want to know whether this is true or not
There is something I would like to mention, Surfactant production in fetal lungs begin at 20 weeks but the amount produced is insuffiecietnt up till the 26-27th week. So actually 34 weeks is alittle bit exaggerated?
Thank you for these videos Dr Strong. As a former physicist now medical student I absolutely loved these videos. If I wish to go into more details about the applications of physics to medicine would you have any recommended resources?
darkenergylambda Thanks for the message. Unfortunately, I don't have any recommended resources for physics in medicine. It was that lack of resources that was one of my motivations for this specific topic as an entire video series.
This video is fascinating and the concepts are crystal clear. Thank you! Tangentially, is there any consensus as to why alveoli are different sizes? It seems identically sized alveoli would be preferential and our lungs should have evolved in that fashion.
+Beegslove I would assume that's part of the explanation. Also, there is variability in the mechanical forces that act on different parts of the lung, which result in termporal and regional differences in alveolar size. As just one example, at night, when you are lying down on your back, your heart (which is an anterior structure) and which is relatively dense, compresses the lung tissue underneath it, resulting in something called atelectasis (mentioned in the video). Retrocardiac (i.e. behind the heart) atelectasis causes those alveoli to be underinflated relative to the alveoli in adjacent regions of the lung. Then during the day, when you are upright, that regional difference goes away.
I don't understand all those positive comments. Yes, the video is nice, yes, there is water in the alveoli (with its surface tension), but the Laplace's law is about wall tension, not about surface tension of fluids.
According to the law of Laplace the result of a low surface tension and a large radius is not a lower collaps pressure. The large alveoli with its large radius has a higher surface tension in relation to the smaller alveoli. Therefore the collaps pressure in the larger alveoli will be higher and in the smaller alveoli lower. Both alveoli will be more equalized (homeostasis) and ventilated.
