What respiratory targets should be recommended in patients with brain injury and respiratory failure?

Excerpt

Acute brain injury (ABI) as a consequence of hypoxia, trauma, or stroke is a major cause of disability and death. Mechanical ventilation (MV) affects cerebral hemodynamics via different mechanisms. First, it can optimize the blood level of oxygen and the arterial partial pressure of carbon dioxide (PaCO₂), which is a potent modulator of intracranial pressure (ICP) owing to its effect on cerebrovascular tone and consequently cerebral perfusion pressure. Hypercapnia mainly triggers vasodilatation and increases ICP whereas hypocapnia causes vasoconstriction. Second, increased intrathoracic pressure caused by application of positive end-expiratory pressure (PEEP) may impair venous return, thus reducing mean arterial pressure and/or increasing ICP. Consequently, in ABI patients, it has become traditional to target a combination of high tidal volume (Vt) (> 9 ml/kg) and low PEEP [1]. Concurrent acute respiratory failure or acute respiratory distress syndrome (ARDS) in ABI is multifactorial, its causes including aspiration, chest trauma, ABI-induced lung inflammation with reduced pulmonary compliance, and ventilator-induced lung injury (VILI), and it is associated with a worse outcome [2]. VILI is a modifiable risk factor, amenable to the use of lung protective ventilation (LPV), an approach that includes the application of low Vt and high PEEP levels [3]. Clearly, therefore, in cases where ABI and respiratory failure coexist, it is necessary to determine which is the optimal ventilator strategy. The aim of this editorial is to review briefly the current evidence on the use of ventilator settings to achieve respiratory targets (including oxygen and PaCO₂ levels) in patients with ABI and acute respiratory failure or ARDS. …