UWorld question #1543

[DarkHorizon]

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The explanation to this question is confusing me, if some can please explain it to me, it would be much appreciated.

The question presents a patient with interstitial lung disease and asks why the expiratory airflow has increased. The answer was increased radial traction on the airway.

The explanation then stated that increasing in radius will decease the resistance 4 folds, and hence will increase the airflow, which makes sense. It then went on to say that, " in a normal individual, high lung volumes are associated with decreased lung airway resistance due to increased radial traction (outward pulling), and conversely low lung volumes are associated with high airway resistance."

I am a bit confused because interstitial lung diseases usually have low lung volumes, a fact even stated by them in the next paragraph. So wouldn't this radial traction principle be inapplicable to them? I know that low lung volumes are due to low compliance, I think I am mixing these two topics, if someone can explain it better, it'll be great!

 

[kstreet]

For pts with fibrotic lungs, they do have low volumes but the expiratory flow rate remains high because of the increased elastic recoil caused by all that fibrosis.

To visualize this point, just breathe in real deeply as much as you can, then at your peak just let out a little bit of air and note that the flow rate is pretty high since you are at your peak volume and peak radial traction.

Breathe out just a tiny bit, and then breathe back in. That's how I imagine it'd be like to have restrictive lung dz.

So, normally you have this increased expiratory flow rate because of:
1. decreased airway resistance(with all that air filling up your lungs and making the airways wider) and
2. because of that radial traction that is your chestwall pulling outward and thus letting your lungs easily release air when you want to expire at peak volume

...people with restrictive lung dz instead have just masses of fibrotic tissue that provide that outward radial traction that would mimic basically breathing to your peak volume. And so when they breathe out, it comes out super quick.

 

[BlondDoctor]

The question presents a patient with interstitial lung disease and asks why the expiratory airflow has increased. The answer was increased radial traction on the airway.

The explanation then stated that increasing in radius will decease the resistance 4 folds, and hence will increase the airflow, which makes sense. It then went on to say that, " in a normal individual, high lung volumes are associated with decreased lung airway resistance due to increased radial traction (outward pulling), and conversely low lung volumes are associated with high airway resistance."

!

The increase in radial traction is because the airways are tethered tightly to the lung parenchyma due to fibrosis, this "outward pulling" on the airways increases the radius despite there being a lower lung volume ie more open at each volume compared to a normal lung.

 

[krs881]

As I get going on this step 1 studying adventure, I find it pretty amazing that the top search result on google for "radial traction" is another med student confused about the very same question that I was just confused about, posted almost a year ago. No one else in their right mind - no doctor, no PhD, no person who gets to decide what the hell they care to spend time thinking about - is concerned with radial traction!

 

[Phloston]

Firstly, we need to define radial traction: the capacity for the small airways to remain patent during expiration due to extra-airway forces.

Hagen–Poiseuille's law (dP = 8uLQ/pi(r)^4) discusses pressure-drop over the length of a hypothetical tube-system. Variants of this law may be used such that, in terms of quantifying intra-airway pressure at one location, versus along the entire length of the airway, we would instead just take the pressure-length integral at that particular location, instead of looking at the entire area under the curve. This integral would be the absolute intra-airway pressure at any given point in time (and therefore, length) along the airway.

After one intra-airway location is chosen, a pressure-time curve can be made that correlates with cross-sectional area (r) of the airway.

In pure interstitial lung disease, compliance (ability to expand outward) decreases because fibrosis inhibits expansion. In contrast, elasticity (ability to close) remains virtually the same because overall alveolar surface area is unchanged, despite demonstrating areas of fibrosis.

The fibrosis external to the airways may provide a source of attachment chastening closure, thereby decreasing elasticity slightly. Technically, one would reason that this would increase FEV1 because of the augmented airway patency. However, in interstitial lung disease (which demonstrates increased relative FEV1/FVC) FEV1 and FVC actually both decrease, with FVC merely decreasing more secondary to decreased IRV. The only reason FEV1 decreases on an absolute scale is because the airways are already closer to closure when expiration is initiated, so even though external fibrosis serves as a force to keep them patent, the reduced cross-sectional area at the onset of expiration is sufficient to induce a greater pressure drop per unit time in comparison to healthy lung. So smaller airways earlier in the expiration process curtail absolute FEV1. In other words, on an expiratory pressure vs time plot, with radius as a function of Hagen–Poiseuille's law, the x-value at the onset of expiration is merely shifted to the right.

Therefore, radial traction (RT) is clinically insignificant because although it reflects extra-airway-induced impediment of airway closure, overarching factors such as decreased lung volume at onset of expiration (interstitial lung disease) and early dynamic small-airway closure (COPD) mask the impact of positive or negative RT.