Browsing by Author "Cornejo, Rodrigo"
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- ItemEstimation of changes in cyclic lung strain by electrical impedance tomography: Proof-of-concept study(2021) Cornejo, Rodrigo; Iturrieta, Pablo Cristián; Olegári, Tayran M. M.; Hurtado Sepúlveda, Daniel; Kajiyama, Carolina; Arellan, Daniel; Bruhn, Alejandro; Guiñez, Dannette; Cerda, María A.; Brito, Roberto; Gajardo, Abraham I. J.; Lazo, Marioli; López, Lorena; Morais, Caio C. A.; Gonzále, Sedric; Zavala, Miguel; Rojas, Verónica; Medel, Juan N.; Ramos, Cristóbal; Estuardo, Nivia
- ItemHigh-volume hemofiltration as salvage therapy in severe hyperdynamic septic shock(2006) Cornejo, Rodrigo; Downey Concha, Patricio; Castro López, Ricardo; Romero, Carlos; Regueira Heskia, Tomás Emilio; Vega Stieb, Jorge Enrique; Castillo Fuenzalida, Luis Benito; Andresen Hernández, Max Alfonso; Dougnac Labatut, Alberto; Bugedo Tarraza, Guillermo; Hernández Poblete, Glenn Wilson
- ItemImpact of emergency intubation on central venous oxygen saturation in critically ill patients: a multicenter observational study(2009) Hernández P., Glenn; Rovegno Echavarria, Maxiliano; Retamal Montes, Jaime; Aranguiz, Ignacio; Castro, Ricardo; Bruhn, Alejandro; Peña, Hector; Cornejo, Rodrigo; Navarro, Jose LuisAbstract Introduction Central venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2. Methods In this prospective multicenter observational study, we included 103 septic and non-septic patients with a central venous catheter in place and in whom emergency intubation was required. A common intubation protocol was used and we evaluated several parameters including ScvO2 before and 15 minutes after emergency intubation. Statistical analysis included chi-square test and t test. Results ScvO2 increased from 61.8 ± 12.6% to 68.9 ± 12.2%, with no difference between septic and non-septic patients. ScvO2 increased in 84 patients (81.6%) without correlation to changes in arterial oxygen saturation (SaO2). Seventy eight (75.7%) patients were intubated with ScvO2 less than 70% and 21 (26.9%) normalized the parameter after the intervention. Only patients with pre-intubation ScvO2 more than 70% failed to increase the parameter after intubation. Conclusions ScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.Abstract Introduction Central venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2. Methods In this prospective multicenter observational study, we included 103 septic and non-septic patients with a central venous catheter in place and in whom emergency intubation was required. A common intubation protocol was used and we evaluated several parameters including ScvO2 before and 15 minutes after emergency intubation. Statistical analysis included chi-square test and t test. Results ScvO2 increased from 61.8 ± 12.6% to 68.9 ± 12.2%, with no difference between septic and non-septic patients. ScvO2 increased in 84 patients (81.6%) without correlation to changes in arterial oxygen saturation (SaO2). Seventy eight (75.7%) patients were intubated with ScvO2 less than 70% and 21 (26.9%) normalized the parameter after the intervention. Only patients with pre-intubation ScvO2 more than 70% failed to increase the parameter after intubation. Conclusions ScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.Abstract Introduction Central venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2. Methods In this prospective multicenter observational study, we included 103 septic and non-septic patients with a central venous catheter in place and in whom emergency intubation was required. A common intubation protocol was used and we evaluated several parameters including ScvO2 before and 15 minutes after emergency intubation. Statistical analysis included chi-square test and t test. Results ScvO2 increased from 61.8 ± 12.6% to 68.9 ± 12.2%, with no difference between septic and non-septic patients. ScvO2 increased in 84 patients (81.6%) without correlation to changes in arterial oxygen saturation (SaO2). Seventy eight (75.7%) patients were intubated with ScvO2 less than 70% and 21 (26.9%) normalized the parameter after the intervention. Only patients with pre-intubation ScvO2 more than 70% failed to increase the parameter after intubation. Conclusions ScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.Abstract Introduction Central venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2. Methods In this prospective multicenter observational study, we included 103 septic and non-septic patients with a central venous catheter in place and in whom emergency intubation was required. A common intubation protocol was used and we evaluated several parameters including ScvO2 before and 15 minutes after emergency intubation. Statistical analysis included chi-square test and t test. Results ScvO2 increased from 61.8 ± 12.6% to 68.9 ± 12.2%, with no difference between septic and non-septic patients. ScvO2 increased in 84 patients (81.6%) without correlation to changes in arterial oxygen saturation (SaO2). Seventy eight (75.7%) patients were intubated with ScvO2 less than 70% and 21 (26.9%) normalized the parameter after the intervention. Only patients with pre-intubation ScvO2 more than 70% failed to increase the parameter after intubation. Conclusions ScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.
- ItemImplementation of a norepinephrine-based protocol for management of septic shock: a pilot feasibility study(2006) Hernández P., Glenn; Bruhn, Alejandro; Romero Patiño, Carlos; Larrondo Gálvez, Francisco Andrés; De la Fuente Sanhueza, René; Cornejo, Rodrigo; Castillo Fuenzalida, Luis Benito; Bugedo Tarraza, GuillermoBackground: The subject of the best vasopressor for hemodynamic management of septic shock (SS) is controversial. One of the difficulties in planning such studies is that physicians are reluctant to use one vasopressor exclusively, and there is considerable variation in practice. The aim of this study was to test the feasibility of implementing a single pressor-based algorithm (in this case, norepinephrine [NE]). Methods: A NE-based algorithm was applied prospectively to 100 consecutive SS patients. A formal training program was implemented before starting the protocol and applied to 72 physicians and nurses involved in intensive care unit (ICU) patient care. Compliance, protocol violations, probable adverse effects, and outcome were evaluated on a daily basis by an independent group of fellows and a research nurse. Results: In 100 patients, there were 7,139 hours of algorithm use. Only 13 protocol violations were observed, mostly in the timing of inotropic drugs. Senior staff physicians or busy night shifts accounted for most of these violations. ICU mortality was 33%, which is comparable to that predicted by Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores. Adverse events probably related to NE were not observed. Conclusions: The present algorithm, applied after a strict training program, obtained an overall good acceptance and compliance with very few protocol violations in more than 7,000 hours of use. Safety was demonstrated by a global mortality comparable to that predicted by severity scores and absence of specific drugrelated morbidity. The implementation of a single pressor-based algorithm for SS is feasible and safe.
- ItemLung Opening and Closing during Ventilation of Acute Respiratory Distress Syndrome(AMER THORACIC SOC, 2010) Caironi, Pietro; Cressoni, Massimo; Chiumello, Davide; Ranieri, Marco; Quintel, Michael; Russo, Sebastiano G.; Cornejo, Rodrigo; Bugedo, Guillermo; Carlesso, Eleonora; Russo, Riccarda; Caspani, Luisa; Gattinoni, LucianoRationale The effects of high positive end-expiratory pressure (PEEP) strictly depend on lung recruitability, which varies widely during acute respiratory distress syndrome (ARDS). Unfortunately, increasing PEEP may lead to opposing effects on two main factors potentially worsening the lung injury, that is, alveolar strain and intratidal opening and closing, being detrimental (increasing the former) or beneficial (decreasing the latter).
- ItemPhysiological effects of high-flow nasal cannula oxygen therapy after extubation: a randomized crossover study(2023) Basoalto Escobar, Roque Ignacio; Damiani Rebolledo, L. Felipe; Jalil, Yorschua; Bachmann, María Consuelo; Oviedo, Vanessa; Alegría Vargas, Leyla; Valenzuela, Emilio Daniel; Rovegno Echavarria, Maxiliano; Ruiz-Rudolph, Pablo; Cornejo, Rodrigo; Retamal Montes, Jaime; Bugedo Tarraza, Guillermo; Thille, Arnaud W.; Bruhn, AlejandroAbstract: Background: Prophylactic high-flow nasal cannula (HFNC) oxygen therapy can decrease the risk of extubation failure. It is frequently used in the postextubation phase alone or in combination with noninvasive ventilation. However, its physiological effects in this setting have not been thoroughly investigated. The aim of this study was to determine comprehensively the effects of HFNC applied after extubation on respiratory effort, diaphragm activity, gas exchange, ventilation distribution, and cardiovascular biomarkers. Methods: This was a prospective randomized crossover physiological study in critically ill patients comparing 1 h of HFNC versus 1 h of standard oxygen after extubation. The main inclusion criteria were mechanical ventilation for at least 48 h due to acute respiratory failure, and extubation after a successful spontaneous breathing trial (SBT). We measured respiratory effort through esophageal/transdiaphragmatic pressures, and diaphragm electrical activity (ΔEAdi). Lung volumes and ventilation distribution were estimated by electrical impedance tomography. Arterial and central venous blood gases were analyzed, as well as cardiac stress biomarkers. Results: We enrolled 22 patients (age 59 ± 17 years; 9 women) who had been intubated for 8 ± 6 days before extubation. Respiratory effort was significantly lower with HFNC than with standard oxygen therapy, as evidenced by esophageal pressure swings (5.3 [4.2–7.1] vs. 7.2 [5.6–10.3] cmH2O; p < 0.001), pressure–time product (85 [67–140] vs. 156 [114–238] cmH2O*s/min; p < 0.001) and ΔEAdi (10 [7–13] vs. 14 [9–16] µV; p = 0.022). In addition, HFNC induced increases in end-expiratory lung volume and PaO2/FiO2 ratio, decreases in respiratory rate and ventilatory ratio, while no changes were observed in systemic hemodynamics, Troponin T, or in amino-terminal pro-B-type natriuretic peptide. Conclusions: Prophylactic application of HFNC after extubation provides substantial respiratory support and unloads respiratory muscles.
- ItemRecomendaciones de la Sociedad Chilena de Medicina Intensiva para la prevención de tromboembolismo venoso en pacientes críticos médico-quirúrgicos adultos(2016) Figueroa, Gastón; Labarca, Eduardo; Cornejo, Rodrigo; Ruiz, Carolina; Sánchez, Juan Eduardo; Castro López, Ricardo; Huerta, Gustavo; Pedreros, César; Regueira Heskia, Tomás; Romero, Carlos
- ItemSpontaneous breathing promotes lung injury in an experimental model of alveolar collapse(2022) Bachmann, María Consuelo; Cruces, Pablo; Díaz, Franco; Oviedo, Vanessa; Goich, Mariela; Fuenzalida, José; Damiani Rebolledo, L. Felipe; Basoalto, Roque; Jalil, Yorschua F.; Carpio Cordero, David; Hamidi Vadeghani, Niki; Cornejo, Rodrigo; Rovegno Echavarria, Maximiliano; Bugedo Tarraza, Guillermo; Bruhn, Alejandro; Retamal Montes, JaimeVigorous spontaneous breathing has emerged as a promotor of lung damage in acute lung injury, an entity known as “patient self-inflicted lung injury”. Mechanical ventilation may prevent this second injury by decreasing intrathoracic pressure swings and improving regional air distribution. Therefore, we aimed to determine the effects of spontaneous breathing during the early stage of acute respiratory failure on lung injury and determine whether early and late controlled mechanical ventilation may avoid or revert these harmful effects. A model of partial surfactant depletion and lung collapse was induced in eighteen intubated pigs of 32 ±4 kg. Then, animals were randomized to (1) SB‐group: spontaneous breathing with very low levels of pressure support for the whole experiment (eight hours), (2) Early MV-group: controlled mechanical ventilation for eight hours, or (3) Late MV-group: first half of the experiment on spontaneous breathing (four hours) and the second half on controlled mechanical ventilation (four hours). Respiratory, hemodynamic, and electric impedance tomography data were collected. After the protocol, animals were euthanized, and lungs were extracted for histologic tissue analysis and cytokines quantification. SB-group presented larger esophageal pressure swings, progressive hypoxemia, lung injury, and more dorsal and inhomogeneous ventilation compared to the early MV-group. In the late MV-group switch to controlled mechanical ventilation improved the lung inhomogeneity and esophageal pressure swings but failed to prevent hypoxemia and lung injury. In a lung collapse model, spontaneous breathing is associated to large esophageal pressure swings and lung inhomogeneity, resulting in progressive hypoxemia and lung injury. Mechanical ventilation prevents these mechanisms of patient self-inflicted lung injury if applied early, before spontaneous breathing occurs, but not when applied late.
- ItemSpontaneous breathing promotes lung injury in an experimental model of alveolar collapse(2022) Bachmann Barrón, María Consuelo; Cruces, Pablo; Díaz, Franco; Orellana Oviedo, Vanessa Ivonne; Goich, Mariela; Fuenzalida, José; Damiani Rebolledo, L. Felipe; Basoalto Escobar, Roque Ignacio; Jalil Contreras, Yorschua Frederick; Carpio Cordero, David Bernardo; Hamidi Vadeghani, Majd Niki; Cornejo, Rodrigo; Rovegno Echavarria, David Maximiliano; Bugedo Tarraza, Guillermo; Bruhn Cruz, Alejandro; Retamal Montes, JaimeVigorous spontaneous breathing has emerged as a promotor of lung damage in acute lung injury, an entity known as “patient self-inflicted lung injury”. Mechanical ventilation may prevent this second injury by decreasing intrathoracic pressure swings and improving regional air distribution. Therefore, we aimed to determine the effects of spontaneous breathing during the early stage of acute respiratory failure on lung injury and determine whether early and late controlled mechanical ventilation may avoid or revert these harmful effects. A model of partial surfactant depletion and lung collapse was induced in eighteen intubated pigs of 32 ±4 kg. Then, animals were randomized to (1) SB‐group: spontaneous breathing with very low levels of pressure support for the whole experiment (eight hours), (2) Early MV-group: controlled mechanical ventilation for eight hours, or (3) Late MV-group: first half of the experiment on spontaneous breathing (four hours) and the second half on controlled mechanical ventilation (four hours). Respiratory, hemodynamic, and electric impedance tomography data were collected. After the protocol, animals were euthanized, and lungs were extracted for histologic tissue analysis and cytokines quantification. SB-group presented larger esophageal pressure swings, progressive hypoxemia, lung injury, and more dorsal and inhomogeneous ventilation compared to the early MV-group. In the late MV-group switch to controlled mechanical ventilation improved the lung inhomogeneity and esophageal pressure swings but failed to prevent hypoxemia and lung injury. In a lung collapse model, spontaneous breathing is associated to large esophageal pressure swings and lung inhomogeneity, resulting in progressive hypoxemia and lung injury. Mechanical ventilation prevents these mechanisms of patient self-inflicted lung injury if applied early, before spontaneous breathing occurs, but not when applied late.