ACUTE RESPIRATORY DISTRESS SYNDROME

Direct Lung Injury

Indirect Lung Injury

Pneumonia
Aspiration of gastric contents
Pulmonary contusion
Near- drowning
Toxic inhalation injury

Sepsis
Severe trauma
Multiple bone fractures
Flail Chest
Head trauma
Burns
Multiple transfusions
Drug overdose
Pancreatitis
Post cardiopulmonary by-pass

Clinical Lung Injury

Alveolar Epithelial Damage

Endothelial Damage

Type II pneumocyte
damage

Platelet aggregation

Attract/activate neutrophils

Increase capillary
permeability

Release of mediators
Extravasation of fluid

Decreased surfactant
production
Alveolar collapse

Increase permeability

Increase alveolar permeability

Increase vascular

Fluid and protein move into

the alveoli

Decrease blood volume

Decrease cardiac output

Atelectasis
Impaired lung compliance

Pulmonary edema

Ischemia

Regeneration of the alveolar

membrane with thick
epithelial cells

Severe organ dysfunction

Eventual scarring and loss

of functional lung tissue

ACUTE RESPIRATORY
DISTRESS SYNDROME

Decrease tissue perfusion

Myocardial depression,
decreased cerebral perfusion
& decreased renal perfusion
V/Q mismatch, R-L shunting

DEATH

Sources:
Smetzer, S.C., & Bare, B. (2011). Brunner & Suddarths Textbook of Medical Surgical Nursing, USA: Lippincott Williams &
Wilkins.
Porth, C. M. (2011). Essential Pathophysiology, China: Lippincott Williams & Wilkins.
Black, J. M., & Hawks, J. H. (2005). Medical- Surgical Nursing Clinical Management for Positive Outcomes. Philippines:
Elsevier.
Huether, S. E., & McCane, K. L. (2008). Understanding Pathophysiology. Missouri: Mosby.
Hogan, M. A. (2008) Prentice Hall Nursing Reviews & Rationales Pathophysilohy. (2nd ed.). New Jersey; Pearson Education Inc..

ACUTE RESPIRATORY DISTRESS SYNDROME

Acute Respiratory Distress Syndrome is acute respiratory failure caused by many factors such as
shock, trauma, burns, bacterial or viral pathogens, aspiration of fluids and toxic injury. [1]
Acute respiratory distress syndrome (ARDS; previously called adult respiratory distress
syndrome) is a clinical syndrome characterized by a sudden and progressive pulmonary edema,
increasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygen supplementation,
and reduced lung compliance. These signs occur in the absence of left-sided heart failure.
Patients with ARDS usually require mechanical ventilation with a higher-than normal airway
pressure. [2]SMELTZER

ETIOLOGY AND RISK FACTORS

The major cause of death in ARDS is nonpulmonary multiple-system organ failure, often with
sepsis. [3]SMELTZER

PATHOPHYSIOLOGY
Alveolar walls are severely impaired; pulmonary capillaries are injured or there is damage to
alveolar lining. The result is increased permeability of alveolar blood vessels, which allows fluid
to accumulate in alveolar spaces and alveoli become airless; a tremendous strain is placed on the
heart and cardiac complications are likely. Fluid in alveoli causes a decrease in surfactant and
increased surface tension, leading to a loss of lung compliance, decreased ventilation and
hypoxia; lungs become stiff and noncompliant because of alveolar collapse. As alveoli are
damaged, hypoxia ensues and eventually cell injury and death occurs. Inflammatory reactions
can occur as alveoli and capillaries are damaged. The inflammation causes release of cytokines
that leads to damage of capillaries and alveoli nearby, the hyaline membranes from inside alveoli
and further hinder exchange of oxygen and carbon dioxide. A spontaneous pneumothorax could
occur. Supplemental oxygen does not improve the condition, a hall mark of diagnosing AROS. [4]

Hogan, M. A. Prentice Hall Nursing Reviews & Rationales Pathophysilohy. (2nd ed.). New Jersey; Pearson Education Inc.,
2008, page 515
2&3

Smetzer, S.C., & Bare, B. Brunner & Suddarths Textbook of Medical Surgical Nursing, USA: Lippincott Williams & Wilkins,
2011, page 544
4

Hogan, M. A. Prentice Hall Nursing Reviews & Rationales Pathophysilohy. (2nd ed.). New Jersey; Pearson Education Inc.,
2008, pages 515-516

ARDS occurs as a result of an inflammatory trigger that initiates the release of cellular and
chemical mediators, causing injury to the alveolar capillary membrane. This results in leakage of

fluid into the alveolar interstitial spaces and alterations in the capillary bed. Severe ventilation
perfusion mismatching occurs in ARDS. Alveoli collapse because of the inflammatory infiltrate,
blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitial fluid
and bronchial obstruction. The lung compliance becomes markedly decreased (stiff lungs), and
the result is a characteristic decrease in functional residual capacity and severe hypoxemia. The
blood returning to the lung for gas exchange is pumped through the nonventilated,
nonfunctioning areas of the lung, causing a shunt to develop. This means that blood is interfacing
with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe,
refractory hypoxemia. [5]SMELTZER

Smetzer, S.C., & Bare, B. Brunner & Suddarths Textbook of Medical Surgical Nursing, USA: Lippincott Williams & Wilkins,
2011, page 544