Annals of translational medicine
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Over the past decade, the use of veno-venous extracorporeal membrane oxygenation (VV-ECMO) for respiratory support has widely expanded as a treatment strategy for patients with acute respiratory distress syndrome (ARDS). Despite considerable attention has been given to the indications, the timing and the management of patients undergoing ECMO for refractory respiratory hypoxemic failure, little is known regarding the management of mechanical ventilation (MV) in this group of patients. ⋯ However, literature is lacking regarding the best strategies and MV settings, including positive end expiratory pressure (PEEP), tidal volume (VT), respiratory rate (RR) and plateau pressure (PPLAT). The aim of this review is to summarize current evidence, the rationale and provide recommendations about the best ventilator strategy to adopt in patients with ARDS undergoing VV-ECMO support.
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Mechanical ventilation applies physical stresses to the tissues of the lung and thus may give rise to ventilator-induced lung injury (VILI), particular in patients with acute respiratory distress syndrome (ARDS). The most dire consequences of VILI result from injury to the blood-gas barrier. ⋯ Recent mathematical/computational modeling studies have shown that the way in which EL varies as a function of both time and positive end-expiratory pressure (PEEP) reflects the nature and degree of lung injury, and can even be used to infer the separate contributions of volutrauma and atelectrauma to VILI. Interrogating such models for minimally injurious regimens of mechanical ventilation that apply to a particular lung may thus lead to personalized approaches to the ventilatory management of ARDS.
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Despite the recognition of its iatrogenic potential, mechanical ventilation remains the mainstay of respiratory support for patients with acute respiratory distress syndrome (ARDS). The low volume ventilation has been recognized as the only method to reduce mortality of ARDS patients and plateau pressure as the lighthouse for delivering safe ventilation. Recent investigations suggest that a ventilation based on lung mechanics (tidal ventilation tailored to the available lung volume able to receive it, i.e., driving pressure) is a successful approach to improve outcome. ⋯ Ventilation-induced lung injury (which includes the self-inflicted lung injury of a spontaneously breathing patient) can therefore be prevented by the adoption of measures promoting an increase of ventilable lung and its homogeneity and by delivering lower levels of mechanical power. Prone position promotes lung homogeneity without increasing the delivered mechanical power. This review describes the recent developments on respiratory mechanics in ARDS patients, providing both bedside and research insights from the most updated evidence.
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Review
Should we titrate ventilation based on driving pressure? Maybe not in the way we would expect.
Mechanical ventilation maintains adequate gas exchange in patients during general anaesthesia, as well as in critically ill patients without and with acute respiratory distress syndrome (ARDS). Optimization of mechanical ventilation is important to minimize ventilator induced lung injury and improve outcome. Tidal volume (VT), positive end-expiratory pressure (PEEP), respiratory rate (RR), plateau pressures as well as inspiratory oxygen are the main parameters to set mechanical ventilation. ⋯ No clear data are currently available about the interpretation and clinical use of ∆P during assisted ventilation. In conclusion, ∆P is an indicator of severity of the lung disease, is related to VT size and associated with complications and mortality. We advocate the use of ∆P to optimize individually VT but not PEEP in mechanically ventilated patients with and without ARDS.
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The first reported human anaphylactic death is considered to be the Pharaoh Menes death, caused by a wasp sting. Currently, anaphylactic cardiovascular events represent one of most frequent medical emergencies. Rapid diagnosis, prompt and appropriate treatment can be life saving. ⋯ Therefore, differentiating the decrease of cardiac output due to myocardial tissue hypoperfusion from systemic vasodilation and leakage of plasma, from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combined antiallergic, anti-ischemic and antithrombotic treatment seems currently beneficial. Simultaneous measurements of peripheral arterial resistance and coronary blood flow with newer diagnostic techniques including cardiac magnetic resonance imaging (MRI) and myocardial scintigraphy may help elucidating the pathophysiology of anaphylactic cardiovascular collapse, thus rendering treatment more rapid and effective.