graph do not coincide. In plain words. at identical intrapleural pressure, the volume of lung is Iess in inspiratory phase than that in expiratory phases. This type of curve is called hysteresis curve by mathematicians (GK hysteresis = to lag behind). So, the difference in the stretchability between inspiratory and expiratory phase accounts for the hysteresis loop of the compliance. The compliance increases in emphysema. but decreases in fibrosis of the lung and pulmonary edema (see applied physiology, later in the chapter for furthe details). Two Items an used. The static compliance and the specific compliance. The static compliance is what has been described above. Obviously, the compliance also depends upon volume of the lung (at low volume, the compliance is high). When the compliance, is determined and values are expressed with reference to the lung volume, it is then called 'specific compliance'. Specific compliance. There is a term, 'relaxation volume. The point at the end of a quiet expiration is called ralaxation volume. At this,point, intrapulmonary and mtrapleural pressures are zero i.e. exactly atmospheric . At ralaxation volume. the lung still contains some air called functional residual capacity (normally about 2500 Ml). On either side of the ralaxation volume point, upto limited range, the pressure volume curve more or less linear (fig 4.2.3). Fig 4.2.3. To illustrate the principle of specific compliance. Specific compliance is the compliance of the lung at ralaxation volume expressed per liter of the functional residual capacity, that is specific compliance - compliance/ functional residual capacity. For example, let the (static) compliance of a man is 0-21/ cm of H2O and his functional residual capacity is 2500 ml. his specific compliance will be 0.08 liter/per cm H2O/liter (0.081 cm H2O-1 liter -1) Compliance of the chest wall and of the excised lung. In experimental animals. lungs can be taken out of the thoracic cavity
and stretchability or compliance of the lungs alone can be measured. lt is seen that the excised lung has a rather low compliance (i.e. it is rather stiff). On the other hand, in experimental animals , the compliance of the thoracic wall minus the lungs also can be seen. It is seen that the thoracic wall alone (minus the lungs) has a high compliance. Stated simply. this means that, if not opposed, the lungs try to collapse whereas the chest wall tends to expand out. The compliance of an intact man or animal (i.e. chest wall plus the lungs), is the resultant of these two opposing forces. In amphysema the lung considerably loses its elastic recoil, (i.e. the tendancy to collapse is Iost), leaving the tendency of the chest wall to expand. unopposed. In emphysema, therefore chest wall remains expanded. Loss of elasticity causes increase of static compliance in emphysema. Factors influencing compliance These are (a) factors present in the pulmonary tissue, (b) factor presents in the chest wall. The factors residing in the pulmonary tissue are - These are (a) factors present in the pulmonary tissue, (b)factors present in the chest wall i) elastic fibers of the lung (ii) surface tension within the alveoli, (iii) interdependence These three factors taken together constitute the the 'elastic recoil' of the lung. Elastic recoil, opposes the streaching of the lung Hence, reduction of elastic recoil = rise in compliance and vice versa Elastic fibers of the lung is a major cause of its elastic recoil. One property of the elastic fiber is that like a strip of India rubber, it elongates when stretched but recoils back to its original (resting) length when the stretch is with draw. During inspiration these elastic fibers are elongated but because of their tendency to -ecoil, it oppooses the expansion (for further details, see 'emphysema chap 6, sac IV). Surface tension within the alveoli is due to the fact that alveoli contain a very thin film of fluid lining their inner side (fig 4.2.4) Fig. 4.2.4. To illustrate the effect of surface tension. If the intraalveolar surface lension rises sufficiently the alveolus collapses. The individual molecules of this fluid, because of the surface tension. try to come closer to each other and the result is that the alveolus tends to collapse as shown in fig 4.2.4. This force too, ultimately opposes the expansion of the lung. Following Laplace's law (see also fig 5.12.1). it can be shown that in a spherical body. Iike alveolus, P=2( EMBED Equation 3 V r where. P is the
Pressure that causes the alveolus to collapse, (EMBED Equation 3) is the surface tension and r is the radius.that is P is pressure
high (and the alveolus collapses) when y is high or r is low. It follows in conditions (i) where the surface tension of the fluid Iining the interior of the alveolus is high (as in 'hyaline membrane disease'), or (ii) where the radius of the alveoli becomes very small, the lung, as a whole strongly resists its expansion (It should be noted that there is another effect of rise of surface tension of the intra alveaolar fluid. if raised sufficiently, it overcomes the colloidal tension of plasma (of the blood of surface capillaries of the lung) and draws fluid from the capillary to alveoli (pulmonary edema)] [N. B. P in the above equation may be called, trans alveolar pressure ] Surfactant. Within the alveolus, there is a material, called surfactant, which reduced surface tension exerted by the alveolar fluid As early as in 1929, von Neergard suspected the presence of a sort of such thing but it was Pattle 1956 who proved the existance of surface tension radusing agent in the alveolar fluid. The surfactant is chemically a mixture of phospholipids (chiefly dip almity "lecithin) and protein. it is secreted by the
and stretchability or compliance of the lungs alone can be measured. lt is seen that the excised lung has a rather low compliance (i.e. it is rather stiff). On the other hand, in experimental animals , the compliance of the thoracic wall minus the lungs also can be seen. It is seen that the thoracic wall alone (minus the lungs) has a high compliance. Stated simply. this means that, if not opposed, the lungs try to collapse whereas the chest wall tends to expand out. The compliance of an intact man or animal (i.e. chest wall plus the lungs), is the resultant of these two opposing forces. In amphysema the lung considerably loses its elastic recoil, (i.e. the tendancy to collapse is Iost), leaving the tendency of the chest wall to expand. unopposed. In emphysema, therefore chest wall remains expanded. Loss of elasticity causes increase of static compliance in emphysema. Factors influencing compliance These are (a) factors present in the pulmonary tissue, (b) factor presents in the chest wall. The factors residing in the pulmonary tissue are - These are (a) factors present in the pulmonary tissue, (b)factors present in the chest wall i) elastic fibers of the lung (ii) surface tension within the alveoli, (iii) interdependence These three factors taken together constitute the the 'elastic recoil' of the lung. Elastic recoil, opposes the streaching of the lung Hence, reduction of elastic recoil = rise in compliance and vice versa Elastic fibers of the lung is a major cause of its elastic recoil. One property of the elastic fiber is that like a strip of India rubber, it elongates when stretched but recoils back to its original (resting) length when the stretch is with draw. During inspiration these elastic fibers are elongated but because of their tendency to -ecoil, it oppooses the expansion (for further details, see 'emphysema chap 6, sac IV). Surface tension within the alveoli is due to the fact that alveoli contain a very thin film of fluid lining their inner side (fig 4.2.4) Fig. 4.2.4. To illustrate the effect of surface tension. If the intraalveolar surface lension rises sufficiently the alveolus collapses. The individual molecules of this fluid, because of the surface tension. try to come closer to each other and the result is that the alveolus tends to collapse as shown in fig 4.2.4. This force too, ultimately opposes the expansion of the lung. Following Laplace's law (see also fig 5.12.1). it can be shown that in a spherical body. Iike alveolus, P=2( EMBED Equation 3 V r where. P is the
Pressure that causes the alveolus to collapse, (EMBED Equation 3) is the surface tension and r is the radius.that is P is pressure
high (and the alveolus collapses) when y is high or r is low. It follows in conditions (i) where the surface tension of the fluid Iining the interior of the alveolus is high (as in 'hyaline membrane disease'), or (ii) where the radius of the alveoli becomes very small, the lung, as a whole strongly resists its expansion (It should be noted that there is another effect of rise of surface tension of the intra alveaolar fluid. if raised sufficiently, it overcomes the colloidal tension of plasma (of the blood of surface capillaries of the lung) and draws fluid from the capillary to alveoli (pulmonary edema)] [N. B. P in the above equation may be called, trans alveolar pressure ] Surfactant. Within the alveolus, there is a material, called surfactant, which reduced surface tension exerted by the alveolar fluid As early as in 1929, von Neergard suspected the presence of a sort of such thing but it was Pattle 1956 who proved the existance of surface tension radusing agent in the alveolar fluid. The surfactant is chemically a mixture of phospholipids (chiefly dip almity "lecithin) and protein. it is secreted by the
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