Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Pulmonary Edema II: Pathophysiology

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...

Cerebral Edema l: Introduction

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...

Cerebral Edema ll: Pathophysiology

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

Cytotoxic Edema: Pathophysiology

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

Pneumothorax II: Pathophysiology

Pneumothorax II: Pathophysiology

Pneumothorax means the presence of air in the pleural space — the thin potential gap between the visceral and parietal pleura. This condition disrupts the normal pressure balance that keeps the lungs inflated, leading to partial or complete collapse of the affected lung.Normal physiologyUnder normal conditions, the pleural space maintains a slightly negative intrapleural pressure, which keeps the lungs expanded against the chest wall. This negative pressure creates a delicate balance between...

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The effect of IL-1 blockers on exertional leg pain in familial Mediterranean fever patients: an exploratory study.

Rheumatology (Oxford, England)·2026

Same author

A single dose of anakinra for arresting familial Mediterranean fever attacks: a proof-of-concept study.

Clinical and experimental rheumatology·2025

Same author

Non-canonical manifestations of FMF in homozygous M694V MEFV genotype: Insights from a large patient cohort.

Seminars in arthritis and rheumatism·2025

Same author

Renal outcomes and survival in amyloidosis associated with familial Mediterranean fever: A longitudinal study.

Seminars in arthritis and rheumatism·2025

Same author

Diagnostic Challenges and Solutions in Systemic Amyloidosis.

International journal of molecular sciences·2023

Same author

Screening for Fabry's disease in a high-risk subpopulation of FMF.

European journal of medical research·2022

Search research articles

Related Experiment Video

Updated: Jul 6, 2026

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

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

Published on: April 7, 2021

[Neurogenic pulmonary edema].

Alexey Naimushin¹, Avi Livneh

¹Department of Medicine F, Sheba Medical Center, Tel-Hashomer, Israel.

|March 25, 2008

Summary

This summary is machine-generated.

A stroke patient developed acute pulmonary edema, a form of left heart failure, shortly after admission. This neurogenic pulmonary edema was linked to the cerebral stroke and treated with diuretics.

More Related Videos

Point-of-Care Lung Ultrasound in Adults: Image Acquisition

Point-of-Care Lung Ultrasound in Adults: Image Acquisition

Published on: March 3, 2023

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

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: Jul 6, 2026

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

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

Published on: April 7, 2021

Point-of-Care Lung Ultrasound in Adults: Image Acquisition

Point-of-Care Lung Ultrasound in Adults: Image Acquisition

Published on: March 3, 2023

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

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:

Neurology
Cardiology
Pulmonology

Background:

Cerebral stroke is a significant neurological event.
Acute left heart failure can manifest with respiratory distress.

Observation:

A patient admitted for cerebral stroke presented with acute dyspnea.
Physical examination revealed fine rales, and chest radiography showed pulmonary congestion.
Cardiac evaluations, including electrocardiogram and cardiac enzymes, were normal.

Findings:

The patient was diagnosed with acute pulmonary edema, attributed to the cerebral stroke.
Neurogenic pulmonary edema is associated with various neurological conditions, including ischemic stroke.
The underlying mechanism may involve sympathetic nervous system overactivity or increased pulmonary vessel permeability.

Implications:

This case highlights the potential link between neurological events and cardiac complications.
Early recognition and management of neurogenic pulmonary edema are crucial.
Treatment involves conventional methods such as diuretics and after-load reduction.