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Related Concept Videos

Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Alveoli and Alveolar Ducts01:26

Alveoli and Alveolar Ducts

The respiratory zone of the human body, which stands in contrast to the conducting zone, comprises the structures that actively participate in the exchange of gases. The initiation of this zone is marked by the terminal bronchioles converging into respiratory bronchioles, the tiniest bronchiole classification. The respiratory bronchioles give way to the alveolar ducts that opens into a congregation of alveoli. Actively involved in gas exchange, alveoli resemble tiny sacs similar to clusters of...
Respiratory Volumes and Capacities01:22

Respiratory Volumes and Capacities

The respiratory system is responsible for the intake of oxygen and the expulsion of carbon dioxide from the body. Respiratory volumes describe the volume of air in the lungs at different phases of the respiratory cycle. Tidal volume is the air breathed in and out during normal, quiet breathing. Inspiratory reserve volume is the air that can be forcefully inspired beyond the tidal volume. In contrast, expiratory reserve volume refers to the air that can be expelled from the lungs after a normal...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
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...
Van der Waals Equation01:10

Van der Waals Equation

The ideal gas law is an approximation that works well at high temperatures and low pressures. The van der Waals equation of state (named after the Dutch physicist Johannes van der Waals, 1837−1923) improves it by considering two factors.
First, the attractive forces between molecules, which are stronger at higher densities and reduce the pressure, are considered by adding to the pressure a term equal to the square of the molar density multiplied by a positive coefficient a. Second, the volume...

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Related Experiment Video

Updated: Jul 7, 2026

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

The alveolar edema equation.

John C Grotberg1, Francesco Romanò2, James B Grotberg3

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States.

Frontiers in Physiology
|July 6, 2026
PubMed
Summary
This summary is machine-generated.

This study models pulmonary edema fluid dynamics, revealing how fluid reaches lung lymphatics and challenging textbook pressure values. It provides equations for predicting fluid pressure and flow, aiding in personalized therapy for pulmonary edema.

Keywords:
Starling equationacute respiratory distress (ARDS)alveolar interstitiumalveolar surface tensioncardiogenic pulmonary edema (CPE)positive end-expiratory pressure (PEEP)pulmonary edema clearance

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

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Bedside Ultrasound for Guiding Fluid Removal in Patients with Pulmonary Edema: The Reverse-FALLS Protocol
07:59

Bedside Ultrasound for Guiding Fluid Removal in Patients with Pulmonary Edema: The Reverse-FALLS Protocol

Published on: July 28, 2018

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Last Updated: Jul 7, 2026

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

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)

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Bedside Ultrasound for Guiding Fluid Removal in Patients with Pulmonary Edema: The Reverse-FALLS Protocol
07:59

Bedside Ultrasound for Guiding Fluid Removal in Patients with Pulmonary Edema: The Reverse-FALLS Protocol

Published on: July 28, 2018

Area of Science:

  • Pulmonary Physiology
  • Fluid Dynamics
  • Medical Physics

Background:

  • Pulmonary edema, characterized by excess alveolar fluid, impairs gas exchange and increases mortality.
  • Fluid clearance from the lungs involves reabsorption into the interstitium and transport via capillaries or lymphatics.
  • The precise mechanism of lymphatic fluid transport in pulmonary edema has remained unclear since 1896.

Purpose of the Study:

  • To resolve the long-standing puzzle of how pulmonary edema fluid reaches lung lymphatics.
  • To develop a fluid mechanical model of the alveolar interstitium to analyze edema formation and clearance.
  • To re-evaluate and correct established values for alveolar interstitial pressures.

Main Methods:

  • A 2D computational fluid dynamics model of an alveolar interstitial strip was developed.
  • The model incorporated fluid flow in alveolar capillaries, interstitial space, and the alveolar liquid layer.
  • Governing equations were coupled using Starling equations at both capillary and alveolar membranes, including surface tension effects.

Main Results:

  • The study resolves the mechanism of lymphatic fluid transport in pulmonary edema.
  • Derived equations predict interstitial fluid pressure and cross-flow rates for edema and clearance.
  • Contrary to traditional views, the alveolar membrane filtration coefficient, not the capillary membrane, controls cross-flow rate magnitude.

Conclusions:

  • A novel understanding of pulmonary edema fluid dynamics and lymphatic transport is presented.
  • The derived "alveolar edema equation" predicts critical capillary pressure for edema formation and aligns with clinical data.
  • Findings support personalized PEEP (Positive End-Expiratory Pressure) therapy for prophylactic edema prevention or clearance.