Pulmonary hypertension pathophysiology

Pulmonary Hypertension Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Pulmonary hypertension from other Diseases
Epidemiology & Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History & Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Pulmonary hypertension pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Google Images
American Roentgen Ray Society Images of Pulmonary hypertension pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Pulmonary hypertension pathophysiology
CDC on Pulmonary hypertension pathophysiology
Pulmonary hypertension pathophysiology in the news
Blogs on Pulmonary hypertension pathophysiology
Directions to Hospitals Treating Pulmonary hypertension
Risk calculators and risk factors for Pulmonary hypertension pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Assistant Editor(s)-in-Chief: Ralph Matar,

Overview

There are different types and causes of pulmonary hypertension, however most of them share the same pathophysiology: An initiating factor leads to increased resistance in the pulmonary vasculature. As a consequence, the right ventricle adapts by increasing right ventricular systolic pressures to preserve the cardiac output from the right heart. With time, increasing right ventricular systolic pressures will subsequently result in chronic changes in the pulmonary circulation and progressive remodeling of the vessel walls further exacerbating the pulmonary hypertension.

The ability of the right ventricle to adapt to increased pulmonary vascular resistance is influenced by several factors, including the age of the patient at onset, rapidity of onset of pulmonary hypertension and coexisting hypoxemia.

All classes of pulmonary hypertension are associated with narrowing and obliteration of the pulmonary arterioles due to thickening of the intima by fibromuscular dysplasia.This constant finding has created increased our interest in the role of endothelial injury and the release of vasoactive mediators in the pathogenesis of pulmonary hypertension.These mediators include both vasoconstrictors and vasodilators.The main vasoconstrictor is Endothelin, whereas Nitric Oxide (NO), PGI2 and endothelium derived hyperpolarizing factor (EDHF) are vasodilators of which NO is the most potent in reversing the effects of Endothelin.