If the patient has a P/F ratio of <100 and oxygenation is marginal, paralysis and sedation are recommended and a recruitment maneuver should be attempted. Not all patients recruit successfully however, and it may be necessary to accept lower oxygenation in those with severe lung injury. Injurious ventilator strategies only transiently improve oxygenation and cause significant long-term pulmonary compromise. There is also evidence that 48 h of paralysis in patients with ARDS may improve outcome primarily due to enhancing synchrony. This not an issue however in those breathing spontaneously with PSV.

Opioid analgesia not only provides pain relief but promotes endotracheal tube tolerance by peripheral cough suppression and central respiratory depression. Hypnotic sedation (with propofol or benzodiazepines) should be minimized and used for the shortest period and at the lowest dose possible to ensure a calm but not comatose patient. Hypnotic sedation should only be used for procedural sedation, severe agitation, or when neuromuscular paralysis is utilized, to avoid the medicolegal hazard of awake paralysis.

Avoiding hypnotic sedation facilitates early mobilization, which is an essential component of the weaning and recovery process, and reduces subsequent cognitive deficit and post-traumatic stress arising from the ICU experience. Hypnotic sedation may be required with a P/F ratio <100, where paralysis is required and for delirium or extreme agitation (if a cause has been sought and if possible corrected and pain and discomfort have been addressed). Analgesia is essential and should be titrated to levels of adequate pain control. Early involvement of the physiotherapist is essential for management of the chest and to ensure maintenance of general range of the movement.

Interventions include restrictive fluid management, recruitment and paralysis (as discussed above), and alternative ventilatory modes such as airway pressure release ventilation (APRV) and extra corporeal membrane oxygenation (ECMO).

Patients with TBI should have the end-tidal CO₂ controlled for approximately 48 h (neuroprotective ventilation) to optimize neuronal recovery. On the one hand, hyperventilation lowers intracranial pressure (ICP) by causing cerebral vasoconstriction, but the latter decreases cerebral flow and intracerebral blood volume, leading to ischemia if prolonged. It is not recommended that chronic prophylactic hyperventilation be used, although short term it may be of value preoperatively.

Similarly controversial has been the use of PEEP. It does appear however that when PEEP is set at levels lower than ICP, it does not have a significant effect on ICP. Given the potential for patients with severe trauma to develop ARDS, it is advisable that PEEP be used to prevent derecruitment as described above.

Patients ventilated for chest trauma, or post major abdominal trauma, are at risk for pulmonary complications due to alterations in thoracic compliance. Capillary leak reduces chest wall compliance, and this has the potential to increase intrathoracic pressures, which along with increased intra-abdominal pressures reduce venous return. Venous pressures may be falsely elevated due to reduced abdominal compliance, pneumothorax, hemothorax, or chest wall injuries. If coupled with intravascular volume depletion, hypotension may ensue. Progression of lung contusion, particularly in the face of fluid overload, reduces lung compliance. All of these factors may act in concert to increase measured ventilator pressures (volume modes) or reduce tidal volume (pressure modes) and reduce oxygenation or carbon dioxide clearance.

Therefore it is essential to monitor: