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DISTRESS SYNDROME
and
OXYGEN THERAPY
ARDS
PaO2/FIO2 < 200 mmHg
ARDS
Epidemiology
Incidence:
5 71 per 100,000
Financial cost:
$5,000,000,000 per annum
ARDS
Pathophysiology
Profound inflammatory response
Diffuse alveolar damage
acute exudative phase (1-7 days)
proliferative phase (3-10 days)
chronic/fibrotic phase (> 1-2 weeks)
Interstitial/alveolar edema
Severe hypoxemia
due to intra-pulmonary shunt (V/Q = 0)
shunt ~ 25% - 50%
Increased airway resistance
ARDS
Pathophysiology
High ventilatory demands
high metabolic state
increased VD/VT
decreased lung compliance
NORMAL ALVEOLUS
Type I cell
Alveolar
macrophage
Endothelial
Cell
RBCs Type II
cell
Capillary
ARDS
Acute Exudative Phase
Basement membrane
disruption
Type I pneumocytes
destroyed
Type II pneumocytes
preserved
Surfactant deficiency
inhibited by fibrin
decreased type II production
Microatelectasis/alveolar
collapse
ARDS
Acute Exudative Phase
Basement membrane
disruption
Type I pneumocytes
destroyed
Type II pneumocytes
preserved
Surfactant deficiency
inhibited by fibrin
decreased type II production
Microatelectasis/alveolar
collapse
ARDS
Acute Exudative Phase
Basement membrane
disruption
Type I pneumocytes
destroyed
Type II pneumocytes
preserved
Surfactant deficiency
inhibited by fibrin
decreased type II production
Microatelectasis/alveolar
collapse
ARDS
Proliferative Phase
Type II pneumocyte
proliferate
differentiate into
Type I cells
reline alveolar walls
Fibroblast
proliferation
interstitial/alveolar
fibrosis
ARDS
Fibrotic Phase
Characterized by:
local fibrosis
vascular obliteration
Repair process:
resolution vs fibrosis
ARDS
Etiology
ARDS
Clinical Features
Acute dyspnea/tachypnea/cyanosis/cough
rhonchi/wheezing
Resistant hypoxemia
PaO2/FIO2 < 200 mmHg
CXR
diffuse, bilateral infiltrates
No evidence of LV failure
(PAWP < 18 mmHg
Management
Search and treatment of disorders precipitating ARDS
Respiratory support
Hemodynamic therapy
Specific therapy to lung damages
Supportive therapy
Anti inflammatory agents (Steroids may have a role)
Antioxidants
Surfactant replacement
Increased alveolar fluid removal
Effect sodium channels
Activate Na+-K+-ATPase pump
Respiratory Support
(Mechanical Ventilation)
NOT without risks, difficulty and hazards
Ventilator induced lung injury (VILI)
Ventilator associated pneumonia (VAP)
Decision to initial mechanical ventilation
Hazards conditional
Possible clinical considering
Benefits and goal
ARDS
Prognosis
Mortality
30% - 50%
Death from respiratory failure = 15% - 18%
Most common cause of death - sepsis/infection
Outcomes
Majority have near-normal lung function
Small % develop pulmonary fibrosis
Neuropsychiatric sequelae may be high