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Recently, there has been increasing attention to bidirectional information exchange between the brain and lungs. Typical physiological data is communicated by channels like the circulation and sympathetic nervous system. However, communication between the brain and lungs can also occur in pathological conditions. Studies have shown that severe traumatic brain injury (TBI), cerebral hemorrhage, subarachnoid hemorrhage (SAH), and other brain diseases can lead to lung damage. Conversely, severe lung diseases such as acute respiratory distress syndrome (ARDS), pneumonia, and respiratory failure can exacerbate neuroinflammatory responses, aggravate brain damage, deteriorate neurological function, and result in poor prognosis. A brain or lung injury can have adverse effects on another organ through various pathways, including inflammation, immunity, oxidative stress, neurosecretory factors, microbiome and oxygen. Researchers have increasingly concentrated on possible links between the brain and lungs. However, there has been little attention given to how the interaction between the brain and lungs affects the development of brain or lung disorders, which can lead to clinical states that are susceptible to alterations and can directly affect treatment results. This review described the relationships between the brain and lung in both physiological and pathological conditions, detailing the various pathways of communication such as neurological, inflammatory, immunological, endocrine, and microbiological pathways. Meanwhile, this review provides a comprehensive summary of both pharmacological and non-pharmacological interventions for diseases related to the brain and lungs. It aims to support clinical endeavors in preventing and treating such ailments and serve as a reference for the development of relevant medications.

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Background: Patients with acute brain injury (ABI) are a peculiar population because ABI does not only affect the brain but also other organs such as the lungs, as theorized in brain-lung crosstalk models. ABI patients often require mechanical ventilation (MV) to avoid the complications of impaired respiratory function that can follow ABI; MV should be settled with meticulousness owing to its effects on the intracranial compartment, especially regarding positive end-expiratory pressure (PEEP). This scoping review aimed to (1) describe the physiological basis and mechanisms related to the effects of PEEP in ABI; (2) examine how clinical research is conducted on this topic; (3) identify methods for setting PEEP in ABI; and (4) investigate the impact of the application of PEEP in ABI on the outcome. Methods: The five-stage paradigm devised by Peters et al. and expanded by Arksey and O'Malley, Levac et al., and the Joanna Briggs Institute was used for methodology. We also adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) extension criteria. Inclusion criteria: we compiled all scientific data from peer-reviewed journals and studies that discussed the application of PEEP and its impact on intracranial pressure, cerebral perfusion pressure, and brain oxygenation in adult patients with ABI. Exclusion criteria: studies that only examined a pediatric patient group (those under the age of 18), experiments conducted solely on animals; studies without intracranial pressure and/or cerebral perfusion pressure determinations, and studies with incomplete information. Two authors searched and screened for inclusion in papers published up to July 2023 using the PubMed-indexed online database. Data were presented in narrative and tubular form. Results: The initial search yielded 330 references on the application of PEEP in ABI, of which 36 met our inclusion criteria. PEEP has recognized beneficial effects on gas exchange, but it produces hemodynamic changes that should be predicted to avoid undesired consequences on cerebral blood flow and intracranial pressure. Moreover, the elastic properties of the lungs influence the transmission of the forces applied by MV over the brain so they should be taken into consideration. Currently, there are no specific tools that can predict the effect of PEEP on the brain, but there is an established need for a comprehensive monitoring approach for these patients, acknowledging the etiology of ABI and the measurable variables to personalize MV. Conclusion: PEEP can be safely used in patients with ABI to improve gas exchange keeping in mind its potentially harmful effects, which can be predicted with adequate monitoring supported by bedside non-invasive neuromonitoring tools.

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Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the body's ability to counteract their harmful effects, playing a key role in the pathogenesis of brain and lung-related diseases. This review comprehensively examines the intricate mechanisms by which oxidative stress influences cellular and molecular pathways, contributing to neurodegenerative, cardiovascular, and respiratory disorders. Emphasizing the detrimental effects on both brain and lung health, we discuss innovative diagnostic biomarkers, such as 8-hydroxy-2'-deoxyguanosine (8-OHdG), and the potential of antioxidant therapies. For these topics, we provide insights into future research directions in the field of oxidative stress treatment, including the development of personalized treatment approaches, the discovery and validation of novel biomarkers, and the development of new drug delivery systems. This review not only provides a new perspective on understanding the role of oxidative stress in brain and lung-related diseases but also offers new insights for future clinical treatments.

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Extracerebral complications, especially pulmonary and cardiovascular, are frequent in brain-injured patients and are major outcome determinants. Two major pathways have been described: brain-lung and brain-heart interactions. Lung injuries after acute brain damages include ventilator-associated pneumonia (VAP), acute respiratory distress syndrome (ARDS) and neurogenic pulmonary œdema (NPE), whereas heart injuries can range from cardiac enzymes release, ECG abnormalities to left ventricle dysfunction or cardiogenic shock. The pathophysiologies of these brain-lung and brain-heart crosstalk are complex and sometimes interconnected. This review aims to describe the epidemiology and pathophysiology of lung and heart injuries in brain-injured patients with the different pathways implicated and the clinical implications for critical care physicians.

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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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Major pulmonary disorders may occur after brain injuries as ventilator-associated pneumonia, acute respiratory distress syndrome or neurogenic pulmonary edema. They are key points for the management of brain-injured patients because respiratory failure and mechanical ventilation seem to be a risk factor for increased mortality, poor neurological outcome and longer intensive care unit or hospital length of stay. Brain and lung strongly interact via complex pathways from the brain to the lung but also from the lung to the brain. Several hypotheses have been proposed with a particular interest for the recently described "double hit" model. Ventilator setting in brain-injured patients with lung injuries has been poorly studied and intensivists are often fearful to use some parts of protective ventilation in patients with brain injury. This review aims to describe the epidemiology and pathophysiology of lung injuries in brain-injured patients, but also the impact of different modalities of mechanical ventilation on the brain in the context of acute brain injury.