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Compliance of the Respiratory System

الكلية كلية طب حمورابي     القسم الكلية ذات القسم الواحد     المرحلة 2
أستاذ المادة امجد حسن عباس المنصوري       14/11/2016 06:58:07
Compliance of the Respiratory System
Lung Compliance
Lung compliance expresses the dispensability of the lungs, that is, how easily the lungs expand when trans-pulmonary pressure increases. It is expressed by the following equation:
C = ?V/?P
where
C = lung compliance
?V = increase in lung volume (mL)
?P = increase in trans-pulmonary pressure (mm Hg).
– Compliance is inversely related to stiffness.
– Compliance is inversely related to the elastic recoil, or elastance, of the lung. Recoil causes the lungs to return to their previous volume when stretching ceases following an increase in trans-pulmonary pressure. It is mediated by surface tension in the alveoli and by elastic fibers in the
lung connective tissue.
Compliance of the Lung–Chest Wall Combination
Because the lungs and chest wall expand and contract together, the overall compliance of the respiratory system is that of the lung–chest wall combination. The compliance of the lung–chest wall combination is lower than the compliance of the lungs alone or chest wall alone.
– The compliance of the lung–chest wall combination varies with lung volume. Compliance is highest at the normal resting volume (functional residual capacity [FRC]) and decreases at both very low and very high volumes.
– At low volumes, compression of the chest wall reduces compliance.
– At high volumes, the increased stretch of elastic tissues in the lung parenchyma causes the lungs to get stiffer (less compliant). High trans-pulmonary pressure is required to drive this increase in volume, but it is not responsible for the decrease in compliance.



Changes in lung compliance in disease states
– Lung compliance is decreased in pulmonary fibrosis because the interstitium surrounding the alveoli becomes infiltrated with inelastic collagen.
– Lung compliance is increased in emphysema because many small alveoli are replaced by fewer but larger coalesced air spaces that have less elastic recoil.

Surface Tension in the Alveoli
Surface tension is due to the cohesive forces between water molecules at the air–water interface in the alveoli of lungs. It acts to contract the alveoli and is a major contributor to the force of elastic recoil of the lung.
If there were no opposing force, surface tension would cause the alveoli to collapse (atelectasis).
However, the collapsing force is opposed by trans-pulmonary pressure, which is always positive, allowing the alveoli to remain open.
According to the law of Laplace, the trans-pulmonary pressure P (in dynes/cm2) required to prevent collapse of an alveolus is directly proportional to surface tension T (in dynes/cm), and inversely
proportional to alveolar radius r (in cm), as expressed by
P = 2T/r
– All alveoli in a given region of the lungs have about the same trans-pulmonary pressure. If they all had the same surface tension, the Laplace relationship predicts that the smaller alveoli would collapse and force their volume into larger alveoli. However, surface tension is reduced by
pulmonary surfactant, and the reduction is greater in small alveoli than in larger ones because small alveoli concentrate the surfactant. Thus, the increased tendency to collapse because of small radius is just balanced by a greater reduction in surface tension.
Surfactant
Surfactant is a complex substance, consisting of proteins and phospholipids (mainly dipalmitoyl lecithin), that is produced in type II pneumocytes. It lines alveoli and lowers surface tension by the same mechanism as detergents and soaps (i.e., it coats the water surface and reduces cohesive
interactions between water molecules).
As an extension of its role in lowering surface tension, surfactant also produces the following effects:
– It increases compliance at all lung volumes, which allows for easier lung inflation and greatly decreases the work of breathing.
– It reduces the otherwise highly negative pressure in the interstitial space, which reduces the rate of filtration from pulmonary capillaries. This assists in maintaining lungs without excessive water.
Failure of surfactant production and/or excessive surfactant breakdown occurs in neonatal respiratory distress syndrome (RDS).


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