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Atelectasis II: Pathophysiology

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...

Acute Respiratory Failure-II

Acute Respiratory Failure-II

Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:

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Updated: Jun 16, 2026

Preparation and Structural Evaluation of Epithelial Cell Monolayers in a Physiologically Sized Microfluidic Culture Device

Preparation and Structural Evaluation of Epithelial Cell Monolayers in a Physiologically Sized Microfluidic Culture Device

Published on: July 1, 2022

Modeling Sepsis-Associated ARDS Using a Lung Endothelial Microphysiological System.

Nai-Wen Liang, Carole Wilson, Brooke Davis

Biorxiv : the Preprint Server for Biology

|October 24, 2023

Summary

This summary is machine-generated.

This study used a lung endothelial microphysiological system (MPS) to analyze sepsis patient plasma. The MPS revealed increased endothelial permeability and inflammation markers, suggesting a new way to study acute respiratory distress syndrome (ARDS).

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Last Updated: Jun 16, 2026

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Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome ARDS

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Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome ARDS

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Published on: September 7, 2016

Area of Science:

Biomedical Engineering
Critical Care Medicine
Vascular Biology

Background:

Acute respiratory distress syndrome (ARDS) from non-pulmonary sources involves endothelial activation, difficult to assess in critical care.
Preclinical models often fail to translate to human therapies due to interspecies differences in inflammatory responses.
Microphysiological systems (MPS) offer higher fidelity to human responses and better predict drug efficacy than traditional cultures.

Conclusions:

The lung endothelial MPS effectively models sepsis-induced endothelial dysfunction.
This MPS approach may allow detailed investigation of mechanisms driving ARDS in sepsis patients.
It offers a promising platform for understanding endothelial responses in critical illness.