Gattinoni, Luciano

[["dc.bibliographiccitation.firstpage","413"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Critical Care Clinics"],["dc.bibliographiccitation.lastpage","422"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Vasques, Francesco"],["dc.contributor.author","Duscio, Eleonora"],["dc.contributor.author","Cipulli, Francesco"],["dc.contributor.author","Romitti, Federica"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2020-12-10T14:22:56Z"],["dc.date.available","2020-12-10T14:22:56Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.ccc.2018.03.011"],["dc.identifier.issn","0749-0704"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71782"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Extracorporeal Gas Exchange"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","252"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Care Medicine"],["dc.bibliographiccitation.lastpage","264"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Chiumello, Davide"],["dc.contributor.author","Cressoni, Massimo"],["dc.contributor.author","Carlesso, Eleonora"],["dc.contributor.author","Caspani, Maria L."],["dc.contributor.author","Marino, Antonella"],["dc.contributor.author","Gallazzi, Elisabetta"],["dc.contributor.author","Caironi, Pietro"],["dc.contributor.author","Lazzerini, Marco"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2018-11-07T09:44:43Z"],["dc.date.available","2018-11-07T09:44:43Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective: Positive end-expiratory pressure exerts its effects keeping open at end-expiration previously collapsed areas of the lung; consequently, higher positive end-expiratory pressure should be limited to patients with high recruitability. We aimed to determine which bedside method would provide positive end-expiratory pressure better related to lung recruitability. Design: Prospective study performed between 2008 and 2011. Setting: Two university hospitals (Italy and Germany). Patients: Fifty-one patients with acute respiratory distress syndrome. Interventions: Whole lung CT scans were taken in static conditions at 5 and 45 cm H2O during an end-expiratory/end-inspiratory pause to measure lung recruitability. To select individual positive end-expiratory pressure, we applied bedside methods based on lung mechanics (ExPress, stress index), esophageal pressure, and oxygenation (higher positive end-expiratory pressure table of lung open ventilation study). Measurements and Main Results: Patients were classified in mild, moderate and severe acute respiratory distress syndrome. Positive end-expiratory pressure levels selected by the ExPress, stress index, and absolute esophageal pressures methods were unrelated with lung recruitability, whereas positive end-expiratory pressure levels selected by the lung open ventilation method showed a weak relationship with lung recruitability (r(2) = 0.29; p < 0.0001). When patients were classified according to the acute respiratory distress syndrome Berlin definition, the lung open ventilation method was the only one which gave lower positive end-expiratory pressure levels in mild and moderate acute respiratory distress syndrome compared with severe acute respiratory distress syndrome (8 2 and 11 +/- 3 cm H2O vs 15 +/- 3 cm H2O; p < 0.05), whereas ExPress, stress index, and esophageal pressure methods gave similar positive end-expiratory pressure values in mild, moderate, and severe acute respiratory distress syndrome. The positive end-expiratory pressure selected by the different methods were unrelated to each other with the exception of the two methods based on lung mechanics (ExPress and stress index). Conclusions: Bedside positive end-expiratory pressure selection methods based on lung mechanics or absolute esophageal pressures provide positive end-expiratory pressure levels unrelated to lung recruitability and similar in mild, moderate, and severe acute respiratory distress syndrome, whereas the oxygenation-based method provided positive end-expiratory pressure levels related with lung recruitability progressively increasing from mild to moderate and severe acute respiratory distress syndrome."],["dc.identifier.doi","10.1097/CCM.0b013e3182a6384f"],["dc.identifier.isi","000329863400020"],["dc.identifier.pmid","24196193"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34453"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1530-0293"],["dc.relation.issn","0090-3493"],["dc.title","Bedside Selection of Positive End-Expiratory Pressure in Mild, Moderate, and Severe Acute Respiratory Distress Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","76"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Intensive Care Medicine"],["dc.bibliographiccitation.lastpage","78"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Tonetti, Tommaso"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2020-12-10T14:08:46Z"],["dc.date.available","2020-12-10T14:08:46Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1007/s00134-017-4770-8"],["dc.identifier.eissn","1432-1238"],["dc.identifier.issn","0342-4642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70555"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Intensive care medicine in 2050: ventilator-induced lung injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","752"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Lancet Respiratory Medicine"],["dc.bibliographiccitation.lastpage","754"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Camporota, Luigi"],["dc.contributor.author","Vasques, Francesco"],["dc.contributor.author","Sanderson, Barnaby"],["dc.contributor.author","Barrett, Nicholas A"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2021-04-14T08:24:32Z"],["dc.date.available","2021-04-14T08:24:32Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/S2213-2600(20)30279-4"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81322"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","2213-2600"],["dc.title","Identification of pathophysiological patterns for triage and respiratory support in COVID-19"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","551"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Intensive Care Medicine"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Pesenti, Antonio"],["dc.contributor.author","Berra, Lorenzo"],["dc.contributor.author","Bartlett, Robert"],["dc.date.accessioned","2020-12-10T14:09:48Z"],["dc.date.available","2020-12-10T14:09:48Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00134-018-5162-4"],["dc.identifier.eissn","1432-1238"],["dc.identifier.issn","0342-4642"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70563"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ted Kolobow"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","86"],["dc.bibliographiccitation.journal","CRITICAL CARE"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2018-11-07T10:15:38Z"],["dc.date.available","2018-11-07T10:15:38Z"],["dc.date.issued","2016"],["dc.description.abstract","The Berlin definition criteria applied at positive end-expiratory pressure (PEEP) 5 cm H2O reasonably predict lung edema and recruitabilty. To maintain viable gas exchange, the mechanical ventilation becomes progressively more risky going from mild to severe acute respiratory distress syndrome (ARDS). Tidal volume, driving pressure, flow, and respiratory rate have been identified as causes of ventilation-induced lung injury. Taken together, they represent the mechanical power applied to the lung parenchyma. In an inhomogeneous lung, stress risers locally increase the applied mechanical power. Increasing lung homogeneity by PEEP and prone position decreases the harm of mechanical ventilation, particularly in severe ARDS."],["dc.identifier.doi","10.1186/s13054-016-1268-7"],["dc.identifier.isi","000373669800001"],["dc.identifier.pmid","27048605"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40846"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1364-8535"],["dc.relation.issn","1466-609X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","How ARDS should be treated"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","31"],["dc.bibliographiccitation.journal","European Journal of Internal Medicine"],["dc.bibliographiccitation.lastpage","33"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Busana, Mattia"],["dc.contributor.author","Camporota, Luigi"],["dc.date.accessioned","2022-04-01T10:02:24Z"],["dc.date.available","2022-04-01T10:02:24Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.ejim.2021.09.004"],["dc.identifier.pii","S0953620521003046"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105899"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.issn","0953-6205"],["dc.rights.uri","https://www.elsevier.com/tdm/userlicense/1.0/"],["dc.title","Standardised PaO2/FiO2 ratio in COVID-19: Added value or risky assumptions?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","464"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Applied Physiology"],["dc.bibliographiccitation.lastpage","473"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Langer, Thomas"],["dc.contributor.author","Brusatori, Serena"],["dc.contributor.author","Carlesso, Eleonora"],["dc.contributor.author","Zadek, Francesco"],["dc.contributor.author","Brambilla, Paolo"],["dc.contributor.author","Ferraris Fusarini, Chiara"],["dc.contributor.author","Duska, Frantisek"],["dc.contributor.author","Caironi, Pietro"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Fasano, Mauro"],["dc.contributor.author","Grasselli, Giacomo"],["dc.date.accessioned","2021-10-01T09:58:11Z"],["dc.date.available","2021-10-01T09:58:11Z"],["dc.date.issued","2021"],["dc.description.abstract","Patients with sepsis are poorly protected against acute respiratory acid-base derangements due to a lower noncarbonic buffer power, which is caused both by a reduction in the major noncarbonic buffers, i.e. hemoglobin and albumin, and by a reduced buffering capacity of albumin. Electrolyte shifts from and to the red blood cells determining acute variations in strong ion difference are the major buffering mechanism during acute respiratory acid-base disorders."],["dc.description.abstract","Patients with sepsis have typically reduced concentrations of hemoglobin and albumin, the major components of noncarbonic buffer power ( β). This could expose patients to high pH variations during acid-base disorders. The objective of this study is to compare, in vitro, noncarbonic β of patients with sepsis with that of healthy volunteers, and evaluate its distinct components. Whole blood and isolated plasma of 18 patients with sepsis and 18 controls were equilibrated with different CO 2 mixtures. Blood gases, pH, and electrolytes were measured. Noncarbonic β and noncarbonic β due to variations in strong ion difference ( β SID ) were calculated for whole blood. Noncarbonic β and noncarbonic β normalized for albumin concentrations ( β NORM ) were calculated for isolated plasma. Representative values at pH = 7.40 were compared. Albumin proteoforms were evaluated via two-dimensional electrophoresis. Hemoglobin and albumin concentrations were significantly lower in patients with sepsis. Patients with sepsis had lower noncarbonic β both of whole blood (22.0 ± 1.9 vs. 31.6 ± 2.1 mmol/L, P < 0.01) and plasma (0.5 ± 1.0 vs. 3.7 ± 0.8 mmol/L, P < 0.01). Noncarbonic β SID was lower in patients (16.8 ± 1.9 vs. 24.4 ± 1.9 mmol/L, P < 0.01) and strongly correlated with hemoglobin concentration ( r = 0.94, P < 0.01). Noncarbonic β NORM was lower in patients [0.01 (−0.01 to 0.04) vs. 0.08 (0.06–0.09) mmol/g, P < 0.01]. Patients with sepsis and controls showed different amounts of albumin proteoforms. Patients with sepsis are exposed to higher pH variations for any given change in CO 2 due to lower concentrations of noncarbonic buffers and, possibly, an altered buffering function of albumin. In both patients with sepsis and healthy controls, electrolyte shifts are the major buffering mechanism during respiratory acid-base disorders. NEW & NOTEWORTHY Patients with sepsis are poorly protected against acute respiratory acid-base derangements due to a lower noncarbonic buffer power, which is caused both by a reduction in the major noncarbonic buffers, i.e. hemoglobin and albumin, and by a reduced buffering capacity of albumin. Electrolyte shifts from and to the red blood cells determining acute variations in strong ion difference are the major buffering mechanism during acute respiratory acid-base disorders."],["dc.description.abstract","Patients with sepsis are poorly protected against acute respiratory acid-base derangements due to a lower noncarbonic buffer power, which is caused both by a reduction in the major noncarbonic buffers, i.e. hemoglobin and albumin, and by a reduced buffering capacity of albumin. Electrolyte shifts from and to the red blood cells determining acute variations in strong ion difference are the major buffering mechanism during acute respiratory acid-base disorders."],["dc.description.abstract","Patients with sepsis have typically reduced concentrations of hemoglobin and albumin, the major components of noncarbonic buffer power ( β). This could expose patients to high pH variations during acid-base disorders. The objective of this study is to compare, in vitro, noncarbonic β of patients with sepsis with that of healthy volunteers, and evaluate its distinct components. Whole blood and isolated plasma of 18 patients with sepsis and 18 controls were equilibrated with different CO 2 mixtures. Blood gases, pH, and electrolytes were measured. Noncarbonic β and noncarbonic β due to variations in strong ion difference ( β SID ) were calculated for whole blood. Noncarbonic β and noncarbonic β normalized for albumin concentrations ( β NORM ) were calculated for isolated plasma. Representative values at pH = 7.40 were compared. Albumin proteoforms were evaluated via two-dimensional electrophoresis. Hemoglobin and albumin concentrations were significantly lower in patients with sepsis. Patients with sepsis had lower noncarbonic β both of whole blood (22.0 ± 1.9 vs. 31.6 ± 2.1 mmol/L, P < 0.01) and plasma (0.5 ± 1.0 vs. 3.7 ± 0.8 mmol/L, P < 0.01). Noncarbonic β SID was lower in patients (16.8 ± 1.9 vs. 24.4 ± 1.9 mmol/L, P < 0.01) and strongly correlated with hemoglobin concentration ( r = 0.94, P < 0.01). Noncarbonic β NORM was lower in patients [0.01 (−0.01 to 0.04) vs. 0.08 (0.06–0.09) mmol/g, P < 0.01]. Patients with sepsis and controls showed different amounts of albumin proteoforms. Patients with sepsis are exposed to higher pH variations for any given change in CO 2 due to lower concentrations of noncarbonic buffers and, possibly, an altered buffering function of albumin. In both patients with sepsis and healthy controls, electrolyte shifts are the major buffering mechanism during respiratory acid-base disorders. NEW & NOTEWORTHY Patients with sepsis are poorly protected against acute respiratory acid-base derangements due to a lower noncarbonic buffer power, which is caused both by a reduction in the major noncarbonic buffers, i.e. hemoglobin and albumin, and by a reduced buffering capacity of albumin. Electrolyte shifts from and to the red blood cells determining acute variations in strong ion difference are the major buffering mechanism during acute respiratory acid-base disorders."],["dc.identifier.doi","10.1152/japplphysiol.00787.2020"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90006"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.relation.eissn","1522-1601"],["dc.relation.issn","8750-7587"],["dc.title","Low noncarbonic buffer power amplifies acute respiratory acid-base disorders in patients with sepsis: an in vitro study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","130"],["dc.bibliographiccitation.journal","CRITICAL CARE"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2018-11-07T10:14:17Z"],["dc.date.available","2018-11-07T10:14:17Z"],["dc.date.issued","2016"],["dc.description.abstract","Partial extracorporeal CO2 removal allows a decreasing tidal volume without respiratory acidosis in patients with acute respiratory distress syndrome. This, however, may be associated with worsening hypoxemia, due to several mechanisms, such as gravitational and reabsorption atelectasis, due to a decrease in mean airway pressure and a critically low ventilation-perfusion ratio, respectively. In addition, an imbalance between alveolar and artificial lung partial pressures of nitrogen may accelerate the process. Finally, the decrease in the respiratory quotient, leading to unrecognized alveolar hypoxia and monotonous low plateau pressures preventing critical opening, may contribute to hypoxemia."],["dc.identifier.doi","10.1186/s13054-016-1310-9"],["dc.identifier.isi","000375649100001"],["dc.identifier.pmid","27170273"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40594"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1364-8535"],["dc.relation.issn","1466-609X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Ultra-protective ventilation and hypoxemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2187"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Intensive Care Medicine"],["dc.bibliographiccitation.lastpage","2196"],["dc.bibliographiccitation.volume","46"],["dc.contributor.author","Chiumello, Davide"],["dc.contributor.author","Busana, Mattia"],["dc.contributor.author","Coppola, Silvia"],["dc.contributor.author","Romitti, Federica"],["dc.contributor.author","Formenti, Paolo"],["dc.contributor.author","Bonifazi, Matteo"],["dc.contributor.author","Pozzi, Tommaso"],["dc.contributor.author","Palumbo, Maria Michela"],["dc.contributor.author","Cressoni, Massimo"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Meissner, Konrad"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Camporota, Luigi"],["dc.contributor.author","Marini, John J."],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2021-04-14T08:32:14Z"],["dc.date.available","2021-04-14T08:32:14Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00134-020-06281-2"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83854"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-1238"],["dc.relation.issn","0342-4642"],["dc.title","Physiological and quantitative CT-scan characterization of COVID-19 and typical ARDS: a matched cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]