Browsing by Author "Damiani Rebolledo, L. Felipe"
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- ItemAutomated detection and quantification of reverse triggering effort under mechanical ventilation(2021) Pham, Tài; Montanya, Jaume; Telias, Irene; Piraino, Thomas; Magrans, Rudys; Coudroy, Rémi; Damiani Rebolledo, L. Felipe; Mellado Artigas, Ricard; Madorno, Matías; Blanch, LluisAbstract Background Reverse triggering (RT) is a dyssynchrony defined by a respiratory muscle contraction following a passive mechanical insufflation. It is potentially harmful for the lung and the diaphragm, but its detection is challenging. Magnitude of effort generated by RT is currently unknown. Our objective was to validate supervised methods for automatic detection of RT using only airway pressure (Paw) and flow. A secondary objective was to describe the magnitude of the efforts generated during RT. Methods We developed algorithms for detection of RT using Paw and flow waveforms. Experts having Paw, flow and esophageal pressure (Pes) assessed automatic detection accuracy by comparison against visual assessment. Muscular pressure (Pmus) was measured from Pes during RT, triggered breaths and ineffective efforts. Results Tracings from 20 hypoxemic patients were used (mean age 65 ± 12 years, 65% male, ICU survival 75%). RT was present in 24% of the breaths ranging from 0 (patients paralyzed or in pressure support ventilation) to 93.3%. Automatic detection accuracy was 95.5%: sensitivity 83.1%, specificity 99.4%, positive predictive value 97.6%, negative predictive value 95.0% and kappa index of 0.87. Pmus of RT ranged from 1.3 to 36.8 cmH20, with a median of 8.7 cmH20. RT with breath stacking had the highest levels of Pmus, and RTs with no breath stacking were of similar magnitude than pressure support breaths. Conclusion An automated detection tool using airway pressure and flow can diagnose reverse triggering with excellent accuracy. RT generates a median Pmus of 9 cmH2O with important variability between and within patients. Trial registration BEARDS, NCT03447288.
- ItemDuration of diaphragmatic inactivity after endotracheal intubation of critically ill patients(2021) Sklar, Michael Chaim; Damiani Rebolledo, L. Felipe; Madotto, Fabiana; Jonkman, Annemijn; Rauseo, Michela; Soliman, Ibrahim; Telias, Irene; Dubo, Sebastian; Chen, Lu; Rittayamai, NuttapolAbstract Background In patients intubated for mechanical ventilation, prolonged diaphragm inactivity could lead to weakness and poor outcome. Time to resume a minimal diaphragm activity may be related to sedation practice and patient severity. Methods Prospective observational study in critically ill patients. Diaphragm electrical activity (EAdi) was continuously recorded after intubation looking for resumption of a minimal level of diaphragm activity (beginning of the first 24 h period with median EAdi > 7 µV, a threshold based on literature and correlations with diaphragm thickening fraction). Recordings were collected until full spontaneous breathing, extubation, death or 120 h. A 1 h waveform recording was collected daily to identify reverse triggering. Results Seventy-five patients were enrolled and 69 analyzed (mean age ± standard deviation 63 ± 16 years). Reasons for ventilation were respiratory (55%), hemodynamic (19%) and neurologic (20%). Eight catheter disconnections occurred. The median time for resumption of EAdi was 22 h (interquartile range 0–50 h); 35/69 (51%) of patients resumed activity within 24 h while 4 had no recovery after 5 days. Late recovery was associated with use of sedative agents, cumulative doses of propofol and fentanyl, controlled ventilation and age (older patients receiving less sedation). Severity of illness, oxygenation, renal and hepatic function, reason for intubation were not associated with EAdi resumption. At least 20% of patients initiated EAdi with reverse triggering. Conclusion Low levels of diaphragm electrical activity are common in the early course of mechanical ventilation: 50% of patients do not recover diaphragmatic activity within one day. Sedatives are the main factors accounting for this delay independently from lung or general severity. Trial Registration ClinicalTrials.gov (NCT02434016). Registered on April 27, 2015. First patients enrolled June 2015.
- ItemEccentric Contractions of the Diaphragm During Mechanical Ventilation(2023) García Valdés, Patricio Hernán; Fernandez Mincone, Tiziana Rita; Jalil Contreras, Yorschua Frederick; Peñailillo, Luis; Damiani Rebolledo, L. FelipeDiaphragm dysfunction is a highly prevalent phenomenon in patients receiving mechanical ventilation, mainly due to ventilatory over-assistance and the development of diaphragm disuse atrophy. Promoting diaphragm activation whenever possible and facilitating an adequate interaction between the patient and the ventilator is encouraged at the bedside to avoid myotrauma and further lung injury. Eccentric contractions of the diaphragm are defined as muscle activation while muscle fibers are lengthening within the exhalation phase. There is recent evidence that suggests that eccentric activation of the diaphragm is very frequent and may occur during post-inspiratory activity or under different types of patient-ventilator asynchronies, which include ineffective efforts, premature cycling, and reverse triggering. The consequences of this eccentric contraction of the diaphragm may have opposite effects, depending on the level of breathing effort. For instance, during high or excessive effort, eccentric contractions can result in diaphragm dysfunction and injured muscle fibers. Conversely, when eccentric contractions of the diaphragm occur along with low breathing effort, a preserved diaphragm function, better oxygenation, and more aerated lung tissue are observed. Despite this controversial evidence, evaluating the level of breathing effort at the bedside seems crucial and is highly recommended to optimize ventilatory therapy. The impact of eccentric contractions of the diaphragm on the patient's outcome remains to be elucidated.
- 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.