Annals of translational medicine
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A protective ventilation strategy is based on separation of lung and chest wall mechanics and determination of transpulmonary pressure. So far, this has required esophageal pressure measurement, which is cumbersome, rarely used clinically and associated with lack of consensus on the interpretation of measurements. We have developed an alternative method based on a positive end expiratory pressure (PEEP) step procedure where the PEEP-induced change in end-expiratory lung volume is determined by the ventilator pneumotachograph. ⋯ Thus, the most crucial factors of ventilator induced lung injury can be determined by a simple PEEP step procedure. The measurement procedure can be repeated with short intervals, which makes it possible to follow the course of the lung disease closely. By the PEEP step procedure we may also obtain information (decision support) on the mechanical consequences of changes in PEEP and tidal volume performed to improve oxygenation and/or carbon dioxide removal.
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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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There is clear evidence that early causal therapy improves outcome in sepsis and septic shock, whereas recent studies on supportive hemodynamic therapy have produced very conflictive results. The objective of the present study was to determine whether a supportive hemodynamic therapy guided by clinically relevant invasive monitoring improves survival and organ function in a high-lethality model of septic shock in sheep as compared to sole causal therapy including surgical and antimicrobial treatment. ⋯ The present data suggest that sole causal sepsis therapy without hemodynamic support worsens outcome even more than natural evolution of sepsis and combined causal and supportive therapy. This underlines the importance of early hemodynamic stabilization in parallel with antibiotic and surgical treatment of the sepsis focus.
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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.
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Fluid administration is the first-line therapy in patients with acute circulatory failure. The main goal of fluid administration is to increase the cardiac output and ultimately the oxygen delivery. Nevertheless, the decision to administer fluids or not should be carefully considered, since half of critically ill patients are fluid unresponsive, and the deleterious effects of fluid overload clearly documented. ⋯ Other tests such as passive leg raising or end-expiratory occlusion act as an internal volume challenge. To reliably predict fluid responsiveness, physicians must choose among these different dynamic tests, depending on their respective limitations and on the cardiac output monitoring technique which is used. In this review, we will summarize the most recent findings regarding the prediction of fluid responsiveness in ventilated patients.