The Intern At Work: Internal Medicine
Aug 9, 2026 · 15 min · 8 segments
Send us Fan Mail In this episode, we discuss updates to diagnosing and managing Acute Respiratory Distress Syndrome (ARDS). Written by Dr. Jason…
[upbeat music] Time for a minute physiology.
ARDS is a clinical syndrome that represents respiratory failure and diffuse alveolar damage due to an exaggerated host response to injury or infection.
ARDS begins with an inflammatory or exudative phase after being triggered by an event such as trauma, aspiration, sepsis, or pancreatitis.
Initially, pro-inflammatory pathways are activated, and neutrophils migrate into the alveoli and interstitium, releasing pro-inflammatory cytokines.
This inflammatory signaling damages both the alveolar epithelium and the capillary endothelium and disrupts the alveolar capillary membrane, leading to increased permeability.
This is the defining pathophysiological event in early ARDS, and it leads to pulmonary edema, flooding the interstitium and alveoli.
Coexisting epithelial cell injury also impairs alveolar fluid clearance and surfactant production, leading to alveolar collapse and poor lung compliance.
Simultaneously, procoagulant signaling leads to fibrin deposition and microvascular thrombosis.
Clinically, these processes produce the hallmarks of ARDS, which are severe refractory hypoxemia from extreme VQ mismatching, stiff noncompliant lungs, and bilateral pulmonary opacities on radiography.
Recovery from ARDS depends on the slow clearance of alveolar edema, resolution of inflammation, and the repair of the alveolar capillary barrier.
In an attempt to heal the damaged epithelium, fibrotic pathways are also activated early.
After the inflammatory or exudative phase of ARDS, patients can transition into the so-called fibroproliferative phase.
Here, fibroblasts and alveolar cells proliferate and lung fibrosis can occur.
Up to ten percent of surviving patients can progress to lung fibrosis with restrictive physiology.
However, in the majority of patients, pulmonary function can return to near normal within six to twelve months despite the initial severe lung injury.
[upbeat music] Time for a minute physiology.
ARDS is a clinical syndrome that represents respiratory failure and diffuse alveolar damage due to an exaggerated host response to injury or infection.
ARDS begins with an inflammatory or exudative phase after being triggered by an event such as trauma, aspiration, sepsis, or pancreatitis.
Initially, pro-inflammatory pathways are activated, and neutrophils migrate into the alveoli and interstitium, releasing pro-inflammatory cytokines.
This inflammatory signaling damages both the alveolar epithelium and the capillary endothelium and disrupts the alveolar capillary membrane, leading to increased permeability.
This is the defining pathophysiological event in early ARDS, and it leads to pulmonary edema, flooding the interstitium and alveoli.
Coexisting epithelial cell injury also impairs alveolar fluid clearance and surfactant production, leading to alveolar collapse and poor lung compliance.
Simultaneously, procoagulant signaling leads to fibrin deposition and microvascular thrombosis.
Clinically, these processes produce the hallmarks of ARDS, which are severe refractory hypoxemia from extreme VQ mismatching, stiff noncompliant lungs, and bilateral pulmonary opacities on radiography.
Recovery from ARDS depends on the slow clearance of alveolar edema, resolution of inflammation, and the repair of the alveolar capillary barrier.
In an attempt to heal the damaged epithelium, fibrotic pathways are also activated early.
After the inflammatory or exudative phase of ARDS, patients can transition into the so-called fibroproliferative phase.
Here, fibroblasts and alveolar cells proliferate and lung fibrosis can occur.
Up to ten percent of surviving patients can progress to lung fibrosis with restrictive physiology.
However, in the majority of patients, pulmonary function can return to near normal within six to twelve months despite the initial severe lung injury.
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