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Kim Petersen Thanks! Shall try to record and upload more & more videos, with greater frequency. Also, please let me know, if any point needs a further discussion. Regards,
Thank you very much! There's just one thing I don't understand. You say that people with COPD exhale slowly to avoid too rapid a drop in airway pressure. But this seems to imply that with a faster flow we can reach a pressure of 0 (atmospheric) before reaching the mouth. And that the air could therefore stagnate (for lack of a gradient) before reaching the mouth.
No. That won’t happen. Alveolar pressure (P1) is positive (say, + 20 for forceful expiration). And atmospheric pressure (P2) is zero. Air flows from P1 to P2. So, howsoever one breathes, pressure won’t become zero within the airways.
Sir is there symphate afferent parasymphatetic afferent ....if yes is it mylinated ....sensation from visera are carried by autonomic or sensory nerve . If..autonomic nerve will carry .but they relay in lateral or dorsal root ganglion and will they too have 1st 2nd 3rd ordor neuron..
There are somatic sensory nerves emerging from the viscera. These fibers will carry the somatic sensations (like, pain). There are autonomic afferent fibers (mainly parasympathetic), which too carry some of the sensations. E.g., distension of the viscera. In some cases, sympathetic fibers carry pain sensations (like, from bladder). The autonomic fibers go via different routes, to carry the signals to some thalamic nuclei and reticular formation in brain stem.
Nicely explained sir...👌👌 What is the physiology of EPP during huffing?how it helps to remove secreations from the lung.you told about slow expiration will help the patient to achieve epp gradually but what is the mechanism of huffing in which the patient expires forcefully?
Plsss Sir a question: we say that in normal health people EPP is in first 7 generation so there's no dynamic compression but at the same time we say that RV is there even after forceful expiration because of closure of airways due to dynamic compression i mean why would there be closure of airways if EPp is in 7 first generation? I'm confused, I'm gonna be very grateful if u can clear my doubt
@@houriak848 Residual volume and EPP are separate matters. EPP is in cartilagenous airways. Once EPP is reached, AIRFLOW will remain constant. However, it’s a continuous column of air. It’s not a bolus of air that is moving from one point to another. From alveolus to nose , it’s a continuous column of air. When smaller airways begin to close due to weight of the lung, eventually the air will stop coming out and residual volume will stay inside lungs.
@@VivekSirsPhysiology but sir in lung volume and capacities u said " even after forceful expiration some amount of air remain in the lung due to closure of airways by dynamic compression" dynamic compression that means it happened in non cartilagenous Airways cuz there's " closure" and in healthy person I thought that won't happen " dynamic compression" in cartilagenous ones
@@VivekSirsPhysiology if u don't mind Sir I came through this paragraph " the forced expiratory effort continues, the equal pressure point is "likely to move down the airway from larger to smaller airways". This movement happens because, as the muscular effort increases, intrapleural pressure increases and because, as lung volume decreases, alveolar elastic recoil pressure decreases. As the equal pressure point moves down the airway, dynamic compression increases and the airways ultimately begin to collapse. This airways closure can be demonstrated only at especially low lung volumes in healthy subjects, " I think that with max forceful expiration equal pressure point won't be at 7 first generation it will be lower in small airways even in healthy ppl and that's why there's RV Plss sir check this It's book " pulmonary physiology" Michael G levitzky page 39
COPDs are associated with drying up of secretions, and consequent formation of mucus plugs that would cause further narrowing/blockade of airways. Pressure will be dissipated faster, during expiration, in an attempt to dislodge the mucus plugs. Result would be the same; shift of EPP downstream (to the lower or smaller airways).
Yes , it does. The intrapleural pressure determines how much will be the recoil force (pressure) would be there on the lungs. And that, in turn, would determine where the EPP would occur. In short, it's not a very fixed point; it does shift. (Though in normal individuals, it stays in the cartilagenous airways.)
anangsha datta Intra alveolar pressure has to be positive at the start of expiration. Reason - At the start of expiration, thoracic cage starts recoiling inward. It compresses the alveoli, and hence alveolar pressure rises above zero (i.e., it becomes positive). With quiet breathing, it may be just + 1 cm H2O. With the start of forceful expiration, it may be +20 or +30 cm H2O. Atmospheric pressure is zero. Alveolar pressure HAS TO BE above that (more than zero, or positive) if air has to flow from alveoli to the atmosphere (during expiration). The transpulmonary pressure acting on the tissue architecture generates the interstitial pressure.
In COPD patients, there is narrowing of airways. Breathing pattern is altered, with more of forceful exhalation. Hence, dissipation of pressure too is different. Hence, EPP shifts. (It’s the dissipation of pressure head, during the airflow, that determines the EPP.)
@@Nitish-tu2cm Chronic bronchitis and emphysema both are under the category of COPD. In emphysema there is destruction of the elastic tissue (due to increasing residual volume), resulting in an increased compliance.
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@@dhruvsharma8357 Kya baat hai….! Thanks….!!
Amazing explanation . I looked everywhere but you explained it so easily. Could not understand from the book . Thank you !!
Thanks for the comment!
So thankful for this wonderful explanation 🥺🥺
Absolutely great - I will show my students this. Thx
Kim Petersen Thanks! Shall try to record and upload more & more videos, with greater frequency.
Also, please let me know, if any point needs a further discussion.
Regards,
Thank you very much for this structured explanation of the EPP!
I loved the explanation. Thank you sir..
Best explanation...thankyu very much sir
This is the best explanation .Amazing ! Thank you
What an explanation! Excellent!
Excellent explanation sir.. I was searchng for this topic for ma finl dnb respi xam preprtn.. 🙏🏻🙏🏻🙏🏻thnku sir
Thanks for explanation! Very helpful!
Such a lucid explanation...Thank you so much😊
Thanks,
Regards,
Great video sir keep making these
Thank you very much! There's just one thing I don't understand. You say that people with COPD exhale slowly to avoid too rapid a drop in airway pressure. But this seems to imply that with a faster flow we can reach a pressure of 0 (atmospheric) before reaching the mouth. And that the air could therefore stagnate (for lack of a gradient) before reaching the mouth.
No. That won’t happen. Alveolar pressure (P1) is positive (say, + 20 for forceful expiration). And atmospheric pressure (P2) is zero. Air flows from P1 to P2. So, howsoever one breathes, pressure won’t become zero within the airways.
You are awesome. Many thanks to you
Thanks for the comment...!
thank you very much for thisss
Sir is there symphate afferent parasymphatetic afferent ....if yes is it mylinated ....sensation from visera are carried by autonomic or sensory nerve . If..autonomic nerve will carry .but they relay in lateral or dorsal root ganglion and will they too have 1st 2nd 3rd ordor neuron..
There are somatic sensory nerves emerging from the viscera. These fibers will carry the somatic sensations (like, pain). There are autonomic afferent fibers (mainly parasympathetic), which too carry some of the sensations. E.g., distension of the viscera. In some cases, sympathetic fibers carry pain sensations (like, from bladder). The autonomic fibers go via different routes, to carry the signals to some thalamic nuclei and reticular formation in brain stem.
Kindly share us the reference text books for this concept
Nicely explained sir...👌👌
What is the physiology of EPP during huffing?how it helps to remove secreations from the lung.you told about slow expiration will help the patient to achieve epp gradually but what is the mechanism of huffing in which the patient expires forcefully?
Plsss Sir a question: we say that in normal health people EPP is in first 7 generation so there's no dynamic compression but at the same time we say that RV is there even after forceful expiration because of closure of airways due to dynamic compression i mean why would there be closure of airways if EPp is in 7 first generation?
I'm confused, I'm gonna be very grateful if u can clear my doubt
@@houriak848 Residual volume and EPP are separate matters. EPP is in cartilagenous airways. Once EPP is reached, AIRFLOW will remain constant. However, it’s a continuous column of air. It’s not a bolus of air that is moving from one point to another.
From alveolus to nose , it’s a continuous column of air. When smaller airways begin to close due to weight of the lung, eventually the air will stop coming out and residual volume will stay inside lungs.
@@VivekSirsPhysiology but sir in lung volume and capacities u said " even after forceful expiration some amount of air remain in the lung due to closure of airways by dynamic compression" dynamic compression that means it happened in non cartilagenous Airways cuz there's " closure" and in healthy person I thought that won't happen " dynamic compression" in cartilagenous ones
@@houriak848 Why would there be any residual volume?
It's because air is unable to come out.
Why is air unable to come out?
@@VivekSirsPhysiology if u don't mind Sir I came through this paragraph " the forced expiratory effort continues, the equal pressure point is "likely to
move down the airway from larger to smaller airways". This movement happens
because, as the muscular effort increases, intrapleural pressure increases and because,
as lung volume decreases, alveolar elastic recoil pressure decreases. As the equal pressure point moves down the airway, dynamic compression increases and the airways
ultimately begin to collapse. This airways closure can be demonstrated only at especially low lung volumes in healthy subjects, " I think that with max forceful expiration equal pressure point won't be at 7 first generation it will be lower in small airways even in healthy ppl and that's why there's RV
Plss sir check this
It's book " pulmonary physiology" Michael G levitzky page 39
@@houriak848 Ok. I’ll check it. Thx.
In COPD there is removal of secretions how does this relate to the equal pressure point
COPDs are associated with drying up of secretions, and consequent formation of mucus plugs that would cause further narrowing/blockade of airways. Pressure will be dissipated faster, during expiration, in an attempt to dislodge the mucus plugs. Result would be the same; shift of EPP downstream (to the lower or smaller airways).
sir. does intrplueral pressure in any way affect the equal pressure point.?
Yes , it does. The intrapleural pressure determines how much will be the recoil force (pressure) would be there on the lungs. And that, in turn, would determine where the EPP would occur. In short, it's not a very fixed point; it does shift. (Though in normal individuals, it stays in the cartilagenous airways.)
Closing volume??? Sir
Yes. Closing volume (and closing capacity) is discussed in some other video.
Why intra alveolar pressure is positive . What generates the interstitial pressure?
anangsha datta Intra alveolar pressure has to be positive at the start of expiration. Reason - At the start of expiration, thoracic cage starts recoiling inward. It compresses the alveoli, and hence alveolar pressure rises above zero (i.e., it becomes positive). With quiet breathing, it may be just + 1 cm H2O. With the start of forceful expiration, it may be +20 or +30 cm H2O.
Atmospheric pressure is zero. Alveolar pressure HAS TO BE above that (more than zero, or positive) if air has to flow from alveoli to the atmosphere (during expiration).
The transpulmonary pressure acting on the tissue architecture generates the interstitial pressure.
🎉🎉
excuse me, why is it that the equal pressure point shifts downwards into the smaller airway passages in the COPD patient?
In COPD patients, there is narrowing of airways. Breathing pattern is altered, with more of forceful exhalation. Hence, dissipation of pressure too is different. Hence, EPP shifts. (It’s the dissipation of pressure head, during the airflow, that determines the EPP.)
What is copd
Bronchitis
Emphysema
In which increases in compliance due to decrease in elastic tissu
@@Nitish-tu2cm Chronic bronchitis and emphysema both are under the category of COPD.
In emphysema there is destruction of the elastic tissue (due to increasing residual volume), resulting in an increased compliance.
Kindly share us the reference text books for this concept
Berne & Levy (6th edition) has explained this concept well.