End-Expiratory Lung Volume in Patients with Acute Respiratory Distress Syndrome: A Time Course Analysis

Mechanical ventilation (MV) is a lifesaving supportive intervention in the management of acute respiratory distress syndrome (ARDS), buying time while the primary precipitating cause is being corrected. However, MV can contribute to a worsening of the primary lung injury, known as ventilation-induced lung injury (VILI), which could have an important impact on outcome. The ARDS lung is characterized by diffuse and heterogeneous lung damage and is particularly prone to suffer the consequences of an excessive mechanical stress imposed by higher airway pressures and volumes during MV. Of major concern is cyclic overdistension, affecting those lung segments receiving a proportionally higher tidal volume in an overall reduced lung volume. Theoretically, healthier lung regions are submitted to a larger stress and cyclic deformation and thus at high risk for developing VILI. Clinicians have difficulties in detecting VILI, particularly cyclic overdistension at the bedside, since routine monitoring of gas exchange and lung mechanics are relatively insensitive to this mechanism of VILI. Expired CO2 kinetics integrates relevant pathophysiological information of high interest for monitoring. CO2 is produced by cell metabolism in large daily quantities. After diffusing to tissue capillaries, CO2 is transported first by the venous and then by pulmonary circulation to the lung. Thereafter diffusing from capillaries to lung alveoli, it is finally convectively transported by lung ventilation for its elimination to the atmosphere. Modern readily clinically available sensor technology integrates information related to pulmonary ventilation, perfusion, and gas exchange from the single analysis of expired CO2 kinetics measured at the airway opening. Current volumetric capnography (VCap), the representation of the volume of expired CO2 in one single breath, informs about pulmonary perfusion, end-expiratory lung volume, dead space, and pulmonary ventilation inhomogeneities, all intimately related to cyclic overdistension during MV. Additionally, the recently described capnodynamic method provides the possibility to continuously measure the end-expiratory lung volume and effective pulmonary blood flow. All this information is accessed non-invasively and breath-by-breath helping clinicians to personalize ventilatory settings at the bedside and minimize overdistension and cyclic deformation of lung tissue.

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Positive end-expiratory pressure-induced recruited lung volume measured by volume-pressure curves in acute respiratory distress syndrome: a physiologic systematic review and meta-analysis

Intensive Care Medicine ◽

10.1007/s00134-020-06226-9 ◽

2020 ◽

Vol 46 (12) ◽

pp. 2212-2225 ◽

Cited By ~ 1

Author(s):

Emanuele Turbil ◽

Nicolas Terzi ◽

Martin Cour ◽

Laurent Argaud ◽

Sharon Einav ◽

...

Keyword(s):

Systematic Review ◽

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Lung Volume ◽

Distress Syndrome ◽

Meta Analysis ◽

Positive End Expiratory Pressure ◽

Volume Pressure Curves

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The complex kinetics of blood endocan during the time course of sepsis and acute respiratory distress syndrome

Critical Care ◽

10.1186/s13054-019-2383-z ◽

2019 ◽

Vol 23 (1) ◽

Cited By ~ 1

Author(s):

Alexandre Gaudet ◽

Erika Parmentier ◽

Sylvain Dubucquoi ◽

Julien Poissy ◽

Thibault Duburcq ◽

...

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Time Course ◽

Distress Syndrome ◽

Kinetics Of

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Substance P and neutral endopeptidase in development of acute respiratory distress syndrome following fire smoke inhalation

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00388.2003 ◽

2004 ◽

Vol 287 (4) ◽

pp. L859-L866 ◽

Cited By ~ 17

Author(s):

Simon S. Wong ◽

Nina N. Sun ◽

R. Clark Lantz ◽

Mark L. Witten

Keyword(s):

Acute Respiratory Distress Syndrome ◽

Substance P ◽

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Time Course ◽

Distress Syndrome ◽

Neutral Endopeptidase ◽

Smoke Inhalation ◽

Plasma Extravasation ◽

Fire Smoke

To characterize the tachykininergic effects in fire smoke (FS)-induced acute respiratory distress syndrome (ARDS), we designed a series of studies in rats. Initially, 20 min of FS inhalation induced a significant increase of substance P (SP) in bronchoalveolar lavage fluid (BALF) at 1 h and persisted for 24 h after insult. Conversely, FS disrupted 51.4, 55.6, 46.3, and 43.0% enzymatic activity of neutral endopeptidase (NEP, a primary hydrolyzing enzyme for SP) 1, 6, 12, and 24 h after insult, respectively. Immunolabeling density of NEP in the airway epithelium largely disappeared 1 h after insult due to acute cell damage and shedding. These changes were also accompanied by extensive influx of albumin and granulocytes/lymphocytes in BALF. Furthermore, levels of BALF SP and tissue NEP activity dose dependently increased and decreased, respectively, following 0, low (10 min), and high (20 min) levels of FS inhalation. However, neither the time-course nor the dose-response study observed a significant change in the highest affinity neurokinin-1 receptor (NK-1R) for SP. Finally, treatment (10 mg/kg im) with SR-140333B, an NK-1R antagonist, significantly prevented 20-min FS-induced hypoxemia and pulmonary edema 24 h after insult. Further examination indicated that SR-140333B (1.0 or 10.0 mg/kg im) fully abolished early (1 h) plasma extravasation following FS. Collectively, these findings suggest that a combination of sustained SP and NEP inactivity induces an exaggerated neurogenic inflammation mediated by NK-1R, which may lead to an uncontrolled influx of protein-rich edema fluid and cells into the alveoli as a consequence of increased vascular permeability.

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