ACUTE RESPIRATORY

DISTRESS SYNDROME
 DEFENITION

ARDS is a sudden & progressive

form of acute respiratory failure in
which the alveolar capillary membrane
becomes damaged and more permeable
to intravascular fluid.
 ARDS

The alveoli fill with fluid, resulting in

severe dyspnea, hypoxemia refractory to
supplemental oxygen, reduced lung
compliance and diffuse pulmonary
infiltrates.
 INCIDENCE
The incidence of the ARDS in the United
States is estimated at more than 1,50,000
cases annually. Despite supportive therapy
the mortality rate from ARDS is
approximately 50%.
 ETIOLOGY
Direct lung injury
Common causes
Aspiration of gastric contents or other substances
Viral or bacterial pneumonia
Less common causes
Chest trauma
Embolism (fat or air)
Inhalation of toxic substances
Near- drowning
O2 toxicity
Radiation pneumonia
 Indirect lung injury
Common causes
Sepsis (especially gram- negative infection)
Severe massive trauma
Less common causes
Acute pancreatitis
Anaphylaxis
Cardiopulmonary bypass
DIC
Multiple blood transfusion
Narcotic drug over dose (e.g. heroin)
Nonpulmonary systemic disease
Severe head injury
Shock states
 Injury to alveolar capillary membrane
Release of inflammatory
Damaged type II mediators
alveolar cell
Increased alveolo-
Surfactant capillary
Membrane Vascular
production permeability narrowing
&obstruction
Outward migration of
Alveolar compliance blood cells &fluids
from capillaries
& recoil
Pulmonary edema
Atelectasis
Bronchoconstriction
Hyaline membrane
formation
Impairment in
gas exchange
Lung
compliance Pulmonary
ARDS HTN
 PATHOPHYSIOLOGY

Injury or exudative phase [1-7 days]

interstitial & alveolar edema
Reparative/proliferative phase[1-2 wks]
influx of neutrophils, monocytes, lymphocte and fibroblast
proliferation
Fibrotic phase [2-3 wks]
remodelled by collagenous & fibrous tissue
 PATHOPHYSIOLOGY

Injury or exudative phase [1-7 days]

-Neutrophils damage vascular endothelium, causing increased
capillary permeability and leak into interstitial space.
-Next, fluid enters alveoli causing an intrapulmonary shunt.
-Alveolar type I & type II cells are damaged(surfactant
production impaired), leading to atelectasis.
-Interstitial & alveolar edema are the characteristic features
of this phase.
 PATHOPHYSIOLOGY

. Reparative/proliferative phase[1-2 wks]

-Influx of neutrophils, monocytes, lymphocte and fibroblast
proliferation
-Increased pulmonary vascular resistance & pulmonary
hypertension develop as inflammatory cells destroy the
pulmonary vasculature.
-The diseased lung is characterised by dense, fibrous tissue.
-Lung compliance decreases, hypoxemia worsens.
 PATHOPHYSIOLOGY

Fibrotic phase [2-3 wks]

- Lung is completely remodelled by collagenous & fibrous
tissue.
- There is diffuse scarring & fibrosis.
- Surface area for gas exchange is significantly reduced
CLINICAL MANIFESTATION
In the initial phase
Do not experience any respiratory symptoms
Dyspnea
Tachypnoea
Cough
Restlessness
Chest auscultation:- May be normal or show
fine, scattered crackles
ABG :- Mild hypoxia, respiratory alkalosis
Chest x-ray:-Normal or scattered interstitial
infiltration.
 As ARDS progresses
Tachycardia
Diaphoresis
Change in sensorium
Cyanosis
Chest auscultation :-scattered to diffuse
crackles & rhonchi
Chest x-ray :-Diffuse and extensive bilateral
interstitial & alveolar infiltrates.
ABG :-Normal or decreased PaO2
Pulmonary function test:-Decreased
compliance & decreased lung volume.
 As ARDS progresses
o Profound respiratory distress requiring
Endotracheal intubation
Positive pressure ventilation
o Severe hypoxemia
o Hypercapnia.
o Metabolic acidosis.
o Chest x-ray:- white lung, pleural effusion.
DIAGNOSTIC EVALUATION
Predisposing conditions
Refractory hypoxemia (PaO2 <50
mm Hg on FiO2 > 40%)
Chest x-ray(white lung)
Pulmonary artery wedge
pressure<18 mm Hg
 COMPLICATIONS
Infection
Respiratory complications O2 toxicity,
barotrauma, emboli, fibrosis
GI paralytic ileus, stress ulcers
Renal failure
Cardiac arrythmias, decreased cardiac output
Hematologic anemia, DIC
ET intubation complications tracheal stenosis,
laryngeal ulcers
COLLABORATIVE THERAPY

Respirative therapy

Medical Supportive therapy

 Respirative therapy
O2 administration via nasal cannula and
simple face mask
ET intubation & Mechanical ventilation
FiO2 maintained at >60%, PEEP at 5 cm of
H2O.
Position strategies, from supine to prone
improves oxygenation, lateral rotation
therapy (slow, continuous side to side turning
of patient using the bed frame)
 Medical supportive therapy
Maintenance of cardiac output & tissue
perfusion
Continuous hemodynamic monitoring necessary
Insertion of arterial catheter for ABG and
monitoring of BP
Pulmonary catheter for pulmonary artery pressure &
PAWP
If CO falls, crystalloids or colloids are given
Dopamine, dobutamine may also be used
Maintenance of fluid balance
Daily weights, I/O chart monitoring
Mild fluid restriction, diuretics used as necessary
 NURSING DIAGNOSIS

1. Ineffective airway clearance related to excessive

secretions, decreased level of consciousness
2. Ineffective breathing pattern related to pain, anxiety
& decreased level of consciousness
3. Impaired gas exchange related to V/Q mismatch &
diffuse infiltration.
4. Risk for imbalanced fluid volume related to increase
in peripheral or pulmonary fluid.
5. Anxiety related to dyspnea, intubation & uncertain
out comes.
CONCLUSION