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Cormack, Ch. 6; Guyton and Hall, Chs. 37-39. 2/21/00

W. Crone (303 FTZ, 629-7439, cronewil@hvcc.edu, http://www.hvcc.edu/academ/faculty/crone/index.html)

possible web site: http://www.vh.org/Providers/ClinRef/FPHandbook/03.html

(U. of Iowa Family Practice Handbook chapter on pulmonary medicine: quick access to many items)

The respiratory system: conducting zone: bringing warm, filtered humidified air in, and a respiratory zone, with many alveoli (< 1mm diameter) in lung, for total surface area of 85 m2 (3). Ventilation is a mechanical process. Gas exchange occurs by diffusion from differential concentrations of O2 and CO2.

Air movement in/out of lungs occurs as a result of changes in lung volumes bringing on pressure differences. The intrapleural space is potential in health patients, with the parietal and visceral pleurae wet and sticking to each other, as a result of a subatmospheric pleural pressure. Therefore, if the thoracic wall changes in size, so should the lungs. Air enters lungs in inspiration because atmospheric pressure (760 mm Hg at sea level) is greater than alveolar (intrapulmonary) pressure, which is negative (-3 mm Hg) with inspiration. In contrast, air leaves lungs in expiration because intrapulmonary pressure is greater than atmospheric pressure (+3 mm Hg). Boyle's Law: the pressure of a gas is inversely proportional to its volume.

Inspiration is mostly diaphragmatic, and expiration is usually passive with relaxation of the diaphragm and external intercostal muscles, but in forced expiration, the internal intercostals and abdominal muscles can raise interpulmonary pressure +20-30 mm Hg above atmospheric.

Physical properties of the lung: compliance to expand when stretched; elasticity to shrink when not stretched. Compliance (D V/D P): lungs are very compliant normally. Elasticity: tendency of structure to return to initial size after distension. A major component (two-thirds) (3) of lung elasticity is surface tension of fluid in alveoli: There is normally a thin layer of fluid in the alveoli. Typically, there is a slightly negative interstitial pressure set up by pulmonary capillaries and lymphatics.2 A wetting layer of the alevolar epithelial cells is maintained by actively transporting Na+ in and Cl- out. The CFTR (cystic fibrosis transmembrane regulator) is altered in cystic fibrosis.1

Normally, this thin film has an attraction to itself, with this surface tension raising the pressure inside of the alveolus. Law of LaPlace: P = (2 X T)/r (the smaller the radius, the higher the pressure).

The lung gets around this by surfactant (surface active agent). Surfactant is produced by type II alveolar cells (pneumocytes), in contrast to the flattened type I alveolar cells (pneumocytes) that line most of the surface of the alveoli. As the alveoli get small in diameter, the surfactant molecules crowd together, so that alveoli do not collapse during expiration, and also are easier to inflate with the next breath. Without surfactant: hyaline membrane disease can result (surface tension forces plasma fluid into alveoli for that shiny"membrane" appearance).2

Spirometry, or pulmonary function tests, to follow these mechanics.

a) tidal volume: amount of air moved in quiet breathing

b) vital capacity: maximum amount of air exhaled after maximum inhalation

c) inspiratory and expiratory reserve volumes above and below tidal volume

d) residual volume left in lungs after maximum expiration

Spirometry can assist in diagnosing classes of lung diseases:1

restrictive lung diseases, e.g., pulmonary fibrosis. Vital capacity reduced, but rate of forcible exhalation normal.

obstructive lung diseases, e.g., asthma. Vital capacity normal, but increased airway resistance. FEV (forced expiratory volume). % of vital capacity exhaled in 1 sec, or FEV1.0. If < 80%, then obstructive disease.

Dalton's Law: total pressure of gas mixture = sum of partial pressure of each gas in mixture.

Henry's Law: the volume of a gas that will dissolve in a liquid at a given temperature is proportional to the gas partial pressure.

Pressure of"wet" atmosphere in humidified respiratory tract = Pressure (N2) + Pressure (O2) + Pressure (CO2) + Pressure (H2O). Liquid and gas should be at equilibrium (blood and alveolar air).

In other words, if arterial PaO2 is very different than the Alveolar PAO2, then there's something wrong with gas exchange. Arterial blood should have fairly stable PaO2 and PaCO2, and so should be useful to measure (as compared to venous blood-why?).

  1. SI Fox, Human Physiology, 6th ed. (WCB McGraw-Hill, Boston, 1999), pp. 488, 494.
  2. AC Guyton, JE Hall, Textbook of Medical Physiology, 9th ed. (WB Saunders Co., Philadelphia, 1996), pp. 496, 541.
  3. W Kapit et al., The Physiology Coloring Book, 2nd ed, (Addison Wesley Longman, Inc., San Francisco, 2000), plates 49, 50.

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Please send comments and questions to: cronewil@hvcc.edu


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This web page updated on March 14, 2000