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Introduction

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Objectives

  1. Discuss the pathophysiology of hypoxemia.

  2. Discuss the physiologic effects of positive end-expiratory pressure (PEEP).

  3. Discuss the indications for the application of PEEP.

  4. Discuss the application, monitoring, and withdrawal of PEEP in acute respiratory distress syndrome.

  5. Discuss the overall management of oxygenation in critically ill patients.

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The principles associated with management of oxygenation are more complex than those associated with ventilation. Provided that cardiovascular function and V̇co2 are constant, increases in alveolar ventilation generally result in decreases in Paco2 and vice versa. Oxygenation status, although dependent on Fio2, is also affected by cardiopulmonary disease, positive end-expiratory pressure (PEEP), and mean airway pressure (P̄aw). In this chapter, the aspects of mechanical ventilation that affect oxygenation are discussed, as well as approaches to these techniques during patient management.

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Pathophysiology of Hypoxemia

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Normal Pao2 is 80 to 100 mm Hg when breathing room air at sea level, with hypoxemia defined as a Pao2 of < 80 mm Hg. To maintain normal tissue oxygenation it is necessary to provide an adequate Fio2, appropriate matching of ventilation and perfusion (V̇/Q̇), sufficient hemoglobin, adequate cardiac output, and appropriate O2 unloading to the tissue. A breakdown at any stage in this process may result in tissue hypoxia. At sea level, hypoxemia results from one of a number of alterations in cardiopulmonary function. Specifically, hypoxemia is caused by shunt, V̇/Q̇ mismatch, diffusion defect, and hypoventilation. Hypoxemia is also worsened by cardiovascular compromise. A reasonable target Pao2 in mechanically ventilated patients is 55 to 80 mm Hg (Spo2 88%-95%).

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Shunt

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Shunt is perfusion without ventilation. When present, venous blood (shunted blood) mixes with arterialized blood in the pulmonary veins or left heart causing a decrease in Pao2 of blood leaving the left heart. Because the majority of O2 is carried by hemoglobin, even a small shunt (Figure 13-1) can result in significant hypoxemia. Increasing Fio2 improves oxygenation only in the settings of small shunt. A large shunt is unresponsive to an Fio2 increase. Improvement in oxygenation in the setting of a large shunt is usually focused on resolution of the shunt (eg, decompression of a pneumothorax, resolution of a pneumonia, re-expansion of atelectasis, diuresis). The use of PEEP, recruitment maneuvers, and maneuvers to elevate P̄aw might improve oxygenation in this setting. A common, but often unrecognized, cause of shunt in mechanically ventilated patients is a patent foramen ovale. A functionally closed foramen ovale may open during mechanical ventilation and acute respiratory failure.

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Figure 13-1

Comparison of the theoretical Fio2 – Pao2 relationships with 0%, 15% and 30% shunts. These relationships were calculated assuming normal ventilation, hemoglobin of 15 g, C(a – v̄)O2 difference of 5 vol %, and normal cardiac output, metabolic rate, pH and Pco2. Note that as shunt increases, the Pa...

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