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Related Concept Videos

Mechanical Ventilation II: Invasive Ventilation01:23

Mechanical Ventilation II: Invasive Ventilation

Ventilators are essential medical equipment used to aid patients with respiratory difficulties. Their primary function is to assist or replace spontaneous breathing by providing mechanical ventilation. There are two general classes of mechanical ventilators: negative-pressure and positive-pressure ventilators.
Negative-Pressure Ventilators
Negative-pressure ventilators create a vacuum around the chest or body to draw air into the lungs, simulating breathing. This method does not require an...
Mechanical Ventilation I: Indication and Settings01:29

Mechanical Ventilation I: Indication and Settings

Mechanical ventilation is a life-saving technique for managing acute respiratory failure and other respiratory complications. The process involves using a machine known as a ventilator to supply oxygen to the lungs and assist in removing carbon dioxide. It serves as a bridge to long-term mechanical ventilation or a temporary measure until ventilatory support is discontinued. The ventilator can maintain this function for a prolonged period, providing critical support for patients until they can...
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:
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...
Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
Acute Respiratory Failure-III01:30

Acute Respiratory Failure-III

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 causing...

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Related Experiment Video

Updated: May 13, 2026

Characterization of the Isolated, Ventilated, and Instrumented Mouse Lung Perfused with Pulsatile Flow
10:02

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Published on: April 29, 2011

Pulmonary vascular dysfunction induced by high tidal volume mechanical ventilation.

Carmen Menendez1, Leticia Martinez-Caro, Laura Moreno

  • 1Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense de Madrid, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos, Madrid, Spain.

Critical Care Medicine
|March 22, 2013
PubMed
Summary

High tidal volume ventilation causes pulmonary vascular dysfunction, impairing blood vessel responses and increasing hypoxic vasoconstriction. A poly-(adenosine diphosphate-ribose) polymerase inhibitor prevented these harmful effects in a rat model.

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Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
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Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise
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Last Updated: May 13, 2026

Characterization of the Isolated, Ventilated, and Instrumented Mouse Lung Perfused with Pulsatile Flow
10:02

Characterization of the Isolated, Ventilated, and Instrumented Mouse Lung Perfused with Pulsatile Flow

Published on: April 29, 2011

Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)
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Surfactant Depletion Combined with Injurious Ventilation Results in a Reproducible Model of the Acute Respiratory Distress Syndrome (ARDS)

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Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise
07:09

Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise

Published on: February 20, 2017

Area of Science:

  • Pulmonary Medicine
  • Vascular Physiology
  • Critical Care Medicine

Background:

  • Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) involve elevated pulmonary artery pressure and ventilation-perfusion mismatch.
  • Understanding pulmonary vascular function changes during ventilator-induced ALI is crucial for patient management.

Purpose of the Study:

  • To analyze alterations in pulmonary vascular function in a rat model of ventilator-induced ALI.
  • To investigate the potential protective effects of a poly-(adenosine diphosphate-ribose) polymerase inhibitor.

Main Methods:

  • Male Sprague-Dawley rats were subjected to low tidal volume (control), high tidal volume, or high tidal volume plus a poly-(adenosine diphosphate-ribose) polymerase inhibitor (3-aminobenzamide).
  • Pulmonary artery vascular rings were assessed using isometric tension recording.
  • Lung messenger RNA and protein expression were analyzed via RT-PCR and Western blot.

Main Results:

  • High tidal volume ventilation impaired pulmonary artery responses to phenylephrine and acetylcholine, linked to inducible nitric oxide synthase induction.
  • 3-aminobenzamide prevented these vascular impairments, as well as hypoxemia and hypotension.
  • Hypoxic pulmonary vasoconstriction increased, while responses to serotonin and Kv currents remained unaffected by high tidal volume.

Conclusions:

  • Ventilator-induced ALI leads to pulmonary vascular dysfunction, characterized by reduced alpha-adrenergic vasoconstriction and endothelium-dependent vasodilation, alongside enhanced hypoxic pulmonary vasoconstriction.
  • 3-aminobenzamide demonstrated a protective effect against these ventilator-induced vascular changes.