Harmful effects of mechanical ventilation on neurocognitive functions

Bilotta, Federico; Giordano, Giovanni; Sergi, P.; Pugliese, Francesco

doi:10.1186/s13054-019-2546-y

Cited by 27 publications

(32 citation statements)

References 13 publications

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“…36 Finally, the potential consequences of low assistance include excessive respiratory muscle load and limbic, paralimbic, and cerebellar activation in the brain that can promote air hunger. [37][38][39][40][41]…”

Section: Flow Starvationmentioning

confidence: 99%

Monitoring Asynchrony During Invasive Mechanical Ventilation

et al. 2020

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Mechanical ventilation in critically ill patients must effectively unload inspiratory muscles and provide safe ventilation (ie, enhancing gas exchange, protect the lungs and the diaphragm). To do that, the ventilator should be in synchrony with patient's respiratory rhythm. The complexity of such interplay leads to several concerning issues that clinicians should be able to recognize. Asynchrony between the patient and the ventilator may induce several deleterious effects that require a proper physiological understanding to recognize and manage them. Different tools have been developed and proposed beyond the careful analysis of the ventilator waveforms to help clinicians in the decision-making process. Moreover, appropriate handling of asynchrony requires clinical skills, physiological knowledge, and suitable medication management. New technologies and devices are changing our daily practice, from automated real-time recognition of asynchronies and their distribution during mechanical ventilation, to smart alarms and artificial intelligence algorithms based on physiological big data and personalized medicine. Our goal as clinicians is to provide care of patients based on the most accurate and current knowledge, and to incorporate new technological methods to facilitate and improve the care of the critically ill.

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Section: Flow Starvationmentioning

confidence: 99%

Monitoring Asynchrony During Invasive Mechanical Ventilation

et al. 2020

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“…MV could be a pivotal mechanism that increases the risk for long-term cognitive impairment, but the complex effects and pathophysiology of MV on neuroinflammation-as well as related neurocognitive adverse outcomes-are not fully understood [3].…”

Section: Dear Editormentioning

confidence: 99%

Mechanical ventilation and long-term neurocognitive impairment after acute respiratory distress syndrome

2020

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“…Recent pre-clinical studies have shown that short-term mechanical ventilation contributes to pathophysiological hallmarks of Alzheimer's Disease (AD) [1][2][3][4][5] . While these data provide mechanistic insights to explain the high rates of cognitive decline after mechanical ventilation, they reveal additional unexpected results.…”

Section: Introductionmentioning

confidence: 99%

Physiological Emergence of Amyloid-β During the Acute Cerebral Stress of Mechanical Ventilation Reduces Peri-Hippocampal and Cortical Blood-Brain Barrier Permeability and Neuronal Injury

Gezalian¹,

Rajput²,

Sparrow³

et al. 2020

Preprint

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Background: Prior published data show that short-term mechanical ventilation contributes to pathological hallmarks of Alzheimer’s Disease (AD) by increasing cerebral accumulation of the amyloid-β1-40 (Aβ1-40) peptide and neuroinflammation while unexpectedly decreasing blood-brain barrier permeability. In this study, we hypothesized that the acute cerebral immunochallenge of mechanical ventilation promotes physiological emergence of Aβ1-40 to regions of acute vascular disruption, resulting in reduced neuronal injury.Methods: Immunohistology was used to assess the regional relationship between cerebral Aβ1-40 accumulation, acute vascular disruption, and neuronal inflammation and apoptosis as measured by cleaved caspase-3 (CC3) expression from mechanically ventilated double transgenic AD-model (ADtg) mice and compared to mechanically ventilated wild-type (WT) controls.Results: There was significantly decreased expression of CC3 in regions of cortical and hippocampal Aβ1-40 accumulation in mechanically ventilated ADtg animals (p=0.0224). In contrast, CC3 expression was significantly increased in cortical and hippocampal regions of mechanically ventilated WT controls (p=0.0260). Aβ1-40 accumulation occurred in regions of acute vascular disruption in a characteristic banding pattern and reduced blood-brain barrier permeability. The banding pattern was significantly increased in ADtg mice subjected to mechanical ventilation compared to non-mechanically ventilated ADtg mice (p=0.0002). Additionally, no evidence of irreversible neurological injury is seen in mechanically ventilated ADtg and WT mice, as demonstrated by the absence of TUNEL positive staining. Conclusions: This study provides first evidence that acute short-term mechanical ventilation-induced cerebral immunochallenge promotes physiological emergence of Aβ1-40 to reduce blood-brain barrier permeability and neuronal injury. While it is expected that sustained or long-term activation of this normally protective pathway leads to dysregulated Aβ1-40 accumulation, neurodegeneration, and cognitive impairment, these data suggest that a window of opportunity may exist within which implementation of timely interventions may limit cognition-relevant cerebral injury.

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Harmful effects of mechanical ventilation on neurocognitive functions

Cited by 27 publications

References 13 publications

Monitoring Asynchrony During Invasive Mechanical Ventilation

Monitoring Asynchrony During Invasive Mechanical Ventilation

Mechanical ventilation and long-term neurocognitive impairment after acute respiratory distress syndrome

Physiological Emergence of Amyloid-β During the Acute Cerebral Stress of Mechanical Ventilation Reduces Peri-Hippocampal and Cortical Blood-Brain Barrier Permeability and Neuronal Injury

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