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A 45-year-old man with no significant past medical history presents to the intensive care unit (ICU) after a motor vehicle collision. Upon presentation to the Emergency Department (ED), he was endotracheally intubated for airway protection, with a Glasgow Coma Scale (GCS) of 7 (E1V2M4). Intubation was accomplished without any incidence of hypotension or hypoxia; however, the patient was actively vomiting at presentation and vomitus was noted at his vocal cords during direct laryngoscopy. His trauma work up included computed tomography (CT) scans of the head, cervical spine, chest, abdomen, and pelvis, as well as a chest radiograph. This demonstrated bifrontal contusions on CT and suspected diffuse axonal injury (DAI). No other injuries were discovered. He presents to your ICU early in the night with the following settings on the mechanical ventilator: assist control/volume-targeted mode (AC/VC), tidal volume, 650 cc; positive end-expiratory pressure (PEEP), 5 cm H2O; respiratory rate, 14; and a fraction of inspired oxygen (Fio2) of 0.50. On these settings, you note that his peak inspiratory pressure is 29 cm H2O, and his inspiratory plateau pressure is 25 cm H2O. The patient’s vital signs are as follows: heart rate, 115; blood pressure, 120/80 mm Hg; respiratory rate, 14; oxygen saturation, 92%; and temperature, 99.5°F. Also, as you review the graphics package on the ventilator, you note smooth waveforms, with no evidence of intrinsic PEEP and no evidence of dysynchrony. As you receive the report from the Emergency Medicine physician, you note the concerns for aspiration, and you review his chest radiograph and chest CT, which both show a suggestion of aspiration to the bilateral lower lobes. You are happy with his current status, but you wonder how his head injury and potential lung injury will progress. As you settle in for an interesting call night, you notice that his inspiratory plateau pressure is now 35 cm H2O and his Fio2 is 0.80.

Regardless of the indication for endotracheal intubation and initiation of mechanical ventilation, a mechanical ventilator in and of itself, does not treat much. However, it does have great potential for harm. Effective mechanical ventilation should prioritize limitation of ventilator-associated lung injury (VALI) almost as much as oxygenation, and maintenance of normal carbon dioxide levels should be a lower priority in the grand majority of patients.1 Keen knowledge of basic and advanced principles can allow the clinician to use the mechanical ventilator for its maximum therapeutic potential and minimize iatrogenic injury, while the process that led to respiratory failure is allowed to heal. It cannot be stressed enough that knowledge of cardiopulmonary physiology, heart-lung interactions, and the effects of mechanical ventilator settings on cerebral oxygenation and blood flow, will allow the clinician flexibility when titrating support to an individual patient at the bedside. Although the clinician should be intimately familiar with guidelines and large clinical trials, they are only as good as ...

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