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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...
Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure01:16

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure

Oxygen therapy has emerged as a significant tool in enhancing the quality of life for patients suffering from pulmonary arterial hypertension (PAH). While this therapy has principally been studied on patients with significant hypoxemia, this therapeutic approach helps prevent potential organ damage and can be administered in the comfort of one's home.
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue, improving...
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:
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Portal Hypertension01:22

Portal Hypertension

Portal hypertension is an increase in blood pressure within the portal venous system. Normally, this pressure is less than 5 mmHg. It is considered clinically significant when it rises above 10 mmHg. At this threshold, complications from altered blood flow and venous congestion emerge.EtiologyPortal hypertension arises from conditions that impede blood flow through the liver. The most common cause is cirrhosis, in which chronic liver injury leads to fibrotic scarring. This fibrosis narrows or...
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...

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Related Experiment Video

Updated: Jun 7, 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 hypertension.

X-Q Xu1, Z-C Jing

  • 1Dept of Pulmonary Circulation, Shanghai Pulmonary Hospital, Tongji University, China.

European Respiratory Review : an Official Journal of the European Respiratory Society
|October 20, 2010
PubMed
Summary

High-altitude pulmonary hypertension (HAPH) affects people living at high elevations. Further research is needed to define its prevalence, understand its pathogenesis involving nitric oxide, endothelin-1, and genetic factors, and confirm effective treatments beyond migration.

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Last Updated: Jun 7, 2026

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

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Published on: May 11, 2015

The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats
07:29

The Left Pneumonectomy Combined with Monocrotaline or Sugen as a Model of Pulmonary Hypertension in Rats

Published on: March 8, 2019

Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat
08:34

Left Atrial Stenosis Induced Pulmonary Venous Arterialization and Group 2 Pulmonary Hypertension in Rat

Published on: November 18, 2018

Area of Science:

  • Cardiovascular Physiology
  • Altitude Medicine
  • Pulmonary Circulation

Background:

  • High-altitude pulmonary hypertension (HAPH) is a condition impacting populations at high elevations.
  • The exact prevalence and underlying mechanisms of HAPH require further investigation.
  • Current understanding of HAPH pathogenesis is limited, particularly regarding genetic factors.

Purpose of the Study:

  • To review the current understanding of high-altitude pulmonary hypertension.
  • To identify gaps in knowledge regarding HAPH prevalence, pathogenesis, and treatment.
  • To highlight areas for future research in HAPH.

Main Methods:

  • Literature review of existing studies on high-altitude pulmonary hypertension.
  • Analysis of proposed pathogenetic mechanisms including nitric oxide, endothelin-1, and prostaglandin I₂.
  • Evaluation of diagnostic tools and current therapeutic strategies for HAPH.

Main Results:

  • HAPH prevalence at high altitudes is not well-defined.
  • Nitric oxide reduction may play a role, but endothelin-1 and prostaglandin I₂ pathways need more study.
  • Genetic contributions to HAPH are suggested but not confirmed.
  • Exertional dyspnea is common; right heart failure signs appear late.
  • Echocardiography is a useful screening tool; right heart catheterization is diagnostic.

Conclusions:

  • Migration to lower altitudes remains the primary management for HAPH.
  • Phosphodiesterase 5 inhibitors and acetazolamide show therapeutic promise.
  • The efficacy of endothelin-receptor antagonists for HAPH is currently unproven.