Arterial Hypoxemia

Published on 22/03/2015 by admin

Last modified 22/04/2025

Print this page

This article have been viewed 2127 times

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).

Figure 8-1 Oxygen saturation varies with the PaO₂ in a nonlinear relationship and is affected by temperature, PaCO₂, pH, and 2,3-diphosphoglycerate (2,3-DPG) concentration.

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

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 increases with either an increase in production or a decrease in alveolar ventilation. Alveolar ventilation represents that portion of the minute ventilation undergoing blood-gas exchange and is represented by the product of respiratory rate and tidal volume minus dead space. Medications such as narcotics and sedatives that reduce the respiratory rate, and processes such as neuromotor weakness that reduce tidal volume, are common causes of hypercarbia.

To summarize, if the alveolar oxygen tension is reduced, then arterial hypoxemia is due to factors responsible for the low alveolar oxygen tension. If alveolar oxygen tension is normal, then hypoxemia is the result of either a ventilation/perfusion imbalance or a diffusion abnormality.

Diffusion Abnormalities

Diffusion abnormalities are the least likely cause of hypoxemia in the ICU, but they can occur as a result of an increase in the thickness of the capillary membrane, a reduction in total alveolar surface area, or a reduction in the capillary transit time. Increases in sympathetic tone due to fever, anemia, work of breathing, or sepsis can increase cardiac output and heart rate, resulting in faster transpulmonary transit times. With less opportunity for alveolar oxygen to diffuse into red blood cells, diffusing capacity is reduced. When capillary transit time is faster, the mean capillary arterial oxygen partial pressure decreases, and the diffusing capacity is reduced.

Ventilation/Perfusion Mismatch

The most common cause of hypoxemia is ventilation/perfusion mismatch. When perfusion is reduced as a result of a decrease in cardiac output or obstruction from pulmonary emboli, the percent of alveoli with adequate blood flow is reduced, increasing functional dead space. If minute ventilation remains constant, the primary blood gas abnormality is an increase in carbon dioxide (PCO₂ = carbon dioxide production/respiratory rate × tidal volume − dead space).

When ventilation is reduced relative to perfusion, alveolar oxygenation decreases and results in arterial hypoxemia. This problem occasionally occurs with bronchospasm or bronchitis. Patients with ventilation/perfusion abnormalities generally respond to increasing the FIO₂. When there is no ventilation (as opposed to reduced ventilation), increasing the FIO₂ is not beneficial.

The portion of cardiac output that does not participate in gas exchange is called the shunt fraction. The normal shunt fraction is approximately 3%, and this small amount of shunt is due to the bronchial arterial circulation. When alveoli are not ventilated, such as occurs with pulmonary edema, pneumonia, or atelectasis, the shunt fraction increases. As the shunt fraction increases, PaO₂ decreases (Figure 8-2), and there is a blunted response to increasing the FIO_2.When the shunt fraction is above 50%, there is little response to increasing FIO₂ (Figure 8-3).

Figure 8-2 Decrease in PaO₂ with increasing shunt fraction.

Figure 8-3 Blunted response to increasing the inspired oxygen concentration. A patient with a shunt greater than 50% has little response to increasing FIO₂.

Patients with refractory hypoxemia and a clear chest radiograph are often evaluated for a pulmonary embolus. In patients with otherwise previously normal lungs, pulmonary emboli are associated with modest decreases in arterial oxygenation; however, the major pathophysiology is an increase in dead space, which results in hypercarbia unless minute ventilation increases. The hypoxemia caused by pulmonary emboli is due to regional ventilation/perfusion abnormalities and responds to supplemental oxygen. If a patient with a pulmonary embolus has refractory hypoxemia unresponsive to supplemental oxygenation, an echocardiogram should be performed to rule out a patent foramen ovale, which creates a right-to-left intracardiac shunt in response to the acute increase in pulmonary artery pressure.

Other causes of refractory hypoxemia with a clear chest radiograph are intracardiac shunts and intrapulmonary shunts resulting from either arterial-venous malformations or end-stage liver disease. Often the cause of refractory hypoxemia without radiographic findings on the plain chest film is atelectasis, which is not seen on the typical anteroposterior portable study obtained in the ICU.

It also is relatively common for patients to develop significant hypoxemia when they are started on an intravenous vasodilator such as sodium nitroprusside. Infusion of sodium nitroprusside interferes with normal hypoxic vasoconstriction, leading to increased perfusion of poorly ventilated areas of the lung. As a result, shunt fraction increases.

Because calculating the shunt fraction, QsCQ_t = CcO₂/CCO₂ − CVO₂, requires arterial and mixed venous blood gases for calculation of C_CaO₂ (arterial) and C_VO₂ (venous) oxygen contents, and because capillary oxygen cannot be directly measured, other indices have been used to estimate the extent of pulmonary gas exchange abnormality. These indices include the alveolar-to-arterial (A-a) PO₂ gradient and the arterial-to-alveolar PO₂ ratio.

Alveolar-Arterial Partial Pressure of Oxygen Gradient

The difference between the alveolar PO₂ and the arterial PO₂ (i.e., the A-a gradient) often is used to estimate the extent of pulmonary pathophysiology and to rule out hypoxemia due to low alveolar PO₂ as the cause of arterial hypoxemia.^4,⁵ A patient with a reduced alveolar PO₂ (e.g., secondary to breathing room air at high altitude) would have a normal A-a gradient, whereas a patient with ventilation/perfusion mismatching would have a widened A-a gradient. A patient with a PaO₂ of 48 mm Hg and a PaCO₂ of 80 mm Hg would have an alveolar PO₂ on room air of 50 mm Hg; the normal A-a gradient of 2 mm Hg is consistent with reduced alveolar PO₂, and causes of hypercarbia need to be ruled out and reversed.