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

Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

2.9K
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
2.9K
Disorders of Acid-Base Balance01:29

Disorders of Acid-Base Balance

253
The human body maintains a precise pH range of arterial blood between 7.35 and 7.45. Deviations result in either acidosis (pH < 7.35) or alkalosis (pH > 7.45). These conditions are further classified as respiratory or metabolic disorders based on their underlying cause.
Respiratory Acidosis and Alkalosis
Respiratory acidosis occurs due to an increase in the partial pressure of carbon dioxide PCO2 in the blood. It often arises from shallow breathing or impaired gas exchange caused by...
253
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

239
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...
239
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

381
Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
381
Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.01:25

Chronic Obstructive Pulmonary Disease-III: Symptoms and Complications.

2.9K
Understanding the variety of primary symptoms and systemic complications that characterize chronic obstructive pulmonary disease (COPD) is crucial for healthcare professionals.
Symptoms of COPD can be classified as primary or systemic. Primary symptoms relate to reduced airflow, while systemic or extrapulmonary symptoms relate to COPD's broader impact on the body.
Primary Symptoms of COPD:
2.9K
Diagnosing Acidosis and Alkalosis01:24

Diagnosing Acidosis and Alkalosis

290
Diagnosing acid-base imbalances involves systematically analyzing arterial blood samples, focusing on three key measurements: pH, bicarbonate (HCO3−) concentration, and carbon dioxide partial pressure (PCO2). This analysis follows a four-step process that helps identify the imbalance's underlying cause and nature.
First, the pH level is assessed to determine whether the blood pH is normal (7.35–7.45), low (acidosis), or high (alkalosis).
Next, the PCO2  and...
290

You might also read

Related Articles

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

Sort by
Same author

A Novel Application-Based Test for Rapid Screening of Olfactory Dysfunction.

JAMA otolaryngology-- head & neck surgery·2026
Same author

Recovery is missing in the pandemic treaty.

BMJ (Clinical research ed.)·2024
Same author

Cholesterol and M2 Rendezvous in Budding and Scission of Influenza A Virus.

Sub-cellular biochemistry·2023
Same author

Influence of Landscape Patterns on Exposure to Lassa Fever Virus, Guinea.

Emerging infectious diseases·2023
Same author

The Impact of COVID Vaccination on Symptoms of Long COVID: An International Survey of People with Lived Experience of Long COVID.

Vaccines·2022
Same author

Long COVID in children.

The Lancet. Child & adolescent health·2021

Related Experiment Video

Updated: Aug 1, 2025

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
07:40

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

9.0K

Hypothesis: inflammatory acid-base disruption underpins Long Covid.

Vicky van der Togt1, Jeremy S Rossman1,2

  • 1Research-Aid Networks, Chicago, IL, United States.

Frontiers in Immunology
|May 1, 2023
PubMed
Summary

Long Covid, or Post-Acute Sequelae of COVID-19 (PASC), may stem from acid-base disruptions caused by anaerobic respiration. This study proposes testing this hypothesis by monitoring acid-base markers in PASC patients.

Keywords:
COVID-19Long CovidPASCSARS-CoV-2acid-baseacidosisinflammation

More Related Videos

Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome
04:45

Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome

Published on: June 2, 2022

2.3K
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.2K

Related Experiment Videos

Last Updated: Aug 1, 2025

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation
07:40

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

9.0K
Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome
04:45

Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome

Published on: June 2, 2022

2.3K
Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

5.2K

Area of Science:

  • Infectious Diseases
  • Metabolic Medicine
  • Physiology

Background:

  • The underlying mechanisms of Long Covid (Post-Acute Sequelae of COVID-19; PASC) remain unknown, lacking validated diagnostics and therapeutics.
  • SARS-CoV-2 infection can lead to widespread tissue damage, inflammation, and metabolic changes, impairing microvascular circulation and causing hypoxia.
  • Hypoxia, combined with viral-induced metabolic shifts, promotes cellular anaerobic respiration and systemic acid-base balance dysregulation in both acute and PASC patients.

Purpose of the Study:

  • To propose and outline a testable hypothesis for the mechanism of PASC.
  • To investigate the role of acid-base disruption in PASC pathogenesis.
  • To suggest a potential avenue for developing diagnostics and therapeutics for PASC.

Main Methods:

  • Longitudinal evaluation of acid-base balance markers in PASC patients and control groups.
  • Monitoring of key physiological and metabolic indicators over a one-month period.
  • Comparative analysis of acid-base markers between PASC patients and healthy controls.

Main Results:

  • Preliminary data indicate systemic dysregulation of acid-base balance markers in PASC patients.
  • Evidence suggests a shift towards anaerobic respiration contributing to metabolic changes.
  • Impaired microvascular circulation and hypoxia are observed in affected individuals.

Conclusions:

  • The study hypothesizes that acid-base disruption, driven by anaerobic respiration, underlies PASC symptoms across multiple organ systems.
  • Testing this hypothesis through longitudinal monitoring of acid-base markers is proposed.
  • Confirmation could significantly advance understanding and treatment strategies for PASC.