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Transpulmonary pressure: importance and limits.

ABSTRACT: Transpulmonary pressure (PL) is computed as the difference between airway pressure and pleural pressure and separates the pressure delivered to the lung from the one acting on chest wall and abdomen. Pleural pressure is measured as esophageal pressure (PES) through dedicated catheters provided with esophageal balloons. We discuss the role of PL in assessing the effects of mechanical ventilation in patients with acute respiratory distress syndrome (ARDS). In the supine position, directly measured PL represents the pressure acting on the alveoli and airways. Because there is a pressure gradient in the pleural space from the non-dependent to the dependent zones, the pressure in the esophagus probably represents the pressure at a mid-level between sternal and vertebral regions. For this reason, it has been proposed to set the end-expiratory pressure in order to get a positive value of PL. This improves oxygenation and compliance. PL can also be estimated from airway pressure plateau and the ratio of lung to respiratory elastance (elastance-derived method). Some data suggest that this latter calculation may better estimate PL in the nondependent lung zones, at risk for hyperinflation. Elastance-derived PL at end-inspiration (PLend-insp) may be a good surrogate of end-inspiratory lung stress for the "baby lung", at least in non-obese patients. Limiting end-inspiratory PL to 20-25 cmH2O appears physiologically sound to mitigate ventilator-induced lung injury (VILI). Last, lung driving pressure (∆PL) reflects the tidal distending pressure. Changes in PL may also be assessed during assisted breathing to take into account the additive effects of spontaneous breathing and mechanical breaths on lung distension. In summary, despite limitations, assessment of PL allows a deeper understanding of the risk of VILI and may potentially help tailor ventilator settings.

SUBMITTER: Grieco DL

PROVIDER: S-EPMC5537111 | biostudies-other | 2017 Jul

REPOSITORIES: biostudies-other

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Project description:OBJECTIVES:In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying "one" autoregulation-guided cerebral perfusion pressure target-called "cerebral perfusion pressure optimal". We investigated whether a cerebral perfusion pressure autoregulation range-which uses a continuous estimation of the "lower" and "upper" cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with pressure reactivity index)-has prognostic value. DESIGN:Single-center retrospective analysis of prospectively collected data. SETTING:The neurocritical care unit at a tertiary academic medical center. PATIENTS:Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol. INTERVENTIONS:None. METHODS AND MAIN RESULTS:Cerebral perfusion pressure-pressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this "U-shaped curve" crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001). CONCLUSIONS:Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical.

Project description:BACKGROUND: Many bacteria of clinical importance survive and may grow in different environments. Antibiotic pollution may exert on them a selective pressure leading to an increase in the prevalence of resistance. OBJECTIVES: In this study we sought to determine whether environmental concentrations of antibiotics and concentrations representing action limits used in environmental risk assessment may exert a selective pressure on clinically relevant bacteria in the environment. METHODS: We used bacterial inhibition as an assessment end point to link antibiotic selective pressures to the prevalence of resistance in bacterial populations. Species sensitivity distributions were derived for three antibiotics by fitting log-logistic models to end points calculated from minimum inhibitory concentration (MIC) distributions based on worldwide data collated by the European Committee on Antimicrobial Susceptibility Testing (EUCAST). To place bacteria represented in these distributions in a broader context, we performed a brief phylogenetic analysis. The potentially affected fraction of bacterial genera at measured environmental concentrations of antibiotics and environmental risk assessment action limits was used as a proxy for antibiotic selective pressure. Measured environmental concentrations and environmental risk assessment action limits were also directly compared to wild-type cut-off values. RESULTS: The potentially affected fraction of bacterial genera estimated based on antibiotic concentrations measured in water environments is ? 7%. We estimated that measured environmental concentrations in river sediments, swine feces lagoons, liquid manure, and farmed soil inhibit wild-type populations in up to 60%, 92%, 100%, and 30% of bacterial genera, respectively. At concentrations used as action limits in environmental risk assessment, erythromycin and ciprofloxacin were estimated to inhibit wild-type populations in up to 25% and 76% of bacterial genera. CONCLUSIONS: Measured environmental concentrations of antibiotics, as well as concentrations representing environmental risk assessment action limits, are high enough to exert a selective pressure on clinically relevant bacteria that may lead to an increase in the prevalence of resistance.

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Transpulmonary pressure: importance and limits.

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