Mechanical ventilation guided by esophageal pressure in acute lung injury.

BACKGROUND: Survival of patients with acute lung injury or the acute respiratory distress syndrome (ARDS) has been improved by ventilation with small tidal volumes and the use of positive end-expiratory pressure (PEEP); however, the optimal level of PEEP has been difficult to determine. In this pilot study, we estimated transpulmonary pressure with the use of esophageal balloon catheters. We reasoned that the use of pleural-pressure measurements, despite the technical limitations to the accuracy of such measurements, would enable us to find a PEEP value that could maintain oxygenation while preventing lung injury due to repeated alveolar collapse or overdistention. METHODS: We randomly assigned patients with acute lung injury or ARDS to undergo mechanical ventilation with PEEP adjusted according to measurements of esophageal pressure (the esophageal-pressure-guided group) or according to the Acute Respiratory Distress Syndrome Network standard-of-care recommendations (the control group). The primary end point was improvement in oxygenation. The secondary end points included respiratory-system compliance and patient outcomes. RESULTS: The study reached its stopping criterion and was terminated after 61 patients had been enrolled. The ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen at 72 hours was 88 mm Hg higher in the esophageal-pressure-guided group than in the control group (95% confidence interval, 78.1 to 98.3; P=0.002). This effect was persistent over the entire follow-up time (at 24, 48, and 72 hours; P=0.001 by repeated-measures analysis of variance). Respiratory-system compliance was also significantly better at 24, 48, and 72 hours in the esophageal-pressure-guided group (P=0.01 by repeated-measures analysis of variance). CONCLUSIONS: As compared with the current standard of care, a ventilator strategy using esophageal pressures to estimate the transpulmonary pressure significantly improves oxygenation and compliance. Multicenter clinical trials are needed to determine whether this approach should be widely adopted. (ClinicalTrials.gov number, NCT00127491.)

Oxygen supplies during a mass casualty situation.

Mass casualty and pandemic events pose a substantial challenge to the resources available in our current health care system. The ability to provide adequate oxygen therapy is one of the systems that could be out-stripped in certain conditions. Natural disasters can disrupt manufacturing or delivery, and pandemic events can increase consumption beyond the available supply. Patients may require manual resuscitation, basic oxygen therapy, or positive-pressure ventilation during these scenarios. Available sources of oxygen include bulk liquid oxygen systems, compressed gas cylinders, portable liquid oxygen (LOX) systems, and oxygen concentrators. The last two are available in a variety of configurations, which include personal and home systems that are suitable for individual patients, and larger systems that can provide oxygen to multiple patients or entire institutions. Bulk oxygen systems are robust and are probably sustainable during periods of high consumption, but are at risk if manufacturing or delivery is disrupted. Compressed gas cylinders offer support during temporary periods of need but are not a solution for extended periods of therapy. Personal oxygen concentrators and LOX systems are limited in their application during mass casualty scenarios. Large-capacity oxygen concentrators and LOX systems may effectively provide support to alternative care sites or larger institutions. They may also be appropriate selections for governmental emergency-response scenarios. Careful consideration of the strengths and limitations of each of these options can reduce the impact of a mass casualty event.

Cytokine release following recruitment maneuvers.

BACKGROUND: There are reports of rigors and/or clinical deterioration following recruitment maneuvers (RMs), leading us to question whether the use of sustained high-pressure inflation could lead to release of inflammatory mediators. METHODS: Prospective cohort study of 26 patients with ARDS receiving mechanical ventilation. A single RM was performed during which the mean airway pressure was increased to 40 cm H2O and held constant for a period of 30 s. The concentration of nine cytokines (interleukin [IL]-1, IL-6, IL-8, IL-10, tumor necrosis factor [TNF]-alpha, Fas ligand, vascular endothelial growth factor, TNF receptor 1, TNF receptor 2) was measured longitudinally at three time points: prior to initiation of the RM, 5 min after the RM, and 60 min after the RM. RESULTS: RMs were tolerated well from a hemodynamic perspective. Oxygenation improved as reflected by an increased Pao2/fraction of inspired oxygen (Fio2) ratio from 140+/-49 at baseline to 190+/-78 (mean+/-SD) at 5 min after the RM (p=0.01). At 60 min, the increase in Pao2/Fio2 ratio, to 172+/-76, was no longer significant (p=0.1). There were no important changes in the levels of any of the measured cytokines at 5 min or 60 min following RM as compared with the baseline levels. CONCLUSIONS: The results of our study demonstrate that recruitment maneuvers are well tolerated in patients with ARDS. Our data suggest no major hemodynamic or immunologic evidence of deterioration within the first hour of RM. In particular, cytokines, previously related to worsening lung injury and distal organ failure in patients with ARDS, are not elevated by use of an RM. Registered at: www.clinicaltrials.gov as NCT00127491.

Attitudes of respiratory therapists and nurses about measures to prevent ventilator-associated pneumonia: a multicenter, cross-sectional survey study.

OBJECTIVE: To understand the reported practices of and adherence to evidence-based guidelines for the prevention of ventilator-associated pneumonia (VAP) among respiratory therapists (RTs) and registered nurses (RNs) in academic and nonacademic intensive care units. METHODS: We conducted a multicenter, cross-sectional survey. We first obtained demographic information about health care professionals in a nonidentifiable method. We next questioned the practice patterns of RTs and RNs for preventing VAP based on evidence-supported guidelines. The participants were RTs and RNs working in academic and nonacademic intensive care units; 278 respondents participated in this study (172 RTs and 106 RNs). There were no interventions. RESULTS: The 3 major findings were: (1) both the RTs and the RNs reported that they frequently practice VAP-prevention measures, (2) the rate of adherence to ineffective measures (eg, routine changes of the ventilator circuit, disposable catheters) is also relatively high, which suggests that the evidence is not translated into bedside practice, (3) a substantial proportion of participants did not know the VAP rate in their institution, which might make it difficult to convince bedside practitioners to apply evidence-based practice, and might reflect a lack of infection-control/surveillance programs at hospitals. CONCLUSION: Consumers, the Centers for Disease Control and Prevention, and other organizations are currently trying to implement mandatory reporting of hospital infections, including VAP rate. Without a definition of VAP suited to individual institutions, an organized data-collection and reporting method, and team-based approaches to preventing and treating VAP, hospitals may not be able to meet these requests and track improvement efforts. Prevention measures need to be translated to bedside practice to improve the outcomes of critically ill patients.

Esophageal pressures in acute lung injury: do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress?

Acute lung injury can be worsened by inappropriate mechanical ventilation, and numerous experimental studies suggest that ventilator-induced lung injury is increased by excessive lung inflation at end inspiration or inadequate lung inflation at end expiration. Lung inflation depends not only on airway pressures from the ventilator but, also, pleural pressure within the chest wall. Although esophageal pressure (Pes) measurements are often used to estimate pleural pressures in healthy subjects and patients, they are widely mistrusted and rarely used in critical illness. To assess the credibility of Pes as an estimate of pleural pressure in critically ill patients, we compared Pes measurements in 48 patients with acute lung injury with simultaneously measured gastric and bladder pressures (Pga and P(blad)). End-expiratory Pes, Pga, and P(blad) were high and varied widely among patients, averaging 18.6 +/- 4.7, 18.4 +/- 5.6, and 19.3 +/- 7.8 cmH(2)O, respectively (mean +/- SD). End-expiratory Pes was correlated with Pga (P = 0.0004) and P(blad) (P = 0.0104) and unrelated to chest wall compliance. Pes-Pga differences were consistent with expected gravitational pressure gradients and transdiaphragmatic pressures. Transpulmonary pressure (airway pressure - Pes) was -2.8 +/- 4.9 cmH(2)O at end exhalation and 8.3 +/- 6.2 cmH(2)O at end inflation, values consistent with effects of mediastinal weight, gravitational gradients in pleural pressure, and airway closure at end exhalation. Lung parenchymal stress measured directly as end-inspiratory transpulmonary pressure was much less than stress inferred from the plateau airway pressures and lung and chest wall compliances. We suggest that Pes can be used to estimate transpulmonary pressures that are consistent with known physiology and can provide meaningful information, otherwise unavailable, in critically ill patients.

Esophageal and transpulmonary pressures in acute respiratory failure.

OBJECTIVE: Pressure inflating the lung during mechanical ventilation is the difference between pressure applied at the airway opening (Pao) and pleural pressure (Ppl). Depending on the chest wall's contribution to respiratory mechanics, a given positive end-expiratory and/or end-inspiratory plateau pressure may be appropriate for one patient but inadequate or potentially injurious for another. Thus, failure to account for chest wall mechanics may affect results in clinical trials of mechanical ventilation strategies in acute respiratory distress syndrome. By measuring esophageal pressure (Pes), we sought to characterize influence of the chest wall on Ppl and transpulmonary pressure (PL) in patients with acute respiratory failure. DESIGN: Prospective observational study. SETTING: Medical and surgical intensive care units at Beth Israel Deaconess Medical Center. PATIENTS: Seventy patients with acute respiratory failure. INTERVENTIONS: Placement of esophageal balloon-catheters. MEASUREMENTS AND MAIN RESULTS: Airway, esophageal, and gastric pressures recorded at end-exhalation and end-inflation Pes averaged 17.5 +/- 5.7 cm H2O at end-expiration and 21.2 +/- 7.7 cm H2O at end-inflation and were not significantly correlated with body mass index or chest wall elastance. Estimated PL was 1.5 +/- 6.3 cm H2O at end-expiration, 21.4 +/- 9.3 cm H2O at end-inflation, and 18.4 +/- 10.2 cm H2O (n = 40) during an end-inspiratory hold (plateau). Although PL at end-expiration was significantly correlated with positive end-expiratory pressure (p < .0001), only 24% of the variance in PL was explained by Pao (R = .243), and 52% was due to variation in Pes. CONCLUSIONS: In patients in acute respiratory failure, elevated esophageal pressures suggest that chest wall mechanical properties often contribute substantially and unpredictably to total respiratory impedance, and therefore Pao may not adequately predict PL or lung distention. Systematic use of esophageal manometry has the potential to improve ventilator management in acute respiratory failure by providing more direct assessment of lung distending pressure.