Person: Vidal Melo, Marcos
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Vidal Melo
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Marcos
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Vidal Melo, Marcos
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Publication Potentially modifiable respiratory variables contributing to outcome in ICU patients without ARDS: a secondary analysis of PRoVENT(Springer International Publishing, 2018) Simonis, Fabienne D.; Barbas, Carmen S. V.; Artigas-Raventós, Antonio; Canet, Jaume; Determann, Rogier M.; Anstey, James; Hedenstierna, Goran; Hemmes, Sabrine N. T.; Hermans, Greet; Hiesmayr, Michael; Hollmann, Markus W.; Jaber, Samir; Martin-Loeches, Ignacio; Mills, Gary H.; Pearse, Rupert M.; Putensen, Christian; Schmid, Werner; Severgnini, Paolo; Smith, Roger; Treschan, Tanja A.; Tschernko, Edda M.; Vidal Melo, Marcos; Wrigge, Hermann; de Abreu, Marcelo Gama; Pelosi, Paolo; Schultz, Marcus J.; Neto, Ary Serpa; Dixon, BarryBackground: The majority of critically ill patients do not suffer from acute respiratory distress syndrome (ARDS). To improve the treatment of these patients, we aimed to identify potentially modifiable factors associated with outcome of these patients. Methods: The PRoVENT was an international, multicenter, prospective cohort study of consecutive patients under invasive mechanical ventilatory support. A predefined secondary analysis was to examine factors associated with mortality. The primary endpoint was all-cause in-hospital mortality. Results: 935 Patients were included. In-hospital mortality was 21%. Compared to patients who died, patients who survived had a lower risk of ARDS according to the ‘Lung Injury Prediction Score’ and received lower maximum airway pressure (Pmax), driving pressure (ΔP), positive end-expiratory pressure, and FiO2 levels. Tidal volume size was similar between the groups. Higher Pmax was a potentially modifiable ventilatory variable associated with in-hospital mortality in multivariable analyses. ΔP was not independently associated with in-hospital mortality, but reliable values for ΔP were available for 343 patients only. Non-modifiable factors associated with in-hospital mortality were older age, presence of immunosuppression, higher non-pulmonary sequential organ failure assessment scores, lower pulse oximetry readings, higher heart rates, and functional dependence. Conclusions: Higher Pmax was independently associated with higher in-hospital mortality in mechanically ventilated critically ill patients under mechanical ventilatory support for reasons other than ARDS. Trial Registration ClinicalTrials.gov (NCT01868321). Electronic supplementary material The online version of this article (10.1186/s13613-018-0385-7) contains supplementary material, which is available to authorized users.Publication Effects of ventilation strategy on distribution of lung inflammatory cell activity(BioMed Central, 2013) de Prost, Nicolas; Costa, Eduardo L; Wellman, Tyler; Musch, Guido; Tucci, Mauro R; Winkler, Tilo; Harris, R Scott; Venegas, Jose; Kavanagh, Brian P; Vidal Melo, MarcosIntroduction: Leukocyte infiltration is central to the development of acute lung injury, but it is not known how mechanical ventilation strategy alters the distribution or activation of inflammatory cells. We explored how protective (vs. injurious) ventilation alters the magnitude and distribution of lung leukocyte activation following systemic endotoxin administration. Methods: Anesthetized sheep received intravenous endotoxin (10 ng/kg/min) followed by 2 h of either injurious or protective mechanical ventilation (n = 6 per group). We used positron emission tomography to obtain images of regional perfusion and shunting with infused 13N[nitrogen]-saline and images of neutrophilic inflammation with 18F-fluorodeoxyglucose (18F-FDG). The Sokoloff model was used to quantify 18F-FDG uptake (Ki), as well as its components: the phosphorylation rate (k3, a surrogate of hexokinase activity) and the distribution volume of 18F-FDG (Fe) as a fraction of lung volume (Ki = Fe × k3). Regional gas fractions (fgas) were assessed by examining transmission scans. Results: Before endotoxin administration, protective (vs. injurious) ventilation was associated with a higher ratio of partial pressure of oxygen in arterial blood to fraction of inspired oxygen (PaO2/FiO2) (351 ± 117 vs. 255 ± 74 mmHg; P < 0.01) and higher whole-lung fgas (0.71 ± 0.12 vs. 0.48 ± 0.08; P = 0.004), as well as, in dependent regions, lower shunt fractions. Following 2 h of endotoxemia, PaO2/FiO2 ratios decreased in both groups, but more so with injurious ventilation, which also increased the shunt fraction in dependent lung. Protective ventilation resulted in less nonaerated lung (20-fold; P < 0.01) and more normally aerated lung (14-fold; P < 0.01). Ki was lower during protective (vs. injurious) ventilation, especially in dependent lung regions (0.0075 ± 0.0043/min vs. 0.0157 ± 0.0072/min; P < 0.01). 18F-FDG phosphorylation rate (k3) was twofold higher with injurious ventilation and accounted for most of the between-group difference in Ki. Dependent regions of the protective ventilation group exhibited lower k3 values per neutrophil than those in the injurious ventilation group (P = 0.01). In contrast, Fe was not affected by ventilation strategy (P = 0.52). Lung neutrophil counts were not different between groups, even when regional inflation was accounted for. Conclusions: During systemic endotoxemia, protective ventilation may reduce the magnitude and heterogeneity of pulmonary inflammatory cell metabolic activity in early lung injury and may improve gas exchange through its effects predominantly in dependent lung regions. Such effects are likely related to a reduction in the metabolic activity, but not in the number, of lung-infiltrating neutrophils.Publication Intraoperative protective mechanical ventilation and risk of postoperative respiratory complications: hospital based registry study(BMJ Publishing Group Ltd., 2015) Ladha, Karim; Vidal Melo, Marcos; McLean, Duncan J; Wanderer, Jonathan P; Grabitz, Stephanie D; Kurth, Tobias; Eikermann, MatthiasObjective: To evaluate the effects of intraoperative protective ventilation on major postoperative respiratory complications and to define safe intraoperative mechanical ventilator settings that do not translate into an increased risk of postoperative respiratory complications. Design: Hospital based registry study. Setting: Academic tertiary care hospital and two affiliated community hospitals in Massachusetts, United States. Participants: 69 265 consecutively enrolled patients over the age of 18 who underwent a non-cardiac surgical procedure between January 2007 and August 2014 and required general anesthesia with endotracheal intubation. Interventions Protective ventilation, defined as a median positive end expiratory pressure (PEEP) of 5 cmH2O or more, a median tidal volume of less than 10 mL/kg of predicted body weight, and a median plateau pressure of less than 30 cmH2O. Main outcome measure Composite outcome of major respiratory complications, including pulmonary edema, respiratory failure, pneumonia, and re-intubation. Results: Of the 69 265 enrolled patients 34 800 (50.2%) received protective ventilation and 34 465 (49.8%) received non-protective ventilation intraoperatively. Protective ventilation was associated with a decreased risk of postoperative respiratory complications in multivariable regression (adjusted odds ratio 0.90, 95% confidence interval 0.82 to 0.98, P=0.013). The results were similar in the propensity score matched cohort (odds ratio 0.89, 95% confidence interval 0.83 to 0.97, P=0.004). A PEEP of 5 cmH2O and median plateau pressures of 16 cmH2O or less were associated with the lowest risk of postoperative respiratory complications. Conclusions: Intraoperative protective ventilation was associated with a decreased risk of postoperative respiratory complications. A PEEP of 5 cmH2O and a plateau pressure of 16 cmH2O or less were identified as protective mechanical ventilator settings. These findings suggest that protective thresholds differ for intraoperative ventilation in patients with normal lungs compared with those used for patients with acute lung injury.Publication Modeling \(^{18}F-FDG\) Kinetics during Acute Lung Injury: Experimental Data and Estimation Errors(Public Library of Science, 2012) Dittrich, A. Susanne; Winkler, Tilo; Wellman, Tyler James; de Prost, Nicolas; Musch, Guido; Harris, Robert; Vidal Melo, MarcosBackground: There is increasing interest in Positron Emission Tomography (PET) of 2-deoxy-2-[18F]flouro-D-glucose (\(^{18}F-FDG\)) to evaluate pulmonary inflammation during acute lung injury (ALI). We assessed the effect of extra-vascular lung water on estimates of \(^{18}F-FDG\)-kinetics parameters in experimental and simulated data using the Patlak and Sokoloff methods, and our recently proposed four-compartment model. Methodology/Principal Findings Eleven sheep underwent unilateral lung lavage and 4 h mechanical ventilation. Five sheep received intravenous endotoxin (10 ng/kg/min). Dynamic \(^{18}F-FDG\) PET was performed at the end of the 4 h period. \(^{18}F-FDG\) net uptake rate (Ki), phosphorylation rate (k3), and volume of distribution (Fe) were estimated in three isogravitational regions for each method. Simulations of normal and ALI \(^{18}F-FDG\)-kinetics were conducted to study the dependence of estimated parameters on the transport rate constants to (k5) and from (k6) the extra-vascular extra-cellular compartment. The four-compartment model described 85.7% of the studied \(^{18}F-FDG\)-kinetics better than the Sokoloff model. Relative to the four-compartment model the Sokoloff model exhibited a consistent positive bias in Ki (3.32 [1.30–5.65] 10−4/min, p<0.001) and showed inaccurate estimates of the parameters composing Ki (k3 and Fe), even when Ki was similar for those methods. In simulations, errors in estimates of Ki due to the extra-vascular extra-cellular compartment depended on both k5 and k5/k6, with errors for the Patlak and Sokoloff methods of 0.02 [−0.01–0.18] and 0.40 [0.18–0.60] 10−3/min for normal lungs and of −0.47 [−0.89–0.72] and 2.35 [0.85–3.68] 10−3/min in ALI. Conclusions/Significance: \(^{18}F-FDG\) accumulation in lung extra-vascular fluid, which is commonly increased during lung injury, can result in substantial estimation errors using the traditional Patlak and Sokoloff methods. These errors depend on the extra-vascular extra-cellular compartment volume and its transport rates with other compartments. The four-compartment model provides more accurate quantification of \(^{18}F-FDG\)-kinetics than those methods in the presence of increased extra-vascular fluid.Publication Ventilation Defect Formation in Healthy and Asthma Subjects Is Determined by Lung Inflation(Public Library of Science, 2012) Harris, Robert; Fujii-Rios, Hanae; Winkler, Tilo; Musch, Guido; Vidal Melo, Marcos; Venegas, JoseBackground: Imaging studies have demonstrated that ventilation during bronchoconstriction in subjects with asthma is patchy with large ventilation defective areas (Vdefs). Based on a theoretical model, we postulated that during bronchoconstriction, as smooth muscle force activation increases, a patchy distribution of ventilation should emerge, even in the presence of minimal heterogeneity the lung. We therefore theorized that in normal lungs, Vdefs should also emerge in regions of the lung with reduced expansion. Objective: We studied 12 healthy subjects to evaluate whether Vdefs formed during bronchoconstriction, and compared their Vdefs with those observed in 9 subjects with mild asthma. Methods: Spirometry, low frequency (0.15 Hz) lung elastance and resistance, and regional ventilation by intravenous \(^{13}\)NN-saline positron emission tomography were measured before and after a challenge with nebulized methacholine. Vdefs were defined as regions with elevated residual 13NN after a period of washout. The average location, ventilation, volume, and fractional gas content of the Vdefs, relative to those of the rest of the lung, were calculated for both groups. Results: Consistent with the predictions of the theoretical model, both healthy subjects and those with asthma developed Vdefs. These Vdefs tended to form in regions that, at baseline, had a lower degree of lung inflation and, in healthy subjects, tended to occur in more dependent locations than in subjects with asthma. Conclusion: The formation of Vdefs is determined by the state of inflation prior to bronchoconstriction.