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OBJECTIVE: During closed chest compression for cardiac arrest, any increase in coronary perfusion pressure accounts for a proportional increase in myocardial blood flow and therefore the resuscitability of the patient. The objectives of this study were to evaluate the safety, feasibility, and hemodynamic effects of phased chest and abdominal compression-decompression and to compare it with mechanical chest compression during cardiopulmonary resuscitation. DESIGN: In this prospective, single-center, phase II study, we compared patients treated with the Datascope Lifestick Resuscitator with patients who had been treated with mechanical precordial compression. SETTING: Emergency department of a tertiary care university hospital. PATIENTS: We included 31 patients with cardiac arrest who had received cardiopulmonary resuscitation in the emergency department. INTERVENTIONS: The Lifestick device was used in 20 patients. In 11 patients, mechanical chest compression with the Thumper device was used as a control intervention. MEASUREMENTS AND MAIN RESULTS: We evaluated the safety, feasibility, and hemodynamic effects of both interventions and observed, with the help of echocardiography, the mechanisms through which blood flow was generated. We found no significant difference between the use of the Lifestick device and standard chest compression with the Thumper device in resuscitations. Most operators regarded the Lifestick as a feasible alternative to the Thumper. We could observe a mean increase in coronary perfusion pressure of 9.33 mm Hg (interquartile range, 1.96-14.36; p = .08) and an increase of end-tidal CO2 of 10 mm Hg (interquartile range, 5-16; p = .003) (1333Pa [interquartile range, 665-2133]) during resuscitation with the Lifestick compared with using the Thumper. CONCLUSION: In this preliminary study, resuscitation with the Lifestick was found to be safe and feasible. The design of the study and small number of patients included in it limit the conclusions about the hemodynamic effects of the Lifestick. [ABSTRACT FROM AUTHOR]

Objective: Mortality is frequently used as an outcome in critical care trials, being a patient-orientated variable and robust against information/selection bias. Mortality frequency, however, should be measured at a defined time point of follow-up. Practice of meta-analysis shows that follow-up times of trials in critical care medicine differ substantially. This may have substantial implications on potential pooling of effect estimates. We aimed to describe the current practice of mortality follow-up time definitions in a representative sample of published critical care randomized controlled trials and to analyze the influence of different follow-up times on subsequently pooled effect estimates., Data Sources: Cochrane CENTRAL, EMBASE, MEDLINE, PASCAL Biomed, and PsycINFO., Study Selection: Databases were searched for critical care randomized controlled trials published after 2000. A random sample of 50% was drawn for further review., Data Extraction: Study characteristics were extracted, as well as the number and time points of mortality ascertainment. Additional data were extracted from Kaplan-Meier plots, as available., Data Synthesis: Meta-regression and multilevel mixed-effects linear regression were used to analyze the influence of follow-up time (independent variable) on deviation of pooled risk ratios from study baseline (dependent variable). From 9,246 retrieved references, we included 106 studies representing 63,713 participants. Among these, 45 studies (43%) reported more than one time point, with 24 different time points at all, only three (28, 30, and 90 d) being reported in more than 10% of studies. Limiting meta-analyses to only one predefined time point would reduce the number of eligible studies by at least 60%. No influence of time points on meta-analytic summary effect estimates was found., Conclusions: In a large sample of critical care randomized controlled trials, numerous different mortality time points are reported. Mortality time points did not influence pooled point estimates of the effects. Consequently, it seems possible to pool effect estimates, which in turn will increase the precision of these effect estimates.

Objective: The association between cigarette smoke exposure and the acute respiratory distress syndrome in patients with the most common acute respiratory distress syndrome risk factors of sepsis, pneumonia, and aspiration has not been well studied. The goal of this study was to test the association between biomarker-confirmed cigarette smoking and acute respiratory distress syndrome in a diverse cohort., Design: Prospective cohort., Setting: Tertiary care center., Patients: Four hundred twenty-six critically ill patients with acute respiratory distress syndrome risk factors (excluding trauma and transfusion), Interventions: : None., Measurements and Main Results: We obtained smoking histories and measured urine 4-(methylnitrosamino)-1-(3-pyridyl)-1- butanol (a biomarker of cigarette smoke exposure) on urine samples obtained at the time of study enrollment. The association between cigarette smoke exposure and acute respiratory distress syndrome differed based on acute respiratory distress syndrome risk factor (p < 0.02 for interaction). In patients with nonpulmonary sepsis as the primary acute respiratory distress syndrome risk factor (n = 212), 39% of those with acute respiratory distress syndrome were current smokers by history compared with 22% of those without acute respiratory distress syndrome (odds ratio, 2.28; 95% CI, 1.24-4.19; p = 0.008). Likewise, cigarette smoke exposure as measured by urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was significantly associated with acute respiratory distress syndrome in this group. The increased risk of acute respiratory distress syndrome in nonpulmonary sepsis was restricted to patients with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol levels consistent with active smoking and was robust to adjustment for other acute respiratory distress syndrome predictors. Cigarette smoke exposure as measured by history or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol was not associated with acute respiratory distress syndrome in patients with other risk factors (e.g., pneumonia and aspiration)., Conclusions: Cigarette smoking measured both by history and biomarker is associated with an increased risk of acute respiratory distress syndrome in patients with nonpulmonary sepsis. This finding has important implications for tobacco product regulation and for understanding the pathogenesis of acute respiratory distress syndrome.

Objectives: The association between tobacco smoke exposure and critical illness is not well studied, largely because obtaining an accurate smoking history from critically ill patients is difficult. Biomarkers can provide quantitative data on active and secondhand cigarette smoke exposure. We sought to compare cigarette smoke exposure as measured by biomarkers to exposure by self-report in a cohort of critically ill patients and to determine how well biomarkers of cigarette smoke exposure correlate with each other in this population., Design, Setting, and Patients: Serum and urine cotinine and trans-3'-hydroxycotinine, urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol, and hair and nail nicotine levels were measured in 60 subjects enrolled in an observational cohort of critically ill subjects at a tertiary academic medical center in Tennessee. Smoking history was obtained from patients, their surrogates, or the medical chart. Cigarette smoke exposure as measured by biomarkers was compared to exposure by history., Measurements and Main Results: By smoking history, 29 subjects were identified as smokers, 28 were identified as nonsmokers, and 3 were identified as unknown. The combination of serum cotinine and urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified 27 of the 28 nonsmokers by history either as active smokers (n = 6, 21%) or as exposed to secondhand smoke (n = 21, 75%). All biomarker levels were strongly correlated with each other (r = .69-.95, p < .0001)., Conclusions: The combination of serum cotinine and urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol identified considerably more active smokers than did smoking history and detected a high prevalence of secondhand smoke exposure in a critically ill population. These markers will be important for future studies investigating the relationship between active smoking and secondhand smoke exposure and critical illness.