Clinical and morphological features
The pathology is characterized by severe damage to the respiratory system. The main manifestations include pronounced hypoxemia, fluid accumulation in the lung tissue, and infiltration of the parenchyma by blood cells with a predominance of leukocytes. At the initial stage of the syndrome, there are no clinical signs of primary heart failure, which distinguishes it from cardiogenic edema.
In medical literature and practice, this condition has several synonyms: non-cardiogenic pulmonary edema, "wet lung", "shock lung", "stiff lung", or "moist lung". The name emphasizes the similarity of functional, clinical, and morphological changes with respiratory distress syndrome in newborns, although their pathogenesis and manifestations may differ significantly in the early stages.
Causes and etiology
Factors leading to the development of the pathology are divided into infectious and non-infectious. Lung tissue damage can develop directly or indirectly through inflammatory mechanisms.
The following groups of causal factors are distinguished:
- Infectious and inflammatory: sepsis, diffuse pulmonary infections, and autoimmune diseases.
- Traumatic and iatrogenic: severe shock states, as well as post-operative conditions following heart-lung transplantation.
- Aspiration and toxic: inhalation of toxic gases or fluid aspiration.
- Hemodynamic and metabolic: pulmonary edema.
Indirect lung alteration
A special group consists of primarily extrapulmonary forms of the pathology, characterized by indirect alteration of the lung tissue. In this case, lung damage is a direct result of the systemic inflammatory response of the body.
Such conditions arise against the background of:
- Severe soft tissue and internal organ trauma.
- Conditions following heart-lung transplantation.
- Performance of balloon counterpulsation (IABP) or cardiopulmonary bypass.
- Shock states of various origins.
Stages of development of the syndrome
The pathological process is based on diffuse damage to the lung tissue. The initial link in pathogenesis is the activation of the synthesis of biologically active substances with a pronounced pro-inflammatory effect, among which cytokines play a leading role.
The development of the process sequentially includes three stages:
- Stage of exudation.
- Stage of proliferation.
- Stage of pulmonary fibrosis.
Briefly: answers to topical questions
Which specific pro-inflammatory cytokines play a leading role in initiating lung damage in ARDS?
Sources on ARDS indicate that the initial link is the activation of the synthesis of biologically active substances with a pro-inflammatory effect, with cytokines playing the leading role among mediators. A specific list of participating mediators is given in materials on COVID-19, where this process is directly associated with the development of ARDS: IL-1, IL-2, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12, IL-17, IL-18, G-CSF, GM-CSF, TNF-$\alpha$, IFN-$\gamma$-inducible protein 10, IFN-$\alpha$, IFN-$\beta$, MCP-1, and MIP-1$\alpha$.
What morphological and cellular changes occur in the lungs during the proliferation stage?
In the subacute proliferative phase of ARDS, edema and swelling of the capillaries and pulmonary parenchyma gradually decrease. Proliferation of type II alveolar epithelial cells and fibroblasts occurs; fibroblasts migrate into the alveolar exudate. Reparative processes are completed.
Which oxygenation index (ratio) is used to assess the severity of hypoxemia in ARDS?
Oxygenation index — the PaO2/FiO2 ratio. In the respiratory support algorithm for severe community-acquired pneumonia with hypoxemic acute respiratory failure, therapy escalation depends on this index and the severity of the condition:
- PaO2/FiO2 200–300: standard oxygen therapy; high-flow nasal cannula oxygen therapy 30–60 L/min; with concomitant COPD, CHF — non-invasive ventilation (NIV) with CPAP/EPAP 5–10 cm H2O.
- PaO2/FiO2 <150–200: transition to mechanical ventilation; tidal volume 4–8 mL/kg of ideal body weight; PEEP 5–8–10 cm H2O — higher in the event of ARDS development.
- PaO2/FiO2 <100–150: light to deep sedation; neuromuscular blockade.
- PaO2/FiO2 <50–80: consider ECMO.
E-P-F: Exudation, Proliferation, Fibrosis — three successive stages of lung damage in distress syndrome.
Class and exam questions
What are the main synonyms for acute respiratory distress syndrome in adults?
The disease is referred to as non-cardiogenic pulmonary edema, as well as "wet", "heavy", "shock", or "moist" lung.
Are there signs of primary heart failure at the initial stage?
No, at the initial stage of the syndrome, signs of primary heart failure are absent, which allows for differential diagnosis.
Which mediators play a leading role in initiating lung damage?
Cytokines and other biologically active substances with a pro-inflammatory effect play a leading role in the implementation of the pathological process.
What else to study on this topic
- Comparison of adult and neonatal distress syndromes
- Mechanisms of indirect lung alteration
- The role of cytokines in the development of inflammation
- Pathomorphology of the pulmonary fibrosis stage
- Hemodynamic and metabolic risk factors
Master the entire topic in the "Pathophysiology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Acute respiratory distress syndrome" and 4,913 more pages on the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 135 video lessons on the subject
Other topics of section "Chapter 23. Typical Forms of Pathology of the External Respiration System"
Free video lessons: pathophysiologyShort lessons with lecture notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.