Download - Acute Respiratory Distress Syndrome
ACUTE RESPIRATORY DISTRESS SYNDROME
(ARDS)
Timothy G. Janz, MD
Department of Emergency Medicine
Pulmonary/Critical Care Division
Department of Internal Medicine
ARDSDefinitions
• Acute Lung Injury– 150 – 200 mmHg < PaO2/FIO2 < 250 – 300 mmHg
• ARDS– PaO2/FIO2 < 150 – 200 mmHg
ARDSEpidemiology
• Incidence:– 5 – 71 per 100,000
• Financial cost:– $5,000,000,000 per annum
ARDSPathophysiology
• Profound inflammatory response
• Diffuse alveolar damage– acute exudative phase (1-7days)– proliferative phase (3-10 days)– chronic/fibrotic phase (> 1-2 weeks)
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
ARDS Acute Exudative Phase
ARDS Acute Exudative Phase
ARDSProliferative Phase
• Type II pneumocyte– proliferate– differentiate into Type I cells– reline alveolar walls
• Fibroblast proliferation– interstitial/alveolar fibrosis
ARDSProliferative Phase
ARDSFibrotic Phase
• Characterized by:– local fibrosis– vascular obliteration
• Repair process:– resolution vs fibrosis
ARDSPathophysiology
• Interstitial/alveolar edema
• Severe hypoxemia– due to intra-pulmonary shunt (V/Q = 0)– shunt ~ 25% - 50%
• Increased airway resistance
ARDSPathophysiology
• High ventilatory demands– high metabolic state
– increased VD/VT
– decreased lung compliance
• Pulmonary HTN– neurohumoral factors, hypoxia, edema
ARDSEtiology
ARDSEtiology
• Hospital-acquired– infection/sepsis
– massive blood transfusions
– gastric aspiration
• Community-acquired– trauma
– pneumonia
– drugs/aspiration/inhalations
ARDSClinical Phases
• I. Injury Phase
• II. Latent/Lag Phase
• III. ARF Phase
• IV. Recuperative/Terminal Phase
ARDSClinical Features
• Acute dyspnea/tachypnea– rales/rhonchi/wheezing
• Resistant hypoxemia– PaO2/FIO2 < 150 – 200 mmHg
• CXR– diffuse, bilateral infiltrates
• No evidence of LV failure– (PAWP < 18 mmHg)
ARDSClinical Features: CXR
ARDSClinical Features: CXR
ARDSDifferential Diagnosis
• CARDIOGENIC PULMONARY EDEMA
• Bronchopneumonia
• Hypersensitivity pneumonitis
• Pulmonary hemorrhage
• Acute interstitial pneumonia (Hamman-Rich Syndrome)
ARDSDiagnosis
• Resistant hypoxemia– PaO2/FIO2 < 150 – 200 mmHg
• CXR– diffuse, bilateral infiltrates
• No evidence of LV failure– (PAWP < 18 mmHg)
ARDSDiagnosis
ARDSDiagnosis
• Based on clinical criteria– no diagnostic tests
• Confirmatory tests:– PA catheter
• PAWP = normal/reduced
– [bronchial secretion protein]:[serum protein] • ratio > 70% - 80%
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“Open-Lung “ Approach to PEEP
Amato, Am J Respir Crit Care Med 1995; 152:1835
ARDSTreatment: PEEP
• “Open-lung” approach– Not practical– Does not improve outcomes
• Optimal PEEP– ???
– Most cases: PEEP ~ 15 – 20 cmH2O
ARDSOptimal PEEP
• Maximize lung compliance– Crs = Vt/(Pplateau – PEEP)
• 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
ARDSOptimal PEEP
• ARDS Network protocol
FIO2 - 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0
PEEP - 5 5-8 8-10 10 10-14 14 14-18 18-22
ARDS Network, N Engl J Med 2000; 342:1301www.ardsnet.org
ARDSVentilator-Induced Lung Injury
ARDSTreatment:Lung-Protective Ventilation
ARDS Network, N Engl J Med 2000; 342:1301ardsnet.org
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
ARDSTreatment: Lung-Protective Ventilation
• VT = 6 mL/kg
• Limit peak airway pressures < 40 cmH2O
• Limit plateau pressures < 30 cmH2O
ARDSTreatment: Lung-Protective Ventilation
• Complications: (derecruitement)
– Elevated PaCO2
• Limit: pH > 7.20 –7.25
– Worsening hypoxemia• Correction:
– Recruitement maneuver – increasing PEEP
ARDSTreatment: Mechanical Ventilation (MV)
• Pressure controlled ventilation– Controlled airway pressures– Controlled inspiratory times– Patient comfort
• Effectiveness:– PCV = VCV
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
ARDSTreatment: Prone Positioning
Chatte, Am J Respir Crit Care Med 1997; 25:1539
ARDSTreatment: Prone Positioning
ARDSTreatment: Prone Positioning
• 65% responders
• Multiple proposed mechanisms– Improved oxygenation
• Difficult to implement
• No improvement in outcomes
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
ARDSTreatment: Partial Liquid Ventilation
• Used as lavage + conventional MV
• Multiple proposed mechanisms– Improves oxygenation
• No improvement in outcomes
ARDSTreatment: Vasodilators
Gerlach, Eur J Clin Invest 1993; 23:499
ARDSTreatment: Vasodilators
• NO has 83% response rate
• Problems:– Special equipment– Rebound phenomenon – No improvements in outcomes
• Prostacyclin may be better agent
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
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 sequelae – may be high
The End