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      Management and outcome of mechanically ventilated patients after cardiac arrest

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          Abstract

          Introduction

          The aim of this study was to describe and compare the changes in ventilator management and complications over time, as well as variables associated with 28-day hospital mortality in patients receiving mechanical ventilation (MV) after cardiac arrest.

          Methods

          We performed a secondary analysis of three prospective, observational multicenter studies conducted in 1998, 2004 and 2010 in 927 ICUs from 40 countries. We screened 18,302 patients receiving MV for more than 12 hours during a one-month-period. We included 812 patients receiving MV after cardiac arrest. We collected data on demographics, daily ventilator settings, complications during ventilation and outcomes. Multivariate logistic regression analysis was performed to calculate odds ratios, determining which variables within 24 hours of hospital admission were associated with 28-day hospital mortality and occurrence of acute respiratory distress syndrome (ARDS) and pneumonia acquired during ICU stay at 48 hours after admission.

          Results

          Among 812 patients, 100 were included from 1998, 239 from 2004 and 473 from 2010. Ventilatory management changed over time, with decreased tidal volumes (V T) (1998: mean 8.9 (standard deviation (SD) 2) ml/kg actual body weight (ABW), 2010: 6.7 (SD 2) ml/kg ABW; 2004: 9 (SD 2.3) ml/kg predicted body weight (PBW), 2010: 7.95 (SD 1.7) ml/kg PBW) and increased positive end-expiratory pressure (PEEP) (1998: mean 3.5 (SD 3), 2010: 6.5 (SD 3); P <0.001). Patients included from 2010 had more sepsis, cardiovascular dysfunction and neurological failure, but 28-day hospital mortality was similar over time (52% in 1998, 57% in 2004 and 52% in 2010). Variables independently associated with 28-day hospital mortality were: older age, PaO 2 <60 mmHg, cardiovascular dysfunction and less use of sedative agents. Higher V T, and plateau pressure with lower PEEP were associated with occurrence of ARDS and pneumonia acquired during ICU stay.

          Conclusions

          Protective mechanical ventilation with lower V T and higher PEEP is more commonly used after cardiac arrest. The incidence of pulmonary complications decreased, while other non-respiratory organ failures increased with time. The application of protective mechanical ventilation and the prevention of single and multiple organ failure may be considered to improve outcome in patients after cardiac arrest.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s13054-015-0922-9) contains supplementary material, which is available to authorized users.

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          Most cited references34

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          Evolution of mortality over time in patients receiving mechanical ventilation.

          Baseline characteristics and management have changed over time in patients requiring mechanical ventilation; however, the impact of these changes on patient outcomes is unclear. To estimate whether mortality in mechanically ventilated patients has changed over time. Prospective cohort studies conducted in 1998, 2004, and 2010, including patients receiving mechanical ventilation for more than 12 hours in a 1-month period, from 927 units in 40 countries. To examine effects over time on mortality in intensive care units, we performed generalized estimating equation models. We included 18,302 patients. The reasons for initiating mechanical ventilation varied significantly among cohorts. Ventilatory management changed over time (P < 0.001), with increased use of noninvasive positive-pressure ventilation (5% in 1998 to 14% in 2010), a decrease in tidal volume (mean 8.8 ml/kg actual body weight [SD = 2.1] in 1998 to 6.9 ml/kg [SD = 1.9] in 2010), and an increase in applied positive end-expiratory pressure (mean 4.2 cm H2O [SD = 3.8] in 1998 to 7.0 cm of H2O [SD = 3.0] in 2010). Crude mortality in the intensive care unit decreased in 2010 compared with 1998 (28 versus 31%; odds ratio, 0.87; 95% confidence interval, 0.80-0.94), despite a similar complication rate. Hospital mortality decreased similarly. After adjusting for baseline and management variables, this difference remained significant (odds ratio, 0.78; 95% confidence interval, 0.67-0.92). Patient characteristics and ventilation practices have changed over time, and outcomes of mechanically ventilated patients have improved. Clinical trials registered with www.clinicaltrials.gov (NCT01093482).
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            Association between use of lung-protective ventilation with lower tidal volumes and clinical outcomes among patients without acute respiratory distress syndrome: a meta-analysis.

            Lung-protective mechanical ventilation with the use of lower tidal volumes has been found to improve outcomes of patients with acute respiratory distress syndrome (ARDS). It has been suggested that use of lower tidal volumes also benefits patients who do not have ARDS. To determine whether use of lower tidal volumes is associated with improved outcomes of patients receiving ventilation who do not have ARDS. MEDLINE, CINAHL, Web of Science, and Cochrane Central Register of Controlled Trials up to August 2012. Eligible studies evaluated use of lower vs higher tidal volumes in patients without ARDS at onset of mechanical ventilation and reported lung injury development, overall mortality, pulmonary infection, atelectasis, and biochemical alterations. Three reviewers extracted data on study characteristics, methods, and outcomes. Disagreement was resolved by consensus. Twenty articles (2822 participants) were included. Meta-analysis using a fixed-effects model showed a decrease in lung injury development (risk ratio [RR], 0.33; 95% CI, 0.23 to 0.47; I2, 0%; number needed to treat [NNT], 11), and mortality (RR, 0.64; 95% CI, 0.46 to 0.89; I2, 0%; NNT, 23) in patients receiving ventilation with lower tidal volumes. The results of lung injury development were similar when stratified by the type of study (randomized vs nonrandomized) and were significant only in randomized trials for pulmonary infection and only in nonrandomized trials for mortality. Meta-analysis using a random-effects model showed, in protective ventilation groups, a lower incidence of pulmonary infection (RR, 0.45; 95% CI, 0.22 to 0.92; I2, 32%; NNT, 26), lower mean (SD) hospital length of stay (6.91 [2.36] vs 8.87 [2.93] days, respectively; standardized mean difference [SMD], 0.51; 95% CI, 0.20 to 0.82; I2, 75%), higher mean (SD) PaCO2 levels (41.05 [3.79] vs 37.90 [4.19] mm Hg, respectively; SMD, -0.51; 95% CI, -0.70 to -0.32; I2, 54%), and lower mean (SD) pH values (7.37 [0.03] vs 7.40 [0.04], respectively; SMD, 1.16; 95% CI, 0.31 to 2.02; I2, 96%) but similar mean (SD) ratios of PaO2 to fraction of inspired oxygen (304.40 [65.7] vs 312.97 [68.13], respectively; SMD, 0.11; 95% CI, -0.06 to 0.27; I2, 60%). Tidal volume gradients between the 2 groups did not influence significantly the final results. Among patients without ARDS, protective ventilation with lower tidal volumes was associated with better clinical outcomes. Some of the limitations of the meta-analysis were the mixed setting of mechanical ventilation (intensive care unit or operating room) and the duration of mechanical ventilation.
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              Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality.

              Laboratory investigations suggest that exposure to hyperoxia after resuscitation from cardiac arrest may worsen anoxic brain injury; however, clinical data are lacking. To test the hypothesis that postresuscitation hyperoxia is associated with increased mortality. Multicenter cohort study using the Project IMPACT critical care database of intensive care units (ICUs) at 120 US hospitals between 2001 and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic cardiac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and arterial blood gas analysis performed within 24 hours following ICU arrival. Patients were divided into 3 groups defined a priori based on PaO(2) on the first arterial blood gas values obtained in the ICU. Hyperoxia was defined as PaO(2) of 300 mm Hg or greater; hypoxia, PaO(2) of less than 60 mm Hg (or ratio of PaO(2) to fraction of inspired oxygen <300); and normoxia, not classified as hyperoxia or hypoxia. In-hospital mortality. Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%), and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) compared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportion difference, 18% [95% CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95% CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model controlling for potential confounders (eg, age, preadmission functional status, comorbid conditions, vital signs, and other physiological indices), hyperoxia exposure had an odds ratio for death of 1.8 (95% CI, 1.5-2.2). Among patients admitted to the ICU following resuscitation from cardiac arrest, arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia.
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                Author and article information

                Contributors
                sutherasan_yuda@yahoo.com
                openuelas@gmail.com
                alfonso.muriel@hrc.es
                vargas.maria82@gmail.com
                ffrutos@ucigetafe.com
                ibrunetti@tin.it
                raymondos@ards.eu
                davide.dantini@hotmail.it
                niklas.nielsen@med.lu.se
                n.ferguson@utoronto.ca
                bernd.boettiger@uk-koeln.de
                aw.thille@gmail.com
                andrew.davies@monash.edu
                jhurtado@hc.edu.uy
                fernandrios@gmail.com
                capez@intramed.net
                damianalejandro.violi@gmail.com
                cakarn@istanbul.edu.tr
                mga@une.net.co
                dubin98@gmail.com
                mi.kuiper@wxs.nl
                marcreis@uai.com.br
                yskoh@amc.seoul.kr
                r.moreno@mail.telepac.pt
                pamin@vsnl.com
                vtomicic@alemana.cl
                lusoro@ctcinternet.cl
                hhbulow@dadlnet.dk
                anzueto@uthscsa.edu
                aesteban@ucigetafe.com
                ppelosi@hotmail.com
                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                8 May 2015
                8 May 2015
                2015
                : 19
                : 1
                : 215
                Affiliations
                [ ]Department of Medicine, Ramathibodi Hospital, Mahidol University, RAMA VI road, Bangkok, 10400 Thailand
                [ ]Department of Surgical Sciences and Integrated Diagnostics IRCCS AOU San Martino-IST, Largo Rosanna Benzi 8, Genoa, 16131 Italy
                [ ]Hospital Universitario Infanta Cristina and CIBER Enfermedades Respiratorias, Avenida 9 de junio, 2, 28981 Parla Madrid, Spain
                [ ]Biostatistics Unit, Ramón y Cajal Institute and Research Health, IRYCIS, CIBERESP, Hospital Ramón y Cajal Ctra., Colmenar Km 9.100, 28034 Madrid, Spain
                [ ]Department of Neurosciences, Odonthostomatological and Reproductive Sciences, University of Naples, “Federico II”, Naples, 80100 Italy
                [ ]Hospital Universitario de Getafe and CIBER Enfermedades Respiratorias, Carretera de Toledo Km 12.500, 28905 Madrid, Spain
                [ ]Anaesthesiology and Intensive Care Medicine, Medical School Hanover, 544 Carl-Neuberg-Strasse 1, D-30625 Hanover, Germany
                [ ]Dipartimento di Anestesia, Rianimazione e Terapia Intensiva, Universita’ degli Studi di Foggia, Viale Pinto, 1, 71100 Foggia, Italy
                [ ]Department of Anesthesia and Intensive Care, Intensive Care Unit, Helsingborg Hospital, S Vallgatan 5, 251 87 Helsingborg, Sweden
                [ ]Interdepartmental Division of Critical Care Medicine, Department of Medicine, University of Toronto, University Health Network and Mount Sinai Hospital, 585 University Avenue, Toronto, M5G 2N2 ON Canada
                [ ]Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Kerpener Straße 62, 50937 Köln, Germany
                [ ]Cenre Hospitalier Universitaire de Poitiers, Réanimation Médicale, INSERM CIC 1402, Université de Poitiers, Poitiers, 86000 France
                [ ]Department of Epidemiology and Preventive Medicine, ANZIC-RC, Monash University, Commercial Road, Melbourne, 3004 Australia
                [ ]Dept. Pathophysiology, Hospital de Clínicas, Av. Italia s/n. Universidad de la Republica, Montevideo, 11600 Uruguay
                [ ]Department of Intensive Care, Hospital Nacional Prof. Alejandro Posadas El Palomar, Buenos Aires, CP 1684 Argentina
                [ ]Medical Staff-Critical Care, Hospital Prof. Dr. Luis Guemes, Buenos Aires, Argentina
                [ ]Anesthesiology and Intensive Care, Istanbul University, Istanbul Medical Faculty, Millet cad., 34093 Istanbul, Turkey
                [ ]Clínica Medellín & Universidad Pontificia Bolivariana, Medellín, Colombia
                [ ]Medical ICU, Peking Union Medical College Hospital, 1 Shuai Fu Yuan, Beijing, 100730 People’s Republic of China
                [ ]Department of Intensive Care, Medical Center Leeuwarden Henri Dunantweg 2, 8934 AD Leeuwarden, The Netherlands
                [ ]Hospital Universitário São José, Belo Horizonte, Brazil
                [ ]Department of Pulmonary and Critical Care Medicine Asan Medical Center, Univ. of Ulsan College of Medicine, 388-1 Pungnap Dong Songpa Ku Seoul, 138-736 Seoul, Republic of Korea
                [ ]Unidade de Cuidados Intensivos Neurocríticos Hospital de São José Centro Hospitalarde Lisboa Central, E.P.E. R. José António Serrano, 1150-199 Lisbon, Portugal
                [ ]Bombay Hospital Institute of Medical Sciences, 12 New Marine Lines, Mumbai, 400020 India
                [ ]Clínica Las Lilas de Santiago, Santiago, Chile
                [ ]Instituto Nacional del Tórax de Santiago, Santiago, Chile
                [ ]Anaesthesiology and Intensive Care, Holbaek Hospitall, Region Zealand University of Copenhagen, Smedelundsgade, 60 4300 Holbaek, Denmark
                [ ]South Texas Veterans Health Care System and University of Texas Health Science Center, 111 E 7400 Merton Minter blvd, 78229 San Antonio, TX USA
                Article
                922
                10.1186/s13054-015-0922-9
                4457998
                25953483
                0d7d6c25-aba0-4eae-b85b-cbafa9121edb
                © Sutherasan et al. 2015

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 4 February 2015
                : 13 April 2015
                Categories
                Research
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                © The Author(s) 2015

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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