Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

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 II: Diagnostic Studies and Interprofessional Care01:29

Pulmonary Embolism II: Diagnostic Studies and Interprofessional Care

Diagnosing Pulmonary EmbolismDiagnosing pulmonary embolism (PE) involves clinical assessment and advanced imaging tests. The preferred diagnostic tool is the spiral (helical) CT scan or CT angiography (CTA), which uses intravenous contrast media to visualize the pulmonary vasculature and identify emboli.A ventilation-perfusion (V/Q) scan is an alternative for patients unable to receive contrast media. This scan includes both perfusion and ventilation scanning. Perfusion scanning involves...
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...
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...
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...

You might also read

Related Articles

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

Sort by
Same author

The Medical Bookshelf.

Postgraduate medicine·2016
Same author

Lung pathology in high-altitude pulmonary edema.

Wilderness & environmental medicine·2002
Same author

Osteitis deformans (Paget's disease) and calcific disease of the heart valves.

The American journal of cardiology·1998
Same author

High altitude pulmonary edema: hemodynamic aspects.

International journal of sports medicine·1997
Same author

High-altitude pulmonary edema at a ski resort.

The Western journal of medicine·1996
Same author

Diplopia at high altitude.

Wilderness & environmental medicine·1995
Same journal

Dupilumab Emerges as an Effective Antibody Therapy for Eosinophilic Esophagitis.

Annual review of medicine·2026
Same journal

CAR T Cell Toxicities and Emerging Treatment Strategies.

Annual review of medicine·2026
Same journal

Transthyretin Amyloid Cardiomyopathy: A Rapidly Evolving Landscape.

Annual review of medicine·2026
Same journal

Accessibility of Somatic Genetic Testing for Cancer Treatment Decisions.

Annual review of medicine·2026
Same journal

Diffuse Parenchymal Lung Disease: Updates in Pathophysiology and Management.

Annual review of medicine·2026
Same journal

Revascularization for Ischemic Cardiomyopathy: Disproving the 45-Year-Old Concept of Hibernating Myocardium.

Annual review of medicine·2026
See all related articles

Related Experiment Video

Updated: Jun 25, 2026

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets
08:08

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Published on: May 11, 2015

High-altitude pulmonary edema: current concepts

H N Hultgren1

  • 1Division of Cardiovascular Medicine, Stanford University School of Medicine, California 94305, USA.

Annual Review of Medicine
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

High-altitude pulmonary edema (HAPE) is a serious condition affecting unacclimatized individuals at high altitudes. Prompt descent, medication, and oxygen rapidly improve symptoms by addressing pulmonary artery pressure and arterial unsaturation.

More Related Videos

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

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

Related Experiment Videos

Last Updated: Jun 25, 2026

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets
08:08

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Published on: May 11, 2015

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

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

Area of Science:

  • Physiology
  • Altitude Medicine
  • Pulmonary Medicine

Background:

  • High-altitude pulmonary edema (HAPE) affects unacclimatized individuals rapidly exposed to altitudes above 2450m.
  • Commonly observed in climbers and skiers, HAPE presents with dyspnea, cough, and chest tightness within days of arrival.
  • Physical signs include tachypnea, tachycardia, rales, and cyanosis.

Purpose of the Study:

  • To summarize the clinical presentation and physiological characteristics of high-altitude pulmonary edema (HAPE).
  • To elucidate the proposed etiology of HAPE, focusing on hypoxic pulmonary vasoconstriction and capillary injury.

Main Methods:

  • Review of clinical observations and physiological studies during the acute stage of HAPE.
  • Analysis of pulmonary artery pressure, pulmonary artery wedge pressure, cardiac output, and arterial unsaturation.

Main Results:

  • Acute HAPE shows normal pulmonary artery wedge pressure but elevated pulmonary artery pressure and pulmonary arteriolar resistance.
  • Severe arterial unsaturation and typically low cardiac output are observed.
  • Physiological studies reveal extensive, non-uniform hypoxic pulmonary vasoconstriction leading to capillary stress and leakage.

Conclusions:

  • High-altitude pulmonary edema (HAPE) is characterized by elevated pulmonary artery pressure and normal left ventricular filling pressure.
  • The leading hypothesis suggests non-uniform hypoxic pulmonary vasoconstriction causes capillary injury and alveolar edema.
  • Rapid clinical improvement follows descent, nifedipine, and oxygen administration.