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Related Concept Videos

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Obstructive Pulmonary Disease01:24

Chronic Obstructive Pulmonary Disease

COPD is defined as a heterogeneous lung condition marked by persistent respiratory symptoms such as dyspnea, cough, and sputum production, caused by abnormalities in the airways that cause airflow obstruction.
Smoking is a primary risk factor for COPD, with over 80% of patients having a history of it. Patients typically experience progressive dyspnea or labored breathing, frequent coughing, and recurrent pulmonary infections. Many eventually succumb to respiratory failure, characterized by...
COPD: Management Using Bronchodilators and Corticosteroids01:26

COPD: Management Using Bronchodilators and Corticosteroids

Chronic obstructive pulmonary isease (COPD) involves a group of progressive lung disorders characterized by persistent airflow limitation and chronic respiratory symptoms. Asthma-COPD Overlap Syndrome (ACOS), encompassing features of both asthma and Chronic obstructive pulmonary disease (COPD), is a group of progressive lung disorders that includes chronic bronchitis, emphysema, and refractory (non-reversible) asthma. ACOS leads to complex clinical presentations that combine the inflammatory...
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Factors Affecting Pulmonary Ventilation01:19

Factors Affecting Pulmonary Ventilation

Besides the pressure difference between the external environment and the lungs, the airflow rate and ease of pulmonary ventilation are also influenced by three other factors: surface tension of the fluid in the alveoli, compliance of the lungs, and airway resistance.
Alveolar Surface Tension
The alveolar fluid lines the luminal surface of the alveoli and exerts a force called surface tension. This force is caused by the polar water molecules in the liquid being more strongly attracted to each...
Chronic Obstructive Pulmonary Disease II: Emphysema01:23

Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.

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Updated: Jun 21, 2026

Dual Test Gas Pulmonary Diffusing Capacity Measurement During Exercise in Humans Using the Single-Breath Method
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Dual Test Gas Pulmonary Diffusing Capacity Measurement During Exercise in Humans Using the Single-Breath Method

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Inspiratory resistive loading does not increase sympathetic tone in COPD.

Tobias Raupach1, Florian Bahr, Peter Herrmann

  • 1Department of Cardiology and Pneumology, University Hospital Goettingen, Robert-Koch-Strasse 40, D-37075 Goettingen, Germany. raupach@med.uni-goettingen.de

Respiratory Medicine
|July 22, 2009
PubMed
Summary

Increasing breathing effort does not activate sympathetic nerves in healthy individuals or those with chronic obstructive pulmonary disease (COPD). This suggests the respiratory muscle ergoreflex plays a minimal role in sympathoexcitation for COPD patients.

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Home-Based Prescribed Pulmonary Exercise in Patients with Stable Chronic Obstructive Pulmonary Disease
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Published on: August 24, 2019

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Last Updated: Jun 21, 2026

Dual Test Gas Pulmonary Diffusing Capacity Measurement During Exercise in Humans Using the Single-Breath Method
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Published on: February 2, 2024

Home-Based Prescribed Pulmonary Exercise in Patients with Stable Chronic Obstructive Pulmonary Disease
07:10

Home-Based Prescribed Pulmonary Exercise in Patients with Stable Chronic Obstructive Pulmonary Disease

Published on: August 24, 2019

Area of Science:

  • Cardiovascular Physiology
  • Respiratory Medicine
  • Neuroscience

Background:

  • Neurohumoral activation and elevated sympathetic tone are observed in chronic obstructive pulmonary disease (COPD) patients.
  • Increased respiratory muscle work may trigger sympathetic activity via a respiratory muscle ergoreflex.

Purpose of the Study:

  • To investigate the impact of increased inspiratory resistive loading on sympathetic activity in healthy subjects and COPD patients.
  • To determine the role of the respiratory muscle ergoreflex in sympathoexcitation in COPD.

Main Methods:

  • Continuous measurement of sympathetic nerve activity, blood pressure, heart rate, and respiratory movements.
  • Inspiratory resistive loading was applied to increase the work of breathing (tension-time index) in 15 COPD patients and 15 healthy controls.

Main Results:

  • Baseline sympathetic nerve activity was significantly higher in COPD patients compared to controls.
  • Resistive loading increased the work of breathing by approximately 110% in COPD and 130% in controls.
  • No significant alterations in blood gases or sympathetic activity were observed in either group following loading.

Conclusions:

  • Moderately increasing the work of breathing does not influence sympathetic activation in COPD patients or healthy individuals.
  • The respiratory muscle ergoreflex does not appear to be a major contributor to sympathoexcitation in COPD.