Dynamic hyperinflation

[bomgd3]

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Hey everyone,
I have a quick question about pulmonary physiology. Our lung dynamics syllabus has this passage:

The time constant is defined as τ = R x C. Alveoli with long time constants empty slowly. As a result, during exercise when the respiratory rate increases, these alveoli don’t fully empty: air becomes trapped inside, lung volume increases, compliance further decreases and these individuals report marked shortness of breath (a process known as dynamic hyperinflation).

This doesn't make sense to me. If compliance decreases, tau should decrease, and therefore the patient should breathe easier. Thus, the air trapping effect should be homeostatic in nature. The way that this syllabus is written makes it sound as if the decrease in compliance causes a vicious cycle.

My understanding is that dynamic hyperinflation is when a prolonged tau due to high resistance or compliance (like COPD) traps more air with each subsequent breath. The "air trapping effect" where trapped air causes volume to increase, decreasing compliance, is a homeostatic mechanism which opposes dynamic hyperinflation. However, in patients with bad disease, the air trapping effect cannot overcome the prolonged tau.

Do I have this right? Or is the syllabus right, and I'm missing some detail?

 

[greatnt249]

Hey everyone,
I have a quick question about pulmonary physiology. Our lung dynamics syllabus has this passage:


This doesn't make sense to me. If compliance decreases, tau should decrease, and therefore the patient should breathe easier. Thus, the air trapping effect should be homeostatic in nature. The way that this syllabus is written makes it sound as if the decrease in compliance causes a vicious cycle.

My understanding is that dynamic hyperinflation is when a prolonged tau due to high resistance or compliance (like COPD) traps more air with each subsequent breath. The "air trapping effect" where trapped air causes volume to increase, decreasing compliance, is a homeostatic mechanism which opposes dynamic hyperinflation. However, in patients with bad disease, the air trapping effect cannot overcome the prolonged tau.

Do I have this right? Or is the syllabus right, and I'm missing some detail?

Tau merely describes how long it will take alveoli to return to a state of static equilibrium volume given the alveoli's resistance and compliance. I think you are well aware of this, but sometimes it helps to lay it out there in plain terms what an equation is describing.

In COPD, tau increases as a result of increased compliance (such as in emphysema) or increased resistance (such as in a restrictive fibrosis). Therefore, with each "normal" breath, alveolar deflation time will be longer than that of a healthy individual. If this deflation time is longer than the individual's need to take a breath, then air will become trapped in the alveoli, as inspiration began before all the air was exhaled from the alveoli.

Exercise is no different. If you're breathing faster than you can completely exhale the air out, it'll become trapped. Obviously, your lungs can only trap so much air before you reach maximum inspiratory capacity at the peak of each breath. While exhalation should theoretically be "easier" at this stretched capacity of the alveoli, if you can't force the air out faster than you need to take it in, it'll still become trapped. If whatever activity you're performing requires more oxygen than can be provided under these circumstances, then bam, dyspnea until your lungs have a chance to recover and empty the trapped air.

I think the variable you were forgetting in all of this is the respiratory rate; if tau is longer than the individual's need to breathe, air will become trapped. Hopefully the above explanation helps; if it is wrong in any way please (anyone) feel free to correct me (I'm studying for Step I and can use all the help I can get).

 

[bomgd3]

Right, I agree with what you said. If tau is high, there may not be enough time to expire the air before the next breath. What's confusing for me is that the air trapping effect on compliance should actually decrease tau, and therefore should improve matters for the patient (i.e. a homeostatic mechanism). However, the way that it is written in our syllabus, it sounds like the decrease in compliance actually worsens things.

 

[turkeyjerky]

Right, I agree with what you said. If tau is high, there may not be enough time to expire the air before the next breath. What's confusing for me is that the air trapping effect on compliance should actually decrease tau, and therefore should improve matters for the patient (i.e. a homeostatic mechanism). However, the way that it is written in our syllabus, it sounds like the decrease in compliance actually worsens things.

no, you got it. it is a homeostatic mechanism--if it wasn't, then these people would keep trapping air until their chests exploded!

 

[greatnt249]

Right, I agree with what you said. If tau is high, there may not be enough time to expire the air before the next breath. What's confusing for me is that the air trapping effect on compliance should actually decrease tau, and therefore should improve matters for the patient (i.e. a homeostatic mechanism). However, the way that it is written in our syllabus, it sounds like the decrease in compliance actually worsens things.

It does decrease tau, but there's a whole lot more to breathing than just how easy it is to do so. If you exceed the ability to expire air at least as fast as you breathe it in, it'll be trapped. Yes, tau decreases, meaning air will passively expel out of your lungs "easier," but the dyspnea comes from using more oxygen than your respiratory efforts can provide, regardless of how "easy" it is to breathe. Do not conflate ease of breathing with how fast you should be able to do so; they are independent of one another.