ACUTE

RESPIRATORY
DISTRESS
SYNDROME
ACUTE RESPIRATORY DISTRESS SYNDROME

Acute respiratory distress syndrome (ARDS), a severe form of

acute lung injury (ALI), consists of a systemic inflammatory
process that causes increased permeability of the
alveolocapillary membrane and vasoconstriction of the
pulmonary vasculature. This inflammation causes
noncardiogenic pulmonary edema with severely impaired
gas exchange. The mortality rate greater than 40%, mostly
from multisystem organ failure. Of those who survive, many
have long term impairment of lung function.
PATHOPHYSIOLOGY
When an injury occurs to the
lungs, an inflammatory
response is initiated by the
immune system. This response
stimulates the activation of
neutrophils, macrophages, and
endotoxins into the lungs and
the release of protein
mediators.
PATHOPHYSIOLOGY
Permeability of the
alveolocapillary membrane is
increased, allowing large
molecules, such as protein-rich
fluid, to enter into the lung
tissue, which causes the alveoli
to collapse and the lungs to
become very stiff (decreased
compliance). Severe hypoxia
develops, leading to
respiratory acidosis, narrowing
of small airways, and
pulmonary vasoconstriction.
PATHOPHYSIOLOGY
As hypoxia increases, the
patient begins to
hyperventilate, which
creates fatigue and
eventually respiratory
failure. Pulmonary
vasoconstriction can lead
to pulmonary
hypertension with RV
dysfunction and
decreased cardiac output.
ETIOLOGY
1. Pulmonary and/or nonpulmonary insult to the alveolar–
capillary membrane causing protein-rich fluid leakage into
interstitial and alveolar spaces, resulting in edema.
a. Inflammation in the interstitium and alveolar space promotes
atelectasis and lung damage.
b. This is associated with severe hypoxemia and reduced
pulmonary compliance.
c. Fibroproliferative state is often accompanied by capillary
thrombosis, lung fibrosis, and neovascularization follows.
ETIOLOGY
2. Diffuse alveolar damage
with ventilation–perfusion
(V/Q) mismatch caused by
shunting of blood
ETIOLOGY
3. Mechanisms are unclear. Acute lung injury includes both pulmonary
capillary endothelium and alveolar epithelium. Etiologies are numerous
and can be pulmonary or nonpulmonary.
Predisposing factors include (but are not limited to):
• Infections, including sepsis, pneumonia (usually bacterial or aspiration).
• Shock (any cause), trauma, pulmonary contusion, near drowning, direct or
indirect lung injury, burns, pancreatitis.
• Inhaled agents—smoke, high concentration of oxygen, corrosive substances.
• Major surgery including coronary artery bypass graft, fat emboli, lung or
bone marrow transplantation, transfusion of blood products, reperfusion
pulmonary edema.
ETIOLOGY (SPECIFIC CONDITION)
 Acute miliary tuberculosis  Hemodialysis
 Anaphylaxis  Idiosyncratic drug reaction
 Aspiration of gastric
contents
 Coronary artery bypass
grafting
 Diffuse pneumonia
(especially viral)
 Drug overdose
Indirect or direct lung trauma (most common)
 Inhalation of noxious gases and vapors
 Leukemia
 Near drowning
 Oxygen toxicity
 Pancreatitis
 Thrombotic thrombocytopenic purpura
 Uremia
 Venous air embolism
ASSESSMENT FINDINGS
Clinical Manifestations
Acute onset of severe dyspnea, tachypnea, tachycardia,
use of accessory muscles, cyanosis.
Increasing requirements of oxygen therapy. Hypoxemia
refractory to supplemental oxygen therapy.
Scattered crackles and rhonchi heard on auscultation.
Decreased pulmonary compliance, evidenced by
increasing pressure required to ventilate patient on
mechanical ventilator.
DIAGNOSTIC EVALUATION

a. Diagnosis is based on clinical, hemodynamic, and oxygen

criteria. The hallmark signs for ARDS include acute-onset,
severe hypoxemia, despite increasing oxygen therapy,
and chest x-ray exhibiting bilateralinfiltrates.
b. Pulmonary artery catheter readings show pulmonary
artery wedge pressure greater than 18 mm Hg, absence of
left atrial hypertension, and no clinical signs of heart
failure.
MANAGEMENT

1. Current ARDS treatment is

primarily supportive. The
underlying cause for ARDS
should be determined so
appropriate treatment can TREAT THE UNDRLYING CAUSE
be initiated.
MANAGEMENT

2. Mechanical ventilation is nearly always required to

decrease work of breathing and improve oxygenation.
a.Low VT by mechanical ventilation (6 mL/kg of predicted body
weight) reduces mortality compared to high-volume ventilation.
b.Protective ventilation (ie, maximum inspiratory pressure of less
than 35 cm) should be instituted.
c. PEEP should be used to improve PaO2 (keeps the alveoli open,
thereby improving gas exchange). Therefore, a lower oxygen
concentration (FiO2) may be used to maintain satisfactory
oxygenation.
MANAGEMENT

3. Fluid management must be maintained. The patient may be

hypovolemic because of the movement of fluid into the
interstitium of the lung. Pulmonary artery catheter
monitoring and inotropic medication can be helpful.
MANAGEMENT

4. Medications are aimed at

treating the underlying cause.
Corticosteroids are used
infrequently because of
controversial benefits.
MANAGEMENT
5. Adequate nutrition should be initiated early and
maintained.
COMPLICATIONS

1. Infections, such as pneumonia, sepsis.

2. Respiratory complications, such as pulmonary emboli, barotrauma,
oxygen toxicity, subcutaneous emphysema, or pulmonary fibrosis.
3. GI complications, such as stress ulcer, ileus, pancreatitis.
4. Cardiac complications, such as decreased cardiac output and
dysrhythmias.
5. Renal failure, disseminated intravascular coagulation.
6. Multiorgan failure and sepsis, which may result in death.
7. Cognitive impairment.
NURSING INTERVENTIONS
( Care is similar to patient with respiratory failure )

1.Give prescribed drugs and monitor for adverse

effects.
2.Maintain a patent airway, tracheal suctioning, and
endotracheal tube care according to facility policy.
*** PEEP may lower cardiac output, so
monitor for hypotension, tachycardia, and
decreased urine output. To maintain PEEP,
suction only as needed.
NURSING INTERVENTIONS
3. Reposition the patient often; consider prone positioning for alveolar
recruitment.
4. Provide alternative communication means, such as cards or a
notepad.
5. Monitor pulse oximetry, hemodynamics, intake and output,
respiratory status (breath sounds, ABG results), mechanical ventilator
settings, sputum characteristics, level of consciousness, daily weight,
and laboratory studies.
***Monitor the patient for
complications, including cardiac
arrhythmias, disseminated
intravascular coagulation, GI
bleeding, infection, sepsis,
malnutrition, and pneumothorax.