Most patients with ischaemic stroke are managed on the ward or in specialty stroke units, but a significant number requires higher-acuity care and, consequently, admission to the intensive care unit. Mechanical ventilation is frequently performed in these patients due to swallowing dysfunction and airway or respiratory system compromise. Experimental studies have focused on stroke-induced immunosuppression and brain-lung crosstalk, leading to increased pulmonary damage and inflammation, as well as reduced alveolar macrophage phagocytic capability, which may increase the risk of infection. Pulmonary complications, such as respiratory failure, pneumonia, pleural effusions, acute respiratory distress syndrome, lung oedema, and pulmonary embolism from venous thromboembolism, are common and found to be among the major causes of death in this group of patients. Furthermore, over the past two decades, tracheostomy use has increased among stroke patients, who can have unique indications for this procedure—depending on the location and type of stroke—when compared to the general population. However, the optimal mechanical ventilator strategy remains unclear in this population. Although a high tidal volume (VT) strategy has been used for many years, the latest evidence suggests that a protective ventilatory strategy (VT = 6–8 mL/kg predicted body weight, positive end-expiratory pressure and rescue recruitment manoeuvres) may also have a role in brain-damaged patients, including those with stroke. The aim of this narrative review is to explore the pathophysiology of brain-lung interactions after acute ischaemic stroke and the management of mechanical ventilation in these patients.

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Purpose:The optimal ventilatory settings in patients after cardiac arrest and their association with outcome remain unclear. The aim of this study was to describe the ventilatory settings applied in the first 72 h of mechanical ventilation in patients after out-of-hospital cardiac arrest and their association with 6-month outcomes.Methods: Preplanned sub-analysis of the Target Temperature Management-2 trial. Clinical outcomes were mortality and functional status (assessed by the Modified Rankin Scale) 6 months after randomization.Results: A total of 1848 patients were included (mean age 64 [Standard Deviation, SD = 14] years). At 6 months, 950 (51%) patients were alive and 898 (49%) were dead. Median tidal volume (V T ) was 7 (Interquartile range, IQR = 6.2-8.5) mL per Predicted Body Weight (PBW), positive end expiratory pressure (PEEP) was 7 (IQR = 5-9) cmH 2 0, plateau pressure was 20 cmH 2 0 (IQR = 17-23), driving pressure was 12 cmH 2 0 (IQR = 10-15), mechanical power 16.2 J/min (IQR = 12.1-21.8), ventilatory ratio was 1.27 (IQR = 1.04-1.6), and respiratory rate was 17 breaths/minute (IQR = 14-20). Median partial pressure of oxygen was 87 mmHg (IQR = 75-105), and partial pressure of carbon dioxide was

Purpose of review The aim of this review is to provide an update on the pathophysiology and treatment of severe traumatic brain injury (TBI)-related complications on extracranial organs. Recent findings Extracranial complications are common and influence the outcome from TBI. Significant improvements in outcome in a sizeable proportion of patients could potentially be accomplished by improving the ability to prevent or reverse nonneurological complications such as pneumonia, cardiac and kidney failure. Prompt recognition and treatment of systemic complications is therefore fundamental to care of this patient cohort. However, the role of extracranial pathology often has been underestimated in outcome assessment since most clinicians focus mainly on intracranial lesions and injury rather than consider the systemic effects of TBI. Summary Robust evidence about pathophysiology and treatment of extracranial complications in TBI are lacking. Further studies are warranted to precisely understand and manage the multisystem response of the body after TBI.