Phase of acute injury and exudation
The triggering mechanism of the syndrome involves biologically active substances that cause massive activation of alveolar macrophages, neutrophils, and other granulocytes. These cells adhere to the endothelium of the microvasculature and release lysosomal enzymes, cytotoxic agents, and reactive oxygen species, triggering lipid peroxidation processes.
The main targets for damage are:
- Capillary endothelium
- Alveolar epithelium (including type I alveolar cells)
- Basement membrane of the blood-air barrier
- Surfactant (its depletion develops)
Such destruction leads to a sharp increase in the permeability of the barrier to proteins, including fibrin, and blood formed elements. As a result, interstitial and alveolar edema rapidly increases, gas exchange is impaired, and respiratory hypoxia develops.
Pathophysiology and vascular disorders
A crucial role in the development of the pathology is played by damage to type II alveolar cells, which are responsible for surfactant production. Their destruction leads to alveolar collapse, atelectasis formation, a rapid drop in lung compliance, and an increase in intrapulmonary shunting of blood.
Pronounced vascular disorders develop in the pulmonary microvasculature, leading to pulmonary hypertension. Its causes are vascular occlusion by multiple thrombi and pronounced vasospasm. Spastic reactions are sustained by mediators:
- Hypoxia
- Thromboxane $A_2$
- Leukotrienes
- Kinin and endothelin
Morphologically, this period is characterized by infiltration of the lung tissue by macrophages and lymphocytes, as well as proliferation of cells and the interstitial matrix.
Fibrotic stage and systemic manifestations
In the areas of most intense damage, the fibrotic stage forms. Excessive influx of proteins and erythrocytes into the alveoli, combined with leukocyte migration, stimulates the synthesis of collagen, argyrophilic, and elastic fibers and extracellular matrix, leading to local pulmonary fibrosis.
Systemic changes encompass multiple organs and functions:
- Respiratory system: tachypnea, increased minute ventilation, and decreased lung volumes (TLC, RV, VC, FRC).
- Acid-base balance: early respiratory alkalosis is replaced by hypercapnia and acidosis.
- Hemodynamics: a compensatory increase in cardiac output at the start is replaced by its decrease in the terminal phase.
- Multiple organ disorders: signs of acute multiple organ dysfunction syndrome (MODS) join in, determining the severe prognosis.
Briefly: answers to topical questions
What are the clinical stages distinguished in the course of ARDS?
The clinical course of acute respiratory distress syndrome features three successive phases.
- Acute phase — the exudative stage lasting about a week. It is characterized by impaired permeability of the alveolar-capillary membrane with the development of non-cardiogenic alveolar and interstitial pulmonary edema.
- Subacute phase — the proliferative stage, lasting from 4 to 10 days. During this period, edema decreases, active proliferation of type II alveolar cells and migrating fibroblasts occurs, and reparative processes are completed.
- Chronic phase — the fibro-proliferative stage. It is distinguished by pronounced interstitial fibrosis, membrane thickening, alveolar obliteration, and microvessel rarefaction, leading to pulmonary hypertension.
What etiological factors (damaging factors) most frequently trigger ARDS?
The development of acute respiratory distress syndrome is most frequently triggered by severe factors of infectious and non-infectious nature.
The main causes include:
- Sepsis — provokes the syndrome in approximately 40% of patients.
- Multiple traumas — cause the pathology in 10–34% of cases, including fractures with the development of fat embolism.
- Aspiration — entry of water into the respiratory tract during drowning or acidic gastric contents (leads to ARDS in 10–36% of cases).
- Massive transfusions — transfusion of large volumes of blood, plasma, or blood substitutes.
- Pneumonia — severe bacterial and viral pulmonary lesions (including atypical pneumonia caused by the SARS-CoV virus).
Five steps of ARDS: Cell activation $\rightarrow$ Enzymes and edema $\rightarrow$ Surfactant failure and atelectasis $\rightarrow$ Pulmonary hypertension $\rightarrow$ Fibrosis and MODS.
Class and exam questions
What mechanism triggers the development of ARDS?
The triggering mechanism is the release of biologically active substances that activate alveolar macrophages and neutrophils, causing damage to the blood-air barrier.
Why does lung compliance drop in ARDS?
Lung compliance decreases due to damage to type II alveolar cells, surfactant depletion, and subsequent alveolar collapse (atelectasis).
How do acid-base balance parameters change over time?
In the initial stages, acute respiratory alkalosis is observed with low partial pressure of oxygen and carbon dioxide, which in later stages is replaced by hypercapnia and acidosis.
What else to study on this topic
- Etiotropic therapy and the use of antibiotics in non-infectious injury
- Mechanisms of pulmonary hypertension development and vascular spasm mediators
- Pathogenetic rationale for respiratory support
- Correction of hemostatic and hemodynamic disorders in the intensive care unit
- Development of acute multiple organ dysfunction in terminal states
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Other topics of section "Chapter 23. Typical Forms of Pathology of the External Respiration System"
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