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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...
Acute Respiratory Failure-II01:21

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:
Pulmonary Embolism I: Introduction01:29

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Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
Pulmonary Embolism I: Introduction01:19

Pulmonary Embolism I: Introduction

A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
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...
Acute Respiratory Failure-III01:30

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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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Updated: May 11, 2026

Point-of-Care Lung Ultrasound in Adults: Image Acquisition
09:17

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

Published on: March 3, 2023

High-altitude pulmonary edema.

Erik R Swenson1, Peter Bärtsch

  • 1VA Puget Sound Health Care System, Department of Medicine, University of Washington, Seattle, Washington, USA. eswenson@u.washington.edu

Comprehensive Physiology
|May 31, 2013
PubMed
Summary
This summary is machine-generated.

High-altitude pulmonary edema (HAPE) is a dangerous altitude illness caused by excessive pulmonary vasoconstriction. Slow ascent and medication can prevent HAPE by managing lung pressures and fluid balance.

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A Large Animal Model for Pulmonary Hypertension and Right Ventricular Failure: Left Pulmonary Artery Ligation and Progressive Main Pulmonary Artery Banding in Sheep
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Last Updated: May 11, 2026

Point-of-Care Lung Ultrasound in Adults: Image Acquisition
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A Large Animal Model for Pulmonary Hypertension and Right Ventricular Failure: Left Pulmonary Artery Ligation and Progressive Main Pulmonary Artery Banding in Sheep
07:02

A Large Animal Model for Pulmonary Hypertension and Right Ventricular Failure: Left Pulmonary Artery Ligation and Progressive Main Pulmonary Artery Banding in Sheep

Published on: July 15, 2021

Area of Science:

  • Physiology
  • Altitude Medicine
  • Pulmonary Circulation

Background:

  • High-altitude pulmonary edema (HAPE) is a severe form of acute altitude illness.
  • It occurs at altitudes above 2500-3000 m due to rapid ascent.
  • HAPE is life-threatening but preventable with acclimatization or prophylaxis.

Purpose of the Study:

  • To review the pathophysiology of HAPE.
  • To discuss the role of pulmonary vascular resistance and hypoxic pulmonary vasoconstriction (HPV).
  • To explore contributing factors and therapeutic strategies for HAPE.

Main Methods:

  • Review of existing literature on HAPE pathophysiology.
  • Analysis of bronchoalveolar lavage and hemodynamic data in humans.
  • Examination of factors influencing pulmonary vascular resistance and fluid balance.

Main Results:

  • HAPE results from excessive HPV, leading to increased pulmonary microvascular pressures.
  • Increased pressure causes alveolar-capillary barrier damage and non-inflammatory edema.
  • Reduced nitric oxide and increased endothelin contribute to excessive HPV in susceptible individuals.

Conclusions:

  • HAPE pathophysiology involves complex interactions of vascular, epithelial, and neural factors.
  • Nonuniform HPV and regional blood flow variations play a key role.
  • Understanding these mechanisms is crucial for developing effective prevention and treatment strategies.