Reverse Triggering during Controlled Ventilation: From Physiology to Clinical Management.

Reverse triggering dyssynchrony is a frequent phenomenon recently recognized in sedated critically ill patients under controlled ventilation. It occurs in at least 30-55% of these patients and often occurs in the transition from fully passive to assisted mechanical ventilation. During reverse triggering, patient inspiratory efforts start after the passive insufflation by mechanical breaths. The most often referred mechanism is the entrainment of the patient's intrinsic respiratory rhythm from the brainstem respiratory centers to periodic mechanical insufflations from the ventilator. However, reverse triggering might also occur because of local reflexes without involving the respiratory rhythm generator in the brainstem. Reverse triggering is observed during the acute phase of the disease, when patients may be susceptible to potential deleterious consequences of injurious or asynchronous efforts. Diagnosing reverse triggering might be challenging and can easily be missed. Inspection of ventilator waveforms or more sophisticated methods, such as the electrical activity of the diaphragm or esophageal pressure, can be used for diagnosis. The occurrence of reverse triggering might have clinical consequences. On the basis of physiological data, reverse triggering might be beneficial or injurious for the diaphragm and the lung, depending on the magnitude of the inspiratory effort. Reverse triggering can cause breath-stacking and loss of protective lung ventilation when triggering a second cycle. Little is known about how to manage patients with reverse triggering; however, available evidence can guide management on the basis of physiological principles.

Impact of Reverse Triggering Dyssynchrony during Lung-Protective Ventilation on Diaphragm Function: An Experimental Model.

Rationale: Reverse triggering dyssynchrony (RT) is a patient-ventilator interaction where a respiratory muscle contraction is triggered by a passive mechanical insufflation. Its impact on diaphragm structure and function is unknown. Objectives: To establish an animal model of RT with lung injury receiving lung-protective ventilation and to assess its impact on the structure and function of the diaphragm. Methods: Lung injury was induced by surfactant depletion and high-stress ventilation in 32 ventilated pigs. Animals were allocated to receive passive mechanical ventilation (Vt: 10 ml/kg; respiratory rate [RR]: 30-35 breaths/min; n = 8) or a more lung-protective strategy (Vt: 6-8 ml/kg; n = 24) with adjustments in RR to facilitate the occurrence of RT for 3 hours. Diaphragm function (transdiaphragmatic pressure [Pdi] during phrenic nerve stimulation [force/frequency curve]) and structure (biopsies) were assessed. The impact of RT on diaphragm function was analyzed according to the breathing effort assessed by the pressure-time product. Measurements and Main Results: Compared with passive ventilation, the protective ventilation group with RT received significantly lower Vt (7 vs. 10 ml/kg) and higher RR (45 vs. 31 breaths/min). An entrainment pattern of 1:1 was the most frequently occurring in 83% of the animals. Breathing effort induced by RT was highly variable across animals. RT with the lowest tercile of breathing effort was associated with 23% higher twitch Pdi compared with passive ventilation, whereas RT with high breathing effort was associated with a 10% lower twitch Pdi and a higher proportion of abnormal muscle fibers. Conclusions: In a reproducible animal model of RT with variable levels of breathing effort and entrainment patterns, RT with high effort is associated with impaired diaphragm function, whereas RT with low effort is associated with preserved diaphragm force.

Positive End-Expiratory Pressure, Pleural Pressure, and Regional Compliance during Pronation: An Experimental Study.

Rationale: The physiological basis of lung protection and the impact of positive end-expiratory pressure (PEEP) during pronation in acute respiratory distress syndrome are not fully elucidated. Objectives: To compare pleural pressure (Ppl) gradient, ventilation distribution, and regional compliance between dependent and nondependent lungs, and investigate the effect of PEEP during supination and pronation. Methods: We used a two-hit model of lung injury (saline lavage and high-volume ventilation) in 14 mechanically ventilated pigs and studied supine and prone positions. Global and regional lung mechanics including Ppl and distribution of ventilation (electrical impedance tomography) were analyzed across PEEP steps from 20 to 3 cm H2O. Two pigs underwent computed tomography scans: tidal recruitment and hyperinflation were calculated. Measurements and Main Results: Pronation improved oxygenation, increased Ppl, thus decreasing transpulmonary pressure for any PEEP, and reduced the dorsal-ventral pleural pressure gradient at PEEP < 10 cm H2O. The distribution of ventilation was homogenized between dependent and nondependent while prone and was less dependent on the PEEP level than while supine. The highest regional compliance was achieved at different PEEP levels in dependent and nondependent regions in supine position (15 and 8 cm H2O), but for similar values in prone position (13 and 12 cm H2O). Tidal recruitment was more evenly distributed (dependent and nondependent), hyperinflation lower, and lungs cephalocaudally longer in the prone position. Conclusions: In this lung injury model, pronation reduces the vertical pleural pressure gradient and homogenizes regional ventilation and compliance between the dependent and nondependent regions. Homogenization is much less dependent on the PEEP level in prone than in supine positon.

Role of Positive End-Expiratory Pressure and Regional Transpulmonary Pressure in Asymmetrical Lung Injury.

Rationale: Asymmetrical lung injury is a frequent clinical presentation. Regional distribution of Vt and positive end-expiratory pressure (PEEP) could result in hyperinflation of the less-injured lung. The validity of esophageal pressure (Pes) is unknown.Objectives: To compare, in asymmetrical lung injury, Pes with directly measured pleural pressures (Ppl) of both sides and investigate how PEEP impacts ventilation distribution and the regional driving transpulmonary pressure (inspiratory - expiratory).Methods: Fourteen mechanically ventilated pigs with lung injury were studied. One lung was blocked while the contralateral one underwent surfactant lavage and injurious ventilation. Airway pressure and Pes were measured, as was Ppl in the dorsal and ventral pleural space adjacent to each lung. Distribution of ventilation was assessed by electrical impedance tomography. PEEP was studied through decremental steps.Measurements and Results: Ventral and dorsal Ppl were similar between the injured and the noninjured lung across all PEEP levels. Dorsal Ppl and Pes were similar. The driving transpulmonary pressure was similar in the two lungs. Vt distribution between lungs was different at zero end-expiratory pressure (≈70% of Vt going in noninjured lung) owing to different respiratory system compliance (8.3 ml/cm H2O noninjured lung vs. 3.7 ml/cm H2O injured lung). PEEP at 10 cm H2O with transpulmonary pressure around zero homogenized Vt distribution opening the lungs. PEEP ≥16 cm H2O equalized distribution of Vt but with overdistension for both lungs.Conclusions: Despite asymmetrical lung injury, Ppl between injured and noninjured lungs is equalized and esophageal pressure is a reliable estimate of dorsal Ppl. Driving transpulmonary pressure is similar for both lungs. Vt distribution results from regional respiratory system compliance. Moderate PEEP homogenizes Vt distribution between lungs without generating hyperinflation.

Dyspnoea and respiratory muscle ultrasound to predict extubation failure.

BACKGROUND: This study investigated dyspnoea intensity and respiratory muscle ultrasound early after extubation to predict extubation failure. METHODS: The study was conducted prospectively in two intensive care units in France and Canada. Patients intubated for at least 48 h were studied within 2 h after an extubation following a successful spontaneous breathing trial. Dyspnoea was evaluated by a dyspnoea visual analogue scale (Dyspnoea-VAS) ranging from 0 to 10 and the Intensive Care Respiratory Distress Observational Scale (IC-RDOS). The ultrasound thickening fraction of the parasternal intercostal and the diaphragm was measured; limb muscle strength was evaluated using the Medical Research Council (MRC) score (range 0-60). RESULTS: Extubation failure occurred in 21 out of 122 enrolled patients (17%). The median (interquartile range (IQR)) Dyspnoea-VAS and IC-RDOS were higher in patients with extubation failure versus success: 7 (4-9) versus 3 (1-5) (p<0.001) and 3.7 (1.8-5.8) versus 1.7 (1.5-2.1) (p<0.001), respectively. The median (IQR) ratio of parasternal intercostal muscle to diaphragm thickening fraction was significantly higher and MRC was lower in patients with extubation failure compared with extubation success: 0.9 (0.4-2.1) versus 0.3 (0.2-0.5) (p<0.001) and 45 (36-50) versus 52 (44-60) (p=0.012), respectively. The thickening fraction of the parasternal intercostal and its ratio to diaphragm thickening showed the highest area under the receiver operating characteristic curve (AUC) for an early prediction of extubation failure (0.81). AUCs of Dyspnoea-VAS and IC-RDOS reached 0.78 and 0.74, respectively. CONCLUSIONS: Respiratory muscle ultrasound and dyspnoea measured within 2 h after extubation predict subsequent extubation failure.

Reverse Triggering Dyssynchrony 24 h after Initiation of Mechanical Ventilation.

BACKGROUND: Reverse triggering is a delayed asynchronous contraction of the diaphragm triggered by passive insufflation by the ventilator in sedated mechanically ventilated patients. The incidence of reverse triggering is unknown. This study aimed at determining the incidence of reverse triggering in critically ill patients under controlled ventilation. METHODS: In this ancillary study, patients were continuously monitored with a catheter measuring the electrical activity of the diaphragm. A method for automatic detection of reverse triggering using electrical activity of the diaphragm was developed in a derivation sample and validated in a subsequent sample. The authors assessed the predictive value of the software. In 39 recently intubated patients under assist-control ventilation, a 1-h recording obtained 24 h after intubation was used to determine the primary outcome of the study. The authors also compared patients' demographics, sedation depth, ventilation settings, and time to transition to assisted ventilation or extubation according to the median rate of reverse triggering. RESULTS: The positive and negative predictive value of the software for detecting reverse triggering were 0.74 (95% CI, 0.67 to 0.81) and 0.97 (95% CI, 0.96 to 0.98). Using a threshold of 1 µV of electrical activity to define diaphragm activation, median reverse triggering rate was 8% (range, 0.1 to 75), with 44% (17 of 39) of patients having greater than or equal to 10% of breaths with reverse triggering. Using a threshold of 3 µV, 26% (10 of 39) of patients had greater than or equal to 10% reverse triggering. Patients with more reverse triggering were more likely to progress to an assisted mode or extubation within the following 24 h (12 of 39 [68%]) vs. 7 of 20 [35%]; P = 0.039). CONCLUSIONS: Reverse triggering detection based on electrical activity of the diaphragm suggests that this asynchrony is highly prevalent at 24 h after intubation under assist-control ventilation. Reverse triggering seems to occur during the transition phase between deep sedation and the onset of patient triggering.

Automated detection and quantification of reverse triggering effort under mechanical ventilation.

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.

Duration of diaphragmatic inactivity after endotracheal intubation of critically ill patients.

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.

Low Spontaneous Breathing Effort during Extracorporeal Membrane Oxygenation in a Porcine Model of Severe Acute Respiratory Distress Syndrome.

BACKGROUND: A lung rest strategy is recommended during extracorporeal membrane oxygenation in severe acute respiratory distress syndrome (ARDS). However, spontaneous breathing modes are frequently used in this context. The impact of this approach may depend on the intensity of breathing efforts. The authors aimed to determine whether a low spontaneous breathing effort strategy increases lung injury, compared to a controlled near-apneic ventilation, in a porcine severe ARDS model assisted by extracorporeal membrane oxygenation. METHODS: Twelve female pigs were subjected to lung injury by repeated lavages, followed by 2-h injurious ventilation. Thereafter, animals were connected to venovenous extracorporeal membrane oxygenation and during the first 3 h, ventilated with near-apneic ventilation (positive end-expiratory pressure, 10 cm H2O; driving pressure, 10 cm H2O; respiratory rate, 5/min). Then, animals were allocated into (1) near-apneic ventilation, which continued with the previous ventilatory settings; and (2) spontaneous breathing: neuromuscular blockers were stopped, sweep gas flow was decreased until regaining spontaneous efforts, and ventilation was switched to pressure support mode (pressure support, 10 cm H2O; positive end-expiratory pressure, 10 cm H2O). In both groups, sweep gas flow was adjusted to keep Paco2 between 30 and 50 mmHg. Respiratory and hemodynamic as well as electric impedance tomography data were collected. After 24 h, animals were euthanized and lungs extracted for histologic tissue analysis. RESULTS: Compared to near-apneic group, the spontaneous breathing group exhibited a higher respiratory rate (52 ± 17 vs. 5 ± 0 breaths/min; mean difference, 47; 95% CI, 34 to 59; P < 0.001), but similar tidal volume (2.3 ± 0.8 vs. 2.8 ± 0.4 ml/kg; mean difference, 0.6; 95% CI, -0.4 to 1.4; P = 0.983). Extracorporeal membrane oxygenation settings and gas exchange were similar between groups. Dorsal ventilation was higher in the spontaneous breathing group. No differences were observed regarding histologic lung injury. CONCLUSIONS: In an animal model of severe ARDS supported with extracorporeal membrane oxygenation, spontaneous breathing characterized by low-intensity efforts, high respiratory rates, and very low tidal volumes did not result in increased lung injury compared to controlled near-apneic ventilation.

Reverse triggering ? a novel or previously missed phenomenon?

BACKGROUND: Reverse triggering (RT) was described in 2013 as a form of patient-ventilator asynchrony, where patient's respiratory effort follows mechanical insufflation. Diagnosis requires esophageal pressure (Pes) or diaphragmatic electrical activity (EAdi), but RT can also be diagnosed using standard ventilator waveforms. HYPOTHESIS: We wondered (1) how frequently RT would be present but undetected in the figures from literature, especially before 2013; (2) whether it would be more prevalent in the era of small tidal volumes after 2000. METHODS: We searched PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials, from 1950 to 2017, with key words related to asynchrony to identify papers with figures including ventilator waveforms expected to display RT if present. Experts labelled waveforms. 'Definite' RT was identified when Pes or EAdi were in the tracing, and 'possible' RT when only flow and pressure waveforms were present. Expert assessment was compared to the author's descriptions of waveforms. RESULTS: We found 65 appropriate papers published from 1977 to now, containing 181 ventilator waveforms. 21 cases of 'possible' RT and 25 cases of 'definite' RT were identified by the experts. 18.8% of waveforms prior to 2013 had evidence of RT. Most cases were published after 2000 (1 before vs. 45 after, p = 0.03). 54% of RT cases were attributed to different phenomena. A few cases of identified RT were already described prior to 2013 using different terminology (earliest in 1997). While RT cases attributed to different phenomena decreased after 2013, 60% of 'possible' RT remained missed. CONCLUSION: RT has been present in the literature as early as 1997, but most cases were found after the introduction of low tidal volume ventilation in 2000. Following 2013, the number of undetected cases decreased, but RT are still commonly missed. Reverse Triggering, A Missed Phenomenon in the Literature. Critical Care Canada Forum 2019 Abstracts. Can J Anesth/J Can Anesth 67 (Suppl 1), 1-162 (2020). https://doi-org.myaccess.library.utoronto.ca/ https://doi.org/10.1007/s12630-019-01552-z .

Specific Training Improves the Detection and Management of Patient-Ventilator Asynchrony.

BACKGROUND: Patient-ventilator asynchrony is common in patients undergoing mechanical ventilation. The proportion of health-care professionals capable of identifying and effectively managing different types of patient-ventilator asynchronies is limited. A few studies have developed specific training programs, but they mainly focused on improving patient-ventilator asynchrony detection without assessing the ability of health-care professionals to determine the possible causes. METHODS: We conducted a 36-h training program focused on patient-ventilator asynchrony detection and management for health-care professionals from 20 hospitals in Latin America and Spain. The training program included 6 h of a live online lesson during which 120 patient-ventilator asynchrony cases were presented. After the 6-h training lesson, health-care professionals were required to complete a 1-h training session per day for the subsequent 30 d. A 30-question assessment tool was developed and used to assess health-care professionals before training, immediately after the 6-h training lecture, and after the 30 d of training (1-month follow-up). RESULTS: One hundred sixteen health-care professionals participated in the study. The median (interquartile range) of the total number of correct answers in the pre-training, post-training, and 1-month follow-up were significantly different (12 [8.75-15], 18 [13.75-22], and 18.5 [14-23], respectively). The percentages of correct answers also differed significantly between the time assessments. Study participants significantly improved their performance between pre-training and post-training (P < .001). This performance was maintained after a 1-month follow-up (P = .95) for the questions related to the detection, determination of cause, and management of patient-ventilator asynchrony. CONCLUSIONS: A specific 36-h training program significantly improved the ability of health-care professionals to detect patient-ventilator asynchrony, determine the possible causes of patient-ventilator asynchrony, and properly manage different types of patient-ventilator asynchrony.

Eccentric Contractions of the Diaphragm During Mechanical Ventilation.

Diaphragm 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.

Mechanical Power of Ventilation: From Computer to Clinical Implications.

Mechanical 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.

Effects of the First Spontaneous Breathing Trial in Children With Tracheostomy and Long-Term Mechanical Ventilation.

BACKGROUND: Weaning and liberation from mechanical ventilation in pediatric patients with tracheostomy and long-term mechanical ventilation constitute a challenging process due to diagnosis heterogeneity and significant variability in the clinical condition. We aimed to evaluate the physiological response during the first attempt of a spontaneous breathing trial (SBT) and to compare variables in subjects who failed or passed the SBT. METHODS: This was a prospective observational study in tracheostomized children with long-term mechanical ventilation admitted to the Hospital Josefina Martinez, Santiago, Chile, between 2014-2020. Cardiorespiratory variables such as breathing pattern, use of accessory respiratory muscles, heart rate, breathing frequency, and oxygen saturation were registered at baseline and throughout a 2-h SBT with or without positive pressure depending on an SBT protocol. Comparison of demographic and ventilatory variables between groups (SBT failure and success) was performed. RESULTS: A total of 48 subjects were analyzed (median [IQR] age of 20.5 [17.0-35.0] months, 60% male). Chronic lung disease was the primary diagnosis in 60% of subjects. Eleven (23%) total subjects failed the SBT (< 2 h), with an average failure time of 69 ± 29 min. Subjects who failed the SBT had a significantly higher breathing frequency, heart rate, and end-tidal CO2 than subjects who succeeded (P < .001). In addition, subjects who failed the SBT had significantly shorter duration of mechanical ventilation before the SBT, higher proportion unassisted SBT, and higher rate of deviation SBT protocol in comparison with subjects who succeeded. CONCLUSIONS: Conducting an SBT to evaluate the tolerance and cardiorespiratory response in tracheostomized children with long-term mechanical ventilation is feasible. Time on mechanical ventilation before the first attempt and type of SBT (with or without positive pressure) could be associated with SBT failure.

Physiological effects of high-flow nasal cannula oxygen therapy after extubation: a randomized crossover study.

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. Trial registration January 15, 2021. NCT04711759.

A deep look into the rib cage compression technique in mechanically ventilated patients: a narrative review. / Desvendando a técnica de compressão torácica em pacientes em ventilação mecânica: uma revisão narrativa.

Defective management of secretions is one of the most frequent complications in invasive mechanically ventilated patients. Clearance of secretions through chest physiotherapy is a critical aspect of the treatment of these patients. Manual rib cage compression is one of the most practiced chest physiotherapy techniques in ventilated patients; however, its impact on clinical outcomes remains controversial due to methodological issues and poor understanding of its action. In this review, we present a detailed analysis of the physical principles involved in rib cage compression technique performance, as well as the physiological effects observed in experimental and clinical studies, which show that the use of brief and vigorous rib cage compression, based on increased expiratory flows (expiratory-inspiratory airflow difference of > 33L/minute), can improve mucus movement toward the glottis. On the other hand, the use of soft and gradual rib cage compression throughout the whole expiratory phase does not impact the expiratory flows, resulting in ineffective or undesired effects in some cases. More physiological studies are needed to understand the principles of the rib cage compression technique in ventilated humans. However, according to the evidence, rib cage compression has more potential benefits than risks, so its implementation should be promoted.

O manejo deficiente das secreções é uma das complicações mais frequentes em pacientes em ventilação mecânica invasiva. A depuração das secreções por meio da fisioterapia respiratória é um aspecto crítico do tratamento desses pacientes. A compressão torácica manual é uma das técnicas de fisioterapia respiratória mais praticadas em pacientes ventilados, mas seu impacto nos desfechos clínicos permanece controverso devido a questões metodológicas e ao pouco conhecimento sobre sua ação. Nesta revisão, apresenta-se uma análise detalhada dos princípios físicos envolvidos na execução da técnica de compressão torácica. Também investigam-se os efeitos fisiológicos observados em estudos experimentais e clínicos, que mostram que o uso de compressão torácica curta e vigorosa, baseada no aumento de fluxos expiratórios (diferença de fluxo aéreo inspiratório-expiratório > 33L/minuto), pode melhorar o movimento do muco em direção à glote. Por outro lado, o uso de compressão torácica suave e gradual ao longo de toda a fase expiratória não afeta os fluxos expiratórios, resultando em efeitos ineficazes ou indesejados em alguns casos. Mais estudos fisiológicos são necessários para entender os princípios da técnica de compressão torácica em pacientes ventilados. No entanto, de acordo com as evidências, a compressão torácica tem mais benefícios potenciais do que riscos, o que incentiva sua implementação.

Acute lung injury secondary to hydrochloric acid instillation induces small airway hyperresponsiveness.

BACKGROUND: Acute respiratory distress syndrome (ARDS) is a severe form of respiratory failure characterized by altered lung mechanics and poor oxygenation. Bronchial hyperresponsiveness has been reported in ARDS survivors and animal models of acute lung injury. Whether this hyperreactivity occurs at the small airways or not is unknown. OBJECTIVE: To determine ex-vivo small airway reactivity in a rat model of acute lung injury (ALI) by hydrochloric acid (HCl) instillation. METHODS: Twelve anesthetized rats were connected to mechanical ventilation for 4-hour, and randomly allocated to either ALI group (HCl intratracheal instillation; n=6) or Sham (intratracheal instillation of 0.9% NaCl; n=6). Oxygenation was assessed by arterial blood gases. After euthanasia, tissue samples from the right lung were harvested for histologic analysis and wet-dry weight ratio assessment. Precision cut lung slice technique (100-200 µm diameter) was applied in the left lung to evaluate ex vivo small airway constriction in response to histamine and carbachol stimulation, using phase-contrast video microscopy. RESULTS: Rats from the ALI group exhibited hypoxemia, worse histologic lung injury, and increased lung wet-dry weight ratio as compared with the sham group. The bronchoconstrictor responsiveness was significantly higher in the ALI group, both for carbachol (maximal contraction of 84.5±2.5% versus 61.4±4.2% in the Sham group, P<0.05), and for histamine (maximal contraction of 78.6±5.3% versus 49.6±5.3% in the Sham group, P<0.05). CONCLUSION: In an animal model of acute lung injury secondary to HCL instillation, small airway hyperresponsiveness to carbachol and histamine is present. These results may provide further insight into the pathophysiology of ARDS.

Patient-ventilator dyssynchronies: Are they all the same? A clinical classification to guide actions.

Patient ventilatory dyssynchrony (PVD) is a mismatch between the respiratory drive of the patient and ventilatory assistance. It is a complex event seen in almost all ventilated patients and at any ventilator mode, with uncertain significance and prognosis. Due to its different pathophysiological mechanisms, there is still not consensual classification to guide us in selecting the best treatment. In the present review we aimed to summarize some clinical data on PVD, and to propose a clinical classification based on the type of PVD, from potentially innocuous to clearly harmful PVD, which could help clinicians in the decision-making process from adjusting ventilator settings to deeply sedate or paralyze the patient. Clearly, further studies are needed addressing risk factors, physiologic mechanisms and direct consequences of PVD in order to help clinicians to design effective and proven strategies at the bedside.