Browsing by Author "Bachmann Barrón, María Consuelo"

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    Effect of decreasing respiratory rate on the mechanical power of ventilation and lung injury biomarkers: a randomized cross-over clinical study in COVID-19 ARDS patients
    (Springer Nature, 2025) Damiani Rebolledo, L. Felipe; Basoalto Escobar, Roque Ignacio; Oviedo Álvarez, Vanessa Andrea; Alegría Vargas, Leyla; Soto Muñoz, Dagoberto Igor; Bachmann Barrón, María Consuelo; Jalil Contreras, Yorschua Frederick; Santis Fuentes, César Antonio; Carpio Cordero, David Bernardo; Ulloa Morrison, Rodrigo; Valenzuela Espinoza, Emilio Daniel; Vera Alarcón, María Magdalena; Schultz, Marcus J.; Retamal Montes, Jaime; Bruhn, Alejandro; Bugedo Tarraza, Guillermo
    Background The respiratory rate (RR) is a key determinant of the mechanical power of ventilation (MP). The effect of reducing the RR on MP and its potential to mitigate ventilator-induced lung injury remains unclear. Objectives To compare invasive ventilation using a lower versus a higher RR with respect to MP and plasma biomarkers of lung injury in COVID-19 ARDS patients. Methods In a randomized cross-over clinical study in COVID-19 ARDS patients, we compared ventilation using a lower versus a higher RR in time blocks of 12 h. Patients were ventilated with tidal volumes of 6 ml/kg predicted body weight, and positive-end-expiratory pressure and fraction of inspired oxygen according to an ARDS network table. Respiratory mechanics and hemodynamics were assessed at the end of each period, and blood samples were drawn for measurements of inflammatory cytokines, epithelial and endothelial lung injury markers. In a subgroup of patients, we performed echocardiography and esophageal pressure measurements. Results We enrolled a total of 32 patients (26 males [81%], aged 52 [44–64] years). The median respiratory rate during ventilation with a lower and a higher RR was 20 [16–22] vs. 30 [26–32] breaths/min (p < 0.001), associated with a lower median minute ventilation (7.3 [6.5–8.5] vs. 11.6 [10–13] L/min [p < 0.001]) and a lower median MP (15 [11–18] vs. 25 [21–32] J/min [p < 0.001]). No differences were observed in any inflammatory (IL-6, IL-8, and TNF-R1), epithelial (s-RAGE and SP-D), endothelial (Angiopoietin-2), or pro-fibrotic activity (TGF-ß) marker between high or low RR. Cardiac function by echocardiography, and respiratory mechanics using esophageal pressure measurements were also not different. Conclusions Reducing the respiratory rate decreases mechanical power in COVID-19 ARDS patients but does not reduce plasma lung injury biomarkers levels in this cross-over study. Study registration This study is registered at clinicaltrials.gov (study identifier NCT04641897)
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    Impact of Awake Prone Positioning on Inspiratory Effort and Work of Breathing. A Physiological Study in Healthy Subjects
    (American Thoracic Society, 2022) Damiani Rebolledo, L. Felipe; Basoalto Escobar, Roque Ignacio; Bachmann Barrón, María Consuelo; Jalil Contreras, Yorschua Frederick; Acuña, V.; Díaz, G.; Mella, J.; García Valdés, Patricio Hernán; Moya Gallardo, Eduardo Sebastián; Villarroel, G.; Retamal Montes, Jaime; Bugedo Tarraza, Guillermo; Bruhn, Alejandro
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    Spontaneous 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, Jaime
    Vigorous 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.