566
U N I T 6
Respiratory Function
the partial pressure (P) of the gases. Thus, oxygen moves
from the alveoli, where the partial pressure of oxygen
(PO
2
) averages 104 mm Hg when breathing room air, to
the blood in the pulmonary capillaries, where the aver-
age PO
2
is only 40 mm Hg.
1
Carbon dioxide moves in
the opposite direction, from the blood in the pulmonary
capillaries, where the partial pressure of carbon dioxide
(PCO
2
) is 45 mm Hg, to the alveolar air, where the PCO
2
is 40 mm Hg.
1
These values vary with tissue metabolism
and the oxygen content of the inspired air.
Perfusion
involves the movement of blood through
the pulmonary circulation, including the pulmonary
capillaries, where gas exchange takes place. Adequate
oxygenation of the blood and removal of CO
2
depend
on perfusion or movement of blood through the pul-
monary blood vessels and appropriate contact between
ventilated alveoli and perfused capillaries of the pulmo-
nary circulation (ventilation and perfusion matching).
Hypoxemia
Hypoxemia refers to a reduction in the PO
2
of the arte-
rial blood. It can result from an inadequate amount of O
2
in the air, disease of the respiratory system, dysfunction
of the neurologic system, or alterations in circulatory
function. The mechanisms whereby respiratory disorders
lead to a significant reduction in PO
2
are hypoventila-
tion, impaired diffusion of gases, inadequate circulation
of blood through the pulmonary capillaries, and mis-
matching of ventilation and perfusion
2,3
(see Chapter 21).
Often, more than one mechanism contributes to hypox-
emia in persons with respiratory or cardiac disease.
Hypoxemia produces its effects through tissue hypoxia
and the compensatory mechanisms that the body uses to
adapt to the lowered oxygen level. Body tissues vary con-
siderably in their vulnerability to hypoxia; those with the
greatest need are the brain and heart. If the PO
2
in these
organs falls belowa critical level, aerobicmetabolismceases
and anaerobic metabolism takes over, with formation and
release of lactic acid. This results in increased serum lactate
levels and a metabolic acidosis (see Chapter 8).
Mild hypoxemia or reduction in the PO
2
of arterial
blood produces few manifestations. Recruitment of
sympathetic nervous system compensatory mechanisms
produces an increase in heart rate, peripheral vasocon-
striction, and a mild increase in blood pressure.
3
This
is because hemoglobin saturation is still approximately
90% when the PO
2
is only 60 mm Hg (see Chapter 21,
Fig. 21-22). More pronounced hypoxemia may produce
personality changes, restlessness, uncoordinated muscle
movements, euphoria, impaired judgment, delirium,
and, eventually, stupor and coma.
Cyanosis
refers to the bluish discoloration of the skin
and mucous membranes resulting from an excessive
concentration of reduced or deoxygenated hemoglobin
in the small blood vessels. It usually is most pronounced
in the lips, nail beds, ears, and cheeks. The degree of cya-
nosis is modified by the amount of cutaneous pigment,
skin thickness, and the state of the cutaneous capillaries.
Cyanosis is more difficult to distinguish in persons with
dark skin and in areas of the body with increased skin
thickness. Although cyanosis may be evident in persons
with respiratory failure, it often is a late sign. A deoxy-
genated hemoglobin concentration of approximately
5 g/dL of deoxygenated hemoglobin is required in the
circulating blood for cyanosis to occur.
1
The absolute
quantity of reduced hemoglobin, rather than the relative
quantity, is important in producing cyanosis. Persons
with anemia are less likely to exhibit cyanosis because
they have less hemoglobin to transport oxygen even
though their cardiac output and lung function are nor-
mal. A person with a high hemoglobin level because of
polycythemia may be cyanotic in the absence of hypoxia.
Cyanosis can be divided into two types: central and
peripheral.
Central cyanosis
is evident in the tongue and
lips. It is caused by an increased amount of deoxygen-
ated hemoglobin in the arterial blood.
Peripheral cyano-
sis
occurs in the extremities and on the tip of the nose or
ears. It is caused by slowing of blood flow to an area of
the body, with increased extraction of oxygen from the
blood. It results from vasoconstriction and diminished
peripheral blood flow, as occurs with cold exposure,
shock, heart failure, or peripheral vascular disease.
The manifestations of chronic hypoxemia may be
insidious in onset and attributed to other causes, par-
ticularly in persons with chronic lung disease. The body
compensates for chronic hypoxemia with increased venti-
lation, pulmonary vessel vasoconstriction, and increased
production of red blood cells. Pulmonary vasoconstric-
tion occurs as a local response to alveolar hypoxia; it
increases pulmonary arterial pressure and improves the
matching of ventilation and perfusion. Increased pro-
duction of red blood cells results from the release of
erythropoietin from the kidneys in response to hypoxia
(see Chapter 13). Other adaptive mechanisms include a
shift to the right in the oxygen dissociation curve, which
increases O
2
release to the tissues (see Chapter 21).
Diagnosis of hypoxemia is based on clinical observa-
tion and diagnostic tests that measure PO
2
levels. The
analysis of arterial blood gases provides a direct mea-
sure of the O
2
content of the blood and is the best indi-
cator of the ability of the lungs to oxygenate the blood.
Mixed venous oxygen saturation (SvO
2
; i.e., oxygen
saturation of hemoglobin in venous blood) reflects the
body’s extraction at the tissue levels. Venous blood sam-
ples can be obtained either through a pulmonary artery
catheter or central line.
Noninvasive measurements of arterial O
2
saturation
of hemoglobin can be obtained using pulse oximetry.
4,5
Reusable clip probes (finger, nasal, ear) and single-use
adhesive probes (finger and forehead) are available.
5
Advantages of the reusable clip probe include the rapid-
ity with which measurements can be obtained and cost-
effectiveness. The adhesive probes allow for more secure
placement and ability to monitor sites other than those
used by the clip probes.
Pulse oximetry uses light-emitting diodes and com-
bines plethysmography (i.e., changes in light absor-
bance and vasodilation) with spectrophotometry.
4,5
Spectrophotometry uses a red-wavelength light that passes
through oxygenated hemoglobin and is absorbed by
