O
oxygen–carbon dioxide exchange The process
by which oxygen passes from the air in the LUNGS
to the HEMOGLOBINin the BLOOD, and carbon diox-
ide from the hemoglobin passes into the air in the
lungs. Oxygen–carbon dioxide exchange is funda-
mental 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 tini-
est blood vessels of the cardiovascular system. The
membranous tissue of an ALVEOLUSis 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 capillar-
ies 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 oxy-
gen–carbon dioxide exchange. Infections such as
INFLUENZAand PNEUMONIAcan cause the alveoli to
fill with fluid, blocking air from reaching the alve-
olar membranes. Inhaled substances, notably ciga-
rette smoke, can clog small bronchioles, prevent-
ing air from reaching the alveoli. Eliminating their
causes usually reverses most if not all of these cir-
cumstances to restore full function (though dam-
age 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. ATELECTASISand BRONCHIECTASISare col-
lapses of lung segments that also block the move-
ment 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 emphysema-
predominant COPD cause scarring and alveolar
rupture. Such structural damage is permanent.
See also CYSTIC FIBROSIS AND THE LUNGS; LUNG
TRANSPLANTATION; OXYGEN SATURATION; OXYGEN THER-
APY.oxygen saturation The percentage of HEMOGLOBIN
molecules in the BLOODthat are bound to oxygen
molecules. Normal oxygen saturation of the arte-
rial blood is 96 to 98 percent. Saturation signifi-
cantly below normal, for instance 88 percent,
indicates RESPIRATORY FAILURE and may be life-
threatening. Oxygen saturation is an essential
measurement for assessing cardiovascular and pul-
monary effectiveness. Inadequate oxygen satura-
tion in the blood is hypoxemia.
The primary method for measuring oxygen sat-
uration is pulse oximetry, which is painless and
noninvasive. The pulse oximeter consists of two216