LEGEND:

Pathophysiology
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Mechanism PATHOPHYSIOLOGY
Phases of ARDS DIRECT LUNG INJURY INDIRECT LUNG INJURY
•Pneumonia • Sepsis
Complications • Lung Trauma (Pulmonary Contusion) • Pancreatitis
• Near Drowning Foreign organisms or chemicals enters the alveoli • Fat Emboli
Signs and symptoms • Chemical pneumonitis from aspiration or
c • Transfusion-related acute lung injury (TRALI)
direct inhalation • Drug overdose
Diagnostic and laboratory findings
Damage the type 1 and type 2 pneumocytes

Management
Activation of immune system. Macrophages act as sentinels for the lungs

Pneumocytes secrete inflammataory cytokines e.g. TNF, IL-1, IL-6, & IL-8

Diffuse damage to the capillary endothelium and alveolar endothelium

After 24 hours of injury Neutrophils leaks into the Presence of cytokines in the site Toxic mediators cause ↑ permeability
further damage to the Fluid leaks Inflammation Fluid wash Dysfunction of
interstitium and enters stimulates the neutrophils to of alveolar Alveolar
type 1 and type 2 in the of alveoli away surfactant
the alveoli secrete toxic mediators e.g. endothelium collapse
pneumocytes alveoli surfactant
reactive O2 species and proteases
EXUDATIVE IL- 8 stimulates V/Q mismatch
PHASE neutrophil recruitment
Hypoxia
Damaged epithelium impairs gas exchange Hypoxemia
Neutrophil infiltration and Dyspnea
proinflammatory cytokines Tachycardia
Pulmonary capillaries do not adequately Pulmonary edema Tachypnea
lead to tissue edema,
dysfunction, and absorb fluid Cyanosis
subsequent destruction of
pulmonary epithelium Deposition of hyaline membranes in the ↓ elasticity in the ↓compliance of
Body attempts to heal lung tissue Impaired gas diffusion
alveoli alveoli the alveoli
After 14 days of
injury

Supply the healing

tissue with NURSING MANAGEMENT:
Hypoxia triggers Formulation of new nutrients and •Assess breath sounds (determine
angiogenesis blood vessels oxygen presence of crackles or rales sound).
•Monitor O2 saturation and symptoms.
PROLIFERATIVE •Monitor respiration and depth of
PHASE Type II alveolar Regenerates ↑PaO2
Differentiates to Repaired lung respiration.
epithelial cell damaged Eupnea ↓PaCO2
type I alveolar tissue •Assess ABG level.
proliferation epithelium ↓O2 requirement
cells •Assess Pt mental status.
Clearing of CXR
•Monitor blood chemistry and fluid levels.
•Assess chest x-ray.
Activation of Production of •Assist pt in a prone position optimizes
fibroblasts collagen and other Collagen deposition respiration.
ECM components •Prepare the client for intubation as
indicated.
•Monitor ventilation alarms and settings.
•For pt prognosed to fibrotic ARDS: Long
term O2supplementation/ventilation.
If it is not successful, •Manage Nutrition.
the tissue transition
to the fibrotic phase

MEDICAL MANAGEMENT:
•No definitive pharmacology
Unresolved infection, ↑PaCO2 treatments
Chronic Activation of Formulation Tissue re- Impaired ↓PaO2
prolonged mechanical •Supportive care: Oxygen therapy
inflammation fibroblasts of scar tissue modelling organ ↓SpO2
ventilation, or continuous •Extracorporeal technique (ECMO)
and function Bilateral opacity of CXR
exposure to irritants •Adjunctive pharmacologic
disruption
treatment:
 Neuromuscular blockade
 Corticosteroids
FIBROTIC Dyspnea  Pulmonary vasodilators
PHASE Distortion and Persistent cough  Anti-inflammatory agents
thickening of the Nail clubbing  Beta agonists
Excessive accumulation of ↑ resistance in the Pulmonary
alveolar walls, Fatigue
collagen and other ECM pulmonary circulation hypertension
narrowing of the Chest pain
proteins in the lung tissue
airways, and the
formation of fibrous SURGICAL MANAGEMENT:
bands  Surgical Lung Biopsy (to diagnose pulmonary
Right sided heart fibrosis).
failure  Extracorporeal membrane oxygenation (ECMO).
 Lung Transplantation