Phloston

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I think I recall something about once you recruit the accessory muscles, the degree of positive pressure in the pleural space during expiration increases more, leading to greater 'compression' of the alveoli. If you're passively breathing, you don't need to exhale as great of a volume per unit time so the intrapleural pressure you need to achieve the volume expulsion is lesser, and the alveoli aren't compressed as much.

As AZ7 has said, I believe that's the specific medical term you're looking for.
 

DrPicard

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You need a bigger force to drive out the same amount of air in a smaller amount of time --> a more positive IPP than normal provides the greater delta-P --> more dynamic compression of the airways as well --> decreased cross sectional radius --> increased resistance --> increased work per unit volume moved out.
 
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How does the RATE effect that? I understand that, the transmittal pressure becomes negative so collapses. Beautiful pic in Constanzo of it, but I don't see how many times a person takes a breath would affect that


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lymphocyte

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In Short, Dynamic Airway Compression.
No. Or, at the very least, can you define what you mean? I'm not a pulmonologist, but I always thought DAC was an expiratory phenomenon.

To a good approximation, airway resistance is the difference in atmospheric pressure and alveolar pressure divided by volumetric flow. You've heard this idea before. Where? Ohm's law. The faster air flows, the greater the resistance.

Higher respiratory rates increases the volumetric flow and therefore increases the resistive work of breathing. This can be a problem, for example, in little tiny tatter tots with crap lungs. You have to ventilate accordingly, since there's a significant metabolic cost to work of breathing.
 
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AZ7

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The way i understood it was that expiration at normal RR is a passive phenomenon, but when we increase the RR we kind of override the normal balance by beginning to use accessory muscle; which is also why the inspiration-expiration transition in this case isn't as smooth. @aspiringmd1015

@lymphocyte It is an expiratory phenomena and RR also effects the resistance to air outflow, which I'm sure you'll agree to, is equally important.
 

lymphocyte

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@lymphocyte It is an expiratory phenomena and RR also effects the resistance to air outflow, which I'm sure you'll agree to, is equally important.
I don't understand what you're saying. Dynamic airway compression limits expiratory air flow. You almost physically can't expire faster. In diseased lungs, this limitation occurs at low expiratory flow rates. That limits exercise capacity, but how does it significantly increase the work of breathing? Expiratory flow is mostly effort-independent across most lung volumes. (As an aside, DAC is why you get breath stacking on COPDers on the vent if the expiratory time is too short.)

Flow rate people. Flow rate. That explains the important relationship between RR and airflow resistance. Ohm's law is the most helpful way to think about things. But we can also get into a discussion about laminar flow vs Reynold's number.

Edit: You even made me dig out John West's Respiratory Physiology because I felt like I was living in crazy world reading the explanations above. "The higher the breathing rate, the faster the flow rates and the greater amount of work" (pg. 121) I also drew a picture to help explain things. WOB has lots of components, but it's helpful to think of just two: resistive and elastic. Resistive work is from the alveoli and lung parenchyma. (Airflow makes up about 80% of the resistive work, so it's massively important. Tissue makes up about 20%, so it matters if you have crap tissue, like in COPD.) Elastance work is from the intercostal muscles, chest wall, and diaphragm. Where the two intersect, you minimise WOB.

Let's think about the clinical implications:
1. What happens as resistive work decreases (i.e. the resistive curve shifts left) as in the case of COPD? Hint: they tend to breath slower.
2. What happens as elastance work increases (i.e. the elastance curve shifts right) as in people with stiff chests? Hint: they tend to be breath faster.

Both 1 and 2 minimise WOB in pathophysiological states, but cause other problems (remember the PaCO2 equation?). So to compensate, you sometimes have to needle the RR off the ideal point and therefore increase WOB--until you can't anymore, and then you have respiratory failure. Welcome to the nightmare that can be asthma. (Check for understanding: why is a normalising PaCO2 a very worrying sign in a severe asthma exacerbation? Do you see how air-flow limitation, RR, airway resistance, WOB, and PaCO2 all tie in together?)

upload_2016-7-31_21-26-6.png

Edit 2: If you still don't believe, me check out this lecture: http://www.physiologylectures.net/index.php?id=28
 
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AZ7

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@lymphocyte Im just doing a poor job of explaining.
And i agree with what you said, even before your lengthy well written following message.
 
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lymphocyte

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@lymphocyte Im just doing a poor job of explaining.
And i agree with what you said, even before your lengthy well written following message.
No worries. It wasn't you. Everybody was going off the rails with their explanations and made me start to doubt myself, hence the double edit.