Evaluating hypoxemia in the critically ill

Evaluating hypoxemia in the critically ill

Hypoxemia frequently occurs in critically ill patients as a result of a derangement in the efficiency of pulmonary oxygen uptake from ambient air. Alterations in pulmonary oxygen uptake are caused by ventilation-perfusion (V./Q. ) abnormalities and/or intrapulmonary shunts resulting in reduced arterial oxygen content, which can lead to tissue hypoxia. Consequently, oxygen delivery and the metabolic activity of various organs are altered.

Clinical conditions associated with hypoxemia and changes in oxygen delivery and consumption include acute respiratory distress syndrome (ARDS), sepsis, and trauma. Clinical worsening leads to progressive hypoxemia that may result in tissue hypoxia, which is implicated in the development of multiorgan failure.1 Thus, critically ill patients with sepsis or ARDS are not only in pulmonary peril but are also very likely to be at increased risk for systemic failure.

Regularly evaluating pulmonary oxygen uptake and delivery in critically ill patients provides information about oxygen transport and metabolic activity of peripheral tissue beds, and may allow early detection of tissue hypoxia.

In this article, we will review the dynamics of tissue oxygen balance. We will also describe various techniques for assessing oxygen delivery and will offer suggestions that may help you to better manage critically ill patients.


The terms "acute lung injury" and "ARDS" are used to describe hyp-oxemic respiratory failure in persons who are critically ill. The proposed mechanisms of abnormal oxygen uptake are alveolar edema and atelectasis, conditions that set the stage for shunting and V./Q. mismatching.2 In patients who have ARDS, hypoxemia is caused primarily by right-to-left intrapulmonary shunting of blood, leading to inefficient pulmonary oxygen uptake. Most patients consume a normal amount of oxygen, and tissue hypoxia rarely occurs unless their condition progresses to a terminal stage.

Other conditions that exacerbate oxygen imbalance and are often present in critically ill, mechanically ventilated patients include hypotension, fever, and anemia (see "Understanding oxygen balance"). Reduced blood flow or abnormal microvascular perfusion distribution is a prominent cause of impaired oxygen delivery and uptake. Febrile patients have increased oxygen demands that may further aggravate hypoxemia. In such an environment, the quantity of oxygen available for tissue delivery is diminished. The resulting tissue hypoxia constitutes a condition in which the cells within the tissue bed use more oxygen, which leads to anaerobic metabolism.3


Initial data using cardiac output and arterial and mixed venous blood oxygen contents suggested that whole body oxygen consumption was dependent on tissue oxygen delivery. This led to the practice of trying to achieve "supranormal" oxygen delivery with the use of vasopressors to increase cardiac output and deliver a greater amount of oxygen to peripheral tissues. This created controversy regarding the best approach to managing oxygen balance in the critically ill patient.

Supranormal delivery describes a strategy in which global oxygen delivery is increased to obtain oxygen delivery, oxygen consumption, and oxygen extraction values that can sustain life. It has been test- ed in clinical trials, with dubious results.

Early studies showed that infusing prostacyclin would increase oxygen delivery without increasing oxygen consumption, improving survival in some critically ill patients.4 This response to prostacyclin was believed to identify patients who had occult tissue hypoxia. The results of this investigation and other nonrandomized studies promulgated the use of vasopressors and inotropes as a means of achieving supranormal oxygen delivery in critically ill patients.5-7

Various investigators noted difficulties in achieving supranormal oxygen delivery.5-7 One problem is the failure to attain target values despite administration of increasing doses of catecholamines. In older or severely ill patients, achieving the target value is difficult. In addition, administration of large doses of dobutamine and norepinephrine to achieve a high cardiac output may lead to tachyarrhythmias, may worsen maldistribution of blood flow, and/or may produce myocardial ischemia.

More recent studies using independent measurements of oxygen consumption and delivery have not revealed a "pathologic" oxygen-supply dependence.8-11 Instead, there is a marked variability in basal whole body oxygen consumption related to the metabolic state of the patient.8-11

Several randomized controlled trials examined the survival benefit of increasing the patient's oxygen delivery to a target cardiac index of more than 4.5 mL/min/m2 and/or mixed venous oxygen saturation (Sv?248-175?O2) of 70% or more. Treatment of patients according to this strategy showed no benefit; to the contrary, mortality was increased.12-16 These studies also showed that using inotropes and vasopressors to increase oxygen to supranormal levels is difficult.14,15

Currently, the use of supranormal oxygen delivery in critically ill patients with existing hypoxia remains largely unjustified by clinical evidence.16 Improvements in global oxygen delivery may be achieved by several means. The first goal is to provide an adequate fraction of inspired oxygen to maintain oxygen saturation at more than 92% or PaO2 at more than 60 mm Hg.

In addition, oxygen-carrying capacity can be improved through the use of packed red blood cell transfusions for volume resuscitation. While the optimal hemoglobin concentration remains unknown, a target value of 10 to 12 g/dL would appear to be appropriate. However, data indicate that lower hemoglobin concentrations (7 to 10 g/dL) may be adequate and that routine transfusions of packed red blood cells to achieve a preselected value are not warranted.17

Alkalemia should be avoided because it impairs dissociation to the tissue. Simultaneously, mechanical ventilatory assistance should be provided using a tidal volume of 6 to 8 mL/kg of ideal body weight, and an attempt should be made to increase end-expiratory lung volume using positive end-expiratory pressure (PEEP) (5 cm H2O). Use of PEEP to increase mean alveolar pressure often succeeds in maintaining an adequate lung volume, thereby improving PaO2.

Low levels of PEEP reduce alveolar atelectasis in dependent portions of the lung and increase PaO2. However, at higher levels of PEEP, cardiac output may decline, leading to decreased oxygen delivery. Thus, optimal PEEP has been defined as the level that optimizes global oxygen delivery.18

PEEP-induced decline in cardiac output may be managed with volume infusion or packed red blood cell transfusion in anemic patients. Other measures involve decreasing oxygen consumption by giving antipyretics for fever and rigors. Minimizing agitation with the use of sedatives may also allow a patient's respiratory pattern to synchronize with the ventilator and avoid excessive muscle activity, thereby diminishing the work and oxygen cost of breathing.


Monitoring the patient for tissue hypoxia may allow early identification and implementation of specific therapies to reverse the process. Tissue hypoxia is assessed on a clinical basis, using biochemical indices, physiologic markers, and specific tissue probes.

Clinical assessment

Assessment of tissue hypoxia begins with a bedside evaluation. Although the physical findings of hypoxia are nonspecific, the presence of hypotension, tachycardia, tachypnea, mental obtundation, oliguria, cyanosis, pallor, and cool extremities provides strong supportive evidence and suggests organ dysfunction. In patients with sepsis, organ dysfunction may occur even in the absence of systemic hypoperfusion. In this case, systemic blood pressure measurements may not reflect specific organ perfusion and oxygen delivery.

The chief limits of bedside clinical assessment are the nonspecific and unquantifiable nature of these findings, as well as interobserver variability. Nonetheless, serial bedside examinations provide information that can be correlated with specific physiologic and biochemical measurements. One report highlighted the finding that the detection of cool extremities can identify patients with hypoperfusion as noted by elevated lactate levels and a relatively low cardiac output.19

Use of a pulmonary artery catheter allows bedside measurement of hemodynamics and Sv?248-175?O2. Measurements of central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output are routinely obtained. The pulmonary artery catheter is useful in determining intravascular volume status and guiding therapy for shock.

While pulmonary artery catheters are widely used in ICUs, there is concern regarding the lack of improvement in patient outcomes.20,21 An observational study involving more than 5700 critically ill medical and surgical patients raised issues concerning patient safety.22 Various reports have indicated that potential problems with the pulmonary artery catheter may be related to patient selection and data interpretation.23-25 Moreover, a prospective randomized trial reported no benefit to therapy directed by the pulmonary artery catheter compared with standard care of elderly, high-risk surgical patients.26


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