Oxygen-carbon dioxide exchange
Oxygen-carbon dioxide - The process by which oxygen passes from the air in the LUNGS to the HEMOGLOBIN in the BLOOD, and carbon dioxide from the hemoglobin passes into the air in the lungs. Oxygen-carbon dioxide exchange is fundamental to life and is the primary function of the lungs. Oxygen-carbon dioxide exchange takes place between the alveoli, the tiny bubblelike sacs deep within the lungs, and the capillaries, the tiniest blood vessels of the cardiovascular system. The membranous tissue of an ALVEOLUS is only one cell or two cells in thickness. A mesh of capillaries encloses each of the 300 million or so alveoli in the lungs. The walls of the capillaries are also only one cell in thickness. Some disease states cause this interface to thicken, thus making the oxygen-carbon dioxide exchange ineffective.
Oxygen and carbon dioxide molecules (as well as the molecules of other gases such as nitrogen and highly toxic carbon monoxide) can easily pass through the walls of the alveoli and the capillaries, moving in the direction of least resistance. Oxygen molecules move from the alveoli into the capillaries with inhalation. Hemoglobin molecules in the erythrocytes (red blood cells) attract the oxygen molecules, binding with them to carry them through the bloodstream. At exhalation carbon dioxide molecules cross the alveolar membrane to join the gases within the alveoli. Exhalation expels the carbon dioxide into the atmosphere.
Factors that influence oxygen-carbon dioxide exchange include the concentration of oxygen in the air, which is about 21 percent at sea level and decreases with elevation.
Numerous pulmonary conditions affect oxygen-carbon dioxide exchange. Infections such as INFLUENZA and PNEUMONIA can cause the alveoli to fill with fluid, blocking air from reaching the alveolar membranes. Inhaled substances, notably cigarette smoke, can clog small bronchioles, preventing air from reaching the alveoli. Eliminating their causes usually reverses most if not all of these circumstances to restore full function (though damage resulting from long-term cigarette smoking or repeated pneumonia can become permanent). Conditions that cause scarring (fibrosis), such as CYSTIC FIBROSIS, SARCOIDOSIS, PNEUMOCONIOSIS, and untreated TUBERCULOSIS, block air from reaching the alveoli. ATELECTASIS and BRONCHIECTASIS are collapses of lung segments that also block the movement of air into the deep lung tissues. Conditions in which the alveoli rupture and form enlarged sacs, such as alpha-1-antitrypsin deficiency (an inherited genetic disorder), destroy the surface area and reduce the effectiveness of the gas exchange. Both late-stage CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) and early emphysemapredominant COPD cause scarring and alveolar rupture. Such structural damage is permanent.