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The maintenance of gas exchange may be tenuous in the injured patient because of dysfunction in three key elements of the respiratory system. First, the central nervous system may be impaired, resulting in inadequate respiratory drive, or inability to maintain patent proximal airways. Second, injury to the torso can produce changes in compliance, ineffective respiratory effort, and pain that impact the patient’s ability to complete the work of breathing. Third, primary and secondary insults to the lung result in ineffective gas exchange.

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In practice, it is common for patients to suffer simultaneous insults, affecting all three elements. Impaired airway patency (e.g., diminished level of consciousness), increased work of breathing (e.g., multiple rib fractures), and impaired gas exchange (e.g., pulmonary contusion, fat emboli syndrome) often coexist in the same patient. Respiratory failure that relates primarily to CNS injury is discussed at length in other chapters and will not be extensively covered here. This chapter will focus on insults that affect work of breathing and gas exchange. The syndrome of postinjury acute respiratory distress syndrome (ARDS) is a major focus.

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The neurohormonal response to injury (ch67) results in a remarkable increase in cellular metabolism. This creates a substantial increase in carbon dioxide (CO2) production that must be matched by increased elimination from the lungs. While a resting adult eliminates 200 cm3/(kg min) of CO2, postinjury hypermetabolism results in CO2 production in the range of 425 cm3/(kg min).1 Thus, the minute ventilation required to maintain eucapnia may rise from a resting rate of approximately 5 L/min to more than 10 L/min. This represents a 100% increase in the work of breathing simply to meet metabolic demands.

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Additionally, injured patients typically have an increase in physiologic and anatomic dead space—ventilated regions that do not participate in gas exchange. In a normal adult, the proportion of each breath that is dead space (Vd/Vt) is approximately 0.35. In the intubated, ventilated patient, the Vd/Vt can be calculated by a number of techniques including the Bohr–Enghoff method (Vd/Vt = [{Paco2 – mean expired CO2}/Paco2]).2 For practical purposes (since mean expired CO2 is not commonly measured), this is a reflection of the minute volume required to achieve a given Paco2. In ventilated patients with pulmonary failure, the Vd/Vt often exceeds 0.6. Simply put, this extra dead space is a burden because each breath is less effective at eliminating CO2, and therefore minute ventilation requirements in the 12–20 L/min range are not uncommon in the postinjury setting.

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The above increase in respiratory demand might be met by a healthy adult; however, the injured patient faces several challenges in completing this additional work. CNS dysfunction from injury impairs respiratory drive, as do many medications routinely used for sedation and analgesia. Decreased thoracic compliance from abdominal distension (e.g., as part ...

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