acute respiratory distress syndrome(ards)
TRANSCRIPT
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ACUTE RESPIRATORY
DISTRESS SYNDROME
(ARDS)
Timothy G. Janz, MD
Department of Emergency Medicine
Pulmonary/Critical Care Division
Department of Internal Medicine
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ARDSDefinitions
Acute Lung Injury
150200 mmHg < PaO2/FIO2 < 250300 mmHg
ARDS
PaO2/FIO2 < 150200 mmHg
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ARDSEpidemiology
Incidence:
571 per 100,000
Financial cost:
$5,000,000,000 per annum
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ARDSPathophysiology
Profound inflammatory response
Diffuse alveolar damage acute exudative phase (1-7days)
proliferative phase (3-10 days)
chronic/fibrotic phase (> 1-2 weeks)
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ARDSAcute 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
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ARDSAcute Exudative Phase
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ARDSAcute Exudative Phase
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ARDSAcute Exudative Phase
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ARDSProliferative Phase
Type II pneumocyte
proliferate
differentiate into Type I cells
reline alveolar walls
Fibroblast proliferation
interstitial/alveolar fibrosis
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ARDSProliferative Phase
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ARDSFibrotic Phase
Characterized by:
local fibrosis
vascular obliteration
Repair process:
resolution vs fibrosis
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ARDSPathophysiology
Interstitial/alveolar edema
Severe hypoxemia
due to intra-pulmonary shunt (V/Q = 0)
shunt ~ 25% - 50%
Increased airway resistance
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ARDSPathophysiology
High ventilatory demands
high metabolic state
increased VD
/VT
decreased lung compliance
Pulmonary HTN
neurohumoral factors, hypoxia, edema
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ARDSEtiology
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ARDSEtiology
Hospital-acquired
infection/sepsis
massive blood transfusions
gastric aspiration
Community-acquired
trauma
pneumonia drugs/aspiration/inhalations
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ARDSClinical Phases
I. Injury Phase
II. Latent/Lag Phase
III. ARF Phase
IV. Recuperative/Terminal Phase
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ARDSClinical Features
Acute dyspnea/tachypnea rales/rhonchi/wheezing
Resistant hypoxemia PaO2/FIO2 < 150200 mmHg
CXR diffuse, bilateral infiltrates
No evidence of LV failure (PAWP < 18 mmHg)
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ARDSClinical Features: CXR
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ARDSClinical Features: CXR
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ARDSDifferential Diagnosis
CARDIOGENIC PULMONARY EDEMA
Bronchopneumonia
Hypersensitivity pneumonitis
Pulmonary hemorrhage
Acute interstitial pneumonia (Hamman-Rich Syndrome)
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ARDSDiagnosis
Resistant hypoxemia PaO2/FIO2 < 150200 mmHg
CXR diffuse, bilateral infiltrates
No evidence of LV failure (PAWP < 18 mmHg)
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ARDSDiagnosis
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ARDSDiagnosis
Based on clinical criteria
no diagnostic tests
Confirmatory tests:
PA catheter
PAWP = normal/reduced
[bronchial secretion protein]:[serum protein] ratio > 70% - 80%
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ARDSTreatment: Standard
Rx underlying cause
Adequate oxygenation/ventilation PaO2 > 60 mmHg; SaO2 > 90%
PEEP usually needed to meet O2 goals
Prevents/corrects alveolar collapse converts: (V/Q = 0) to V/Q mismatch
ARDS
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ARDSOpen-Lung Approach to PEEP
Amato,Am J Respir Crit Care Med1995; 152:183
ARDS
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ARDSTreatment: PEEP
Open-lung approach
Not practical
Does not improve outcomes
Optimal PEEP
???
Most cases: PEEP ~ 1520 cmH2O
ARDS
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ARDSOptimal PEEP
Maximize lung compliance
Crs = Vt/(PplateauPEEP)
Maximize O2
delivery
DO2 = 10 x CO x (1.34 x Hgb x SaO2)
Lowest PEEP to oxygenate @ FIO2 < .60
Empiric approach:
PEEP = 16 cmH2O and Vt = 6 ml/kg
ARDS
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ARDSOptimal PEEP
ARDS Network protocol
FIO2 - 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0PEEP - 5 5-8 8-10 10 10-14 14 14-18 18-22
ARDS Network,N Engl J Med2000; 342:1www.ardsnet.org
ARDS
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ARDSVentilator-Induced Lung Injury
ARDS
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ARDSTreatment:Lung-Protective Ventilation
ARDS Network,N Engl J Med2000; 342:1301ardsnet.org
ARDS
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ARDSTreatment: Lung-Protective Ventilation
VT = 6 mL/kg
Limit plateau pressures < 30 cmH2O Volume controlled ventilation
Limit peak airway pressures < 40 cmH2O
Pressure controlled ventilation
ARDS
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ARDSTreatment: Lung-Protective Ventilation
VT = 6 mL/kg
Limit peak airway pressures < 40 cmH2O
Limit plateau pressures < 30 cmH2O
ARDS
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ARDSTreatment: Lung-Protective Ventilation
Complications: (derecruitement)
Elevated PaCO2
Limit: pH > 7.207.25
Worsening hypoxemia Correction:
Recruitement maneuver
increasing PEEP
ARDS
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ARDSTreatment: Mechanical Ventilation (MV)
Pressure controlled ventilation
Controlled airway pressures
Controlled inspiratory times
Patient comfort
Effectiveness:
PCV = VCV
ARDS
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ARDSTreatment: Alternate Modes of MV
Inverse-ratio ventilation
Airway pressure-release ventilation
Bilevel airway pressure ventilation
Proportional-assist ventilation
High-frequency ventilation
ECMO
Tracheal gas insufflation
ARDS
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ARDSTreatment: Prone Positioning
Chatte,Am J Respir Crit Care Med 1997; 25:153
ARDS
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ARDSTreatment: Prone Positioning
ARDS
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ARDSTreatment: Prone Positioning
65% responders
Multiple proposed mechanisms Improved oxygenation
Difficult to implement
No improvement in outcomes
ARDS
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ARDSTreatment: Partial Liquid Ventilation
Lungs filled to FRC with perflubron 17 times more O2 dissolved than water
Low surface tension
Gravitates to dependent areas of lungs
Nontoxic Minimally absorbed
Eliminated by evaporation
ARDS
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ARDSTreatment: Partial Liquid Ventilation
Used as lavage + conventional MV
Multiple proposed mechanisms
Improves oxygenation
No improvement in outcomes
ARDS
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ARDSTreatment: Vasodilators
Gerlach,Eur J Clin Invest 1993; 23:499
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ARDS
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ARDSTreatment: Other Modalities
Antiinflammatory agents
Steroids may have a role
Antioxidants
Surfactant replacement
Increased alveolar fluid removal
Effect sodium channels
Activate Na+-K+-ATPase pump
ARDS
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ARDSPrognosis
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 sequelaemay be high
The End
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The End