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.