Physiology

Some of the physiologic principles relating to the pulmonary parenchyma were covered briefly in Chapter 1. This chapter further discusses two topics that are important in the pathophysiologic abnormalities resulting from diffuse parenchymal lung disease: gas exchange at the alveolar-capillary level and how disturbances within the pulmonary parenchyma affect the mechanical properties of the lung.

Gas exchange between the alveolus and the capillary depends on passive diffusion of gas from a region of higher partial pressure to one of lower partial pressure. As discussed in Chapter 1, the Po2 in the alveolus normally is approximately 100 mm Hg, and in the blood entering the pulmonary capillary is approximately 40 mm Hg. This difference results in a driving pressure for O2 to diffuse from the alveolus to the pulmonary capillary, where it binds with hemoglobin within the erythrocyte. The barrier to diffusion—which includes the thin cytoplasmic extension of the type I cell, the basement membrane of type I and capillary endothelial cells, and the capillary endothelial cell itself—is extremely thin, measuring approximately 0.5 μm. Some areas of the alveolar wall also contain a thin layer of interstitium, but presumably diffusion and gas exchange occur preferentially at the thinnest region, where the interstitium is sparse or absent.

Although the rate of gas transfer across the alveolar-capillary interface depends on the thickness of the barrier, O2 uptake by the blood is normally complete early during the transit through the capillaries. The total time spent by a red blood cell traveling through the pulmonary capillaries is approximately 0.75 second, and equilibration with O2 occurs within the first third of this time. Therefore, extra time is available for diffusion should disease affect the alveolar-capillary interface and impair the normal process of diffusion. Because CO2 diffuses much more readily than O2, even more ample reserve time is available for its diffusion.

Oxygen uptake and CO2 elimination at the alveolar-capillary interface are completed early during transit of an erythrocyte through the pulmonary vascular bed.

Consequently, although diffuse parenchymal lung diseases do affect gas exchange, impaired diffusion across an abnormal alveolar-capillary interface is not the primary contributor to the disturbance in gas exchange when the patient is at rest. However, when these patients exercise and cardiac output increases, blood flows more rapidly through the pulmonary capillaries, and the combination of a diffusion impairment and a shorter time for diffusion of oxygen may lead to hypoxemia. This issue is considered further in Chapter 9 as part of the discussion of abnormalities in gas exchange in patients with diseases affecting the alveolar wall.

Another important aspect of physiology relating to the lung parenchyma is compliance. As stated in Chapter 1, the lung is elastic and resists expansion like a balloon or a rubber band. Lung compliance relates the volume of gas within the lung and the distending pressure (i.e., transpulmonary pressure) needed to expand the lung to that volume. Diseases affecting the alveolar walls commonly disturb this pressure-volume relationship, making the lung either more stiff (less compliant, more resistant to expansion), or less stiff (more compliant, easier to expand). For the stiffer, less compliant lung, the compliance curve is shifted to the right: a lower volume is achieved for any given transpulmonary pressure. Most of the diseases discussed in this section, which are included in the category of diffuse parenchymal lung disease, affect the compliance of the lung in this way (Fig. 8.3). In contrast, as discussed in Chapter 6 and illustrated in Fig. 6.7, patients with emphysema, whose lungs are less resistant to expansion (i.e., are more compliant), have compliance curves that are shifted to the left. This principle of compliance is important in pulmonary physiology. Chapters 1 and 6 discussed the role of compliance in

determining lung volumes measured by pulmonary function testing, particularly total lung capacity and functional residual capacity. This principle is cited again in Chapter 9, which discusses the pathophysiology of diseases that affect the alveolar walls.

FIGURE 8.3 Compliance curve of lung in diffuse parenchymal lung disease

compared with that of normal lung. In addition to shift of the curve downward and to

right, total lung capacity (TLC) in diffuse parenchymal lung disease (point B on

volume axis) is characteristically less than normal TLC (point A). Maximal pressure

at TLC is called maximal static recoil pressure (Pstmax), represented for normal lung and lung with interstitial disease by points C and D,

respectively. Source: (Compare with Fig. 6.7.)

The compliance curve of the lung in interstitial lung disease is shifted downward and to the right.

Suggested readings

Anatomy

Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/

Albertine K.H. Anatomy of the lungs Broaddus, V.C. Mason, R.J. Ernst, J.D. King, T.E,Jr. Lazarus, S.C. Murray & J.F. et al. Murray and Nadel’s textbook of respiratory medicine 6th ed. 2016; Elsevier Philadelphia 3-21.

Autilio C. & Pérez-Gil J. Understanding the principle biophysics concepts of pulmonary surfactant in health and disease Archives of Disease in Childhood Fetal and Neonatal Edition 2019;104: F443F451.

Hentschel R, Bohlin K, van Kaam A, Fuchs H. & Danhaive O. Surfactant replacement therapy: From biological basis to current clinical practice Pediatric Research 2020;88: 176-183.

King S.D. & Chen S.Y. Recent progress on surfactant protein A: Cellular function in lung and kidney disease development American Journal of Physiology Cell Physiology 2020;319: C316C320.

Knudsen L. & Ochs M. The micromechanics of lung alveoli: Structure and function of surfactant and tissue components Histochemistry and Cell Biology 2018;150: 661-676.

Leslie K.O. & Wick M.R. Practical pulmonary pathology: a diagnostic approach 3rd ed. 2018; Elsevier Philadelphia.

Ruaro B, Salton F, Braga L., et al. The history and mystery of alveolar epithelial type II cells: Focus on their physiologic and pathologic role in lung International Journal of Molecular Sciences 2021;22: 1-16.

Physiology

Cloutier M.M. Respiratory physiology 2nd ed. 2019; Elsevier Philadelphia. Schwartzstein R.M. & Parker M.J. Respiratory physiology: a clinical approach 2006;

Lippincott Williams & Wilkins Philadelphia.

West J.B. & Luks A.M. West’s respiratory physiology - the essentials 11th ed. 2021; Wolters Kluwer Philadelphia.