C h a p t e r 2 3
Disorders of Ventilation and Gas Exchange
595
in ventilation and greater diffusion rate of carbon diox-
ide. Hypoxemia resulting from impaired diffusion can
be partially or completely corrected by the administra-
tion of high concentrations of oxygen. In this case, the
high concentration of oxygen serves to overcome the
decrease in diffusion by establishing a larger alveolar-to-
capillary diffusion gradient.
Hypercapnic/Hypoxemic Respiratory Failure
In the hypercapnic form of respiratory failure, patients
are unable to maintain a level of alveolar ventilation
sufficient to eliminate CO
2
and keep arterial O
2
levels
within normal range. Because ventilation is determined
by a sequence of events ranging from the generation of
impulses in the CNS to movement of air through the con-
ducting airways, there are several stages at which prob-
lems can adversely affect the total minute ventilation.
Hypoventilation or ventilatory failure occurs when the
volume of “fresh” air moving into and out of the lung
is significantly reduced. It is commonly caused by condi-
tions outside the lung such as depression of the respira-
tory center (e.g., drug overdose, brain injury), diseases
of the nerves supplying the respiratory muscles (e.g.,
Guillain-Barré syndrome, spinal cord injury), disorders of
the respiratory muscles (e.g., muscular dystrophy), exac-
erbation of chronic lung disease (e.g., COPD), or thoracic
cage disorders (e.g., severe scoliosis or crushed chest).
Hypoventilation has two important effects on arterial
blood gases. First, it almost always causes an increase
in PCO
2
. The rise in PCO
2
is directly related to the
level of ventilation; reducing the ventilation by one half
causes a doubling of the PCO
2
. Thus, the PCO
2
level is
a good diagnostic measure for hypoventilation. Second,
it may cause hypoxemia, although the hypoxemia that
is caused by hypoventilation can be readily abolished by
the administration of supplemental oxygen.
Clinical Features
Acute respiratory failure is usually manifested by vary-
ing degrees of hypoxemia and hypercapnia. There is no
absolute definition of the levels of PO
2
and PCO
2
that
indicate respiratory failure; however, it is convention-
ally defined as an arterial PO
2
of less than 60 mm Hg,
an arterial PCO
2
of more than 45 mm Hg, or both when
prior blood values have been normal.
71
Again, these cut-
off values are not rigid, but serve as a general guide in
combination with history and physical assessment data.
The signs and symptoms of acute respiratory fail-
ure are those of the underlying disease combined with
those of hypoxemia and hypercapnia.
72,73
Hypoxemia
is accompanied by increased respiratory drive and
increased sympathetic tone. Potential signs include cya-
nosis, restlessness, confusion, anxiety, delirium, fatigue,
tachypnea, hypertension, cardiac arrhythmias, and
tremor. The initial cardiovascular effects are tachycardia
with increased cardiac output and increased blood pres-
sure. Serious cardiac arrhythmias may be triggered. The
pulmonary vasculature constricts in response to low
alveolar PO
2
. If severe, the pulmonary vasoconstriction
may result in acute right ventricular failure with
manifestations such as jugular vein distention and
dependent edema. Profound acute hypoxemia can cause
convulsions, retinal hemorrhages, and permanent brain
damage. Hypotension and bradycardia often are preter-
minal events in persons with hypoxemic respiratory fail-
ure, indicating the failure of compensatory mechanisms.
Many of the adverse consequences of hypercapnia
are the result of respiratory acidosis. Direct effects of
acidosis include depression of cardiac contractility,
decreased respiratory muscle contractility, and arte-
rial vasodilation (see Chapter 8). Raised levels of PCO
2
greatly increase cerebral blood flow, which may result
in headache, increased cerebrospinal fluid pressure, and
sometimes papilledema (see Chapter 38, Fig. 38-9).
The headache is due to dilation of the cerebral vessels.
Additional indicators of hypercapnia are warm and
flushed skin and hyperemic conjunctivae. Hypercapnia
produces nervous system effects similar to those of an
anesthetic—hence the term
carbon dioxide narcosis.
There is progressive somnolence, disorientation, and, if
the condition is left untreated, coma. Mild to moderate
increases in blood pressure are common. Air hunger and
rapid breathing occur when alveolar PCO
2
levels rise to
approximately 60 to 75 mm Hg; as PCO
2
levels reach
80 to 100 mm Hg, the person becomes lethargic and
sometimes semicomatose.
The treatment of respiratory failure focuses on cor-
recting the problem causing impaired gas exchange
when possible and on relieving the hypoxemia and
hypercapnia. A number of treatment modalities are
available, including the establishment of an airway, use
of bronchodilating drugs, and antibiotics for respiratory
infections. Controlled oxygen therapy and mechanical
ventilation are used in treating blood gas abnormalities
associated with respiratory failure.
75
When alveolar ventilation is inadequate to maintain
PO
2
or PCO
2
levels because of respiratory or neuro-
logic failure, mechanical ventilation may be lifesaving.
Usually a nasotracheal, orotracheal, or tracheotomy
tube is inserted into the trachea to provide the airway
needed for mechanical ventilation. There has been
recent interest in noninvasive forms of mechanical ven-
tilation that use a face mask to deliver positive-pressure
ventilation.
76
SUMMARY CONCEPTS
■■
The hallmark of acute lung injury and acute
respiratory distress syndrome is a pronounced
inflammatory response that affects the lung and
may result in systemic organ failure.The acute
inflammatory response results in damage and
dysfunction of the alveolar–capillary membrane
of the lung. Classically, there is interstitial edema
of lung tissue, an increase in surface tension
caused by inactivation of surfactant, collapse of
alveolar structures, a stiff and noncompliant lung
(continued)
