Browsing by Author "Carpio Cordero, David Bernardo"

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    Determinación del nivel de PEEP óptima calculado de acuerdo con mecánica respiratoria y al desempeño cardiovascular en pacientes con síndrome de distres respiratorio agudo, mediante el análisis de la variación cíclica de la impedancia torácica medida por tomografía de impedancia eléctrica
    (2024) Carpio Cordero, David Bernardo; Retamal Montes, Jaime; Hurtado Sepúlveda, Daniel; Pontificia Universidad Católica de Chile. Escuela de Medicina
    La presión positiva al final de la espiración (PEEP) es un componente clave en las estrategias de ventilación mecánica protectora para pacientes con síndrome de distrés respiratorio agudo. Su uso adecuado está relacionado con la mejora de la oxigenación y la mecánica pulmonar, ya que previene el colapso de los alvéolos inestables, optimiza el reclutamiento alveolar y reduce el estrés cíclico, minimizando la apertura y colapso repetitivo de los alvéolos. La determinación del nivel óptimo de la PEEP se realiza mediante una maniobra de reclutamiento alveolar la cual consiste en aumentar progresivamente la presión total en las vías aéreas hasta lograr la apertura de la mayoría de los alvéolos colapsados. Posterior a ello, se reduce gradualmente la PEEP, seleccionando el nivel que esté asociado con la mejor distensibilidad del sistema respiratorio. No obstante, esta maniobra, al generar aumentos supranormales de la presión intratorácica, puede inducir un deterioro hemodinámico, manifestándose como disfunción ventricular derecha y asociarse a un peor pronóstico en pacientes críticos. Nuestro estudio se centró en la monitorización no invasiva de variables hemodinámicas y respiratorias durante una maniobra de reclutamiento alveolar en pacientes con distrés respiratorio agudo, utilizando termodilución transpulmonar para medir el volumen sistólico y tomografía de impedancia eléctrica para evaluar la impedancia pulsátil torácica. 13 Como resultado la maniobra de reclutamiento alveolar produjo cambios cardiopulmonares esperados como cambios en la función cardiaca (GC – GEF), mejoría del intercambio gaseoso (SpO2, SaO2/FiO2), disminución del mismatch pulmonar (QS/QT), homogenización de la ventilación (GI-IR) y optimización de la mecánica pulmonar (DP CRS). Mostró una correlación débil entre la variación de la impedancia pulsátil pulmonar y el volumen sistólico. No obstante, esta correlación mejoró en pacientes con IMC < 30. En conclusión, la metodología demostró ser factible y permitió la observación de los efectos fisiológicos esperados de la interacción cardiopulmonar. Además, se evidenció la viabilidad de evaluar cambios regionales en la relación ventilación-perfusión, subrayando la importancia de ajustar la monitorización hemodinámica según la composición corporal en futuras investigaciones.
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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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    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.