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Related Concept Videos

Breathing01:05

Breathing

The process of breathing, inhaling and exhaling, involves the coordinated movement of the chest wall, the lungs, and the muscles that move them. Two muscle groups with important roles in breathing are the diaphragm, located directly below the lungs, and the intercostal muscles, which lie between the ribs. When the diaphragm contracts, it moves downward, increasing the volume of the thoracic cavity and creating more room for the lungs to expand. When the intercostal muscles contract, the ribs...
Atelectasis II: Pathophysiology01:10

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...
Factors Affecting Pulmonary Ventilation01:19

Factors Affecting Pulmonary Ventilation

Besides the pressure difference between the external environment and the lungs, the airflow rate and ease of pulmonary ventilation are also influenced by three other factors: surface tension of the fluid in the alveoli, compliance of the lungs, and airway resistance.
Alveolar Surface Tension
The alveolar fluid lines the luminal surface of the alveoli and exerts a force called surface tension. This force is caused by the polar water molecules in the liquid being more strongly attracted to each...
Acute Respiratory Failure-V01:29

Acute Respiratory Failure-V

The treatment for acute respiratory failure varies based on factors like the underlying cause, overall health, and severity. A collaborative healthcare team is essential for early detection, often through arterial blood gas analysis. Identifying the cause is the primary goal, with treatment strategies adjusted for ventilation/perfusion (V/Q) mismatch, shunting, or diffusion impairment.
Ensure that patients are monitored continuously for their response to therapy, including changes in...
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without causing...

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Related Experiment Video

Updated: May 14, 2026

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
06:22

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

Published on: April 7, 2021

Annexin A2 Regulates Surfactant Dysfunction During Injurious Ventilation.

Ian D Bentley, Jonathan Fritz, Anusha Kapoor

    Biorxiv : the Preprint Server for Biology
    |May 13, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Annexin A2 regulates lung surfactant function during mechanical ventilation. This protein is crucial for preventing lung stiffness and surfactant dysfunction in ventilator-induced lung injury (VILI).

    More Related Videos

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    Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
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    Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device

    Published on: September 24, 2020

    Related Experiment Videos

    Last Updated: May 14, 2026

    Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
    06:22

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

    Published on: April 7, 2021

    Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome (ARDS)
    07:20

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

    Published on: September 7, 2016

    Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
    09:36

    Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device

    Published on: September 24, 2020

    Area of Science:

    • Pulmonary medicine
    • Molecular biology
    • Biochemistry

    Background:

    • Acute Respiratory Distress Syndrome (ARDS) causes respiratory failure, often necessitating mechanical ventilation.
    • Mechanical ventilation can lead to ventilator-induced lung injury (VILI), exacerbating lung dysfunction.
    • The mechanisms underlying surfactant dysfunction in ARDS and VILI are not fully understood.

    Purpose of the Study:

    • To investigate the role of Annexin A2 (AnxA2) in regulating pulmonary surfactant function during injurious ventilation.
    • To determine if AnxA2 deficiency impacts lung mechanics and surfactant properties following VILI.

    Main Methods:

    • Comparison of lung mechanics and surfactant function between wild-type and AnxA2 knockout (AnxA2-/-) mice subjected to injurious mechanical ventilation.
    • Analysis of lung stiffness, pulmonary barrier permeability, and inflammation.
    • Assessment of surfactant surface tension-lowering properties and composition, specifically focusing on 1-palmitoyl-2-oleoylphosphatidylglycerol (POPG).

    Main Results:

    • AnxA2-/- mice exhibited increased lung stiffness after VILI compared to wild-type mice.
    • Surfactant isolated from AnxA2-/- mice showed impaired surface tension-lowering capacity.
    • A reduction in POPG content was observed in surfactant from AnxA2-/- mice, correlating with altered phase transitions during compression.

    Conclusions:

    • Annexin A2 plays a critical role in maintaining pulmonary surfactant composition and function during injurious ventilation.
    • AnxA2 deficiency leads to lung stiffening and surfactant dysfunction in the context of VILI.
    • Targeting Annexin A2 may offer a novel therapeutic strategy to prevent surfactant dysfunction in mechanically ventilated ARDS patients.