Alveolar Pressure Research Articles

Mechanosensitive Responses of Resident Alveolar

BackgroundThe extent of micromechanical coupling between resident alveolar macrophages (AMs) and the surrounding tissue niche remains unclear. Lung overexpansion due to therapeutic mechanical ventilation imposes distortional stresses on the alveolar epithelium (AE), causing acute lung injury (ALI). Sessile AMs, lying adjacent to the AE, are causally implicated in ALI. However, it is not clear whether micromechanical coupling with the AE induces proinflammatory distortional stresses in sessile AMs. We addressed this question in live mouse lungs by real‐time confocal microscopy (RCM).MethodsFor RCM, we inflated and blood‐perfused mouse lungs at physiological pressures. To detect cytosolic Ca2+ (cCa2+), we microinfused fluo‐4 by alveolar micropuncture. To detect sessile AMs, we microinfused fluorophore‐conjugated anti‐Siglec‐F and anti‐CD11c Abs. To induce transient lung overexpansion, we increased the alveolar pressure from 5 to 15 cmH2O for 15 seconds. We determined alveolar diameter in terms of fluo‐4 fluorescence, which marked the epithelial margins. We determined cell diameter of sessile AMs in terms of Siglec‐F fluorescence, which marked the cell boundary. We detected gap junctional communication (GJC) by fluorescence recovery after photobleaching (FRAP).ResultsSessile AMs were exclusively located in non‐distending microniches of the alveolus and therefore, did not stretch during lung expansion. Nevertheless, a subset of AMs responded to lung overexpansion by transiently increasing cCa2+. The cCa2+ increase initiated in 5 min, reaching peak at two‐times baseline in 20 min, then subsiding to baseline after a further 20 min. Concomitantly, in AE adjacent to AMs, there was marked increase in cCa2+ oscillations, but no increase in mean cCa2+. In lungs with AM‐specific Cx43 deletion, the transient cCa2+ response was blocked in AMs, but not in adjoining AE. FRAP revealed GJC only in cCa2+‐responsive AMs. In paired comparisons, AMs lacking GJC failed to show expansion‐induced Ca2+ responses (p<0.05).ConclusionsWe report the unexpected finding that sessile AMs were exclusively located in immobile microniches of alveoli and therefore did not stretch during lung expansion. Nevertheless, following expansion there was Cx43‐mediated Ca2+communication with the AE, causing cCa2+ increases in sessile AMs. Although further studies are required to evaluate the potentially proinflammatory responses induced by this Ca2+ response, we propose Cx43 of sessile AMs might be a therapeutic target to mitigate lung expansion‐induced ALI.

Respiratory-Cardiovascular Interactions During Mechanical Ventilation: Physiology and Clinical Implications.

Positive-pressure inspiration and positive end-expiratory pressure (PEEP) increase pleural, alveolar, lung transmural, and intra-abdominal pressure, which decrease right and left ventricular (RV; LV) preload and LV afterload and increase RV afterload. The magnitude and clinical significance of the resulting changes in ventricular function are determined by the delivered tidal volume, the total level of PEEP, the compliance of the lungs and chest wall, intravascular volume, baseline RV and LV function, and intra-abdominal pressure. In mechanically ventilated patients, the most important, adverse consequences of respiratory-cardiovascular interactions are a PEEP-induced reduction in cardiac output, systemic oxygen delivery, and blood pressure; RV dysfunction in patients with ARDS; and acute hemodynamic collapse in patients with pulmonary hypertension. On the other hand, the hemodynamic changes produced by respiratory-cardiovascular interactions can be beneficial when used to assess volume responsiveness in hypotensive patients and by reducing dyspnea and improving hypoxemia in patients with cardiogenic pulmonary edema. Thus, a thorough understanding of the physiological principles underlying respiratory-cardiovascular interactions is essential if critical care practitioners are to anticipate, recognize, manage, and utilize their hemodynamic effects. © 2022 American Physiological Society. Compr Physiol 12:1-24, 2022.

The Effect of the Endotracheal Cuff and Alveolar Pressures on Laryngopharyngeal Outcomes in Laparoscopic and Open Gynecological Procedure

The Effect of the Endotracheal Cuff and Alveolar Pressures on Laryngopharyngeal Outcomes in Laparoscopic and Open Gynecological Procedure

A comparative analysis of lung function and spirometry parameters in genotype-controlled natives living at low and high altitude

BackgroundThe reference values for lung function are associated to anatomical and lung morphology parameters, but anthropometry it is not the only influencing factor: altitude and genetics are two important agents affecting respiratory physiology. Altitude and its influence on respiratory function has been studied independently of genetics, considering early and long-term acclimatization.ObjectiveThe objective of this study is to evaluate lung function through a spirometry study in autochthonous Kichwas permanently living at low and high-altitude.MethodologyA cross-sectional study of spirometry differences between genetically matched lowland Kichwas from Limoncocha (230 m) at Amazonian basin and high-altitude Kichwas from Oyacachi (3180 m) in Andean highlands. The sample size estimates permitted to recruited 118 patients (40 men and 78 women) from Limoncocha and 95 (39 men and 56 women) from Oyacachi. Chi-square method was used to analyze association or independence of categorical variables, while Student’s t test was applied to comparison of means within quantitative variables. ANOVA, or in the case that the variables didn’t meet the criteria of normality, Kruskal Wallis test were used to compare more than two groups.ResultsThe FVC and the FEV1 were significantly greater among highlanders than lowlanders (p value < 0.001), with a proportion difference of 15.2% for men and 8.5% for women. The FEV1/FVC was significantly higher among lowlanders than highlanders for men and women. A restrictive pattern was found in 12.9% of the participants.ConclusionResidents of Oyacachi had greater FVC and FEV1 than their peers from Limoncocha, a finding physiologically plausible according to published literature. Lung size and greater ventilatory capacities could be an adaptive mechanism developed by the highlander in response to hypoxia. Our results support the fact that this difference in FVC and FEV1 is a compensatory mechanism towards lower barometric and alveolar partial pressure of oxygen pressure.

Expiratory Peak Flow and Minute Ventilation Are Significantly Increased at High Altitude versus Simulated Altitude in Normobaria.

Simulated altitude (normobaric hypoxia, NH) is used to study physiologic hypoxia responses of altitude. However, several publications show differences in physiological responses between NH and hypobaric conditions at altitude (hypobaric hypoxia, HH). The causality for these differences is controversially discussed. One theory is that the lower air density and environmental pressure in HH compared to NH lead to lower alveolar pressure and therefore lower oxygen diffusion in the lung. We hypothesized that, if this theory is correct, due to physical laws (Hagen-Poiseuille, Boyle), resistance respectively air compression (Boyle) at expiration should be lower, expiratory flow higher, and therefore peak flow and maximum expiratory flow (MEF) 75–50 increased in hypobaric hypoxia (HH) vs. normobaric hypoxia (NH). To prove the hypothesis of differences in respiratory flow as a result of lower alveolar pressure between HH and NH, we performed spirography in NH at different simulated altitudes and the corresponding altitudes in HH. In a cross over study, 6 healthy subjects (2 f/4 m, 28.3 ± 8.2 years, BMI: 23.2 ± 1.9) performed spirography as part of spiroergometry in a normobaric hypoxic room at a simulated altitude of 2800 m and after a seven-hour hike on a treadmill (average incline 14%, average walking speed 1.6 km/h) to the simulated summit of Mauna Kea at 4200 m. After a two-month washout, we repeated the spirometry in HH on the start and top of the Mauna Kea hiking trail, HI/USA. Comparison of NH (simulated 4200 m) and HH at 4200 m resulted in increased pulmonary ventilation during exercise (VE) (11.5%, p < 0.01), breathing-frequency (7.8%, p < 0.01), peak expiratory flow PEF (13.4%, p = 0.028), and MEF50 (15.9%, p = 0.028) in HH compared to NH, whereas VO2max decreased by 2%. At 2800 m, differences were only trendy, and at no altitude were differences in volume parameters. Spirography expresses higher mid expiratory flows and peak flows in HH vs. NH. This supports the theory of lower alveolar and small airway pressure due to a lower air density resulting in a lower resistance.

Static and Dynamic Measurements of Compliance and Driving Pressure: A Pilot Study.

RationaleMonitoring tidal cycle mechanics is key to lung protection. For this purpose, compliance and driving pressure of the respiratory system are often measured clinically using the plateau pressure, obtained after imposing an extended end-inspiratory pause, which allows for relaxation of the respiratory system and redistribution of inflation volume (method A). Alternative methods for estimating compliance and driving pressure utilize the measured pressure at the earliest instance of zero flow (method B), the inspiratory slope of the pressure-time tracing during inflation with constant flow (method C), and the expiratory time constant (method D).MethodsTen passive mechanically ventilated subjects, at a large tertiary referral center, underwent measurements of compliance and driving pressure using the four different methods. The inspiratory tidal volume, inspiratory to expiratory ratio, and positive end expiratory pressures were then adjusted from baseline and the measurements re-obtained.ResultsMethod A yielded consistently higher compliance and lower driving pressure calculations compared to methods B and C. Methods B and C most closely approximated one another. Method D did not yield a consistent reliable pattern.ConclusionStatic measurements of compliance and driving pressure using the plateau pressure may underestimate the maximum pressure experienced by the most vulnerable lung units during dynamic inflation. Utilizing the pressure at zero flow as a static measurement, or the inspiratory slope as a dynamic measurement, may calculate a truer estimate of the maximum alveolar pressure that generates stress upon compromised lung units.

Variations on Ernsting's Post-Decompression Hypoxia Prevention Model.

INTRODUCTION: In the event of decompression using an isobaric differential cockpit pressurization system, oxygen concentration breathed pre-decompression must be greater than required for the given cockpit altitude in order to prevent hypoxia. The model for determining oxygen concentration requirements advanced by Dr. John Ernsting, when graphed against cockpit altitude, creates a hypoxia safety "notch" which has become a standard requirement for aircraft oxygen systems. Although variables in the Ernsting notch model are not fixed, they are often presented as such.METHODS: Model equations are presented to evaluate the effects of different cockpit pressurization, oxygen regulator PBA schedules, and changes to the physiological state of the aircrew.RESULTS: Increased cockpit differential pressure, regulator breathing pressure, and aircrew respiratory quotient decreased pre-decompression oxygen concentration requirements by up to 6%, eliminating the hypoxia safety "notch." Although effects were small, reducing alveolar carbon dioxide pressure decreased oxygen concentration requirements while reducing respiratory quotient increased oxygen concentration requirements. A 10-mmHg increase in the minimal oxygen hypoxia threshold increased the pre-decompression oxygen concentration requirement 8 to 12% depending on cockpit altitude.CONCLUSION: Variation in cockpit and regulator pressure schedules which stray outside the parameters used by Ernsting need to be independently calculated. During flight, an individual's physiological "notch" will be dynamic, wavering in response to changes in metabolic load, respiratory dynamics, and environmental conditions. Consideration of aircrew activity should be factored in when considering minimal oxygen concentration for pre-decompression hypoxia protection in the design of aircrew life support systems.Dart TS, Morse BG. Variations on Ernsting's post-decompression hypoxia prevention model. Aerosp Med Hum Perform. 2022; 93(2):99-105.

Neumomediastino en pacientes con COVID-19

Se considera neumomediastino a la presencia de aire libre en el mediastino. Puede clasificarse en primario o secundario, asociado a entidades torácicas o extratorácicas. Se ha detallado casos eventuales de neumomediastino espontáneo en pacientes con COVID-19 que podría considerarse un indicador potencial de agravamiento de la infección. En la presente revisión se generó una exploración en repositorios como Google Scholar, PubMed, SiELO, Redalyc y Scopus. Aunque se desconoce el mecanismo exacto delneumomediastino en pacientes con neumonía por COVID-19 se detalla el aumento de la presión alveolar y la lesión alveolar difusa, que resulta en mayor propensión de los alvéolos a romperse. Además, la trombosis y la inflamación local alteran la respuesta vasoconstrictora a la hipoxia alveolar y la vasoreactividad.

Pulmonary Interstitial Matrix and Lung Fluid Balance From Normal to the Acutely Injured Lung.

This review analyses the mechanisms by which lung fluid balance is strictly controlled in the air-blood barrier (ABB). Relatively large trans-endothelial and trans-epithelial Starling pressure gradients result in a minimal flow across the ABB thanks to low microvascular permeability aided by the macromolecular structure of the interstitial matrix. These edema safety factors are lost when the integrity of the interstitial matrix is damaged. The result is that small Starling pressure gradients, acting on a progressively expanding alveolar barrier with high permeability, generate a high transvascular flow that causes alveolar flooding in minutes. We modeled the trans-endothelial and trans-epithelial Starling pressure gradients under control conditions, as well as under increasing alveolar pressure (Palv) conditions of up to 25 cmH2O. We referred to the wet-to-dry weight (W/D) ratio, a specific index of lung water balance, to be correlated with the functional state of the interstitial structure. W/D averages ∼5 in control and might increase by up to ∼9 in severe edema, corresponding to ∼70% loss in the integrity of the native matrix. Factors buffering edemagenic conditions include: (i) an interstitial capacity for fluid accumulation located in the thick portion of ABB, (ii) the increase in interstitial pressure due to water binding by hyaluronan (the “safety factor” opposing the filtration gradient), and (iii) increased lymphatic flow. Inflammatory factors causing lung tissue damage include those of bacterial/viral and those of sterile nature. Production of reactive oxygen species (ROS) during hypoxia or hyperoxia, or excessive parenchymal stress/strain [lung overdistension caused by patient self-induced lung injury (P-SILI)] can all cause excessive inflammation. We discuss the heterogeneity of intrapulmonary distribution of W/D ratios. A W/D ∼6.5 has been identified as being critical for the transition to severe edema formation. Increasing Palv for W/D > 6.5, both trans-endothelial and trans-epithelial gradients favor filtration leading to alveolar flooding. Neither CT scan nor ultrasound can identify this initial level of lung fluid balance perturbation. A suggestion is put forward to identify a non-invasive tool to detect the earliest stages of perturbation of lung fluid balance before the condition becomes life-threatening.

This Month in Anesthesiology

This Month in Anesthesiology

PPV May Be a Starting Point to Achieve Circulatory Protective Mechanical Ventilation.

Pulse pressure variation (PPV) is a mandatory index for hemodynamic monitoring during mechanical ventilation. The changes in pleural pressure (Ppl) and transpulmonary pressure (PL) caused by mechanical ventilation are the basis for PPV and lead to the effect of blood flow. If the state of hypovolemia exists, the effect of the increased Ppl during mechanical ventilation on the right ventricular preload will mainly affect the cardiac output, resulting in a positive PPV. However, PL is more influenced by the change in alveolar pressure, which produces an increase in right heart overload, resulting in high PPV. In particular, if spontaneous breathing is strong, the transvascular pressure will be extremely high, which may lead to the promotion of alveolar flooding and increased RV flow. Asynchronous breathing and mediastinal swing may damage the pulmonary circulation and right heart function. Therefore, according to the principle of PPV, a high PPV can be incorporated into the whole respiratory treatment process to monitor the mechanical ventilation cycle damage/protection regardless of the controlled ventilation or spontaneous breathing. Through the monitoring of PPV, the circulation-protective ventilation can be guided at bedside in real time by PPV.

Electrical Impedance Tomography to Set Positive End Expiratory Pressure During Pediatric Extracorporeal Membrane Oxygenation for Respiratory Failure... Is it Feasible?

Electrical Impedance Tomography to Set Positive End Expiratory Pressure During Pediatric Extracorporeal Membrane Oxygenation for Respiratory Failure... Is it Feasible?

This Month in Anesthesiology

This Month in Anesthesiology

In-hospital clinical complications of COVID-19: a brief overview.

In-hospital clinical complications of COVID-19: a brief overview.

Reliable Estimates of Power Delivery During Mechanical Ventilation Utilizing Easily Obtained Bedside Parameters.

Ventilator-induced lung injury (VILI) requires repetitive transfer of energy from the ventilator to the compromised lung. To understand this phenomenon, 2 sets of equations have been developed to partition total inflation energy into harmless and hazardous components using an arbitrary level of alveolar pressure as a threshold beyond which further energy increments may become damaging. One set of equations uses premeasured resistance and compliance as inputs to predict the energy that would be delivered by typical ventilator settings, whereas the other equation set uses observed output values for end-inspiratory peak and plateau pressure of an already completed inflation. Our aim for this study was to compare the relative accuracy of these equation sets against the performance of a physical one-compartment model of the respiratory system, programmed with information readily available at the bedside and ventilated using both constant and decelerating flow profiles. Accordingly, equations of each set were compared against the corresponding energy areas measured by digital planimetry of pressure-volume curves for 76 ventilator and patient parameter combinations and over 500 power calculations. With few exceptions, all equations strongly correlated with their corresponding measurements by planimetry. This validation of threshold-partitioned energy equations suggests their potential utility for implementing practical strategies for VILI avoidance.

LEAKY LUNGS: A COMPLICATION OF COVID-19 PNEUMONIA

TOPIC: Chest Infections TYPE: Medical Student/Resident Case Reports INTRODUCTION: COVID-19 pneumonia can result in complications such as ARDS, septic shock, thromboembolic events, and kidney failure. Spontaneous pneumothorax, pneumomediastinum and subcutaneous emphysema are rare complications. CASE PRESENTATION: A 72-year-old African American female presented with a four day history of dyspnea. She was tachypneic with respiratory rate of 25/min with O2 saturation of 67% on room air, oxygen therapy via nonrebreather mask improved the O2 saturation to 92%. PCR test for SARS-CoV-2 was positive. Laboratory studies revealed a D-dimer-1121 ng/ml, C-reactive protein-15.97mg/dl, ferritin-356.8 and lactate dehydrogenase-337 U/L. Chest X-ray showed focal areas of interstitial and alveolar opacities. A CT scan of chest showed multiple focal ground glass opacities in the bilateral lung fields. She was treated with dexamethasone, remdesivir and supplemental oxygen. Two days later she became more hypoxic and chest X-ray showed increased interstitial opacities and a small pneumomediastinum. She was placed on high flow nasal cannula oxygen therapy. On the fourth day, her condition acutely worsened and she was emergently intubated without any complications and placed on mechanical ventilation with tidal volume of 6ml/kg ideal body weight. Post intubation chest-X-ray showed extensive pneumomediastinum, subcutaneous emphysema and right sided pneumothorax. Bilateral chest tubes were placed. Ultimately the patient passed away. DISCUSSION: COVID-19 pneumonia presents with a wide spectrum of symptoms, ranging from febrile illness to complications like ARDS, respiratory failure, and septic shock. Spontaneous pneumothorax, subcutaneous emphysema and pneumomediastinum are relatively rare complications. We presented a case of COVID-19 pneumonia who developed these complications while getting appropriate treatment. COVID-19 pneumonia can cause diffuse alveolar damage, desquamation of pneumocytes and cellular fibromyositis [1,2]. Increase in alveolar pressure by coughing or Valsalva maneuver can cause marginal alveoli to rupture and leak air into the interstitial space. The air then dissects between the perivascular and the peri-bronchial sheath into the mediastinum, pleural space and subcutaneous tissue causing pneumomediastinum, pneumothorax and subcutaneous emphysema respectively. Higher level of LDH is associated with increased risk of air leak from the lungs [3]. Small pneumothoraces can resolve on their own, but larger require chest tubes. Pneumomediastinum and subcutaneous emphysema are usually self-limiting benign conditions which resolve with bed rest, analgesics, and oxygen therapy [3]. CONCLUSIONS: Sudden deterioration in the oxygenation in COVID-19 patient should prompt clinicians to think of possible air leakage. Management of pneumomediastinum, subcutaneous emphysema and smaller spontaneous pneumothorax is conservative but large and tension pneumothoraces require chest tube. REFERENCE #1: Quincho-Lopez A, Quincho-Lopez DL, Hurtado-Medina FD. Case Report: Pneumothorax and Pneumomediastinum as Uncommon Complications of COVID-19 Pneumonia-Literature Review. Am J Trop Med Hyg. 2020;103(3):1170-1176. doi:10.4269/ajtmh.20-0815 REFERENCE #2: Shan S, Guangming L, Wei L, Xuedong Y. Spontaneous pneumomediastinum, pneumothorax and subcutaneous emphysema in COVID-19: case report and literature review. Rev Inst Med Trop Sao Paulo. 2020;62:e76. Published 2020 Oct 9. doi:10.1590/S1678-9946202062076 REFERENCE #3: Elhakim TS, Abdul HS, Pelaez Romero C, Rodriguez-Fuentes Y. Spontaneous pneumomediastinum, pneumothorax and subcutaneous emphysema in COVID-19 pneumonia: a rare case and literature review. BMJ Case Rep. 2020;13(12):e239489. Published 2020 Dec 12. doi:10.1136/bcr-2020-239489 DISCLOSURES: No relevant relationships by Prakash Adhikari, source=Web Response No relevant relationships by Nikhil Madala, source=Web Response

Inflation instability in the lung: an analytical model of a thick-walled alveolus with wavy fibres under large deformations.

Inflation of hollow elastic structures can become unstable and exhibit a runaway phenomenon if the tension in their walls does not rise rapidly enough with increasing volume. Biological systems avoid such inflation instability for reasons that remain poorly understood. This is best exemplified by the lung, which inflates over its functional volume range without instability. The goal of this study was to determine how the constituents of lung parenchyma determine tissue stresses that protect alveoli from instability-related overdistension during inflation. We present an analytical model of a thick-walled alveolus composed of wavy elastic fibres, and investigate its pressure-volume behaviour under large deformations. Using second-harmonic generation imaging, we found that collagen waviness follows a beta distribution. Using this distribution to fit human pressure-volume curves, we estimated collagen and elastin effective stiffnesses to be 1247 kPa and 18.3 kPa, respectively. Furthermore, we demonstrate that linearly elastic but wavy collagen fibres are sufficient to achieve inflation stability within the physiological pressure range if the alveolar thickness-to-radius ratio is greater than 0.05. Our model thus identifies the constraints on alveolar geometry and collagen waviness required for inflation stability and provides a multiscale link between alveolar pressure and stresses on fibres in healthy and diseased lungs.

SARS-COV-2-RELATED PNEUMOMEDIASTINUM: A RARE PRESENTATION OF AN EQUALLY RARE COMPLICATION

TOPIC: Critical Care TYPE: Fellow Case Reports INTRODUCTION: Pneumomediastinum is a rare entity in viral pneumonias. Only about 1% of patients in the ARDSNet trials developed pneumomediastinum as an early complication in the first four days of mechanical ventilation. With SARS-CoV-1, there were reports of late development of barotrauma complications, but there are very few case reports of pneumomediastinum in the current pandemic. We present a case of a tension pneumomediastinum and pneumoperitoneum as a complication of SARS-CoV-2. CASE PRESENTATION: An 86-year-old female was hospitalized for respiratory failure secondary to COVID-19. She was treated and discharged to a nursing facility requiring supplemental oxygen. Two days later, she developed worsening respiratory failure requiring intubation and mechanical ventilation with pressure-regulated volume control mode. CT imaging on admission revealed only viral pneumonia changes. Despite open lung ventilation strategy, she required plateau pressures of 32cmH20 to maintain adequate gas exchange. Hospital day 10, her respiratory failure worsened with increased plateau pressures of 40cmH20 despite no changes in her ventilator settings. She required paralysis and proning at that time with no changes on chest x-ray and no abnormalities were appreciated on exam other than developing ventilator dyssynchrony. She deteriorated further on hospital day 15 with development of shock and chest x-ray demonstrating possible free air in the mediastinum and abdomen. CT confirmed massive amounts of intraperitoneal, retroperitoneal, and mediastinal air without pneumothorax. Given her poor prognosis, she was transitioned to comfort measures and expired. DISCUSSION: COVID-19-related pneumomediastinum is thought to develop from diffuse alveolar injury and fibrosis leading to increased alveolar pressures, which ultimately rupture. Barotrauma from mechanical ventilation exacerbates this. Patients may be asymptomatic or they may have signs of tachycardia, tachypnea, and/or subcutaneous emphysema with upper chest and neck swelling. Tension pneumomediastinum is an exceedingly rare but life threatening development in critically ill patients. The development of pneumomediastinum related to SARS-CoV-2 seems to occur later in the disease course when compared to ARDSNet trials, however this may be similar to reports in SARS-CoV-1. CONCLUSIONS: Despite the rare occurrence of pneumomediastinum in viral pneumonia, providers should be aware of this potential late complication in SARS-CoV-2 and take measures for prevention and early recognition. Without adjusting treatment, tension pneumomediastinum may develop and lead to a significant increase in mortality. REFERENCE #1: Chu CM, et al. Spontaneous pneumomediastinum in patients with severe acute respiratory syndrome. European Respiratory Journal 2004 23: 802-804;DOI: 10.1183/09031936.04.00096404 REFERENCE #2: Mart M, et al. Pneumomediastinum in Acute Respiratory Distress Syndrome from COVID-19. Am J Respir Crit Care Med Vol 203, Iss 2, pp 237–238. DOI: 10.1164/rccm.202008-3376IM REFERENCE #3: Clancy DJ, et al. Tension pneumomediastinum: a literal form of chest tightness. J Intensive Care Soc 2017;18(1): 52–56. DISCLOSURES: No relevant relationships by Rayan Ihle, source=Web Response No relevant relationships by Mark Radow, source=Web Response

Perioperative Pulmonary Atelectasis: Part I. Biology and Mechanisms.

Pulmonary atelectasis is common in the perioperative period. Physiologically, it is produced when collapsing forces derived from positive pleural pressure and surface tension overcome expanding forces from alveolar pressure and parenchymal tethering. Atelectasis impairs blood oxygenation and reduces lung compliance. It is increasingly recognized that it can also induce local tissue biologic responses, such as inflammation, local immune dysfunction, and damage of the alveolar-capillary barrier, with potential loss of lung fluid clearance, increased lung protein permeability, and susceptibility to infection, factors that can initiate or exaggerate lung injury. Mechanical ventilation of a heterogeneously aerated lung (e.g., in the presence of atelectatic lung tissue) involves biomechanical processes that may precipitate further lung damage: concentration of mechanical forces, propagation of gas-liquid interfaces, and remote overdistension. Knowledge of such pathophysiologic mechanisms of atelectasis and their consequences in the healthy and diseased lung should guide optimal clinical management.

Dynamic lung behavior under high G acceleration monitored with electrical impedance tomography

Objective. During launch and atmospheric re-entry in suborbital space flights, astronauts are exposed to high G-acceleration. These acceleration levels influence gas exchange inside the lung and can potentially lead to hypoxaemia. The distribution of air inside the lung can be monitored by electrical impedance tomography. This imaging technique might reveal how high gravitational forces affect the dynamic behavior of ventilation and impair gas exchange resulting in hypoxaemia. Approach. We performed a trial in a long-arm centrifuge with ten participants lying supine while being exposed to +2, +4 and +6 G x (chest-to-back acceleration) to study the magnitude of accelerations experienced during suborbital spaceflight. Main results. First, the tomographic images revealed that the dorsal region of the lung emptied faster than the ventral region. Second, the ventilated area shifted from dorsal to ventral. Consequently, alveolar pressure in the dorsal area reached the pressure of the upper airways before the ventral area emptied completely. Finally, the upper airways collapsed and the end-expiratory volume increased. This resulted in ventral gas trapping with restricted gas exchange. Significance. At +4 G x , changes in ventilation distribution varied considerably between subjects, potentially due to variation in individual physical conditions. However, at +6 G x all participants were affected similarly and the influence of high gravitational conditions was pronounced.