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.
- ItemEffect of a lung rest strategy during ECMO in a porcine acute lung injury model(2015) Araos, J.; Tapia, Pablo; Alegría, Leyla; García Cañete, Patricia; Rodríguez, F.; Amthauer, M.; Castro, G.; Soto, Dagoberto; Damiani Rebolledo, L. Felipe; Bugedo Tarraza, Guillermo; Bruhn, Alejandro; Cruces, Pablo; Salomon, Tatiana; Erranz, B.; Carreño, P.; Medina, T.
- ItemExtracorporeal membrane oxygenation improves survival in a novel 24-hour pig model of severe acute respiratory distress syndrome(2016) Araos, J.; Alegría Aguirre, Luz Katiushka; Garcia, P.; Damiani Rebolledo, L. Felipe; Tapia, P.; Soto, D.; Salomon, T.; Retamal Montes, Jaime; Bugedo Tarraza, Guillermo; Bruhn, Alejandro; Rodriguez, F.; Amthauer, M.; Erranz, B.; Castro, G.; Carreno, P.; Medina, T.; Cruces, P.
- ItemGeographic latitude and sleep duration: A population-based survey from the Tropic of Capricorn to the Antarctic Circle(2017) Brockmann Veloso, Pablo Edmundo; Gozal, D.; Villarroel del Pino, Luis A.; Damiani Rebolledo, L. Felipe; Nunez, F.; Cajochen, C.
- ItemImpact of a Noninvasive Ventilation Protocol in Hospitalized Children With Acute Respiratory Failure(2017) Jalil, Y.; Damiani Rebolledo, L. Felipe; Astudillo, C.; Villarroel S, G.; Barañao Garcés, Patricio; Bustos, E.; Silva, A.; Méndez Lesser, Manuel
- ItemImpact of television on the quality of sleep in preschool children(2016) Brockmann Veloso, Pablo Edmundo; Diaz, B.; Damiani Rebolledo, L. Felipe; Villarroel del Pino, Luis A.; Nuñez, F.; Bruni, O.
- ItemLong-term effects of adenotonsillectomy in children with obstructive sleep apnoea : protocol for a systematic review(2016) Damiani Rebolledo, L. Felipe; Rada G., Gabriel; Gana Ansaldo, Juan Cristóbal; Brockmann Veloso, Pablo Edmundo; Alberti, Gigliola
- ItemLow Spontaneous Breathing Effort during Extracorporeal Membrane Oxygenation in a Porcine Model of Severe Acute Respiratory Distress Syndrome(2020) Dubo, S.; Oviedo, V.; Garcia, A.; Alegría Aguirre, Luz Katiushka; Garcia, P.; Valenzuela, E. D.; Damiani Rebolledo, L. Felipe; Araos, J.; Medina, T.; Retamal Montes, Jaime; Bachmann, M. C.; Basoalto, R.; Bravo, S.; Soto, D.; Cruces, P.; Guzman, P.; Cornejo, R.; Bugedo Tarraza, Guillermo; Brebi, P.; Bruhn, Alejandro
- ItemMechanical Power of Ventilation: From Computer to Clinical Implications(2023) Damiani Rebolledo, L. Felipe; Basoalto Escobar, Roque Ignacio; Retamal Montes, Jaime Alejandro; Bruhn Cruz, Alejandro Rodrigo; Bugedo Tarraza, Guillermo JaimeMechanical ventilation is a lifesaving intervention that may also induce further lung injury by exerting excessive mechanical forces on susceptible lung tissue, a phenomenon termed ventilator-induced lung injury (VILI). The concept of mechanical power (MP) aims to unify in one single variable the contribution of the different ventilatory parameters that could induce VILI by measuring the energy transfer to the lung over time. Despite an increasing amount of evidence demonstrating that high MP values can be associated with VILI development in experimental studies, the evidence regarding the association of MP and clinical outcomes remains controversial. In the present review, we describe the different determinants of VILI, the concept and computation of MP, and discuss the experimental and clinical studies related to MP. Currently, due to different limitations, the clinical application of MP is debatable. Further clinical studies are required to enhance our understanding of the relationship between MP and the development of VILI, as well as its potential impact on clinical outcomes.
- ItemMetabolic consequences of snoring in adolescents and younger adults : a population study in Chile(2016) Brockmann Veloso, Pablo Edmundo; Damiani Rebolledo, L. Felipe; Smith, D.; Castet, A.; Nunez, F.; Villarroel del Pino, Luis A.; Gozal, D.
- ItemNear-apneic ventilation decreases lung injury and fibroproliferation in an acute respiratory distress syndrome model with extracorporeal membrane oxygenation(2019) Araos, J.; Alegría Aguirre, Luz Katiushka; Garcia, P.; Cruces, P.; Soto, D.; Erranz, B.; Amthauer, M.; Ayala, Pedro; Borzone, Gisella; Damiani Rebolledo, L. Felipe
- 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.
- ItemReverse triggering dyssynchrony and its impact on diaphragm injury during mechanical ventilation.(2020) Damiani Rebolledo, L. Felipe; Bruhn, Alejandro; Brochard, Laurent; Pontificia Universidad Católica de Chile. Escuela de MedicinaMechanical ventilation (MV) is used to sustain life in patients admitted to the intensive care unit for a wide spectrum of indications such as elective surgical procedures, septic shock, multiple organic failure and acute respiratory distress syndrome. Safe and effective ventilation depends on a smooth interaction between these two independent systems: the patient and the mechanical ventilator. Any mismatch between the patient and mechanical ventilator in terms of breath delivery timing, as well as the inability of the ventilator’s flow delivery to match the patient’s flow demand, is referred to as patient-ventilator dyssynchrony (PVD). Reverse Triggering (RT) is a type of PVD where muscle contractions are delayed, starting a certain amount of time after the machine triggered breath and occurring under different entrainment patterns. RT was originally described in 2013, in sedated patients admitted to the intensive care unit. Unfortunately, data about RT until now is scarce and its relevance remains totally uncertain. If any, the relevance of RT might be attributed to 2 main factors: the frequency of this PVD and its potential consequences in both lung and diaphragm injury. The group of different adverse patient–ventilator interactions leading to diaphragm atrophy and injury and resulting in a final common pathway of diaphragm weakness are denominated myotrauma. Particularly, RT is thought to cause eccentric myotrauma, which is a muscle contraction while muscle is lengthening during the ventilator’s expiratory phase while lung volume is decreasing. Based on animal and human studies, the impact of RT (if any) might be mediated by the level of breathing effort. In this thesis we aimed to describe the incidence of RT in patients early after intubation and admission to the intensive care unit and also to study the impact of RT with different levels of breathing effort on diaphragm injury (function and structure) in an animal model of RT with acute respiratory distress syndrome. To determine RT incidence, we conducted ancillary study in patients with continuous monitorization of the electrical activity of the diaphragm (EAdi). We developed a method for automatic detection of reverse triggering using EAdi and airway pressure curve. We additionally compared patients’ demographics, sedation depth and ventilation settings according to the median rate of reverse triggering, including time to transition to assisted ventilation or extubation. We found that our new automatic method presented a good diagnostic accuracy (98% total accuracy). Using a threshold of 1 µV for EAdi, median reverse triggering rate was 8% (range 0.1 to 75) with 44% (17 out of 39) of patients having ≥10% of breaths with reverse triggering. With 3 µV threshold, 26% (10 out of 39) of patients had ≥10% reverse triggered breaths. Importantly, patients who resented more reverse triggering were more likely to be on an assisted mode or extubated in the following 24 hours than patients who had low rate of RT (68% vs 35%; p=0.039). We also developed a 3 hours model of reverse triggering in pigs by modifying tidal volume, respiratory rate and level of sedation. Our approach to induce reverse triggering was not only feasible, but consistently reproducible in all animals, although with different presentations in terms of breathing effort and entrainment pattern. The most frequent entrainment pattern observed was 1:1, occurring in 83% of the total animals. Compared to passive ventilation (no breathing effort), RT group had significantly lower tidal volume (7 vs 10 ml/kg) and higher respiratory rate (45 vs 31 bpm) whereas no differences were found in other cardiorespiratory and sedation variables, nor in lung injury indicators after the study period. In order to study the impact of RT on diaphragm injury, we divided the RT group in 3 subgroups based on the level of breathing effort calculated by the pressure time product. Thus, 4 experimental groups were analyzed: Passive (no breathing effort), RT with low effort, RT with middle effort and RT with high effort. Function of the diaphragm was assessed by the ability to generate force, which correspond to the transdiaphragmatic pressure whilst diaphragm structure was evaluated using histological samples and serum troponin I as biomarker of muscle injury. We found that RT affects diaphragm function in two opposite directions. On one hand, animals with RT and low breathing effort showed a significant increase in force of 10% as compared to baseline. On the other hand, animals with RT and high breathing effort showed a larger decrease in force (34%) as compared to baseline. This difference was significantly different with the other experimental groups. Moreover, histologic analysis of diaphragm myofibers showed that RT with high breathing effort had significant lower myofiber cross-sectional area than passive group. Also, when comparing abnormal myofibers between groups, a significantly lower proportion of small fiber size were found in RT whit high breathing effort in comparison to passive group. No differences were found in serum troponin I neither overtime nor between groups. In conclusion, an EAdi-based automated reverse triggering detection showed that this asynchrony is highly prevalent early after intubation under assist-control ventilation; the incidence depends on the magnitude of the activity detected and that reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering. In addition, the creation of a reverse triggering model revealed this phenomenon very complex, with high variability in terms of entrainment pattern and level of breathing effort. Finally, we have confirmed that RT dyssynchrony affects diaphragm function and this effect is modulated by the level of respiratory effort. Reverse triggering with low breathing effort seems to have a protective role on diaphragm function whereas reverse triggering with high breathing effort may favor eccentric myotrauma.Mechanical ventilation (MV) is used to sustain life in patients admitted to the intensive care unit for a wide spectrum of indications such as elective surgical procedures, septic shock, multiple organic failure and acute respiratory distress syndrome. Safe and effective ventilation depends on a smooth interaction between these two independent systems: the patient and the mechanical ventilator. Any mismatch between the patient and mechanical ventilator in terms of breath delivery timing, as well as the inability of the ventilator’s flow delivery to match the patient’s flow demand, is referred to as patient-ventilator dyssynchrony (PVD). Reverse Triggering (RT) is a type of PVD where muscle contractions are delayed, starting a certain amount of time after the machine triggered breath and occurring under different entrainment patterns. RT was originally described in 2013, in sedated patients admitted to the intensive care unit. Unfortunately, data about RT until now is scarce and its relevance remains totally uncertain. If any, the relevance of RT might be attributed to 2 main factors: the frequency of this PVD and its potential consequences in both lung and diaphragm injury. The group of different adverse patient–ventilator interactions leading to diaphragm atrophy and injury and resulting in a final common pathway of diaphragm weakness are denominated myotrauma. Particularly, RT is thought to cause eccentric myotrauma, which is a muscle contraction while muscle is lengthening during the ventilator’s expiratory phase while lung volume is decreasing. Based on animal and human studies, the impact of RT (if any) might be mediated by the level of breathing effort. In this thesis we aimed to describe the incidence of RT in patients early after intubation and admission to the intensive care unit and also to study the impact of RT with different levels of breathing effort on diaphragm injury (function and structure) in an animal model of RT with acute respiratory distress syndrome. To determine RT incidence, we conducted ancillary study in patients with continuous monitorization of the electrical activity of the diaphragm (EAdi). We developed a method for automatic detection of reverse triggering using EAdi and airway pressure curve. We additionally compared patients’ demographics, sedation depth and ventilation settings according to the median rate of reverse triggering, including time to transition to assisted ventilation or extubation. We found that our new automatic method presented a good diagnostic accuracy (98% total accuracy). Using a threshold of 1 µV for EAdi, median reverse triggering rate was 8% (range 0.1 to 75) with 44% (17 out of 39) of patients having ≥10% of breaths with reverse triggering. With 3 µV threshold, 26% (10 out of 39) of patients had ≥10% reverse triggered breaths. Importantly, patients who resented more reverse triggering were more likely to be on an assisted mode or extubated in the following 24 hours than patients who had low rate of RT (68% vs 35%; p=0.039). We also developed a 3 hours model of reverse triggering in pigs by modifying tidal volume, respiratory rate and level of sedation. Our approach to induce reverse triggering was not only feasible, but consistently reproducible in all animals, although with different presentations in terms of breathing effort and entrainment pattern. The most frequent entrainment pattern observed was 1:1, occurring in 83% of the total animals. Compared to passive ventilation (no breathing effort), RT group had significantly lower tidal volume (7 vs 10 ml/kg) and higher respiratory rate (45 vs 31 bpm) whereas no differences were found in other cardiorespiratory and sedation variables, nor in lung injury indicators after the study period. In order to study the impact of RT on diaphragm injury, we divided the RT group in 3 subgroups based on the level of breathing effort calculated by the pressure time product. Thus, 4 experimental groups were analyzed: Passive (no breathing effort), RT with low effort, RT with middle effort and RT with high effort. Function of the diaphragm was assessed by the ability to generate force, which correspond to the transdiaphragmatic pressure whilst diaphragm structure was evaluated using histological samples and serum troponin I as biomarker of muscle injury. We found that RT affects diaphragm function in two opposite directions. On one hand, animals with RT and low breathing effort showed a significant increase in force of 10% as compared to baseline. On the other hand, animals with RT and high breathing effort showed a larger decrease in force (34%) as compared to baseline. This difference was significantly different with the other experimental groups. Moreover, histologic analysis of diaphragm myofibers showed that RT with high breathing effort had significant lower myofiber cross-sectional area than passive group. Also, when comparing abnormal myofibers between groups, a significantly lower proportion of small fiber size were found in RT whit high breathing effort in comparison to passive group. No differences were found in serum troponin I neither overtime nor between groups. In conclusion, an EAdi-based automated reverse triggering detection showed that this asynchrony is highly prevalent early after intubation under assist-control ventilation; the incidence depends on the magnitude of the activity detected and that reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering. In addition, the creation of a reverse triggering model revealed this phenomenon very complex, with high variability in terms of entrainment pattern and level of breathing effort. Finally, we have confirmed that RT dyssynchrony affects diaphragm function and this effect is modulated by the level of respiratory effort. Reverse triggering with low breathing effort seems to have a protective role on diaphragm function whereas reverse triggering with high breathing effort may favor eccentric myotrauma.Mechanical ventilation (MV) is used to sustain life in patients admitted to the intensive care unit for a wide spectrum of indications such as elective surgical procedures, septic shock, multiple organic failure and acute respiratory distress syndrome. Safe and effective ventilation depends on a smooth interaction between these two independent systems: the patient and the mechanical ventilator. Any mismatch between the patient and mechanical ventilator in terms of breath delivery timing, as well as the inability of the ventilator’s flow delivery to match the patient’s flow demand, is referred to as patient-ventilator dyssynchrony (PVD). Reverse Triggering (RT) is a type of PVD where muscle contractions are delayed, starting a certain amount of time after the machine triggered breath and occurring under different entrainment patterns. RT was originally described in 2013, in sedated patients admitted to the intensive care unit. Unfortunately, data about RT until now is scarce and its relevance remains totally uncertain. If any, the relevance of RT might be attributed to 2 main factors: the frequency of this PVD and its potential consequences in both lung and diaphragm injury. The group of different adverse patient–ventilator interactions leading to diaphragm atrophy and injury and resulting in a final common pathway of diaphragm weakness are denominated myotrauma. Particularly, RT is thought to cause eccentric myotrauma, which is a muscle contraction while muscle is lengthening during the ventilator’s expiratory phase while lung volume is decreasing. Based on animal and human studies, the impact of RT (if any) might be mediated by the level of breathing effort. In this thesis we aimed to describe the incidence of RT in patients early after intubation and admission to the intensive care unit and also to study the impact of RT with different levels of breathing effort on diaphragm injury (function and structure) in an animal model of RT with acute respiratory distress syndrome. To determine RT incidence, we conducted ancillary study in patients with continuous monitorization of the electrical activity of the diaphragm (EAdi). We developed a method for automatic detection of reverse triggering using EAdi and airway pressure curve. We additionally compared patients’ demographics, sedation depth and ventilation settings according to the median rate of reverse triggering, including time to transition to assisted ventilation or extubation. We found that our new automatic method presented a good diagnostic accuracy (98% total accuracy). Using a threshold of 1 µV for EAdi, median reverse triggering rate was 8% (range 0.1 to 75) with 44% (17 out of 39) of patients having ≥10% of breaths with reverse triggering. With 3 µV threshold, 26% (10 out of 39) of patients had ≥10% reverse triggered breaths. Importantly, patients who resented more reverse triggering were more likely to be on an assisted mode or extubated in the following 24 hours than patients who had low rate of RT (68% vs 35%; p=0.039). We also developed a 3 hours model of reverse triggering in pigs by modifying tidal volume, respiratory rate and level of sedation. Our approach to induce reverse triggering was not only feasible, but consistently reproducible in all animals, although with different presentations in terms of breathing effort and entrainment pattern. The most frequent entrainment pattern observed was 1:1, occurring in 83% of the total animals. Compared to passive ventilation (no breathing effort), RT group had significantly lower tidal volume (7 vs 10 ml/kg) and higher respiratory rate (45 vs 31 bpm) whereas no differences were found in other cardiorespiratory and sedation variables, nor in lung injury indicators after the study period. In order to study the impact of RT on diaphragm injury, we divided the RT group in 3 subgroups based on the level of breathing effort calculated by the pressure time product. Thus, 4 experimental groups were analyzed: Passive (no breathing effort), RT with low effort, RT with middle effort and RT with high effort. Function of the diaphragm was assessed by the ability to generate force, which correspond to the transdiaphragmatic pressure whilst diaphragm structure was evaluated using histological samples and serum troponin I as biomarker of muscle injury. We found that RT affects diaphragm function in two opposite directions. On one hand, animals with RT and low breathing effort showed a significant increase in force of 10% as compared to baseline. On the other hand, animals with RT and high breathing effort showed a larger decrease in force (34%) as compared to baseline. This difference was significantly different with the other experimental groups. Moreover, histologic analysis of diaphragm myofibers showed that RT with high breathing effort had significant lower myofiber cross-sectional area than passive group. Also, when comparing abnormal myofibers between groups, a significantly lower proportion of small fiber size were found in RT whit high breathing effort in comparison to passive group. No differences were found in serum troponin I neither overtime nor between groups. In conclusion, an EAdi-based automated reverse triggering detection showed that this asynchrony is highly prevalent early after intubation under assist-control ventilation; the incidence depends on the magnitude of the activity detected and that reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering. In addition, the creation of a reverse triggering model revealed this phenomenon very complex, with high variability in terms of entrainment pattern and level of breathing effort. Finally, we have confirmed that RT dyssynchrony affects diaphragm function and this effect is modulated by the level of respiratory effort. Reverse triggering with low breathing effort seems to have a protective role on diaphragm function whereas reverse triggering with high breathing effort may favor eccentric myotrauma.Mechanical ventilation (MV) is used to sustain life in patients admitted to the intensive care unit for a wide spectrum of indications such as elective surgical procedures, septic shock, multiple organic failure and acute respiratory distress syndrome. Safe and effective ventilation depends on a smooth interaction between these two independent systems: the patient and the mechanical ventilator. Any mismatch between the patient and mechanical ventilator in terms of breath delivery timing, as well as the inability of the ventilator’s flow delivery to match the patient’s flow demand, is referred to as patient-ventilator dyssynchrony (PVD). Reverse Triggering (RT) is a type of PVD where muscle contractions are delayed, starting a certain amount of time after the machine triggered breath and occurring under different entrainment patterns. RT was originally described in 2013, in sedated patients admitted to the intensive care unit. Unfortunately, data about RT until now is scarce and its relevance remains totally uncertain. If any, the relevance of RT might be attributed to 2 main factors: the frequency of this PVD and its potential consequences in both lung and diaphragm injury. The group of different adverse patient–ventilator interactions leading to diaphragm atrophy and injury and resulting in a final common pathway of diaphragm weakness are denominated myotrauma. Particularly, RT is thought to cause eccentric myotrauma, which is a muscle contraction while muscle is lengthening during the ventilator’s expiratory phase while lung volume is decreasing. Based on animal and human studies, the impact of RT (if any) might be mediated by the level of breathing effort. In this thesis we aimed to describe the incidence of RT in patients early after intubation and admission to the intensive care unit and also to study the impact of RT with different levels of breathing effort on diaphragm injury (function and structure) in an animal model of RT with acute respiratory distress syndrome. To determine RT incidence, we conducted ancillary study in patients with continuous monitorization of the electrical activity of the diaphragm (EAdi). We developed a method for automatic detection of reverse triggering using EAdi and airway pressure curve. We additionally compared patients’ demographics, sedation depth and ventilation settings according to the median rate of reverse triggering, including time to transition to assisted ventilation or extubation. We found that our new automatic method presented a good diagnostic accuracy (98% total accuracy). Using a threshold of 1 µV for EAdi, median reverse triggering rate was 8% (range 0.1 to 75) with 44% (17 out of 39) of patients having ≥10% of breaths with reverse triggering. With 3 µV threshold, 26% (10 out of 39) of patients had ≥10% reverse triggered breaths. Importantly, patients who resented more reverse triggering were more likely to be on an assisted mode or extubated in the following 24 hours than patients who had low rate of RT (68% vs 35%; p=0.039). We also developed a 3 hours model of reverse triggering in pigs by modifying tidal volume, respiratory rate and level of sedation. Our approach to induce reverse triggering was not only feasible, but consistently reproducible in all animals, although with different presentations in terms of breathing effort and entrainment pattern. The most frequent entrainment pattern observed was 1:1, occurring in 83% of the total animals. Compared to passive ventilation (no breathing effort), RT group had significantly lower tidal volume (7 vs 10 ml/kg) and higher respiratory rate (45 vs 31 bpm) whereas no differences were found in other cardiorespiratory and sedation variables, nor in lung injury indicators after the study period. In order to study the impact of RT on diaphragm injury, we divided the RT group in 3 subgroups based on the level of breathing effort calculated by the pressure time product. Thus, 4 experimental groups were analyzed: Passive (no breathing effort), RT with low effort, RT with middle effort and RT with high effort. Function of the diaphragm was assessed by the ability to generate force, which correspond to the transdiaphragmatic pressure whilst diaphragm structure was evaluated using histological samples and serum troponin I as biomarker of muscle injury. We found that RT affects diaphragm function in two opposite directions. On one hand, animals with RT and low breathing effort showed a significant increase in force of 10% as compared to baseline. On the other hand, animals with RT and high breathing effort showed a larger decrease in force (34%) as compared to baseline. This difference was significantly different with the other experimental groups. Moreover, histologic analysis of diaphragm myofibers showed that RT with high breathing effort had significant lower myofiber cross-sectional area than passive group. Also, when comparing abnormal myofibers between groups, a significantly lower proportion of small fiber size were found in RT whit high breathing effort in comparison to passive group. No differences were found in serum troponin I neither overtime nor between groups. In conclusion, an EAdi-based automated reverse triggering detection showed that this asynchrony is highly prevalent early after intubation under assist-control ventilation; the incidence depends on the magnitude of the activity detected and that reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering. In addition, the creation of a reverse triggering model revealed this phenomenon very complex, with high variability in terms of entrainment pattern and level of breathing effort. Finally, we have confirmed that RT dyssynchrony affects diaphragm function and this effect is modulated by the level of respiratory effort. Reverse triggering with low breathing effort seems to have a protective role on diaphragm function whereas reverse triggering with high breathing effort may favor eccentric myotrauma.
- ItemSleep spindle activity in children with obstructive sleep apnea as a marker of neurocognitive performance : A pilot study(2018) Brockmann Veloso, Pablo Edmundo; Damiani Rebolledo, L. Felipe; Pincheira, E.; Daiber, F.; Ruiz Poblete, Sergio Marcelo; Aboitiz, Francisco; Ferri, R.; Bruni, O.
- ItemSleep-Disordered Breathing in Adolescents and Younger Adults A Representative Population-Based Survey in Chile(2016) Brockmann Veloso, Pablo Edmundo; Damiani Rebolledo, L. Felipe; Gozal, David
- ItemSleep-disordered breathing in children with Down syndrome : usefulness of home polysomnography(2016) Brockmann Veloso, Pablo Edmundo; Damiani Rebolledo, L. Felipe; Núñez, Felipe; Moya, Ana; Pincheira, Eduardo; Paul Delfau, María de los Ángeles; Lizama C., Macarena
- 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.
- ItemThe airway occlusion pressure (P 0.1) to monitor respiratory drive during mechanical ventilation: increasing awareness of a not-so-new problem(2018) Telias, Irene; Damiani Rebolledo, L. Felipe; Brochard, Laurent