Arterial Hypoxemia

Published on 22/03/2015 by admin

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Last modified 22/03/2015

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8 Arterial Hypoxemia

Respiratory distress with hypoxemia is a common reason for patients to be admitted to the intensive care unit (ICU). Because a patient’s arterial oxygen saturation can be monitored easily using a continuous pulse oximeter, nurses and physicians are alerted immediately to changes in a patient’s oxygen saturation. For these reasons, it is important for healthcare providers to understand the meaning of this measurement, recognize its limitations, and outline a plan for diagnosing and managing patients with hypoxemia.

Arterial hypoxemia is defined as a partial pressure of oxygen in arterial blood (PaO2) less than 80 mm Hg while breathing room air. The PaO2 represents the amount of oxygen in physical solution, whereas the oxygen saturation represents the fractional amount of oxyhemoglobin relative to total hemoglobin concentration. Oxygen saturation varies with the PaO2 in a nonlinear relationship and is affected by temperature, partial pressure of carbon dioxide in arterial blood (PaCO2), pH, and 2,3-diphosphoglycerate concentration (Figure 8-1).

Falsely low saturations can be recorded if there is a poor waveform or if light absorption is decreased by dark blue or black nail polish. Patients with methemoglobinemia can have a falsely low oxygen saturation, whereas patients with carboxyhemoglobinemia can have a falsely elevated oxygen saturation, because the pulse oximeter cannot differentiate carboxyhemoglobin from oxyhemoglobin.1 Finally, because the oxygen-hemoglobin dissociation curve is affected by temperature, pH, partial pressure of carbon dioxide (PCO2), and 2,3-diphosphoglycerate concentration, patients can have a higher or lower saturation for a given PaO2.

Patients who have significant decreases in oxygen saturation attempt to maintain oxygen delivery by increasing cardiac output. Although patients with normal left ventricular function and normal coronary vasculature can tolerate lower oxygen saturation, patients with coronary artery disease or decreased myocardial contractility may not be able to tolerate the compensatory tachycardia. The decision to begin mechanical or noninvasive ventilation should be based on the patient’s cardiopulmonary physiology and not the specific value for the oxygen saturation measurement. PaO2 less than 40 mm Hg or oxygen saturation less than 75% results in tissue hypoxemia, however, despite compensatory increases in cardiac output. Generally, saturations in the low 90s on escalating levels of inspired oxygen concentration indicate impending respiratory failure, and invasive or noninvasive mechanical ventilation is necessary.

Etiologies for hypoxemia are best understood if approached from a physiologic point of view rather than by referring to a list of possible differential diagnoses. Simply stated, hypoxemia results from an imbalance between pulmonary ventilation and pulmonary capillary blood flow.2

image Reduced Alveolar Oxygenation

Alveolar oxygenation is defined by the equation:

where FIO2 is the concentration of inspired oxygen, BP is the barometric pressure, BPH2O is the partial pressure of water, and RQ is the respiratory quotient. The respiratory quotient represents the amount of oxygen consumed relative to the amount of carbon dioxide produced when nutrients are metabolized. RQ is generally assumed to be 0.8. Under normal conditions, where the FIO2 is 21%, BP is 760 mm Hg, BPH2O is 47 mm Hg, and PaCO2 is 40 mm Hg, the Palvo2 = 0.21(760 − 47) − 40/0.8 = 100 mm Hg. According to the equation, several factors may contribute to lower alveolar oxygenation. One is a reduction in barometric pressure, causing hypobaric hypoxemia that affects those climbing at high altitudes.3 The second factor is an increase in PaCO2, which can be explained by the relationship: PaCO2 = carbon dioxide production/respiratory rate (tidal volume − dead space). Accordingly, the PaCO2

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