High Inspiratory Pressures Research Articles

Equine exercise-induced pulmonary hemorrhage: the role of high left-heart pressures secondary to exercise-induced hypervolemia, and high inspiratory pressures.

Exercise-induced pulmonary hemorrhage (EIPH) is common in racehorses. Stress failure of the blood-gas barrier causes EIPH when the transmural pulmonary capillary (Pcap)-alveolar pressure difference (Ptm) exceeds the barrier's stress failure threshold. Why Pcap increases is incompletely understood. We hypothesized that alterations in blood volume (BV) could affect left ventricular (LV) and pulmonary arterial wedge (PAW) pressures and Pcap, and correspondingly affect EIPH severity. Six thoroughbreds with EIPH exercised at the same treadmill speed (≈11.9 m/s [11.1, 12.2]; median [IQR]) before (≈119% V̇o2max; B), 2 h after 14 L depletion of blood (≈132% V̇o2max; D), and 2 h after reinfusing the blood (≈111% V̇o2max; R). LV, pulmonary arterial (PAP), PAW, and intrapleural (Ppl) pressures were measured throughout exercise. Pcap = (PAP + PAW)/2 and Ptm = (Pcap - Ppl). EIPH severity was assessed 60 min postexercise by tracheoendoscopy (EIPHgrade) and bronchoalveolar lavage erythrocyte number (BALRBC). A mixed-effect model and Tukey post hoc test analyzed the effects of BV changes on LV, PAW, Pcap, Ppl, Ptm, and EIPH. P ≤ 0.05 was significant. Peak intrapleural inspiratory pressure (PplI) was high (-41 mmHg), unaffected by changes in BV (P = 0.44), and did not contribute to fluctuations in Ptm and EIPH severity, whereas changes in BV did (EIPHgrade: P = 0.01, BALRBC: P = 0.003). EIPH prevalence was 100% with B and R but 50% with D. MaxPtm was not different between B (146 mmHg [140, 151]) and R (151 mmHg [137, 160]) but was lower for D (128 mmHg [127, 130]; B: P = 0.005, R: P = 0.02). Vascular pressures and Ppl fluctuated constantly during exercise and independently influenced Ptm. Left ventricular end diastolic (LVED) pressure was correlated with Ptm (rrm = 0.90, P = 0.03) and EIPH rrm = 0.82, P = 0.004). Exercise BV was strongly correlated with EIPH severity in racehorses (rrm = 0.86, P = 0.009).NEW & NOTEWORTHY Hypervolemia induced by the infusion of erythrocyte-rich blood stored in the spleen is normal in high-speed thoroughbred exercise and increases capillary-alveolar transmural pressure (Ptm), leading to exercise-induced pulmonary hemorrhage (EIPH). In this study, decreasing blood volume reduced Ptm and EIPH. Large negative inspiratory pressures also contribute to high Ptm and the occurrence of EIPH. Ptm is dynamic and oscillates constantly during exercise. A significant relationship existed between circulating blood volume and EIPH severity in racehorses.

Traumatic nasogastric intubation as a suspected cause of laryngeal obstruction in a horse recovering from emergency laparotomy

AbstractAn 18‐year‐old mare, admitted for colic, underwent an exploratory laparotomy for right dorsal colon displacement. During recovery from anaesthesia, a severe acute onset laryngeal obstruction occurred at standing, requiring orotracheal re‐intubation, which relieved the obstruction. This was followed by secondary pulmonary oedema, treated with furosemide (2 mg/kg intravenously) and oxygen. At re‐extubation, attempted 30 minutes later, the horse re‐obstructed immediately and collapsed, prompting an emergency tracheostomy. Furosemide (2 mg/kg intravenously) and dexamethasone (0.1 mg/kg intravenously) were also administered. The horse stood up thereafter with a patent airway. In the history, to note, nasogastric intubation was particularly difficult at admission, and was identified as a potential cause of laryngeal trauma that may have precipitated laryngeal obstruction due to severe local inflammation. Dynamic laryngeal collapse probably also played a role due to high inspiratory negative pressure generated at the precise timing of standing, similar to exercise.

Pathophysiological profile of non-ventilated lung injury in healthy female pigs undergoing mechanical ventilation

BackgroundLung regions excluded from mechanical insufflation are traditionally assumed to be spared from ventilation-associated lung injury. However, preliminary data showed activation of potential mechanisms of injury within these non-ventilated regions (e.g., hypoperfusion, inflammation).MethodsIn the present study, we hypothesized that non-ventilated lung injury (NVLI) may develop within 24 h of unilateral mechanical ventilation in previously healthy pigs, and we performed extended pathophysiological measures to profile NVLI. We included two experimental groups undergoing exclusion of the left lung from the ventilation with two different tidal volumes (15 vs 7.5 ml/kg) and a control group on bilateral ventilation. Pathophysiological alteration including lung collapse, changes in lung perfusion, lung stress and inflammation were measured. Lung injury was quantified by histological score.ResultsHistological injury score of the non-ventilated lung is significantly higher than normally expanded lung from control animals. The histological score showed lower intermediate values (but still higher than controls) when the tidal volume distending the ventilated lung was reduced by 50%. Main pathophysiological alterations associated with NVLI were: extensive lung collapse; very low pulmonary perfusion; high inspiratory airways pressure; and higher concentrations of acute-phase inflammatory cytokines IL-6, IL-1β and TNF-α and of Angiopoietin-2 (a marker of endothelial activation) in the broncho-alveolar lavage. Only the last two alterations were mitigated by reducing tidal volume, potentially explaining partial protection.ConclusionsNon-ventilated lung injury develops within 24 h of controlled mechanical ventilation due to multiple pathophysiological alterations, which are only partially prevented by low tidal volume.

Developing a Computational Model of Lungs for Patients With Acute Respiratory Distress Syndrome

Abstract Acute respiratory distress syndrome (ARDS) is a condition secondary to direct or indirect insult to lungs, leading to acute respiratory failure, and is associated with high mortality. Majority of the ARDS patients require mechanical ventilation, which acts as double-edged sword. Ventilator induced lung injury (VILI) is considered secondary to high inspiratory pressure and cyclical opening during inspiration, and collapse during expiration as suggested by ARDS network clinical trials. Other mechanism for VILI exist secondary to heterogeneous ventilation. To enumerate these mechanisms leading to VILI, a computational fluids dynamics (CFD) study was performed in this study to explore the flow patterns and the pressure distribution in a human tracheobronchial airway model from third to sixth generation branches. The authors validated the computational methodology and analyzed the results to obtain velocity profiles in the primary and secondary flow directions. The study investigated the role of various flow velocities corresponding to Reynolds number (Re) from 100 to 2000 on the pressure drops along branches and bifurcation zones. The identification of secondary flow patterns was critical in understanding the development of asymmetric velocity profiles in the triple bifurcation geometry. The observed patterns in pressure drops and velocity profiles over the laminar flow regime pave the path toward further development of a numerical model to aid treatment for patients with ARDS.

Sustained vs. Intratidal Recruitment in the Injured Lung During Airway Pressure Release Ventilation: A Computational Modeling Perspective.

During mechanical ventilation, cyclic recruitment and derecruitment (R/D) of alveoli result in focal points of heterogeneous stress throughout the lung. In the acutely injured lung, the rates at which alveoli can be recruited or derecruited may also be altered, requiring longer times at higher pressure levels to be recruited during inspiration, but shorter times at lower pressure levels to minimize collapse during exhalation. In this study, we used a computational model to simulate the effects of airway pressure release ventilation (APRV) on acinar recruitment, with varying inspiratory pressure levels and durations of exhalation. The computational model consisted of a ventilator pressure source, a distensible breathing circuit, an endotracheal tube, and a porcine lung consisting of recruited and derecruited zones, as well as a transitional zone capable of intratidal R/D. Lung injury was simulated by modifying each acinus with an inflation-dependent surface tension. APRV was simulated for an inhalation duration (Thigh) of 4.0 seconds, inspiratory pressures (Phigh) of 28 and 40 cmH2O, and exhalation durations (Tlow) ranging from 0.2 to 1.5 seconds. Both sustained acinar recruitment and intratidal R/D within the subtree were consistently higher for Phigh of 40 cmH2O vs. 28 cmH2O, regardless of Tlow. Increasing Tlow was associated with decreasing sustained acinar recruitment, but increasing intratidal R/D, within the subtree. Increasing Tlow was associated with decreasing elastance of both the total respiratory system and transitional subtree of the model. Our computational model demonstrates the confounding effects of cyclic R/D, sustained recruitment, and parenchymal strain stiffening on estimates of total lung elastance during APRV. Increasing inspiratory pressures leads to not only more sustained recruitment of unstable acini but also more intratidal R/D. Our model indicates that higher inspiratory pressures should be used in conjunction with shorter exhalation times, to avoid increasing intratidal R/D.

Ratchet recruitment in the acute respiratory distress syndrome: lessons from the newborn cry.

Patients with acute respiratory distress syndrome (ARDS) have few treatment options other than supportive mechanical ventilation. The mortality associated with ARDS remains unacceptably high, and mechanical ventilation itself has the potential to increase mortality further by unintended ventilator-induced lung injury (VILI). Thus, there is motivation to improve management of ventilation in patients with ARDS. The immediate goal of mechanical ventilation in ARDS should be to prevent atelectrauma resulting from repetitive alveolar collapse and reopening. However, a long-term goal should be to re-open collapsed and edematous regions of the lung and reduce regions of high mechanical stress that lead to regional volutrauma. In this paper, we consider the proposed strategy used by the full-term newborn to open the fluid-filled lung during the initial breaths of life, by ratcheting tissues opened over a series of initial breaths with brief expirations. The newborn's cry after birth shares key similarities with the Airway Pressure Release Ventilation (APRV) modality, in which the expiratory duration is sufficiently short to minimize end-expiratory derecruitment. Using a simple computational model of the injured lung, we demonstrate that APRV can slowly open even the most recalcitrant alveoli with extended periods of high inspiratory pressure, while reducing alveolar re-collapse with brief expirations. These processes together comprise a ratchet mechanism by which the lung is progressively recruited, similar to the manner in which the newborn lung is aerated during a series of cries, albeit over longer time scales.

Pressure- vs. volume-controlled ventilation and their respective impact on dynamic parameters of fluid responsiveness: a cross-over animal study

Background and goal of studyPulse pressure variation (PPV) and stroke volume variation (SVV), which are based on the forces caused by controlled mechanical ventilation, are commonly used to predict fluid responsiveness. When PPV and SVV were introduced into clinical practice, volume-controlled ventilation (VCV) with tidal volumes (VT) ≥ 10 ml kg− 1 was most commonly used. Nowadays, lower VT and the use of pressure-controlled ventilation (PCV) has widely become the preferred type of ventilation. Due to their specific flow characteristics, VCV and PCV result in different airway pressures at comparable tidal volumes. We hypothesised that higher inspiratory pressures would result in higher PPVs and aimed to determine the impact of VCV and PCV on PPV and SVV.MethodsIn this self-controlled animal study, sixteen anaesthetised, paralysed, and mechanically ventilated (goal: VT 8 ml kg− 1) pigs were instrumented with catheters for continuous arterial blood pressure measurement and transpulmonary thermodilution. At four different intravascular fluid states (IVFS; baseline, hypovolaemia, resuscitation I and II), ventilatory and hemodynamic data including PPV and SVV were assessed during VCV and PCV. Statistical analysis was performed using U-test and RM ANOVA on ranks as well as descriptive LDA and GEE analysis.ResultsComplete data sets were available of eight pigs. VT and respiratory rates were similar in both forms. Heart rate, central venous, systolic, diastolic, and mean arterial pressures were not different between VCV and PCV at any IVFS. Peak inspiratory pressure was significantly higher in VCV, while plateau, airway and transpulmonary driving pressures were significantly higher in PCV. However, these higher pressures did not result in different PPVs nor SVVs at any IVFS.ConclusionVCV and PCV at similar tidal volumes and respiratory rates produced PPVs and SVVs without clinically meaningful differences in this experimental setting. Further research is needed to transfer these results to humans.

Negative pressure pulmonary edema (Review).

Negative pressure pulmonary edema (NPPE) is a complication resulting from acute or chronic upper airway obstruction, often posing challenges in recognition and diagnosis for clinicians. If left untreated, NPPE can lead to hypoxemia, heart failure and even shock. Furthermore, the drug treatment of NPPE remains a subject of controversy. The primary pathophysiological mechanism of NPPE involves the need for high inspiratory pressure to counteract upper airway obstruction, subsequently causing a progressive rise in negative pressure within the pleural cavity. Consequently, this results in increased pulmonary microvascular pressure, leading to the infiltration of pulmonary capillary fluid into the alveoli. NPPE exhibits numerous risk factors and causes, with laryngospasm following anesthesia and extubation being the most prevalent. The diagnosis of NPPE often presents challenges due to confusion with conditions such as gastroesophageal reflux or cardiogenic pulmonary edema, given the similarity in initial factors triggering both diseases. Upper airway patency, positive pressure non-invasive ventilation, supplemental oxygen and re-intubation mechanical ventilation are the foundation of the treatment of NPPE. The present review aims to discuss the etiology, clinical presentation, pathophysiology and management of NPPE.

Differential effects of two-hit models of acute and ventilator-induced lung injury on lung structure, function, and inflammation.

Acute respiratory distress syndrome (ARDS) and acute lung injury have a diverse spectrum of causative factors including sepsis, aspiration of gastric contents, and near drowning. Clinical management of severe lung injury typically includes mechanical ventilation to maintain gas exchange which can lead to ventilator-induced lung injury (VILI). The cause of respiratory failure is acknowledged to affect the degree of lung inflammation, changes in lung structure, and the mechanical function of the injured lung. However, these differential effects of injury and the role of etiology in the structure-function relationship are not fully understood. To address this knowledge gap we caused lung injury with intratracheal hydrochloric acid (HCL) or endotoxin (LPS) 2days prior to ventilation or with an injurious lavage (LAV) immediately prior to ventilation. These injury groups were then ventilated with high inspiratory pressures and positive end expiratory pressure (PEEP) = 0cmH2O to cause VILI and model the clinical course of ARDS followed by supportive ventilation. The effects of injury were quantified using invasive lung function measurements recorded during PEEP ladders where the end-expiratory pressure was increased from 0 to 15cm H2O and decreased back to 0cmH2O in steps of 3cmH2O. Design-based stereology was used to quantify the parenchymal structure of lungs air-inflated to 2, 5, and 10cmH2O. Pro-inflammatory gene expression was measured with real-time quantitative polymerase chain reaction and alveolocapillary leak was estimated by measuring bronchoalveolar lavage protein content. The LAV group had small, stiff lungs that were recruitable at higher pressures, but did not demonstrate substantial inflammation. The LPS group showed septal swelling and high pro-inflammatory gene expression that was exacerbated by VILI. Despite widespread alveolar collapse, elastance in LPS was only modestly elevated above healthy mice (CTL) and there was no evidence of recruitability. The HCL group showed increased elastance and some recruitability, although to a lesser degree than LAV. Pro-inflammatory gene expression was elevated, but less than LPS, and the airspace dimensions were reduced. Taken together, those data highlight how different modes of injury, in combination with a 2nd hit of VILI, yield markedly different effects.

Mitigation and Outcomes of Difficult Bag-Mask Ventilation in Critically Ill Children

AbstractDifficult bag-mask ventilation (BMV) occurs in 10% of pediatric intensive care unit (PICU) tracheal intubations (TI). The reasons clinicians identify difficult BMV in the PICU and the interventions used to mitigate that difficulty have not been well-studied. This is a prospective, observational, single-center study. A patient-specific data form was sent to PICU physicians supervising TIs from November 2019 through December 2020 to identify the presence of difficult BMV, attempted interventions used, and perceptions about intervention success. The dataset was linked and merged with the local TI quality database to assess safety outcomes. Among 305 TIs with response (87% response rate), 267 (88%) clinicians performed BMV during TI. Difficult BMV was reported in 28 of 267 patients (10%). Commonly reported reasons for difficult BMV included: facial structure (50%), high inspiratory pressure (36%), and improper mask fit (21%). Common interventions were jaw thrust (96%) and an airway adjunct (oral airway 50%, nasal airway 7%, and supraglottic airway 11%), with ventilation improvement in 44% and 73%, respectively. Most difficult BMV was identified before neuromuscular blockade (NMB) administration (96%) and 67% (18/27) resolved after NMB administration. The overall success in improving ventilation was 27/28 (96%). TI adverse outcomes (hemodynamic events, emesis, and/or hypoxemia <80%) are associated with the presence of difficult BMV (10/28, 36%) versus non-difficult BMV (20/239, 8%, p< 0.001). Difficult BMV is common in critically ill children and is associated with increased TI adverse outcomes. Airway adjunct placement and NMB use are often effective in improving ventilation.

Synchronized ventilation during resuscitation in pigs does not necessitate high inspiratory pressures to provide adequate oxygenation.

Synchronized ventilation during resuscitation in pigs does not necessitate high inspiratory pressures to provide adequate oxygenation.

Spatiotemporal distribution of cellular injury and leukocytes during the progression of ventilator-induced lung injury.

Supportive mechanical ventilation is a necessary lifesaving treatment for acute respiratory distress syndrome (ARDS). This intervention often leads to injury exacerbation by ventilator-induced lung injury (VILI). Patterns of injury in ARDS and VILI are recognized to be heterogeneous; however, quantification of these injury distributions remains incomplete. Developing a more detailed understanding of injury heterogeneity, particularly how it varies in space and time, can help elucidate the mechanisms of VILI pathogenesis. Ultimately, this knowledge can be used to develop protective ventilation strategies that slow disease progression. To expand existing knowledge of VILI heterogeneity, we document the spatial evolution of cellular injury distribution and leukocyte infiltration, on the micro- and macroscales, during protective and injurious mechanical ventilation. We ventilated naïve mice using either high inspiratory pressure and zero positive end-expiratory pressure ventilation or low tidal volume with positive end-expiratory pressure. Distributions of cellular injury, identified with propidium iodide staining, were microscopically analyzed at three levels of injury severity. Cellular injury initiated in diffuse, quasi-random patterns, and progressed through expansion of high-density regions of injured cells termed "injury clusters." The density profile of the expanding injury regions suggests that stress shielding occurs, protecting the already injured regions from further damage. Spatial distribution of leukocytes did not correlate with that of cellular injury or ventilation-induced changes in lung function. These results suggest that protective ventilation protocols should protect the interface between healthy and injured regions to stymie injury propagation.

Acute cardiac injury (ACI) in COVID-19 pneumonia

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Since the SARS-CoV2 break-out many reports focused on the role of cardiovascular system involvement in the patient’s outcome(1). However, few descriptions exist including only patients with severe ARDS admitted to general ICU. Methods We enrolled adult patients with severe ARDS related to COVID-19 infection consecutively admitted to ICU between February 2020 and March 2021. Acute cardiac injury was defined as a rise and fall of cTnI above the 99th percentile (i.e., ≥ 47 ng/L)(2). Hs-TnI was measured at admission and during ICU stay. Echocardiographic examinations were performed at ICU admission and at the time of worst cTnI. Left ventricular (LV) and right ventricular (RV) systolic dysfunction were defined respectively as LV ejection fraction (LVEF) < 50% and as tricuspid annular plane systolic excursion (TAPSE) < 16 mm. Results A total of 148 patients were included in the analysis. Acute cardiac injury was present in 65 (44.9%) cases at admission. Forty-seven (21.8%) patients had isolated depressed LVEF, 13 (9.0%) had isolated RV systolic dysfunction and 24 (16,4%) presented with biventricular systolic dysfunction. Eithy-two (56.1%) had a worsening of hs-TNI values during the admission of whom a consensual worsening of LVEF and TAPSE was observed in respectively 32 (21.8%) and 28 (19.2%) patients. Cardiac injury at ICU admission yielded an increased risk of in-hospital mortality (OR 1.30 [95% CI 0.71 – 2.38]) (Figure 1 – left panel) as well as the presence of impaired echocardiography (OR 1.85 [95% CI 1.01 – 3.40]) (Figure 1 – right panel). Worst hs-TNI correlated with worst procalcitonin (PCT) values (p <0.001 r20.81) in case of on-going septic shock and 85 % of patients with RV dysfunction had either evidence of pulmonary thrombus at CT scan or high inspiratory peak pressure (> 30 cmH2O) at mechanical ventilation (respectively, p < 0.001 and p <0.01). Bivariable analysis adjusted for the inverse probability of having an impaired echocardiographic exam confirmed the increased risk of in-hospital mortality in patients with cardiac injury (OR 2.01 [95% CI 1.28 – 3.15]) and in presence of altered echocardiography with RV dysfunction yielding a higher risk (OR 2.42 [95% CI 1.29 – 4.55]) compared with biventricular impairment (OR 1.86 [95% CI 0.87 – 4.00]) and isolated LV dysfunction (OR 1.30 [95% CI 0.77 – 2.19]) (Figure 2). Conclusion The use of echocardiography for the detection of cardiac dysfunction, has shown a greater correlation with mortality than the identification of acute cardiac damage using laboratory parameters. Of all the parameters obtained with the echocardiography, right ventricular dysfunction demonstrates the greatest correlation with mortality compared to left or biventricular dysfunction. However, the major cause of LV dysfunction in our population occurred during septic shock while RV dysfunction seemed to be due to pulmonary embolism and/or acute cor pulmonale ARDS-related.

Aerosol delivery through high flow nasal cannula compared to biphasic positive airway pressure, at two different pressure: an in-vitro study

BackgroundBoth non-invasive ventilation and high flow oxygen therapy are preferred over low flow oxygen therapy in many conditions. Nebulizers, for aerosol delivery, can be used within them without interrupting the circuit. The present study aimed to compare the efficiency of drug delivery within high flow nasal cannula (HFNC) and biphasic positive airway pressure (BiPAP) ventilation mode using two different inspiratory positive airway pressures. The aerosol delivery was examined in HFNC system at low flow, 5 L min−1, and BiPAP non-invasive ventilation under 2 different pressures [high pressure; inspiratory positive airway pressure/expiratory positive airway pressure (IPAP/EPAP) of 20/5 cm water, and low pressure; IPAP/EPAP of 10/5 cm water]. The total inhalable dose (TID) was measured by inserting an Aerogen Solo nebulizer installed with 1 mL salbutamol respiratory solution (5000 μg mL−1) within the circuit, and the salbutamol was collected on an inhalation filter placed in a filter holder connected to a breathing simulator. The breathing simulator was adjusted at a tidal volume of 500 mL, respiratory rate of 15 breaths min−1, and inhalation to exhalation (I:E) ratio of 1:1 for the adult setting. In each technique of the three (HFNC, and low, and high-pressures BiPAP), TID was determined 5 times (n = 5). For particle size characterization, cooled Anderson Cascade Impactor (ACI) was inserted instead of the inhalation filter and the breathing simulator with the same scheme. In each technique of the three, particle size characterization was determined 3 times (n = 3).ResultsThe BiPAP mode at low inspiratory pressure had the highest TID, followed by HFNC at flow 5 L min−1, then BiPAP mode at high inspiratory pressure. There was a significant difference only between low and high inspiratory pressure modes of BiPAP mode. Low-inspiratory pressure BiPAP delivered the highest mean ± SD fine particle dose (FPD). It was significantly higher than that delivered in high inspiratory pressure BiPAP, and HFNC. Also, FPD in HFNC was significantly higher than that in high inspiratory pressure BiPAP. HFNC system had the smallest mass median aerodynamic diameter (MMAD) and the highest FPF followed by low then high inspiratory pressure BiPAP.ConclusionsIncreasing the inspiratory positive airway pressure in BiPAP, from 10 to 20 cm water, decreased the total inhalable dose and FPF nearly by half. Low inspiratory pressure BiPAP delivered the highest TID and FPD. The HFNC system at low oxygen flow resulted in the least MMAD, and the highest FPF. Using HFNC delivered a TID that was non-significant from that delivered by low inspiratory pressure BiPAP.Graphical

Is bilevel PAP more effective than CPAP in treating hypercapnic obese patients with COPD and severe OSA?

Commentary on Zheng Y, Yee BJ, Wong K, Grunstein R, Piper A. A pilot randomized trial comparing CPAP versus bilevel PAP spontaneous mode in the treatment of hypoventilation disorder in patients with obesity and obstructive airway disease. J Clin Sleep Med. 20XX;XX(XX):XXX-XXX. doi:10.5664/jcsm.9506.

Long-Term Domiciliary Noninvasive Ventilation for COPD.

COPD can lead to abnormalities in oxygenation as well as ventilation. Thanks to pioneering work by Dr Thomas Petty, supplemental oxygen therapy has been shown to improve morbidity and mortality for individuals with COPD and severe daytime hypoxemia. However, efforts to augment ventilation have been less uniformly successful. Recent studies employing a so-called high-intensity noninvasive ventilation strategy, which used high inspiratory pressures and backup breathing frequency to reduce arterial carbon dioxide levels, have shown improved quality of life and reduced mortality. Thus, efforts are underway to better identify and treat patients with COPD who might benefit from noninvasive ventilation, though many practical questions remain.

Correction: Non-invasive ventilation with pursed lips breathing mode for patients with COPD and hypercapnic respiratory failure: A retrospective analysis

[This corrects the article DOI: 10.1371/journal.pone.0238619.].

Average volume-assured pressure support vs conventional bilevel pressure support in pediatric nocturnal hypoventilation: a case series.

Average volume-assured pressure support (AVAPS) is a modality of noninvasive ventilation that provides a targeted tidal volume by automatically adjusting the inspiratory pressure support within a set range. Pediatric studies evaluating the efficacy of AVAPS in treating nocturnal hypoventilation are confined to case reports. The aim of this study was to compare AVAPS to conventional bilevel positive airway pressure (BPAP) support in improving hypercarbia in a cohort of pediatric patients with nocturnal hypoventilation. Retrospective review of patient records at an established tertiary pediatric sleep laboratory over a 6-year period. Ventilatory and sleep study parameters from AVAPS and conventional BPAP titration studies were compared. AVAPS was used only if hypoventilation was not controlled using conventional BPAP. Inspiratory pressures, tidal volumes, and adherence were downloaded on final titrated ventilatory settings. Comparisons were made using paired t test. A total of 19 patients (11 boys, 8 girls; median age 10.5 years, range 1 to 20 years) were identified. Diagnoses included neuromuscular disease (n = 9), obstructive hypoventilation (n = 5), parenchymal lung disease (n = 4), and congenital central hypoventilation syndrome (n = 2). AVAPS demonstrated significant improvement in peak (P = .009) and mean (P = .001). Transcutaneous CO₂ parameters compared to conventional bilevel. Oxygenation on AVAPS showed positive trend but did not reach statistical significance. AVAPS delivered higher tidal volumes (P = .04) using similar pressures. There was no statistically significant difference in obstructive apnea-hypopnea index, respiratory arousal index, sleep efficiency, and adherence between AVAPS and conventional BPAP. AVAPS was an effective alternative to conventional BPAP in improving hypercarbia in our selective cohort of pediatric patients. Prospective, longitudinal studies are needed to evaluate the benefits of AVAPS feature in the pediatric population.

Effects of the Lower Airway Secretions on Airway Opening Pressures and Suction Pressures in Critically Ill COVID-19 Patients: A Computational Simulation.

In patients with critically ill COVID-19 pneumonia, lower airways are filled with plenty of highly viscous exudates or mucus, leading to airway occlusion. The estimation of airway opening pressures and effective mucus clearance are therefore two issues that clinicians are most concerned about during mechanical ventilation. In this study we retrospectively analyzed respiratory data from 24 critically ill patients with COVID-19 who received invasive mechanical ventilation and recruitment maneuver at Jinyintan Hospital in Wuhan, China. Among 24 patients, the mean inspiratory plateau pressure was 52.4 ± 4.4 cmH2O (mean ± [SD]). Particularly, the capnograms presented an upward slope during the expiratory plateau, indicting the existence of airway obstruction. A computational model of airway opening was subsequently introduced to investigate possible fluid dynamic mechanisms for the extraordinarily high inspiratory plateau pressures among these patients. Our simulation results showed that the predicted airway opening pressures could be as high as 40–50 cmH2O and the suction pressure could exceed 20 kPa as the surface tension and viscosity of secretion simulants markedly increased, likely causing the closures of the distal airways. We concluded that, in some critically ill patients with COVID-19, limiting plateau pressure to 30 cmH2O may not guarantee the opening of airways due to the presence of highly viscous lower airway secretions, not to mention spontaneous inspiratory efforts. Active airway humidification and effective expectorant drugs are therefore strongly recommended during airway management.

YOUNG FEMALE WITH CYSTIC LUNG LESIONS: LAM OR CANNABIS-INDUCED?

SESSION TITLE: Medical Student/Resident Lung Pathology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Lymphangioleiomyomatosis (LAM) is a rare condition of unknown etiology, which causes cystic lung lesions in young women and often presents with dyspnea and pneumothoraces (1). CASE PRESENTATION: A 39-year-old African American female with a past medical history of asthma, marijuana use, and tobacco use presented to the Emergency Room (ER) with non-specific abdominal pain. She underwent computed tomography (CT) of her chest, abdomen, and pelvis and was incidentally found to have bilateral cystic lung lesions. Her abdominal workup was negative and she was discharged with a referral to pulmonology due to concerns for LAM. On follow-up in pulmonology clinic, her history was significant for dyspnea on exertion for several years, as well as worsening dyspnea during a recent pregnancy. A few months later, the patient presented to the ER with chest pain and was found to have a primary spontaneous pneumothorax (PSP) and a chest tube was placed and removed prior to discharge. A few weeks later the patient developed worsening chest pain and dyspnea and was found to have a recurrent pneumothorax. She underwent repeat chest tube placement and her VEGF-D was negative at that time. She underwent pleurodesis with lobectomy of her lingula, and pathology showed smoking-related mild emphysematous changes, subpleural blebs, reactive mesothelium, and no evidence of LAM. Her cystic lesions, dyspnea, and recurrent pneumothoraces were attributed to her heavy cannabis use. DISCUSSION: Our patient had characteristic findings of LAM including dyspnea, recurrent pneumothoraces, and cystic lung disease. However, her VEGF-D was negative and her lingula biopsy results revealed no evidence of LAM; therefore, she was diagnosed with cannabis cystic lung disease. Young females with cystic lung disease are frequently suspected of having LAM, which is rare. When evaluating females with cystic lung disease, common etiologies such as emphysema and cannabis cystic lung disease should be ruled out. Many case reports have documented the appearance of PSP, dyspnea, and upper to middle lobe bullous emphysema in patients who use cannabis (1,2). These findings are heightened in patients who are users of both cannabis and tobacco, such as our patient (1). The mechanism of bullae formation in cannabis users is unknown, but has been attributed to prolonged breath holding during marijuana smoking, which leads to extended exposure to inhaled toxins and subsequent loss of elastic recoil in lung tissue. The mechanism of pneumothoraces has been attributed to repeated Muller’s and Valsalva maneuvers, in addition to high inspiratory pressures causing barotrauma (3). CONCLUSIONS: Common etiologies such as emphysema and cannabis cystic lung disease should be ruled out when evaluating young females with cystic lung lesions. Reference #1: Martinasek MP, McGrogan JB, Maysonet A. A Systematic Review of the Respiratory Effects of Inhalational Marijuana. Respir Care. 2016 Nov;61(11):1543-1551. Reference #2: Underner M, Urban T, Perriot J, Peiffer G, Harika-Germaneau G, Jaafari N. Spontaneous pneumothorax and lung emphysema in cannabis users. Rev Pneumol Clin. 2018 Dec;74(6):400-415 Reference #3: Mishra R, Patel R, Khaja M. Cannabis-induced bullous lung disease leading to pneumothorax. Medicine (Baltimore). 2017 May; 96(19): e6917. DISCLOSURES: No relevant relationships by Nelly Bellamy, source=Web Response Speaker/Speaker's Bureau relationship with Theravance Please note: $1001 - $5000 Added 06/12/2020 by Edward Charbek, source=Web Response, value=Honoraria No relevant relationships by Joseph Cumming, source=Admin input no disclosure on file for Elizabeth Davaro