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Related Concept Videos

Acute Respiratory Failure-II01:21

Acute Respiratory Failure-II

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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:
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Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

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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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Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

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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...
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Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

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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...
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Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

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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
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Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

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Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
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Related Experiment Video

Updated: Apr 18, 2026

Invasive Hemodynamic Monitoring of Aortic and Pulmonary Artery Hemodynamics in a Large Animal Model of ARDS
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Invasive Hemodynamic Monitoring of Aortic and Pulmonary Artery Hemodynamics in a Large Animal Model of ARDS

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Pulmonary vascular dysfunction in ARDS.

Donal Ryan1, Stephen Frohlich1, Paul McLoughlin2

  • 1Department of Anaesthesia and Intensive Care Medicine, St Vincent's University Hospital, Elm Park, Dublin 4, Ireland.

Annals of Intensive Care
|January 17, 2015
PubMed
Summary
This summary is machine-generated.

Pulmonary hypertension in acute respiratory distress syndrome (ARDS) is complex. Elevated pulmonary vascular resistance and transpulmonary gradient may indicate increased mortality risk in ARDS patients.

Keywords:
ARDSAcute cor pulmonaleOutcomePulmonary haemodynamicsPulmonary vascular dysfunctionPulmonary vascular resistance

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Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise
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Lavage-induced Surfactant Depletion in Pigs As a 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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Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome ARDS
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Lavage-induced Surfactant Depletion in Pigs As a Model of the Acute Respiratory Distress Syndrome ARDS

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Area of Science:

  • Critical Care Medicine
  • Pulmonary Medicine
  • Cardiovascular Physiology

Background:

  • Acute respiratory distress syndrome (ARDS) often involves pulmonary hypertension (PH).
  • Multiple factors contribute to PH development in ARDS.
  • Pulmonary haemodynamics are crucial in ARDS management and prognosis.

Purpose of the Study:

  • To systematically review literature on pulmonary haemodynamics and mortality in ARDS (1977-2010).
  • To explore discrepancies in reported associations between pulmonary haemodynamics and mortality.
  • To discuss the influence of mechanical ventilation and other factors on pulmonary arterial pressure and resistance.

Main Methods:

  • Systematic literature search for studies measuring pulmonary haemodynamics and mortality in ARDS.
  • Review of physiological concepts of pulmonary haemodynamics.
  • Analysis of factors influencing pulmonary arterial pressure, pulmonary vascular resistance (PVR), and transpulmonary gradient (TPG).

Main Results:

  • Significant variability exists in reported associations between elevated pulmonary haemodynamics (pulmonary arterial pressure, PVR) and mortality in ARDS.
  • Some studies show strong associations, while others find none.
  • Bull et al. (2010) uniquely reported PVR and TPG independently associated with increased mortality in ARDS with lung-protective ventilation.

Conclusions:

  • Abnormally elevated PVR/TPG may serve as an index of ARDS severity and progression.
  • Existing evidence does not confirm a causal relationship between PVR/TPG and ARDS mortality.
  • Further research is needed to clarify the role of pulmonary vascular dysfunction in ARDS, especially with lung-protective ventilation.