ACUTE RESPIRATORY DISTRESS SYNDROME – DR.

CONTANTINO
Acute respiratory distress syndrome – is clinical
syndrome of severe dyspnea of rapid onset,
hypoxemia, and diffuse pulmonary infiltrates
leading to respiratory failure
ALI- better prognosis, much easy to treat, just
give O2 and treat the cause of ALI
Etiology

- Very common in ICU (80% of patient)

- Sepsis 40-50% - most common cause

Background

Diffuse pulmonary parenchymal injury

Non-cardiogenic pulmonary edema

- Low pressure pulmonary edema

[18mmHg] compare to pulmonary
edema cause by CHF which is high
Pneumonia (~40-50%)
pressure [95mmHg]).
Mortality/morbidity
3 component of ARDS
- Before – 40-70%
1. Severe dyspnea of rapid/acute in onset
- Now – 60% - improve due to various
2. Refractory hypoxemia – difficulty to
mode of mechanical ventilator and the
correct (type 1 RF)
understanding of the cause of the
3. Bilateral infiltrates in chest x-ray
problem
Pathologic hallmark – diffuse alveolar damage - Co-existing organ failure – increase risk
– the primary cause of pathophysiologic of mortality ( sepsis 25%, another
damage in ARDS problem with sepsis 50% mortality)

Diagnostic criteria for ALI and ARDS AGE

Oxygenation Onset Chest Absence of - No age prediction

Radiography left atrial - Adult > children
hypertension
ALI: Acute Bilateral PCWP History
PaO2/FIO2 alveolar or ≤18mmHg or
≤300mmHg interstitial no clinical - Can follow a variety of pulmonary or non-
ARDS: infiltrates evidence of
PaO2/FIO2 increased pulmonary insult
≤200mmHg left atrial - Can follow the predisposing condition from
pressure 4 hrs. to several days
Abbreviation - dyspnea
- ALI- acute lung injury
- PaO2- arterial partial pressure of O2
- FIO2- inspired O2 percentage
- PCWD- pulmonary capillary partial pressure Physical examination
ACUTE RESPIRATORY DISTRESS SYNDROME – DR. CONTANTINO
- Labored breathing and tachypnea
- Cyanosis and moist skin
- Tachycardia
- Hyperventilation
- Scattered crackles
- Increase work of breathing
- Agitation
- Lethargy followed by obtundation
- Epithelial cell regeneration – proliferation of
type 2 pneumocytes that synthesize new
pulmonary surfactant and differentiate into
type 1 pneumocytes
- Fibroblastic traction
- Remodelling
Fibrotic phase – 21 days onward

- Collagen deposit – ventilator dependent pt.

Pathophysiology
- Extensive alveolar duct and interstitial
The natural history of ARDS is marked by 3 fibrosis
phases – exudative, proliferative and fibrotic
Differential diagnosis
Loss of integrity of the alveolar capillary barrier
- CHF and Pulmonary edema – can cause
- due to injury to type 1 pneumocytes
bilateral pleural effusion – non in ARDS
- Pneumonia – fever, productive cough, chills
but can be cause of ARDS
- Smoke inhalation – due to chemical or fire
- Massive smoke inhalation can cause
burn in the airway
Exudative phase – 0-7days - Can develop ARDS

- Severe injury to alveolar capillary Diagnostic

endothelial cells and alveolar epithelial cell
- ABG- most important lab test
(type1 pneumocytes) – leading to the loss
- Documentation of hypoxemia
of surfactant and loss of the normal tight
- Hypocapnea – typical finding
alveolar barrier to fluid and
- Hypercapnia- ventilator failure
macromolecules
- X-ray – diffuse alveolar infiltrates
- Edema fluid that is rich in protein
Accumulates in the interstitial and alveolar
spaces.
- Released of inflammatory cytokines ( IL1,
IL8 and TNF)
- Released of lipid mediator – leukotriene B4
- Inflammatory changes
- Intra-pulmonary shunting

Proliferative phase – 7-21days

- Most patients recover rapidly during this

phase
ACUTE RESPIRATORY DISTRESS SYNDROME – DR. CONTANTINO
- Chest CT
- Permanent pulmonary fibrosis and
symptoms of restrictive lung disease
- Indicator for prognosis – Alveolar
typeIII – marker of pulmonary fibrosis

Treatment

- Conventional mechanical ventilaton

- Supplement O2 – ALI
- Intubation – ARDS
- Mechanical ventilation
A representative computed tomographic scan of the
- Assist control mode
chest during the exudative phase of ARDS in which
dependent alveolar edema and atelectasis
- PEEP- can impede venous return –
predominate causes hypotension
- Use the lowest level
- Echocardiography – exclude cardiogenic - Don’t go for 99% O2 sat
etiology of pulmonary edema
Normal ARDS alveoli
- No pulmonary artery wedge pressure
- Sputum analysis – best obtained from the Decrease area for
LRT shortly after ET intubation ventilation
- Bronchoscopy with bronchoalveolar lavage

Complication

- Restriction lung disease due to fibrosis

- MOF- due to hypotension, hypoxemia PEEP
leading to coma
- Large area for ventilation
- Death
- Permanent lung disease
- O2 toxicity – FIO2 – 48-72 hrs –
superoxide/ O2 radicals can cause
further damage
- Lung protective strategies = PEEP
- Barotrauma – due to decrease lung
- Increased PEEP - 12mmHg – used
compliance
- 15mmHg – can cause
- Use lower tidal volume in
pneumothorax
mechanical ventilator ( can cause
- Reduce left atrial filling pressures with
permissive hypercapnia)
fluid restriction and diuretics – but
- Superinfection
enough to keep the urine output
Prognosis normal

- Mortality rate average of 60%

- Non survivor – usually due from sepsis
that causes MOF
ACUTE RESPIRATORY DISTRESS SYNDROME – DR. CONTANTINO
Other strategies

- High frequency ventilator – ventilating

at extremely high RR
- Prone position – improve arterial
oxygenation, but its effect in survival
and clinical outcome remains uncertain
- Partial liquid ventilation
- ECMO

Fluid management – reduces left atrial filling

pressure

- Important aspect of ARDS mgt

- Limited by hypertension

Corticosteroids- does not improve outcome

- Increased risk for complication