Original Article
Effect of a Protective-Ventilation Strategy on Mortality in the Acute Respiratory Distress Syndrome
N Engl J Med 1998; 338:347-354February 5, 1998
- Abstract
Background
In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome.
Methods
We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection point on the static pressure–volume curve, a tidal volume of less than 6 ml per kilogram, driving pressures of less than 20 cm of water above the PEEP value, permissive hypercapnia, and preferential use of pressure-limited ventilatory modes.
Results
After 28 days, 11 of 29 patients (38 percent) in the protective-ventilation group had died, as compared with 17 of 24 (71 percent) in the conventional-ventilation group (P<0.001). The rates of weaning from mechanical ventilation were 66 percent in the protective-ventilation group and 29 percent in the conventional-ventilation group (P = 0.005); the rates of clinical barotrauma were 7 percent and 42 percent, respectively (P = 0.02), despite the use of higher PEEP and mean airway pressures in the protective-ventilation group. The difference in survival to hospital discharge was not significant; 13 of 29 patients (45 percent) in the protective-ventilation group died in the hospital, as compared with 17 of 24 in the conventional-ventilation group (71 percent, P = 0.37).
Conclusions
As compared with conventional ventilation, the protective strategy was associated with improved survival at 28 days, a higher rate of weaning from mechanical ventilation, and a lower rate of barotrauma in patients with the acute respiratory distress syndrome. Protective ventilation was not associated with a higher rate of survival to hospital discharge.
Media in This Article
Figure 1
Actuarial 28-Day Survival among 53 Patients with the Acute Respiratory Distress Syndrome Assigned to Protective or Conventional Mechanical Ventilation.Table 1
Base-Line Characteristics of the Study Groups.Article Activity
- Article
Mechanical ventilation can damage the lungs.1,2 Lesions at the alveolar–capillary interface,3 alterations in permeability,4 and edema5-7 have repeatedly been shown to occur in animals subjected to adverse patterns of mechanical ventilation.
In clinical practice, however, the “mechanical stretch” caused by conventional ventilation has been found to be detrimental in only a few uncontrolled studies.8-11 Large variations in the susceptibility of individual animal species12 and the apparent success of mechanical ventilation based on a strategy of using the lowest positive end-expiratory pressure (PEEP) that results in acceptable oxygenation13,14 suggest that the devastating effects observed in animals cannot be easily extrapolated to humans.
We recently demonstrated that mechanical lung protection can be provided in patients with the acute respiratory distress syndrome, resulting in better pulmonary function and higher rates of weaning from the ventilator.15 Briefly, lung protection was based on a strategy of maintaining low inspiratory driving pressures (<20 cm of water above PEEP, with low tidal volumes and preferential use of limited airway pressure over regulation of arterial carbon dioxide levels), with the simultaneous circumvention of alveolar collapse through the use of high PEEP to keep end-expiratory pressures above the lower inflection point (PFLEX) on the static pressure–volume curve of the respiratory system. The nearly maximal alveolar recruitment and aeration accomplished with this strategy were intended to minimize shear stresses in the lung tissue during inspiration.15
We have extended our earlier report15 and evaluated the effect of mechanical lung protection on survival. We hypothesized that preventing the persistent collapse of recruitable units (alveolar units anatomically preserved but requiring high opening pressures for aeration) and reducing cyclic lung reopening and stretch during mechanical breaths would result in lower rates of pulmonary complications and mortality at 28 days in patients with the acute respiratory distress syndrome.
Methods
Study Population
Between December 1990 and July 1995, 53 patients with the acute respiratory distress syndrome were prospectively enrolled in the trial (including 28 described previously15). The hemodynamic data in 48 of the patients during the first seven days of the study have been reported elsewhere.16 The study was conducted in two intensive care units in Brazil: one in São Paulo and one in Porto Alegre. The protocol was approved by the hospitals' medical-ethics committees, and informed consent was obtained from each patient or the patient's next of kin.
Each year during the study period, a total of about 60 patients with the acute respiratory distress syndrome were admitted to the two intensive care units. The criteria for enrollment were an underlying disease process known to be associated with the acute respiratory distress syndrome along with a lung-injury score17 of 2.5 or higher (range, 0 [normal] to 4 [most severe]) plus a pulmonary arterial wedge pressure of less than 16 mm Hg. Confirmation that the tip of the pulmonary arterial catheter was in the area of the lung zone where capillary vessels were patent, transmitting left atrial pressures backward, was assessed with two mechanical maneuvers.5,18 The exclusion criteria (listed in decreasing order of frequency) were previous lung or neuromuscular disease, mechanical ventilation for more than one week, uncontrolled terminal disease, previous barotrauma (pneumothorax, pneumomediastinum, or subcutaneous emphysema), previous lung biopsy or resection, an age of more than 70 years or less than 14 years, uncontrollable and progressive acidosis, signs of intracranial hypertension, and documented coronary insufficiency. The primary diagnoses at enrollment are shown in Table 1Table 1
Base-Line Characteristics of the Study Groups..Stabilizing Procedures and Randomization
After enrollment, all patients underwent a standardized regimen of ventilatory–hemodynamic procedures for at least 30 minutes (control period), during which time their initial clinical condition was evaluated and stabilized. This regimen consisted of volume-controlled ventilation (tidal volume, 10 ml per kilogram of body weight), a square-wave inspiratory flow of 50 liters per minute, a respiratory rate of 15 cycles per minute, an inspiratory pause of 0.4 second, an inspiratory oxygen fraction of 1.0, PEEP of 5 cm of water or the minimal value necessary to maintain an arterial oxygen saturation of more than 85 percent, 5 percent albumin administered intravenously until the pulmonary arterial wedge pressure was higher than 9 mm Hg, dobutamine administered intravenously in a fixed dose of 5 μg per kilogram per minute, and norepinephrine administered intravenously whenever the mean arterial pressure remained lower than 60 mm Hg (the minimal dose that kept the pressure at or above 60 mm Hg).
After the patient's condition had been stabilized, respiratory, hemodynamic, and laboratory measurements were performed. These data were used for a base-line comparison of the two groups and for calculating the risk of death according to the severity of illness (Table 1). The physiologic data for Acute Physiology and Chronic Health Evaluation (APACHE) II21 scores were collected during the 24-hour period starting at this time. The worst values during this interval, including the control-period measurements, were recorded, except for blood gas and heart-rate values. To avoid the overestimating effects of subsequent permissive hypercapnia on these variables (since respiratory acidosis and tachycardia usually increase the APACHE score), only the control-period measurements of blood gas and heart rate were considered (adjusted APACHE II score).
Subsequently, a bedside procedure was performed to calculate the inspiratory and static pressure–volume curve without disconnecting the ventilator, as described previously.15,22 A well-defined PFLEX (corresponding to an upward shift in the slope of the curve and signaling an increment in lung compliance) could be determined for 49 patients, but the corresponding value was used to adjust PEEP only in the group assigned to protective mechanical ventilation. Since this was the only curve calculated during the protocol, PEEP was then kept constant in this group until the inspiratory oxygen fraction was less than 0.4.15 After determining the pressure–volume curve, we randomly assigned the patients to one of the two groups. Randomization was performed with sealed envelopes and a 1:1 assignment scheme.
General Ventilatory Support
Protective or conventional mechanical ventilation was rigorously maintained until the patient was extubated or died. Each patient was connected to a closed system for aspirating tracheal secretions; the patient remained connected to the ventilator during aspiration, minimizing temporary drops in airway pressure. In both groups, the target partial pressure of arterial oxygen was 80 mm Hg, and the PEEP level was never set below 5 cm of water, even during weaning from the ventilator. The weaning procedure was the same in the two groups: a gradual decrease in the level of pressure support.15 Patients received ventilation exclusively through endotracheal tubes.
Conventional Approach
We sought to maintain an arterial carbon dioxide level of 35 to 38 mm Hg, independent of airway pressures, and an inspiratory oxygen fraction of less than 0.6 with adequate systemic oxygen delivery. To optimize this compromise, we used a stepwise algorithm for PEEP increments.15,16 Other ventilatory settings were as follows: tidal volume, 12 ml per kilogram (volume-cycled assisted or controlled ventilation); square-wave inspiratory flow rate, 50 to 80 liters per minute (adjusted to avoid auto-PEEP, or abnormal gas trapping leading to an elevated end-respiratory pressure); inspiratory pause, 0.4 second; and backup respiratory rate, 10 to 24 cycles per minute (depending on the value for arterial carbon dioxide). In addition to the administration of sedative drugs to keep the patients comfortable, additional doses of sedatives were given to prevent patient-triggered respiratory rates higher than 24 cycles per minute or arterial carbon dioxide values lower than 25 mm Hg.
Protective Approach
The protective approach was intended to prevent alveolar collapse and overdistention, regardless of arterial carbon dioxide levels, and to maintain an “open lung” independently of hemodynamic conditions. The tidal volume was maintained at a level lower than 6 ml per kilogram, with a respiratory rate of less than 30 cycles per minute, even during pressure support. Permissive hypercapnia and continuous infusions of fentanyl and diazepam were used to prevent discomfort and signs of increased respiratory drive. Initial arterial carbon dioxide levels of up to 80 mm Hg were allowed, and slow intravenous sodium bicarbonate infusions (<50 mmol per hour) were permitted if the arterial pH was less than 7.2.
Driving pressures (PPLAT-PEEP, with PPLAT defined as the plateau pressure after the inspiratory pause) and peak airway pressures were kept below 20 and 40 cm of water, respectively. Only pressure-limited modes of ventilation (pressure-controlled inverse-ratio ventilation [ratio of inspiration to expiration, >1] and pressure-support ventilation, both generating constant airway pressure during inspiration) or combined modes (volume-ensured pressure-support ventilation, in which a constant inspiratory pressure is targeted at the same time that a minimal tidal volume is guaranteed23) were used, according to a stepwise algorithm.15
PEEP was preset at 2 cm of water above PFLEX. When auto-PEEP (defined as the difference between alveolar pressures at end expiration and airway pressures) was present, the total PEEP (external PEEP plus auto-PEEP) was considered and adjusted to equal PFLEX plus 2 cm of water. Finally, if a sharp PFLEX could not be determined on the pressure–volume curve, an empirical total-PEEP value of 16 cm of water was used.15 Recruiting maneuvers — aimed at reaerating alveolar units requiring very high opening pressures — were frequently used, especially after inadvertent disconnections from the ventilator. Continuous positive airway pressures of 35 to 40 cm of water were applied for 40 seconds, followed by a careful return to previous PEEP levels. Finally, pressure-controlled inverse-ratio ventilation was used whenever the inspiratory oxygen fraction was higher than 0.5, in order to decrease minute-volume requirements.24
General Support
All patients were monitored with the Swan–Ganz catheter, and a stepwise algorithm for hemodynamic optimization15,16 was used. Measurements of plasma lactate and mixed venous saturation were used to correct imbalances between oxygen transport and demand. The pulmonary-artery wedge pressure never exceeded 15 mm Hg. Procedures for nutritional support, treatment of infections, and renal dialysis (when needed) were the same in both groups.15,16 Corticosteroids were given only to patients with Pneumocystis carinii pneumonia. No patients received immunotherapy. The protocol for sedation was the same for both groups, with only two sedatives prescribed (fentanyl and diazepam) and only one neuromuscular paralyzing drug (pancuronium). Although larger doses (up to 9 mg per day) were used in the protective-ventilation group, continuous infusions of fentanyl were used in both groups to keep the patients comfortable. All patients received ranitidine (50 mg intravenously every eight hours) as prophylaxis against bleeding.
Statistical Analysis
The primary end point was survival at 28 days. The effect of the protective approach was analyzed with a Cox proportional-hazards model, with the base-line adjusted APACHE II score (adjusted risk of death) included as a covariate.
After the first block of 28 patients had been enrolled, a beneficial effect of the protective approach on pulmonary function became evident,15 and we were concerned about the possibility of subjecting the patients to an unnecessary continuation of the protocol.25 Therefore, we performed an interim analysis after each new block of five patients. We estimated that a maximal sample of 58 patients was required, assuming a type I error of 5 percent, a statistical power of 85 percent, and a survival rate in the protective-ventilation group that would be 2.4 times that in the conventional-ventilation group, according to our initial results.15
To counterbalance the increased chance of prematurely stopping the study because of a type I error, we used the conservative correction for multiplicity proposed by Peto et al.26 and Geller and Pocock,27 with a nominal significance level of <0.001 for an interim analysis, if the study was stopped early, and a significance level of <0.04 for the final analysis, if the study was completed.27
The secondary end points were survival to hospital discharge, occurrence of clinically detectable barotrauma, and weaning rate adjusted for APACHE II score (Cox model). Bonferroni's adjustment for multiple comparisons was performed for each secondary end point. All other statistical tests are described below. All P values (two-tailed) were calculated with the BMDP software package (BMDP Statistical Software, version 7.0, Los Angeles).
Results
The study was stopped during the fifth interim analysis, after 53 patients had been enrolled, because of a significant survival difference between the groups (Table 2Table 2
Study Outcomes According to the Intention-to-Treat Analysis. and Table 3Table 3
Base-Line Factors Influencing the Relative Risk of Death at 28 Days. and Figure 1Figure 1Actuarial 28-Day Survival among 53 Patients with the Acute Respiratory Distress Syndrome Assigned to Protective or Conventional Mechanical Ventilation.). After 28 days, 11 of 29 patients (38 percent) in the protective-ventilation group had died, as compared with 17 of 24 (71 percent) in the conventional-ventilation group (P<0.001). The results were similar when the groups were stratified according to the initial severity of illness or the center where the patient was treated.The difference in weaning rates mirrored the results for survival, with 19 of 29 patients (66 percent) in the protective-ventilation group successfully weaned from the ventilator, as compared with 7 of 24 (29 percent) in the conventional-ventilation group (P = 0.005 after adjustment for multiple comparisons). The rate of clinical barotrauma was also significantly lower in the protective-ventilation group than in the conventional-ventilation group (7 percent vs. 42 percent, P = 0.02 after adjustment for multiple comparisons). The difference in survival to hospital discharge was not significant; 13 of 29 patients in the protective-ventilation group (45 percent) died in the hospital, as compared with 17 of 24 patients in the conventional-ventilation group (71 percent, P = 0.37 after adjustment for multiple comparisons).
Within the first 28 days, the most frequent causes of death were refractory septic shock and progressive respiratory failure (Table 2).15 Fourteen episodes of accidental extubation (usually during repositioning of the patient) occurred in nine patients in the protective-ventilation group, as compared with 10 episodes in seven patients in the conventional-ventilation group. In two of the patients in the protective-ventilation group and one in the conventional-ventilation group, irreversible cardiac events followed these episodes. Although successfully extubated (at >48 hours), four patients in the protective-ventilation group died before hospital discharge: one from massive hemothorax with arterial rupture during attempts at central venous cannulation (on day 7), one from diffuse gastrointestinal bleeding (on day 23), one from intracerebral nocardiosis with brain edema (on day 11), and one from a new episode of nosocomial pneumonia followed by refractory septic shock (on day 68). Except for the episode of arterial rupture, no iatrogenic event related to central lines occurred after study entry.
The values for the respiratory variables measured during the first week of the study are shown in Table 4Table 4
Respiratory Values during the First Week of Mechanical Ventilation.. The objectives of ventilatory support were achieved in 48 of the 53 patients. Although the mean respiratory values suggest good adherence to the protocol, there were minor protocol violations in the care of four patients in the protective-ventilation group and one patient in the conventional-ventilation group. In the patient in the conventional-ventilation group, a tidal volume of 7 ml per kilogram was inadvertently used for 12 hours. Among the violations in the protective-ventilation group, there was an inadvertent use of a tidal volume higher than 7 ml per kilogram during a period of eight hours, a PEEP prematurely reduced in disregard of the protocol, use of antibiotics in disregard of the protocol, and a previous pneumothorax detected during a careful review of radiographs. The exclusion of these five patients from the analysis of mortality had little effect on the mortality rate associated with the protective-ventilation approach (relative risk of death, 0.14 [95 percent confidence interval, 0.05 to 0.38], as compared with 0.19 [95 percent confidence interval, 0.08 to 0.47]). The protective-ventilation approach had significant benefits with regard to oxygenation and lung compliance.Table 3 shows the results of univariate and multivariate analyses of mortality at 28 days according to base-line factors (data collected during the control period before randomization). The APACHE II scores and the ventilatory treatment were the only significant factors. These were the two covariates that had been included a priori in the final multivariate Cox regression model.
Discussion
We found that in a group of patients with severe acute respiratory distress syndrome, the protective approach to mechanical ventilation improved the survival rate at 28 days and the weaning rate but not the rate of survival to hospital discharge. The incidence of barotrauma was significantly lower in the protective-ventilation group than in the conventional-ventilation group, despite the use of higher PEEP levels and higher mean airway pressures.
The complexity of the procedures in this study precluded the use of a protocol in which the investigators were unaware of the treatment assignments. Nevertheless, we believe that the stringent algorithms used for infectious problems, hemodynamic values, nutrition, sedation, dialysis, and general care15 were sufficient to minimize additional bias due to differences in the management of nonrespiratory problems. We demonstrated in a previous analysis that we were able to accomplish the planned hemodynamic goals in most patients in both groups.16 Finally, it is difficult to ascribe the better outcome in the protective-ventilation group to uncontrolled or unrecognized factors, since our staff was much more used to the conventional approach. In fact, a greater number of fatal iatrogenic accidents occurred in the protective-ventilation group than in the conventional-ventilation group. Considering the small size of the study, the conservative nature of Bonferroni's statistical adjustment,27 and the severity of base-line disease in the patients (which was responsible for many of the late deaths), the failure to detect a significant difference in survival to hospital discharge was not surprising.
Despite the use of an appropriate rule for early termination of the study during all interim analyses,26,27 the estimates of relative risk shown in Table 3 may be imprecise. The corrections proposed for multiple sequential analysis can properly control the overall type I error, but they cannot prevent associated distortions of the magnitude of the treatment effect caused by early termination or the small sample.28
Since the effect of the protective-ventilation strategy on survival was observed in the context of many concomitant maneuvers (permissive hypercapnia, lower peak and driving pressures, higher PEEP, a tidal volume of less than 6 ml per kilogram, and so forth), we performed a pooled “retrospective” analysis to determine the key combination of ventilatory variables responsible for the ventilatory treatment effect on mortality at 28 days (data not shown). When the treatment assignment was removed from the Cox mortality model, there were three significant prognostic factors: the APACHE II score, the mean PEEP used during the first 36 hours (with a protective effect indicated by a coefficient of -0.15), and the driving pressures (PPLAT-PEEP) during the first 36 hours (with a deleterious effect of high driving pressures indicated by a coefficient of 0.06). All other respiratory variables were of secondary importance. Higher PEEP values (preferentially above the PFLEX value) and lower driving pressures were independently associated with better survival. High initial PEEP values appeared to be beneficial, even when the PPLAT value increased, as long as the driving pressure did not change disproportionately.
The strong protective effect associated with a high PEEP value is consistent with recent experimental data,7,29-33 and the benefit seems to be more pronounced than the deleterious effect of high distending pressures.7,29,30 Had we not used high PEEP levels (>PFLEX), the results might have been very different, with the isolated reduction in PPLAT potentially causing reabsorption atelectasis, loss of alveolar surface, and hypoxemia in some patients.
Recent evidence suggests that the minimization of ventilator-induced lung injury may have important systemic benefits, decreasing the release of proinflammatory mediators,34-36 the dissemination of infections,37-39 and possible complications related to air embolism.40,41 In addition to preventing progressive respiratory failure, the protective-ventilation approach may be associated with these mechanisms.
Despite the use of higher PEEP values (up to 24 cm of water) and higher mean airway pressures, there was a lower incidence of barotrauma in the protective-ventilation group. The protective-ventilation approach may thus not only improve pulmonary function and oxygenation but also reduce clinically apparent alveolar damage. Another study suggested a protective effect of PEEP against clinical barotrauma.42 The paucity of data in favor of this concept may be explained by the correlation normally found between PEEP and peak pressures.43,44 In our study, however, the use of high PEEP levels did not necessarily result in high peak or plateau pressures.
Presented in part at the International Conference of the American Lung Association and the American Thoracic Society, New Orleans, May 10–15, 1996.
Supported by the Laboratório de Investigação Médica, Hospital das Clínicas, University of São Paulo, and Intermed Equipamento Médico Hospitalar.
We are indebted to Drs. Eduardo C. Meyer, Mauro R. Tucci, Pedro Caruso, Ivany A.L. Schettino, Cristiane Hoelz, Elnara Negri, Chin An Lin, Eloisa A. Silva, Vasco Moskovitz, Laerte Pastore, Fabio Gomes, Sergio Demarzo, Cristiane Morais, Eduardo de Oliveira Fernandes, Marcia Xavier Barreto, Marco Ferreira, Mauro Kaufmann, Luis Alexandre Borges, Jorge Höher, Jairo Othero, Luis A. Azambuja, Gilberto Friedman, Michelle Grunauer, and all the residents working in our units during the study period for their dedication and collaboration in providing care to the patients; to Dr. Rosangela Santoro de Souza Amato for her assistance in the preparation of the manuscript; to Intermed Equipamento Médico Hospitalar and Siemens–Elema for technical support; and especially to Dr. John J. Marini for his stimulating discussions and helpful comments.
Source Information
From the Respiratory Intensive Care Unit, Pulmonary Division, Hospital das Clínicas, University of São Paulo (M.B.P.A., C.S.V.B., D.M.M., R.B.M., G.P.P.S., G.L.-F., R.A.K., D.D., T.Y.T., C.R.R.C.); and the General Intensive Care Unit, Santa Casa de Misericórdia, Porto Alegre (C.M., R.O.) — both in Brazil.
Address reprint requests to Dr. Amato at 135 Rua Dr. Joel Lagos, CEP 05344-000 São Paulo, Brazil.
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Citing Articles
1
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Nicolas Bamat, David Millar, Sanghee Suh, Haresh Kirpalani, Nicolas Bamat. 2012. Positive end expiratory pressure for preterm infants requiring conventional mechanical ventilation for respiratory distress syndrome or bronchopulmonary dysplasia. .
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Sameh M.I. Saad, Zdenka Policova, Edgar J. Acosta, A. Wilhelm Neumann. (2012) Effect of surfactant concentration, compression ratio and compression rate on the surface activity and dynamic properties of a lung surfactant. Biochimica et Biophysica Acta (BBA) - Biomembranes 1818:1, 103-116
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Zhanqi Zhao, Josef Guttmann, Knut Möller. (2012) Adaptive SLICE method: an enhanced method to determine nonlinear dynamic respiratory system mechanics. Physiological Measurement 33:1, 51-64
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Peter J. Papadakos, Marcin Karcz, David Schwaiberger, Burkhard Lachmann. (2012) Lungs in Critical Care: New Look at Old Practices. Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine 79:1, 116-122
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Johannes Bickenbach, Ingeborg Biener, Michael Czaplik, Kay Nolte, Rolf Dembinski, Gernot Marx, Rolf Rossaint, Michael Fries. (2011) Neurological outcome after experimental lung injury. Respiratory Physiology & Neurobiology 179:2-3, 174-180
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Stephen E. Rees. (2011) The Intelligent Ventilator (INVENT) project: The role of mathematical models in translating physiological knowledge into clinical practice. Computer Methods and Programs in Biomedicine 104, S1-S29
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Saeid Eslami, Ameen Abu-Hanna, Marcus J. Schultz, Evert de Jonge, Nicolette F. de Keizer. (2011) Evaluation of consulting and critiquing decision support systems: Effect on adherence to a lower tidal volume mechanical ventilation strategy. Journal of Critical Care
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A. Gil Cano, M.I. Monge García, M. Gracia Romero, J.C. Díaz Monrové. (2011) Incidencia, características y evolución del barotrauma durante la ventilación mecánica con apertura pulmonar. Medicina Intensiva
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Stefan Lundin, Ola Stenqvist. (2011) Electrical impedance tomography. Current Opinion in Critical Care1
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David N. Hager. (2011) High-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Current Opinion in Anaesthesiology1
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William R. Henderson, A. William Sheel. (2011) Pulmonary mechanics during mechanical ventilation. Respiratory Physiology & Neurobiology
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Huan Ye, Qingyuan Zhan, Yanhong Ren, Xiaoyang Liu, Chun Yang, Chen Wang. (2011) Cyclic deformation-induced injury and differentiation of rat alveolar epithelial type II cells. Respiratory Physiology & Neurobiology
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Massimo Bonacchi, Guy Harmelin, Adriano Peris, Guido Sani. (2011) A novel strategy to improve systemic oxygenation in venovenous extracorporeal membrane oxygenation: The “χ-configuration”. The Journal of Thoracic and Cardiovascular Surgery 142:5, 1197-1204
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, Robinder G. Khemani, Katherine Sward, Alan Morris, J. Michael Dean, Christopher J. L. Newth. (2011) Variability in usual care mechanical ventilation for pediatric acute lung injury: the potential benefit of a lung protective computer protocol. Intensive Care Medicine 37:11, 1840-1848
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Flávia K. Foronda, Eduardo J. Troster, Julio A. Farias, Carmen S. Barbas, Alexandre A. Ferraro, Lucília S. Faria, Albert Bousso, Flávia F. Panico, Artur F. Delgado. (2011) The impact of daily evaluation and spontaneous breathing test on the duration of pediatric mechanical ventilation: A randomized controlled trial*. Critical Care Medicine 39:11, 2526-2533
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Gerard F. Curley, Maya Contreras, Brendan Higgins, Cecilia OʼKane, Daniel F. McAuley, Daniel OʼToole, John G. Laffey. (2011) Evolution of the Inflammatory and Fibroproliferative Responses during Resolution and Repair after Ventilator-induced Lung Injury in the Rat. Anesthesiology 115:5, 1022-1032
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Gerardo Tusman, Stephan H. Böhm, David O. Warner, Juraj Sprung. (2011) Atelectasis and perioperative pulmonary complications in high-risk patients. Current Opinion in Anaesthesiology1
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Hamid Aslami, Maria T. Kuipers, Charlotte J.P. Beurskens, Joris J.T.H. Roelofs, Marcus J. Schultz, Nicole P. Juffermans. (2011) Mild hypothermia reduces ventilator-induced lung injury, irrespective of reducing respiratory rate. Translational Research
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M.I. Monge García, A. Gil Cano, M. Gracia Romero, J.C. Díaz Monrové. (2011) Cambios respiratorios y hemodinámicos durante una maniobra de reclutamiento pulmonar mediante incrementos y decrementos progresivos de PEEP. Medicina Intensiva
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John J. Marini. (2011) Recruitment by sustained inflation: time for a change. Intensive Care Medicine 37:10, 1572-1574
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J. Dellamonica, N. Lerolle, C. Sargentini, G. Beduneau, F. Marco, A. Mercat, J. C. M. Richard, J. L. Diehl, J. Mancebo, J. J. Rouby, Q. Lu, G. Bernardin, L. Brochard. (2011) PEEP-induced changes in lung volume in acute respiratory distress syndrome. Two methods to estimate alveolar recruitment. Intensive Care Medicine 37:10, 1595-1604
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Jean-Michel Arnal, Jérémie Paquet, Marc Wysocki, Didier Demory, Stéphane Donati, Isabelle Granier, Gaëlle Corno, Jacques Durand-Gasselin. (2011) Optimal duration of a sustained inflation recruitment maneuver in ARDS patients. Intensive Care Medicine 37:10, 1588-1594
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Andriy I. Batchinsky, Samuel E. Burkett, Thomas B. Zanders, Kevin K. Chung, Dara D. Regn, Bryan S. Jordan, Corina Necsoiu, Ruth Nguyen, Margaret A. Hanson, Michael J. Morris, Leopoldo C. Cancio. (2011) Comparison of airway pressure release ventilation to conventional mechanical ventilation in the early management of smoke inhalation injury in swine*. Critical Care Medicine 39:10, 2314-2321
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Markus Kredel, Joerg Brederlau, Christian Wunder, Thomas E. Wurmb, Peter Kranke, Norbert Roewer, Ralf M. Muellenbach. (2011) High-frequency oscillatory ventilation with and without arteriovenous extracorporeal lung assist in patients with severe respiratory failure. Journal of Critical Care
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Stavros G. Memtsoudis, Anna Maria Bombardieri, Yan Ma, Federico P. Girardi. (2011) The effect of low versus high tidal volume ventilation on inflammatory markers in healthy individuals undergoing posterior spine fusion in the prone position: a randomized controlled trial. Journal of Clinical Anesthesia
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Sven Pulletz, Andy Adler, Matthias Kott, Gunnar Elke, Barbara Gawelczyk, Dirk Schädler, Günther Zick, Norbert Weiler, Inéz Frerichs. (2011) Regional lung opening and closing pressures in patients with acute lung injury. Journal of Critical Care
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Jose P. Garcia, Zachary N. Kon, Charles Evans, Zhongjun Wu, Aldo T. Iacono, Brian McCormick, Bartley P. Griffith. (2011) Ambulatory veno-venous extracorporeal membrane oxygenation: Innovation and pitfalls. The Journal of Thoracic and Cardiovascular Surgery 142:4, 755-761
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Kuo-Chin Kao, Cheng-Ta Yang, Han-Chung Hu, Hui-Ching Ting, Ching-Tzu Huang, Lan-Ti Chou, Hsiu-Feng Hsiao, Li-Fu Li, Ying-Huang Tsai, Chung-Chi Huang. (2011) Resolution of Organ Functional Scores to Predict the Outcome in Adult Acute Respiratory Distress Syndrome Patients Receiving High-Frequency Oscillatory Ventilation. The Journal of Trauma: Injury, Infection, and Critical Care1
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Arturo Briva, Cristina Santos, Leonel Malacrida, Fabiana Rocchiccioli, Juan Soto, Martin Angulo, Carlos Batthyany, Ernesto Cairoli, Hector Piriz. (2011) Adenosine triphosphate–dependent calcium signaling during ventilator-induced lung injury is amplified by hypercapnia. Experimental Lung Research 37:8, 471-481
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P. M. Spieth, A. Guldner, A. R. Carvalho, M. Kasper, P. Pelosi, S. Uhlig, T. Koch, M. Gama de Abreu. (2011) Open lung approach vs acute respiratory distress syndrome network ventilation in experimental acute lung injury. British Journal of Anaesthesia 107:3, 388-397
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Siva Subramanian, Ayman El-Mohandes, Ramasubbareddy Dhanireddy, Matthew A. Koch. (2011) Association of Bronchopulmonary Dysplasia and Hypercarbia in Ventilated Infants with Birth Weights of 500–1,499 g. Maternal and Child Health Journal
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Ayumi Hashimoto, Masaki Kuwabara, Yoshinori Hirasaki, Hiroyuki Tsujimoto, Tsuyoshi Torii, Tatsuo Nakamura, Akeo Hagiwara. (2011) Reduction of air leaks in a canine model of pulmonary resection with a new staple-line buttress. The Journal of Thoracic and Cardiovascular Surgery 142:2, 366-371
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Toshiki Yokoyama, Kenji Tsushima, Hiroshi Yamamoto, Tomonobu Koizumi, Keishi Kubo. (2011) Potential benefits of early continuous positive pressure ventilation in patients with rapidly progressive interstitial pneumonia. Respirologyno-no
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Christine R. Rutter, Elizabeth A. Rozanski, Claire R. Sharp, Lisa L. Powell, Marc Kent. (2011) Outcome and medical management in dogs with lower motor neuron disease undergoing mechanical ventilation: 14 cases (2003-2009). Journal of Veterinary Emergency and Critical Caren/a-n/a
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Juan P. Boriosi, Anil Sapru, James H. Hanson, Jeanette Asselin, Ginny Gildengorin, Vivienne Newman, Katie Sabato, Heidi R. Flori. (2011) Efficacy and safety of lung recruitment in pediatric patients with acute lung injury. Pediatric Critical Care Medicine 12:4, 431-436
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Carl F. Haas. (2011) Mechanical Ventilation with Lung Protective Strategies: What Works?. Critical Care Clinics 27:3, 469-486
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Sammy Ali, Niall D. Ferguson. (2011) High-Frequency Oscillatory Ventilation in ALI/ARDS. Critical Care Clinics 27:3, 487-499
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James E. Lynch, Don Hayes, Joseph B. Zwischenberger. (2011) Extracorporeal CO2 Removal in ARDS. Critical Care Clinics 27:3, 609-625
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B. Taylor Thompson, Gordon R. Bernard. (2011) ARDS Network (NHLBI) Studies: Successes and Challenges in ARDS Clinical Research. Critical Care Clinics 27:3, 459-468
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Jan Florian Heuer, Philip Sauter, Jürgen Barwing, Peter Herrmann, Thomas A. Crozier, Annalen Bleckmann, Tim Beißbarth, Onnen Moerer, Michael Quintel. (2011) Effects of High-frequency Oscillatory Ventilation on Systemic and Cerebral Hemodynamics and Tissue Oxygenation: An Experimental Study in Pigs. Neurocritical Care
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Onnen Moerer, Günter Hahn, Michael Quintel. (2011) Lung impedance measurements to monitor alveolar ventilation. Current Opinion in Critical Care 17:3, 260-267
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Bart Cortjens, Annick A.N.M. Royakkers, Rogier M. Determann, Jeroen D.E. van Suijlen, Stephan S. Kamphuis, Jannetje Foppen, Anita de Boer, Cathrien.W. Wieland, Peter E. Spronk, Marcus J. Schultz, Catherine S.C. Bouman. (2011) Lung-protective mechanical ventilation does not protect against acute kidney injury in patients without lung injury at onset of mechanical ventilation. Journal of Critical Care
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Andriy I. Batchinsky, Bryan S. Jordan, Dara Regn, Corina Necsoiu, William J. Federspiel, Michael J. Morris, Leopoldo C. Cancio. (2011) Respiratory dialysis: Reduction in dependence on mechanical ventilation by venovenous extracorporeal CO2 removal*. Critical Care Medicine 39:6, 1382-1387
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Roberto Santa Cruz, Juan Ignacio Rojas, Rolando Nervi, Roberto Heredia, Agustín Ciapponi, Roberto Santa Cruz. 2011. High versus low positive end-expiratory pressures (PEEP) levels for mechanically ventilated adult patients with acute lung injury and acute respiratory distress syndrome. .
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Sugantha Sundar, Victor Novack, Karinne Jervis, S. Patrick Bender, Adam Lerner, Peter Panzica, Feroze Mahmood, Atul Malhotra, Daniel Talmor. (2011) Influence of Low Tidal Volume Ventilation on Time to Extubation in Cardiac Surgical Patients. Anesthesiology 114:5, 1102-1110
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S.M.K. Rausch, C. Martin, P.B. Bornemann, S. Uhlig, W.A. Wall. (2011) Material model of lung parenchyma based on living precision-cut lung slice testing. Journal of the Mechanical Behavior of Biomedical Materials 4:4, 583-592
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G. TUSMAN, F. SUAREZ-SIPMANN, S. H. BOHM, J. B. BORGES, G. HEDENSTIERNA. (2011) Capnography reflects ventilation/perfusion distribution in a model of acute lung injury. Acta Anaesthesiologica Scandinavica 55:5, 597-606
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Dave A. Dongelmans, Frederique Paulus, Denise P. Veelo, Jan M. Binnekade, Margreeth B. Vroom, Marcus J. Schultz. (2011) Adaptive Support Ventilation May Deliver Unwanted Respiratory Rate–Tidal Volume Combinations in Patients with Acute Lung Injury Ventilated According to an Open Lung Concept. Anesthesiology 114:5, 1138-1143
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R.A. do Amaral, D.M. Tavares, L.S. Lucena, J. Brandão-Neto. (2011) The physical origin of sigmoidal respiratory pressure–volume curves: Alveolar recruitment and nonlinear elasticity. Physica A: Statistical Mechanics and its Applications 390:10, 1791-1799
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Yves Moens, Stephan Böhm. (2011) Ventilating horses: moving away from old paradigms. Veterinary Anaesthesia and Analgesia 38:3, 165-168
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M. Czaplik, R. Rossaint, E. Koch, A. Fahlenkamp, W. Schröder, P. Pelosi, W.M. Kübler, J. Bickenbach. (2011) Methods for quantitative evaluation of alveolar structure during in vivo microscopy. Respiratory Physiology & Neurobiology 176:3, 123-129
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Thomas Bice, Guangxi Li, Michael Malinchoc, Augustine S. Lee, Ognjen Gajic. (2011) Incidence and risk factors of recurrent acute lung injury*. Critical Care Medicine 39:5, 1069-1073
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Göran Hedenstierna, Görel Nyman, Claes Frostell. 2011. Animal Models of Lung Physiology during Anesthesia. .
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Ashwath Sundaresan, J. Geoffrey Chase. (2011) Positive end expiratory pressure in patients with acute respiratory distress syndrome ??? The past, present and future. Biomedical Signal Processing and Control
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Onuma Chaiwat, Monica S. Vavilala, Shaji Philip, Amin Malakouti, Margaret J. Neff, Steven Deem, Miriam M. Treggiari, Jin Wang, John D. Lang. (2011) Intraoperative adherence to a low tidal volume ventilation strategy in critically ill patients with preexisting acute lung injury. Journal of Critical Care 26:2, 144-151
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A. Sablotzki, M. Fuchs, J. Gille, A. Weimann, E. Czeslick. (2011) Therapie der posttraumatischen abdominellen Sepsis. Intensivmedizin und Notfallmedizin 48:3, 199-206
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Arasch Wafaisade, Rolf Lefering, Bertil Bouillon, Samir G. Sakka, Oliver C. Thamm, Thomas Paffrath, Edmund Neugebauer, Marc Maegele. (2011) Epidemiology and risk factors of sepsis after multiple trauma: An analysis of 29,829 patients from the Trauma Registry of the German Society for Trauma Surgery*. Critical Care Medicine 39:4, 621-628
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Terry L. Jones. (2011) A Retrospective Exploration of Patient-Ventilator Monitoring Intensity, Therapeutic Intervention Intensity, and Compliance with Lung Protective Guidelines in a Cohort of Patients with Adult Respiratory Distress Syndrome. Worldviews on Evidence-Based Nursing 8:1, 40-50
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F. J. da Silva Ramos, E. M. de Oliveira, M. Park, G. P. P. Schettino, L. C. P. Azevedo. (2011) Heart-lung interactions with different ventilatory settings during acute lung injury and hypovolaemia: an experimental study. British Journal of Anaesthesia 106:3, 394-402
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Michael A. Matthay, Rachel L. Zemans. (2011) The Acute Respiratory Distress Syndrome: Pathogenesis and Treatment. Annual Review of Pathology: Mechanisms of Disease 6:1, 147-163
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Julia K Weigel, Daniel Steinmann, Philipp Emerich, Claudius A Stahl, Dominik v Elverfeldt, Josef Guttmann. (2011) High-resolution three-dimensional 19 F-magnetic resonance imaging of rat lung in situ : evaluation of airway strain in the perfluorocarbon-filled lung. Physiological Measurement 32:2, 251-262
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Brian Whang, Farzan Filsoufi, Gregory W. Fischer, George Silvay, Ramachandra C. Reddy. (2011) The Left Thoracotomy Approach for Reoperative Cardiac Surgery: Considerations for the Surgeon and Anesthesiologist. Journal of Cardiothoracic and Vascular Anesthesia 25:1, 134-139
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David A Turner, Ira M Cheifetz. (2011) Pediatric acute respiratory failure: areas of debate in the pediatric critical care setting. Expert Review of Respiratory Medicine 5:1, 65-73
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Sérgio N. Nemer, Jefferson B. Caldeira, Leandro M. Azeredo, João Márcio Garcia, Ricardo T. Silva, Darwin Prado, Ricardo G. Santos, Bruno S. Guimarães, Rodrigo A. Ramos, Rosângela A. Noé, Paulo Cesar P. Souza. (2011) Alveolar recruitment maneuver in patients with subarachnoid hemorrhage and acute respiratory distress syndrome: A comparison of 2 approaches. Journal of Critical Care 26:1, 22-27
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Mario Perl, Joanne Lomas-Neira, Fabienne Venet, Chun-Shiang Chung, Alfred Ayala. (2011) Pathogenesis of indirect (secondary) acute lung injury. Expert Review of Respiratory Medicine 5:1, 115-126
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Nicolò Patroniti, Stefano Isgrò, Alberto Zanella. (2011) Clinical management of severely hypoxemic patients. Current Opinion in Critical Care 17:1, 50-56
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Markus Kredel, Ralf M Muellenbach, Nicolas Schlegel, Christian Wunder, Michael Klingelhöfer, Markus Lange, Norbert Roewer, Jens Waschke, Jörg Brederlau. (2011) Pulmonary effects of positive end-expiratory pressure and fluid therapy in experimental lung injury. Experimental Lung Research 37:1, 35-43
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Claude Guerin, Sophie Debord, Véronique Leray, Bertrand Delannoy, Frédérique Bayle, Gael Bourdin, Jean-Christophe Richard. (2011) Efficacy and safety of recruitment maneuvers in acute respiratory distress syndrome. Annals of Intensive Care 1:1, 9
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Carol L Hodgson, David V Tuxen, Andrew R Davies, Michael J Bailey, Alisa M Higgins, Anne E Holland, Jenny L Keating, David V Pilcher, Andrew J Westbrook, David J Cooper, Alistair D Nichol. (2011) A randomised controlled trial of an open lung strategy with staircase recruitment, titrated PEEP and targeted low airway pressures in patients with acute respiratory distress syndrome. Critical Care 15:3, R133
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Helen C. Koenig, Barbara B. Finkel, Satjeet S. Khalsa, Paul N. Lanken, Meeta Prasad, Richard Urbani, Barry D. Fuchs. (2011) Performance of an automated electronic acute lung injury screening system in intensive care unit patients*. Critical Care Medicine 39:1, 98-104
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Guillermo M Albaiceta, Lluis Blanch. (2011) Beyond volutrauma in ARDS: the critical role of lung tissue deformation. Critical Care 15:2, 304
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Carmen Sílvia Valente Barbas. (2011) Introducing automated acute lung injury/acute respiratory distress syndrome electronic screening in intensive care unit practice: Is it the future?*. Critical Care Medicine 39:1, 209-210
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Ashwath Sundaresan, J Chase, Geoffrey M Shaw, Yeong Shiong Chiew, Thomas Desaive. (2011) Model-based optimal PEEP in mechanically ventilated ARDS patients in the Intensive Care Unit. BioMedical Engineering OnLine 10:1, 64
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M. Frass, M. Linkesch, S. Banyai, G. Resch, C. Dielacher, T. Löbl, C. Endler, M. Haidvogl, I. Muchitsch, E. Schuster. (2011) Adjunctive homeopathic treatment in patients with severe sepsis: a randomized, double-blind, placebo-controlled trial in an intensive care unit. Homeopathy 100:1-2, 95-100
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Vitaly Herasevich, Mykola Tsapenko, Marija Kojicic, Adil Ahmed, Rachul Kashyap, Chakradhar Venkata, Khurram Shahjehan, Sweta J. Thakur, Brian W. Pickering, Jiajie Zhang, Rolf D. Hubmayr, Ognjen Gajic. (2011) Limiting ventilator-induced lung injury through individual electronic medical record surveillance*. Critical Care Medicine 39:1, 34-39
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Uwe Erkens. (2011) Maschinelle Beatmung. DoctorConsult - The Journal. Wissen für Klinik und Praxis 1:4, e249-e255
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Megan Way, Gary E. Hill. (2011) Intraoperative End-Tidal Carbon Dioxide Concentrations: What Is the Target?. Anesthesiology Research and Practice 2011, 1-3
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H. Hamakawa, H. Sakai, A. Takahashi, A. Aoyama, J. Zhang, F. Chen, T. Fujinaga, H. Wada, H. Date, T. Bando. (2011) Dynamic Instability of Central Airways and Peripheral Airspace in Rat Lungs Perfused with Cold Preservation Solutions. European Surgical Research 47:3, 159-167
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A. R. Wilkes. (2011) Heat and moisture exchangers and breathing system filters: their use in anaesthesia and intensive care.
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Fernando G Rios, Elissa Estenssoro, Fernando Villarejo, Ricardo Valentini, Liliana Aguilar, Daniel E Pezzola, Pascual Valdez, Miguel Blasco, Cristina Orlandi, Javier Alvarez, Fernando Saldarini, Alejandro Gomez, Pablo E Gomez, Martin Deheza, Alan Zazu, Monica Quinteros, Javier Osatnik, Ariel Chena, Damian Violi, Maria EUGENIA Gonzalez, Guillermo Chiappero. (2011) Lung Function and Organ Dysfunctions in 178 Patients Requiring Mechanical Ventilation,During The 2009 Influenza A(H1N1) Pandemic. Critical Care 15:4, R201
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Ana Fernandez-Bustamante, Cristina L Wood, Zung V Tran, Pierre Moine. (2011) Intraoperative ventilation: incidence and risk factors for receiving large tidal volumes during general anesthesia. BMC Anesthesiology 11:1, 22
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Merja Ålander, Outi Peltoniemi, Tytti Pokka, Tero Kontiokari. (2011) Comparison of pressure-, flow-, and NAVA-Triggering in pediatric and neonatal ventilatory care. Pediatric Pulmonologyn/a-n/a
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Jingen Xia, Bing Sun, Hangyong He, Heng Zhang, Chunting Wang, Qingyuan Zhan. (2011) Effect of spontaneous breathing on ventilator-induced lung injury in mechanically ventilated healthy rabbits: a randomized, controlled, experimental study. Critical Care 15:5, R244
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Robert P Dickson, Robert C Hyzy. (2011) Short people got no reason: gender, height, and disparities in the management of acute lung injury. Critical Care 15:6, 1010
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Eric M. Bershad, José I. Suarez. 2011. Aneurysmal Subarachnoid Hemorrhage. , 589-615.
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Jean Dellamonica, Nicolas Lerolle, Cyril Sargentini, Gaetan Beduneau, Fabiano Di Marco, Alain Mercat, Jean-Christophe M Richard, Jean-Luc Diehl, Jordi Mancebo, Jean-Jacques Rouby, Qin Lu, Gilles Bernardin, Laurent Brochard. (2011) Accuracy and precision of end expiratory lung volume measurements by automated nitrogen washout/washin technique in patients with acute respiratory distress syndrome. Critical Care 15:6, R294
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Jean-Damien Ricard, Didier Dreyfuss, Alexandre T. Rotta, Georges Saumon. 2011. Ventilator-Induced Lung Injury. , 697-705.
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Stéphane Dauger, Philippe Durand, Etienne Javouey, Jean-Christophe Mercier. 2011. Acute Respiratory Distress Syndrome in Children. , 706-716.
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Shekhar T. Venkataraman. 2011. Mechanical Ventilation and Respiratory Care. , 657-688.
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Ismail Abdul Hamid, Antony Simon Hariharan, Nelamangala Ramakrishnaiah Ravi Shankar. (2010) The advent of ECMO and pumpless extracorporeal lung assist in ARDS—a review. Indian Journal of Thoracic and Cardiovascular Surgery 26:4, 280-288
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Carmen Silvia Valente Barbas. (2010) Understanding and avoiding ventilator-induced lung injury: Lessons from an insightful experimental study*. Critical Care Medicine 38:12, 2418-2419
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Marcus H. T. Reinges. (2010) Pros and cons of permissive hypercapnia in patients with subarachnoid haemorrhage and ARDS. Acta Neurochirurgica 152:12, 2173-2174
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Hamid Aslami, Jan M. Binnekade, Janneke Horn, Sandra Huissoon, Nicole P. Juffermans. (2010) The effect of induced hypothermia on respiratory parameters in mechanically ventilated patients. Resuscitation 81:12, 1723-1725
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Naoya Iguchi, Osamu Hirao, Akinori Uchiyama, Takashi Mashimo, Masaji Nishimura, Yuji Fujino. (2010) Evaluation of performance of two high-frequency oscillatory ventilators using a model lung with a position sensor. Journal of Anesthesia 24:6, 888-892
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Jin Won HUH, Sang-Bum HONG, Chae-Man LIM, Younsuck KOH. (2010) Effect of the alveolar recruitment manoeuvre on haemodynamic parameters in patients with acute respiratory distress syndrome: Relationship with oxygenation. Respirology 15:8, 1220-1225
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Hamid Aslami, André Heinen, Joris J. T. H. Roelofs, Coert J. Zuurbier, Marcus J. Schultz, Nicole P. Juffermans. (2010) Suspended animation inducer hydrogen sulfide is protective in an in vivo model of ventilator-induced lung injury. Intensive Care Medicine 36:11, 1946-1952
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Peter A. Dargaville, Peter C. Rimensberger, Inéz Frerichs. (2010) Regional tidal ventilation and compliance during a stepwise vital capacity manoeuvre. Intensive Care Medicine 36:11, 1953-1961
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Miriam Santschi, Philippe Jouvet, Francis Leclerc, France Gauvin, Christopher J. L. Newth, Christopher L. Carroll, Heidi Flori, Robert C. Tasker, Peter C. Rimensberger, Adrienne G. Randolph. (2010) Acute lung injury in children: Therapeutic practice and feasibility of international clinical trials*. Pediatric Critical Care Medicine 11:6, 681-689
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John C. Marshall. (2010) Critical illness is an iatrogenic disorder. Critical Care Medicine 38, S582-S589
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John J. Marini. (2010) Can we prevent the spread of focal lung inflammation?. Critical Care Medicine 38, S574-S581
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Luciano Gattinoni, Alessandro Protti, Pietro Caironi, Eleonora Carlesso. (2010) Ventilator-induced lung injury: The anatomical and physiological framework. Critical Care Medicine 38, S539-S548
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Robert M. Kacmarek, Jesús Villar. (2010) Clinical repercussions of high-frequency percussive ventilation: A burning issue*. Critical Care Medicine 38:10, 2069-2070
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BENJAMIN CONTE, JOËL L'HERMITE, JACQUES RIPART, JEAN-YVES LEFRANT. (2010) Perioperative optimization of oxygen delivery. Transfusion Alternatives in Transfusion Medicine 11, 22-29
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James O'Beirne, Nicholas Murphy, Julia Wendon. 2010. Fulminant Hepatic Failure: Treatment. , 661-684.
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Linda L. Liu, J. Matthew Aldrich, David W. Shimabukuro, Kristina R. Sullivan, John M. Taylor, Kevin C. Thornton, Michael A. Gropper. (2010) Rescue Therapies for Acute Hypoxemic Respiratory Failure. Anesthesia & Analgesia 111:3, 693-702
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Jack Hodd, Alex Doyle, Joseph Carter, John Albarran, Peter Young. (2010) Increasing positive end expiratory pressure at extubation reduces subglottic secretion aspiration in a bench-top model. Nursing in Critical Care 15:5, 257-261
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Robert A. Maxwell, John M. Green, Jimmy Waldrop, Benjamin W. Dart, Philip W. Smith, Donald Brooks, Patricia L. Lewis, Donald E. Barker. (2010) A Randomized Prospective Trial of Airway Pressure Release Ventilation and Low Tidal Volume Ventilation in Adult Trauma Patients With Acute Respiratory Failure. The Journal of Trauma: Injury, Infection, and Critical Care 69:3, 501-511
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Francesco Ventura, Alessandro Bonsignore, Raffaella Gentile, Francesco De Stefano. (2010) Two Fatal Cases of Hidden Pneumonia in Young People*. Journal of Forensic Sciences 55:5, 1380-1383
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Ravi S. Tripathi, James M. Blum, Andrew L. Rosenberg, Kevin K. Tremper. (2010) Pulse oximetry saturation to fraction inspired oxygen ratio as a measure of hypoxia under general anesthesia and the influence of positive end-expiratory pressure. Journal of Critical Care 25:3, 542.e9-542.e13
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