Annals of translational medicine
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Ventilator management of patients with acute respiratory distress syndrome (ARDS) has been characterized by implementation of basic physiology principles by minimizing harmful distending pressures and preventing lung derecruitment. Such strategies have led to significant improvements in outcomes. Positive end expiratory pressure (PEEP) is an important part of a lung protective strategy but there is no standardized method to set PEEP level. ⋯ Although there is some spatial and positional artifact, esophageal pressures in numerous animal and human studies in healthy, obese and critically ill patients appear to be a good estimate for the "effective" pleural pressure. Multiple studies have illustrated the benefit of using esophageal pressures to titrate PEEP in patients with obesity and with ARDS. Esophageal pressure monitoring provides a window into the unique physiology of a patient and helps improve clinical decision making at the bedside.
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Despite being a promising idea that combines several variables related to ventilator-induced lung injury (VILI), the concept of mechanical power (MP) carries a number of limitations, leaves several open questions, lacks proper modelling of positive end-expiratory pressure (PEEP) effects and, more importantly, does not respect the amount of lung tissue subjected to MP. First, the assessment of MP as a measure for development of VILI would have the highest relevance when volume displacement and related pressure changes are measured directly within the lung. Thus, ideally the relationship between MP delivered to the total respiratory system, and that delivered to lung tissue is discerned. ⋯ Fourth, in its current form, MP is modelled with a positive linear relationship with PEEP, which is based on incorrect mathematical modelling to integrate the role of PEEP into MP. Fifth, the present equation used to calculate MP is qualitatively in disagreement with clinical data on VILI. The reduction of MP to its elastic part, might not only result in a higher association with VILI, but also amplifies an indirect U-shaped relationship with PEEP.
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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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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.
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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.