OXYGEN THERAPY IN ACUTE RESPIRATORY FAILURE
ARTERIAL
BLOOD GAS COMPOSITION
Arterial blood gas (ABG) findings can be explained by the carbon dioxide: oxygen diagram shown at the top of the illustration. Because there is no uptake or excretion of nitrogen during respiration and the alveolar partial pressure of water vapor is a function of body temperature only, there is a reciprocal relationship between the alveolar Pco2 and Po2, as indicated by the alveolar gas composition line. Because prolonged survival is not possible when the PaO2 is less than 20 mm Hg, the range of arterial gas tensions compatible with life is confined to the yellow triangle. Initial ABG values of air-breathing patients with decompensated chronic obstructive pulmonary disease (COPD) fall in the upper shaded blue area. With higher oxygen concentrations, the alveolar gas composition line is shifted to the right, and much higher PaCO2 values are possible.
Fortunately, because of the shape of the hemoglobin
dissociation curve, only a small increase in oxygen tension is necessary to
produce a marked increase in arterial oxygen content. In most patients, a 15-mm
Hg increase in arterial oxygen tension can be produced by increasing the
inspired oxygen fraction by only 4% to 7%. Administration of low oxygen
concentrations (24%-35%) and low flows (1-3 L/min) can be achieved by use of a
nasal cannula (see Plate 5-13). Care must be given to supplying enough oxygen
to achieve adequate oxygenation (SaO2 >90%) without
causing too much CO2 retention, which may occur during acute exacerbations
in patients with severe COPD. Contrary to popular belief, CO2
retention in COPD is caused by a worsening mismatch of ventilation and
perfusion in the presence of excessive oxygen with a resulting increase in dead
space ventilation, as well as an increased offloading of CO2 by
hemoglobin, rather than a reduced drive to breathe.
CARE AND MONITORING DURING OXYGEN THERAPY
Although measurement
of AGBs is
of prime importance in patients receiving oxygen for
acute respiratory failure, a reduction in cardiac output, hemoglobin
concentration, or local
blood flow, a
shift in position
of the oxygen dissociation curve, or an increase in tissue requirements
can result in inadequate oxygen delivery to the tissues even if the PaO2 is normal. Although there is no specific way
to assess the level of tissue oxygenation, tissue hypoxia probably exists if
the mixed venous Po2 is less than 35 mm Hg. Monitoring and
correcting abnormalities of cardiovascular
function and hemoglobin concentration minimize tissue hypoxia.
Oxygen requirements may change during therapy, and a
patient’s respiratory, cardiovascular, and mental status should be evaluated
often. Patients should be observed during sleep, when their breathing patterns
may be different. Sedation should be avoided.
Pulse oximetry is a convenient and noninvasive method
for monitoring oxyhemoglobin saturation; however, its limitations must be appreciated. The
method does not allow direct measurement of Po2, Pco2, or
pH, and accuracy may be affected by many factors, including skin pigmentation,
adequate capillary blood flow, external light conditions, and alternative
hemoglobin species such as carboxy- and methemoglobin. New pulse oximeters that
use co-oximetry to determine the presence of these other hemoglobin species are being introduced into
clinical practice.
