Potential for the lung recruitment and the risk of lung overdistension during 21 days of mechanical ventilation in patients with COVID-19 after noninvasive ventilation failure: the COVID-VENT observational trial.

BACKGROUND: Data on the lung respiratory mechanics and gas exchange in the time course of COVID-19-associated respiratory failure is limited. This study aimed to explore respiratory mechanics and gas exchange, the lung recruitability and risk of overdistension during the time course of mechanical ventilation. METHODS: This was a prospective observational study in critically ill mechanically ventilated patients (n = 116) with COVID-19 admitted into Intensive Care Units of Sechenov University. The primary endpoints were: «optimum¼ positive end-expiratory pressure (PEEP) level balanced between the lowest driving pressure and the highest SpO2 and number of patients with recruitable lung on Days 1 and 7 of mechanical ventilation. We measured driving pressure at different levels of PEEP (14, 12, 10 and 8 cmH2O) with preset tidal volume, and with the increase of tidal volume by 100 ml and 200 ml at preset PEEP level, and calculated static respiratory system compliance (CRS), PaO2/FiO2, alveolar dead space and ventilatory ratio on Days 1, 3, 5, 7, 10, 14 and 21. RESULTS: The «optimum¼ PEEP levels on Day 1 were 11.0 (10.0-12.8) cmH2O and 10.0 (9.0-12.0) cmH2O on Day 7. Positive response to recruitment was observed on Day 1 in 27.6% and on Day 7 in 9.2% of patients. PEEP increase from 10 to 14 cmH2O and VT increase by 100 and 200 ml led to a significant decrease in CRS from Day 1 to Day 14 (p < 0.05). Ventilatory ratio was 2.2 (1.7-2,7) in non-survivors and in 1.9 (1.6-2.6) survivors on Day 1 and decreased on Day 7 in survivors only (p < 0.01). PaO2/FiO2 was 105.5 (76.2-141.7) mmHg in non-survivors on Day 1 and 136.6 (106.7-160.8) in survivors (p = 0.002). In survivors, PaO2/FiO2 rose on Day 3 (p = 0.008) and then between Days 7 and 10 (p = 0.046). CONCLUSION: Lung recruitability was low in COVID-19 and decreased during the course of the disease, but lung overdistension occurred at «intermediate¼ PEEP and VT levels. In survivors gas exchange improvements after Day 7 mismatched CRS. TRIAL REGISTRATION: ClinicalTrials.gov, NCT04445961 . Registered 24 June 2020-Retrospectively registered.

The POOR Get POORer: A Hypothesis for the Pathogenesis of Ventilator-induced Lung Injury.

Protective ventilation strategies for the injured lung currently revolve around the use of low Vt, ostensibly to avoid volutrauma, together with positive end-expiratory pressure to increase the fraction of open lung and reduce atelectrauma. Protective ventilation is currently applied in a one-size-fits-all manner, and although this practical approach has reduced acute respiratory distress syndrome deaths, mortality is still high and improvements are at a standstill. Furthermore, how to minimize ventilator-induced lung injury (VILI) for any given lung remains controversial and poorly understood. Here we present a hypothesis of VILI pathogenesis that potentially serves as a basis upon which minimally injurious ventilation strategies might be developed. This hypothesis is based on evidence demonstrating that VILI begins in isolated lung regions manifesting a Permeability-Originated Obstruction Response (POOR) in which alveolar leak leads to surfactant dysfunction and increases local tissue stresses. VILI progresses topographically outward from these regions in a POOR-get-POORer fashion unless steps are taken to interrupt it. We propose that interrupting the POOR-get-POORer progression of lung injury relies on two principles: 1) open the lung to minimize the presence of heterogeneity-induced stress concentrators that are focused around the regions of atelectasis, and 2) ventilate in a patient-dependent manner that minimizes the number of lung units that close during each expiration so that they are not forced to rerecruit during the subsequent inspiration. These principles appear to be borne out in both patient and animal studies in which expiration is terminated before derecruitment of lung units has enough time to occur.

Expired Tidal Volume Variation in Extremely Low Birth Weight and Very Low Birth Weight Infants on Volume-Targeted Ventilation.

In a prospective study we describe the delivery of small tidal volumes to extremely low birth weight (ELBW) and very low birth weight (VLBW) infants using a volume-targeted ventilation mode (VTV). Tidal volume delivery was consistent for both ELBW and VLBW infants independent of gestational age, birth weight, and the target volume.

Ventilator-Induced Lung Injury as a Dynamic Balance Between Epithelial Cell Damage and Recovery.

Acute respiratory distress syndrome (ARDS) has a high mortality rate that is due in part to ventilator-induced lung injury (VILI). Nevertheless, the majority of patients eventually recover, which means that their innate reparative capacities eventually prevail. Since there are currently no medical therapies for ARDS, minimizing its mortality thus amounts to achieving an optimal balance between spontaneous tissue repair versus the generation of VILI. In order to understand this balance better, we developed a mathematical model of the onset and recovery of VILI that incorporates two hypotheses: (1) a novel multi-hit hypothesis of epithelial barrier failure, and (2) a previously articulated rich-get-richer hypothesis of the interaction between atelectrauma and volutrauma. Together, these concepts explain why VILI appears in a normal lung only after an initial latent period of injurious mechanical ventilation. In addition, they provide a mechanistic explanation for the observed synergy between atelectrauma and volutrauma. The model recapitulates the key features of previously published in vitro measurements of barrier function in an epithelial monolayer and in vivo measurements of lung function in mice subjected to injurious mechanical ventilation. This provides a framework for understanding the dynamic balance between factors responsible for the generation of and recovery from VILI.

Ventilation-Induced Lung Injury (VILI) in Neonates: Evidence-Based Concepts and Lung-Protective Strategies.

Supportive care with mechanical ventilation continues to be an essential strategy for managing severe neonatal respiratory failure; however, it is well known to cause and accentuate neonatal lung injury. The pathogenesis of ventilator-induced lung injury (VILI) is multifactorial and complex, resulting predominantly from interactions between ventilator-related factors and patient-related factors. Importantly, VILI is a significant risk factor for developing bronchopulmonary dysplasia (BPD), the most common chronic respiratory morbidity of preterm infants that lacks specific therapies, causes life-long morbidities, and imposes psychosocial and economic burdens. Studies of older children and adults suggest that understanding how and why VILI occurs is essential to developing strategies for mitigating VILI and its consequences. This article reviews the preclinical and clinical evidence on the pathogenesis and pathophysiology of VILI in neonates. We also highlight the evidence behind various lung-protective strategies to guide clinicians in preventing and attenuating VILI and, by extension, BPD in neonates. Further, we provide a snapshot of future directions that may help minimize neonatal VILI.

Positive airway pressure longer than 24 h is associated with histopathological volutrauma in severe COVID-19 pneumonia-an ESGFOR based narrative case-control review.

Background and Objective: A thorough understanding of the pathogenic mechanisms elicited by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) still requires further research. Until recently, only a restricted number of autopsies have been performed, therefore limiting the accurate knowledge of the lung injury associated with SARS-CoV-2. A multidisciplinary European Society of Clinical Microbiology and Infectious Diseases (ESCMID) Study Group of Forensic and Post-mortem Microbiology-ESGFOR team conducted a non-systematic narrative literature review among coronavirus 2019 disease (COVID-19) pneumonia cases assessing the histopathological (HP) effects of positive airways pressure. HP lung features were recorded and compared between mechanically ventilated (>24 hours) and control (ventilation <24 hours) patients. A logistic regression analysis was performed to identify associations between mechanical ventilation (MV) and HP findings. Methods: A PubMed and MEDLINE search was conducted in order to identify studies published between March 1st 2020 and June 30th 2021. Key Content and Findings: Seventy patients (median age: 69 years) from 24 studies were analysed, among whom 38 (54.2%) underwent MV longer than 24 hours. Overall, main HP features were: diffuse alveolar damage (DAD) in 53 (75.7%), fibrosis (interstitial/intra-alveolar) in 43 (61.4%), vascular damage-including thrombosis/emboli- in 41 (58.5%), and endotheliitis in only 8 (11.4%) patients. Association of DAD, fibrosis and vascular damage was detected in 30 (42.8%) patients. Multivariate analysis, adjusted by age and gender, identified MV >24 hours as an independent variable associated with DAD (OR =5.40, 95% CI: 1.48-19.62), fibrosis (OR =3.88, 95% CI: 1.25-12.08), vascular damage (OR =5.49, 95% CI: 1.78-16.95) and association of DAD plus fibrosis plus vascular damage (OR =6.99, 95% CI: 2.04-23.97). Conclusions: We identified that patients mechanically ventilated >24 hours had a significantly higher rate of pulmonary injury on histopathology independently of age and gender. Our findings emphasize the importance of maintaining a protective ventilator strategy when subjects with COVID-19 pneumonia undergo intubation.

Novel Ventilation Strategies to Reduce Adverse Pulmonary Outcomes.

Extremely preterm infants who must suddenly support their own gas exchange with lungs that are incompletely developed and lacking adequate amount of surfactant and antioxidant defenses are susceptible to lung injury. The decades-long quest to prevent bronchopulmonary dysplasia has had limited success, in part because of increasing survival of more immature infants. The process must begin in the delivery room with gentle assistance in establishing and maintaining adequate lung aeration, followed by noninvasive support and less invasive surfactant administration. Various modalities of invasive and noninvasive support have been used with varying degree of effect and are reviewed in this article.

Recent Advances in Bronchopulmonary Dysplasia.

Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that occurs in preterm infants, usually those receiving substantial respiratory support with either mechanical ventilation or supplementation with oxygen. The pathogenesis of BPD is multifactorial, and the clinical phenotype is variable. BPD is associated with substantial mortality and short- and long-term morbidity. The incidence of BPD has remained stable or increased, as advances in neonatal care have led to improved survival of more extremely preterm infants. Extensive basic science, translational, and clinical research focusing on BPD has improved the current understanding of the factors that contribute to BPD pathogenesis. However, despite a better understanding of its pathophysiology, BPD continues to be challenging to prevent and manage adequately. The current review aims to provide a clinically useful synopsis of evidence on the prevention and management of BPD in preterm infants.

Lung Protection During Mechanical Ventilation in the Premature Infant.

Mechanical ventilation can be life-saving for the premature infant, but is often injurious to immature and underdeveloped lungs. Lung injury is caused by atelectrauma, oxygen toxicity, and volutrauma. Lung protection must include appropriate lung recruitment starting in the delivery suite and throughout mechanical ventilation. Strategies include open lung ventilation, positive end-expiratory pressure, and volume-targeted ventilation. Respiratory function monitoring, such as capnography and ventilator graphics, provides clinicians with continuous real-time information and an adjunct to optimize lung-protective ventilatory strategies. Further research is needed to assess which lung-protective strategies result in a decrease in long-term respiratory morbidity.

The Difference Between Set and Delivered Tidal Volume: A Lung Simulation Study.

BACKGROUND: Precise control of tidal volume is one of the keys in limiting ventilator-induced lung injury and ensuring adequate ventilation in mechanically ventilated neonates. The aim of the study was to compare the tidal volume (mVT) measured from the expiratory limb of the ventilator with the actual tidal volume (aVT) that would be delivered to the patient using a lung model to simulate a neonate. METHODS: This study was conducted using the ASL5000 lung simulator. Three combinations of parameters were set: resistance (cmH2O/L/sec) and compliance (mL/cmH2O) of 50 and 2 (Group 1), 100 and 1 (Group 2), and 150 and 0.5 (Group 3), respectively. The ASL5000 was connected to each of the ventilators including one anesthesia machine ventilator (Drager Fabius GS) and two ICU ventilators (Servo-i Universal and Evita Infinity V500). Each ventilator was evaluated with a set tidal volume of 30 mL (sVT) and a respiratory rate of 25 breathes/minute in both the volume-controlled ventilation (VCV) and dual-controlled ventilation (DCV) modes. RESULTS: The discrepancies between sVT, mVT and aVT were highest with the Fabius anesthesia machine ventilator and increased in the simulated lung injury groups. When comparing the ICU ventilators, the difference was greater the Servo-i and increased when using the DCV mode and with simulated lung injury. CONCLUSION: Accurate tidal volumes were achieved only with the Infinity ICU ventilator. This was true regardless of mode of ventilation and even during simulated lung injury.

Atelectrauma Versus Volutrauma: A Tale of Two Time-Constants.

OBJECTIVES: Elucidate how the degree of ventilator-induced lung injury due to atelectrauma that is produced in the injured lung during mechanical ventilation is determined by both the timing and magnitude of the airway pressure profile. DESIGN: A computational model of the injured lung provides a platform for exploring how mechanical ventilation parameters potentially modulate atelectrauma and volutrauma. This model incorporates the time dependence of lung recruitment and derecruitment, and the time-constant of lung emptying during expiration as determined by overall compliance and resistance of the respiratory system. SETTING: Computational model. SUBJECTS: Simulated scenarios representing patients with both normal and acutely injured lungs. MEASUREMENTS AND MAIN RESULTS: Protective low-tidal volume ventilation (Low-Vt) of the simulated injured lung avoided atelectrauma through the elevation of positive end-expiratory pressure while maintaining fixed tidal volume and driving pressure. In contrast, airway pressure release ventilation avoided atelectrauma by incorporating a very brief expiratory duration () that both prevents enough time for derecruitment and limits the minimum alveolar pressure prior to inspiration. Model simulations demonstrated that has an effective threshold value below which airway pressure release ventilation is safe from atelectrauma while maintaining a tidal volume and driving pressure comparable with those of Low-Vt. This threshold is strongly influenced by the time-constant of lung-emptying. CONCLUSIONS: Low-Vt and airway pressure release ventilation represent markedly different strategies for the avoidance of ventilator-induced lung injury, primarily involving the manipulation of positive end-expiratory pressure and , respectively. can be based on exhalation flow values, which may provide a patient-specific approach to protective ventilation.

Pressure-controlled Volume Guaranteed Mode Improves Respiratory Dynamics during Laparoscopic Cholecystectomy: A Comparison with Conventional Modes.

BACKGROUND: Pneumoperitoneum and altered positioning 1in laparoscopic cholecystectomy predispose to alterations in cardiorespiratory physiology. We compared the effects of volume controlled, pressure controlled, and the newly introduced pressure controlled-volume guaranteed ventilation (PCV-VG) modes of ventilation on respiratory mechanics and oxygenation during laparoscopic cholecystectomy. MATERIALS AND METHODS: Seventy-five physical status American Society of Anesthesiologists Classes I and II patients with normal lungs undergoing laparoscopic cholecystectomy were randomly allocated to receive volume controlled ventilation (VCV), pressure-controlled ventilation (PCV), or PCV-VG modes of ventilation during general anesthesia. In all modes of ventilation, the tidal volume was set at 8 mL/kg, and respiratory rate was set at 12 breaths/min with inspired oxygen of 0.4. After pneumoperitoneum, respiratory rate was adjusted to maintain an end-tidal carbon dioxide between 32 and 37 mm Hg. The peak airway pressures, compliance, the mean airway pressures, oxygen saturation, end tidal carbon dioxide and hemodynamics were recorded at the time of intubation (T1), 15 min after pneumoperitoneum (T2) and after desufflation (T3) and were compared. Arterial oxygen tension, arterial carbon dioxide tension at T2 and T3 were compared. RESULTS: PCV-VG and PCV mode resulted in lower peak airway pressures than VCV (23.04 ± 3.43, 24.52 ± 2.79, and 27.24 ± 2.37 cm of water, respectively, P = 0.001). Compliance was better preserved in the pressure mediated modes than VCV (fall from baseline was 42%, 29%, and 30% in VCV, PCV, and PCV-VG). The arterial to end-tidal carbon dioxide gradient was lower in PCV-VG and PCV compared to VCV. No difference in oxygenation and hemodynamics were observed. CONCLUSION: PCV and PCV-VG modes are superior to VCV mode in providing adequate oxygenation at lower peak inspiratory pressures.

Ventilator-induced lung injury during controlled ventilation in patients with acute respiratory distress syndrome: less is probably better.

INTRODUCTION: Mechanical ventilation is required to support respiratory function in the acute respiratory distress syndrome (ARDS), but it may promote lung damage, a phenomenon known as ventilator-induced lung injury (VILI). Areas covered: Several mechanisms of VILI have been described, such as: inspiratory and/or expiratory stress inducing overdistension (volutrauma); interfaces between collapsed or edema-filled alveoli with surrounding open alveoli, acting as stress raisers; alveoli that repetitively open and close during tidal breathing (atelectrauma); and peripheral airway dynamics. In this review, we discuss: the definition and classification of ARDS; ventilatory parameters that act as VILI determinants (tidal volume, respiratory rate, positive end-expiratory pressure, peak, plateau, driving and transpulmonary pressures, energy, mechanical power, and intensity); and the roles of prone positioning and muscle paralysis. We seek to provide an up-to-date overview of the evidence in the field from a clinical perspective. Expert commentary: To prevent VILI, mechanical ventilation strategies should minimize inspiratory/expiratory stress, dynamic/static strain, energy, mechanical power, and intensity, as well as mitigate the hemodynamic consequences of positive-pressure ventilation. In patients with moderate to severe ARDS, prone positioning can reduce lung damage and improve survival. Overall, volutrauma seems to be more harmful than atelectrauma. Extracorporeal support should be considered in selected cases.

Opening pressures and atelectrauma in acute respiratory distress syndrome.

PURPOSE: Open lung strategy during ARDS aims to decrease the ventilator-induced lung injury by minimizing the atelectrauma and stress/strain maldistribution. We aim to assess how much of the lung is opened and kept open within the limits of mechanical ventilation considered safe (i.e., plateau pressure 30 cmH2O, PEEP 15 cmH2O). METHODS: Prospective study from two university hospitals. Thirty-three ARDS patients (5 mild, 10 moderate, 9 severe without extracorporeal support, ECMO, and 9 severe with it) underwent two low-dose end-expiratory CT scans at PEEP 5 and 15 cmH2O and four end-inspiratory CT scans (from 19 to 40 cmH2O). Recruitment was defined as the fraction of lung tissue which regained inflation. The atelectrauma was estimated as the difference between the intratidal tissue collapse at 5 and 15 cmH2O PEEP. Lung ventilation inhomogeneities were estimated as the ratio of inflation between neighboring lung units. RESULTS: The lung tissue which is opened between 30 and 45 cmH2O (i.e., always closed at plateau 30 cmH2O) was 10 ± 29, 54 ± 86, 162 ± 92, and 185 ± 134 g in mild, moderate, and severe ARDS without and with ECMO, respectively (p < 0.05 mild versus severe without or with ECMO). The intratidal collapses were similar at PEEP 5 and 15 cmH2O (63 ± 26 vs 39 ± 32 g in mild ARDS, p = 0.23; 92 ± 53 vs 78 ± 142 g in moderate ARDS, p = 0.76; 110 ± 91 vs 89 ± 93, p = 0.57 in severe ARDS without ECMO; 135 ± 100 vs 104 ± 80, p = 0.32 in severe ARDS with ECMO). Increasing the applied airway pressure up to 45 cmH2O decreased the lung inhomogeneity slightly (but significantly) in mild and moderate ARDS, but not in severe ARDS. CONCLUSIONS: Data show that the prerequisites of the open lung strategy are not satisfied using PEEP up to 15 cmH2O and plateau pressure up to 30 cmH2O. For an effective open lung strategy, higher pressures are required. Therefore, risks of atelectrauma must be weighted versus risks of volutrauma. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT01670747 ( www.clinicaltrials.gov ).

Driving pressure and mechanical power: new targets for VILI prevention.

Several factors have been recognized as possible triggers of ventilator-induced lung injury (VILI). The first is pressure (thus the 'barotrauma'), then the volume (hence the 'volutrauma'), finally the cyclic opening-closing of the lung units ('atelectrauma'). Less attention has been paid to the respiratory rate and the flow, although both theoretical considerations and experimental evidence attribute them a significant role in the generation of VILI. The initial injury to the lung parenchyma is necessarily mechanical and it could manifest as an unphysiological distortion of the extracellular matrix and/or as micro-fractures in the hyaluronan, likely the most fragile polymer embedded in the matrix. The order of magnitude of the energy required to break a molecular bond between the hyaluronan and the associated protein is 1.12×10-16 Joules (J), 70-90% higher than the average energy delivered by a single breath of 1L assuming a lung elastance of 10 cmH2O/L (0.5 J). With a normal statistical distribution of the bond strength some polymers will be exposed each cycle to an energy large enough to rupture. Both the extracellular matrix distortion and the polymer fractures lead to inflammatory increase of capillary permeability with edema if a pulmonary blood flow is sufficient. The mediation analysis of higher vs. lower tidal volume and PEEP studies suggests that the driving pressure, more than tidal volume, is the best predictor of VILI, as inferred by increased mortality. This is not surprising, as both tidal volume and respiratory system elastance (resulting in driving pressure) may independently contribute to the mortality. For the same elastance driving pressure is a predictor similar to plateau pressure or tidal volume. Driving pressure is one of the components of the mechanical power, which also includes respiratory rate, flow and PEEP. Finding the threshold for mechanical power would greatly simplify assessment and prevention of VILI.

Predicting ventilator-induced lung injury using a lung injury cost function.

Managing patients with acute respiratory distress syndrome (ARDS) requires mechanical ventilation that balances the competing goals of sustaining life while avoiding ventilator-induced lung injury (VILI). In particular, it is reasonable to suppose that for any given ARDS patient, there must exist an optimum pair of values for tidal volume (VT) and positive end-expiratory pressure (PEEP) that together minimize the risk for VILI. To find these optimum values, and thus develop a personalized approach to mechanical ventilation in ARDS, we need to be able to predict how injurious a given ventilation regimen will be in any given patient so that the minimally injurious regimen for that patient can be determined. Our goal in the present study was therefore to develop a simple computational model of the mechanical behavior of the injured lung in order to calculate potential injury cost functions to serve as predictors of VILI. We set the model parameters to represent normal, mildly injured, and severely injured lungs and estimated the amount of volutrauma and atelectrauma caused by ventilating these lungs with a range of VT and PEEP. We estimated total VILI in two ways: 1) as the sum of the contributions from volutrauma and atelectrauma and 2) as the product of their contributions. We found the product provided estimates of VILI that are more in line with our previous experimental findings. This model may thus serve as the basis for the objective choice of mechanical ventilation parameters for the injured lung.

Did studies on HFOV fail to improve ARDS survival because they did not decrease VILI? On the potential validity of a physiological concept enounced several decades ago.

High frequency oscillatory ventilation (HFOV) has been the subject of extensive physiological research for 30 years and even more so of an intense debate on its potential usefulness in the treatment of acute respiratory distress syndrome (ARDS). This technique has been enthusiastically promoted by some teams until two high-quality randomized clinical trials in adults with ARDS showed that HFOV did not decrease and might have even increased mortality. As a consequence of these results, physiological concepts such as atelectrauma and biotrauma on which ARDS management with HFOV were based should be reexamined. In contrast, the concept of volutrauma, i.e., end-inspiratory overdistension, as the cause for ventilator-induced lung injury might help explain excess mortality during mechanical ventilation of ARDS when inspiratory volumes are too high. This is what might have happened during one of the recent studies on HFOV. Failure of this complex technique must be put in perspective with the dramatic improvement of ARDS prognosis with very simple interventions such as tidal volume reduction, early pharmacological paralysis, and prone positioning which all limited end-inspiratory volume.

Ventilator-Induced Lung Injury (VILI) in Acute Respiratory Distress Syndrome (ARDS): Volutrauma and Molecular Effects.

Acute Respiratory Distress Syndrome (ARDS) is a clinical condition secondary to a variety of insults leading to a severe acute respiratory failure and high mortality in critically ill patients. Patients with ARDS generally require mechanical ventilation, which is another important factor that may increase the ALI (acute lung injury) by a series of pathophysiological mechanisms, whose common element is the initial volutrauma in the alveolar units, and forming part of an entity known clinically as ventilator-induced lung injury (VILI). Injured lungs can be partially protected by optimal settings and ventilation modes, using low tidal volume (VT) values and high positive-end expiratory pressure (PEEP). The benefits in ARDS outcomes caused by these interventions have been confirmed by several prospective randomized controlled trials (RCTs) and are attributed to reduction in volutrauma. The purpose of this article is to present an approach to VILI pathophysiology focused on the effects of volutrauma that lead to lung injury and the 'mechanotransduction' mechanism. A more complete understanding about the molecular effects that physical forces could have, is essential for a better assessment of existing strategies as well as the development of new therapeutic strategies to reduce the damage resulting from VILI, and thereby contribute to reducing mortality in ARDS.

A biomechanical model of pendelluft induced lung injury.

Lung ventilation using high frequency oscillatory techniques have been documented to attain adequate gas exchange through various gas transport mechanisms. Among them, the pendelluft flow is considered one of the most crucial mechanisms. In this work, we computationally investigate the induction of abnormal mechanical stresses and a regionally trapped volume of gas due to pendelluft flow. Large eddy simulation was used to model the turbulence in an upper tracheobronchial lung geometry that was derived from CT scans. The pendelluft flow was captured by modeling physiological boundary conditions at the truncated level of the lung model that is sensitive to the coupled resistance and compliance of individual patients. The flow-volume and volume-pressure loops are characterized by irregular shapes and suggest abnormal regional lung ventilation. Incomplete loops were observed indicating gas trapping in these regions signifying a potential for local injury due to incomplete ventilation from a residual volume build-up at the end of the expiration phase. In addition, the gas exchange between units was observed to create a velocity gradient causing a region of high wall shear stress surrounding the carina ridges. The recurrence of the pendelluft flow could cause a rupture to the lung epithelium layer. The trapped gas and wall shear stress were observed to amplify with increasing compliance asymmetry and ventilator operating frequency. In general, despite the significant contribution of the pendelluft flow to the gas exchange augmentation there exists significant risks of localized lung injury, phenomena we describe as pendelluft induced lung injury or PILI.

Expansibilidade torácica na avaliação do volume corrente em recém-nascidos prematuros ventilados / Chest expansion for assessing tidal volume in premature newborn infants on ventilators

OBJETIVOS: Avaliar se a observação clínica da expansibilidade torácica prediz o volume corrente em neonatos sob ventilação mecânica e se a experiência do examinador interfere no resultado. MÉTODOS: Estudo observacional que incluiu médicos de baixa experiência (1° ano de residência em pediatria), moderada experiência (2° ano de residência em pediatria, 1° ano de especialização em neonatologia ou em terapia intensiva pediátrica) e experientes (2° ano de especialização em neonatologia, pós-graduandos ou assistentes com experiência mínima de 4 anos em neonatologia). Estes observaram a expansibilidade torácica de recém-nascidos em ventilação mecânica e responderam qual o volume corrente fornecido aos bebês. O volume corrente ofertado foi calculado, indexado ao peso atual do paciente e considerado adequado se entre 4-6 mL/kg, insuficiente se abaixo de 4 mL/kg e excessivo se acima de 6 mL/kg. Para análise dos resultados, foi utilizado o qui-quadrado. RESULTADOS: Foram realizadas 111 avaliações em 21 recém-nascidos, e as respostas fornecidas concordaram com o volume mensurado em 23,1, 41,3 e 65,7 por cento para os médicos de baixa, moderada experiência e experientes, respectivamente. Esses resultados evidenciam que os três grupos não são estatisticamente iguais (p = 0,013) e que o grupo de médicos experientes apresenta maior concordância que os de baixa e moderada experiência (p = 0,007). CONCLUSÃO: A análise clínica da expansibilidade torácica realizada por médicos de baixa e moderada experiência apresenta pouca concordância com o volume corrente ofertado aos recém-nascidos em ventilação mecânica. Embora a experiência dos médicos tenha resultado em maior concordância, a expansibilidade torácica deve ser interpretada com cautela.

OBJECTIVES: To investigate whether clinical observation of chest expansion predicts tidal volume in neonates on mechanical ventilation and whether observer experience interferes with results. METHODS: An observational study that enrolled less experienced physicians in the first year of pediatric residency, moderately experienced (second year pediatric residency, first year of neonatology or pediatric intensive care specialization) or who were already experienced (second year neonatology specialization, graduate students or primary physician supervisors with minimum experience of 4 years in neonatology). These professionals observed the chest expansion of newborn infants on mechanical ventilation and estimated the tidal volume being supplied to the babies. True tidal volume given was calculated, indexed by the patient's current weight, and considered adequate between 4 and 6 mL/kg, insufficient below 4 mL/kg and excessive over 6 mL/kg. Results were analyzed using chi-square test. RESULTS: One hundred and eleven assessments were carried out with 21 newborn infants and the estimates given were in agreement with measured volume in 23.1, 41.3 and 65.7 percent for less, moderately and experienced physicians, respectively. These results are evidence that the three groups are not statistically equal (p = 0.013) and that the group of fully-experienced physicians have a better level of agreement than those with little or moderate experience (p = 0.007). CONCLUSIONS: Clinical analysis of chest expansion by physicians with less or moderate experience exhibit a low level of agreement with the tidal volume given to newborn infants on mechanical ventilation. Although increased experience did result in higher levels of agreement, chest expansion must still be interpreted with caution.