Intraplueral pressure

[Kobebucsfan]

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In which condition would intrapleural pressure be more negative than normal after inspiration is complete, i.e., at end of inspiration when there is no airflow?

A.Asthma
B.Emphysema
C.Intrapulmonary airway obstruction
D.Partial paralysis of diaphragm due to trauma
E.Pulmonary fibrosis



The correct answer is E. When there is no airflow, the only factors that influence intrapleural pressure are the elastic recoil of the lung and chest wall. Fibrosis increases inward recoil of the lung, which causes more negative intrapleural pressure to occur.



Can someone explain this for me, im more confused after reading the explanation

 

[worldbeater]

I didn't get a very favorable response last time when I posted about restrictive and obstructive breathing patterns, but it has worked for every pulmonary question I have done on practice questions. So here we go:

At the end of inspiration there is no airflow -> you have a problem breathing IN -> restrictive breathing pattern

Pulmonary fibrosis is the only restrictive disease/pattern listed here. Other examples of restrictive patterns that have a problem when breathing in are: anxiety, pregnancy, gram negative sepsis, pulmonary embolism. Pulmonary fibrosis will also present on x-ray as a coarse reticular pattern.

Asthma and Intrapulmonary airway obstruction are obstructive patterns. Emphysema is a restrictive to obstructive pattern. Paralysis of diaphragm is a problem breathing in, I would guess, so it has a restrictive pattern but it's not as common of an answer as pulmonary fibrosis.

Just for more depth, a restrictive pattern means you a problem breathing in -> your pO2 drops from the normal 75-105 -> your respiratory rate increases to bring more oxygen in -> you are blowing off CO2, so it will be less than the normal 33-45 -> ABG presents with respiratory alkalosis, since CO2 is an acid

For the heart: you have a decreased pO2 in the blood -> causes pulmonary vessels to constrict (only area in the body this happens, due to attempt to ventilate the "working" portions of the lung) -> resistance increases due to pulmonary hypertension -> pressure increases -> blood flow (amount of blood) goes down -> pulmonary capillary wedge pressure (measures amount of blood) goes down -> S2 split is narrow and loud due to decrease in flow

Resistance problem leads to right ventricle hypertrophy -> increase contraction -> causes an S4 that gets louder on inspiration

 

[dempty]

I can try to explain the given explanation a little further.

We also know that the pleural fluid between the parietal and visceral pleura acts as a "glue" (sort of...surface tension, vacuum formation) to hold keep the lungs and chest wall in close proximity. Finally, we know that the natural tendency of the lungs and of the chest wall is to collapse and expand, respectively (think of pneumothorax).

I think this can be boiled down to two surfaces and a vacuum. The more force each surface has in an opposing direction, the more "negative" the pressure in the vacuum needs to be to equilibrate the forces.

When we inspire, we have an increase in the force pulling the lungs in against the outward pull of the chest wall. This is due to the elastance of the lungs causing the lungs to recoil inward against the outward pull of the chest wall (these forces find an equilibrium).

In a lung with fibrosis, the lung compliance has further decreased (elastance, inward recoil, increased). At the same point of inspiration, there is a bigger inward "pull" acting on the lungs against the outward tendency of the chest wall. The intrapleural pressure is more now more negative than in a normal lung.


This is how I understand it, and hopefully it adds a little clarity for you as well.


As for D, the partial paralysis of the diaphragm-- I would suspect this makes intrapleural pressure less negative than normal. If you can't use (part of) the diaphragm to expand the chest cavity and increase the expansion of the lungs (increasing their desire to spring inward), your intrapleural pressure isn't as negative as it is under normal conditions.

Feel free to correct anything I might have mixed up!

 

[DrPicard]

Its really simple. There are two forces acting on the lungs,

Recoil, which wants to collapse the them into a smaller volume and is a property of the lung parenchyma and connective tissue and
IPP, which wants to expand the lungs. Think of the negative IPP as a pressure that tries to "suck" the lungs outwards into a larger volume.

In a steady state, when the lungs volume isn't changing, IPP must equal recoil. If the lung is collapsing into a smaller volume, recoil is greater than IPP. Similarly, to expand the lungs, the body must create an IPP that applies a stronger force than recoil.

The only tricky thing is that the more negative the IPP, the greater its force, since its trying to suck the lungs outwards.

With pul fibrosis -> increases in interstitial connective tissue -> increased recoil. Hence a stronger (or a more negative) IPP is required to expand the lungs.

At the end of inspiration, since the lungs aren't expanding, it stands to reason that IPP = recoil at that point in time, just that these values will be raised relative to a person with normal lungs.

 

[thehundredthone]

The correct answer is E. When there is no airflow, the only factors that influence intrapleural pressure are the elastic recoil of the lung and chest wall. Fibrosis increases inward recoil of the lung, which causes more negative intrapleural pressure to occur.

Think of the fibrosis as increased adherent matter between the lung and pleura. This is constantly pulling the lung (and thus visceral pleura) inward. At the same time, the parietal pleura is attached chest wall. The end result is that there is increased negative pressure within this compartment (like trying to pull apart two sides of a deflated balloon). The other mentioned conditions do not exert any such forces on the pleura at the end of inspiration.