Articles: respiratory-distress-syndrome.
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Sirtuin6 (SIRT6) has been demonstrated to be involved in a range of physiological processes and diseases, while its role in acute respiratory distress syndrome (ARDS) remains unclear. Therefore, this study focused on the role and underlying mechanism of SIRT6 in ARDS with the aim of identifying potential therapeutic targets. In this study, we found that SIRT6 was significantly decreased in lipopolysaccharide (LPS)-induced A549 cells and a murine model. ⋯ In vivo, the SIRT6-specific inhibitor OSS_128167 also significantly accelerated LPS-induced loss of tight junction proteins, lung inflammation, and apoptosis. Meanwhile, the SIRT6-specific inhibitor OSS_128167 also activated the ERK1/2 pathway and inhibited lung autophagy. These results suggested that SIRT6 could ameliorate the loss of tight junction proteins, inflammation, and apoptosis in LPS-induced ARDS by inhibiting the ERK1/ 2 pathway and enhancing autophagy, indicating that SIRT6 plays a beneficial role in ARDS and might be a potential therapeutic target for ARDS.
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The relationship between indices of mechanical ventilation and pulmonary artery pressures remains ill-defined in ARDS. As our understanding of mechanical ventilation has progressed, there is now a greater appreciation of the impact of high driving pressures and mechanical power in perpetuating lung injury. However, the relationship between the newer derived indices of mechanical ventilation and pulmonary artery pressure is unclear. We performed a post hoc analysis of the Fluid and Catheters Treatment Trial (FACTT) trial to investigate the associations between mechanical ventilation indices in ARDS patients and the prevalence of pulmonary hypertension. This may help elucidate future clinical targets for more, right ventricular protective, mechanical ventilation strategies. ⋯ The associations identified between mPAP and mechanical ventilation variables in this analysis would suggest that classical ARDS lung protective strategies, including low tidal volume ventilation and permissive hypercapnia, may negatively impact the management of the subset of ARDS patients with associated right ventricular dysfunction or ACP. Additionally, respiratory rates above 17 cycles per minute show an incremental increase in mPAP. Therefore, increases in tidal volume (within the limitation of driving pressure < 18 cmH20) may represent a more right ventricular protective way to control CO2 and pH.
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A diagnosis of ARDS serves as a pretext for several perilous clinical practices. Clinical trials demonstrated that tidal volume 12 ml/kg increases patient mortality, but 6 ml/kg has not proven superior to 11 ml/kg or anything in between. Present guidelines recommend 4 ml/kg, which foments severe air hunger, leading to prescription of hazardous (yet ineffective) sedatives, narcotics and paralytic agents. ⋯ Each of three pillars of the prevailing Berlin definition is extremely flimsy and the source of confusion and unscientific practices. For doctors at the bedside, none of the revisions have enhanced patient care over that using the original 1967 description of Ashbaugh and colleagues. Bedside doctors are better advised to diagnose ARDS on the basis of pattern recognition and instead concentrate their vigilance on resolving the numerous hidden dangers that follow inevitably once a diagnosis has been made.
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Cardiac arrest (CA) is a major cause of morbidity and mortality frequently associated with neurological and systemic involvement. Supportive therapeutic strategies such as mechanical ventilation, hemodynamic settings, and temperature management have been implemented in the last decade in post-CA patients, aiming at protecting both the brain and the lungs and preventing systemic complications. A lung-protective ventilator strategy is currently the standard of care among critically ill patients since it demonstrated beneficial effects on mortality, ventilator-free days, and other clinical outcomes. ⋯ The management of hemodynamics and temperature in post-CA patients represents critical steps for obtaining clinical improvement. The aim of this review is to summarize and discuss current evidence on how to optimize mechanical ventilation in post-CA patients. We will provide ten tips and key insights to apply a lung-protective ventilator strategy in post-CA patients, considering the interplay between the lungs and other systems and organs, including the brain.
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Observational Study
Risk factors and long-term prognosis for postoperative hypoxemia in patients with acute type A aortic dissection: A retrospective observational study.
Hypoxemia is 1 of the most common complications in the patients with acute Type A aortic dissection (ATAAD). This study aimed to summarize the risk factors, management strategies and long-term prognosis for postoperative hypoxemia in ATAAD patients. Baseline characteristics and clinical data of all the patients were collected. ⋯ Logistic regression analysis revealed that PaO2/FiO2 before extubating (OR: 0.985, P < .001), paraplegia (OR: 10.994, P = .019), acute renal failure (OR: 12.590, P < .001), re-operation (OR: 4.721, P = .014) and re-admission to intensive care unit (OR: 13.727, P = .001) were independent risk factors for long-term mortality. Our results showed that overweight and prolonged CPB time were risk factors for postoperative hypoxemia in ATAAD patients. While PaO2/FiO2 before extubating were independent risk factors for long-term mortality, indicating that active correction of hypoxemia and maintain a higher PaO2/FiO2 before extubating may help to improve the prognosis of the ATAAD patients.