ARDS University of Washington Department of Respiratory Care Services Skills Day May, 2006.
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Transcript of ARDS University of Washington Department of Respiratory Care Services Skills Day May, 2006.
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ARDS
University of Washington
Department of Respiratory Care Services
Skills Day May, 2006
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CASE PRESENTATION
• A 62 year old woman with a history of coronary artery disease comes to the ER with shortness of breath over the past 8 hours. A CXR reveals a bilateral alveolar filling process and her arterial blood gas shows marked hypoxemia despite a 70 % high flow mask.
• A PA catheter is placed to assess the cause of the bilateral infiltrates.
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CASE PRESENTATION
• SVR - 500 dynes/sec/cm2
• PA - 21/ 13 mm Hg
• PAOP - 11 mm Hg
• CO - 9 LPM You should:
1) Consider a inotrope such as dobutamine as she is in CHF.
2) Administer dopamine IV, evaluate carefully for a source of infection and cover with broad spectrum antibiotics
3) Consider volume infusion with normal saline to treat her volume depletion.
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CASET PRESENTATION• She develops progressive hypoxemia
despite 100 % non-rebreather mask and is intubated.
• The most appropriate ventilator management would include the following settings:
A) VT = 600ml, PEEP = 15cmH2OB) VT = 600 ml, PEEP = 5 cmH2OC) VT = 400 ml, PEEP = 10 cmH2OD) VT = 400 ml, PEEP = 17.5 cmH2O
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ARDS Definition
• American-European Consensus Conference-1994– Acute onset of respiratory symptoms (with associated
predisposing factor)
– Bilateral infiltrates on CXR
– PCWP ≤18 or the absence of clinical evidence of LA hypertension
– PaO2/FiO2 ratio:· ≤ 200 = ARDS
· ≤ 300 = ALI (acute lung injury)
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ARDSPredisposing Factors
–Direct Lung Injury
· Pneumonia
· Aspiration
· Lung contusion
· Near-drowning
· Inhalation injury
· Fat emboli
–Indirect lung injury
·Sepsis
·Severe trauma
·Acute pancreatitis
·Blood transfusions
·Cardiopulmonary bypass
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PATHOGENESIS• Target organ injury from host’s inflammatory response and
uncontrolled liberation of inflammatory mediators
• Localized manifestation of SIRS
• Neutrophils and macrophages play major roles
• Complement activation
• Cytokines: TNF-, IL-1, IL-6
• Platelet activation factor
• Eicosanoids: prostacyclin, leukotrienes, thromboxane
• Free radicals
• Nitric oxide
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PATHOPHYSIOLOGY
• Abnormalities of gas exchange
• Oxygen delivery and consumption
• Cardiopulmonary interactions
• Multiple organ involvement
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ABNORMALITIES OF GAS EXCHANGE
• Hypoxemia: HALLMARK of ARDS– Increased capillary permeability
– Interstitial and alveolar exudate
– Surfactant damage
– Decreased FRC
– Diffusion defect and right to left shunt
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ARDS STAGES
• Acute or Exudative Phase
• Proliferative or Subacute Phase
• Chronic Phase
–Scarring
–Recovery
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ARDS STAGES
• Acute, exudative phase– rapid onset of respiratory failure after trigger
– diffuse alveolar damage with inflammatory cell infiltration
– hyaline membrane formation
– capillary injury
– protein-rich edema fluid in alveoli
– disruption of alveolar epithelium
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NORMAL ALVEOLUS
Type I cell
EndothelialCell
RBC’s
Capillary
Alveolarmacrophage
Type IIcell
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ACUTE PHASE OF ARDS
Type I cell
EndothelialCell
RBC’s
Capillary
Alveolarmacrophage
Type IIcell
Neutrophils
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Proliferative Phase
• Subacute, Proliferative phase:
– persistent hypoxemia
– development of hypercarbia
– fibrosing alveolitis
– further decrease in pulmonary compliance
– pulmonary hypertension
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Chronic Phase
• Chronic phase
– obliteration of alveolar and bronchiolar spaces and pulmonary capillaries
• Recovery phase
– gradual resolution of hypoxemia
– improved lung compliance
– resolution of radiographic abnormalities
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ARDS Treatments
• Decades of Ineffective Treatments– Steroids
– NSAIDs
– Pentoxyphlline
– Nitric oxide
– surfactant
– ……….
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Low Tidal Volume Strategies in ARDSLow Tidal Volume Strategies in ARDS
• High lung inflation volumes over distend more compliant portions of the lung.
• In the past our high tidal volume strategies may have actually caused lung injury (“ventilator lung”).
• Using lower lung volumes may prevent over distension and reduce ventilator induced lung injury.
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ARDS NETWORK
• Clinical Trials Network > 20 centers nationwide• Multiple Trials• Initial Study “ARMA”• Randomized to 6 ml/kg (IBW) vs. 12 ml/kg and
plateau pressure <30 cm• Study was halted early due to significant survival
improvement in one group
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New England Journal of Medicine 2000;342:1301-8
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Mortality Prior to Hospital DischargeMortality Prior to Hospital Discharge
0
10
20
30
40
50
Mortality (Percent)
6 ml/kg 12 ml/kg
P=0.0054
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What about PEEP ?
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• 549 ARDS Patients
• Randomized to high or low PEEP levels– 5 versus 12 cm PEEP
– ? Differences in mortality, ventilator, ICU and hospital days
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High vs. Low PEEP Protocol
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High vs. Low PEEP
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Where do I set PEEP ?
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Recruitment Maneuvers
• Hyperinflation maneuvers to open collapse lung
• Some parts of lung are open, some are collapsed
• Detrimental effects:– “Baby lungs” can be overdistended
– Collapsed portions can put traction on normal portions causing injury
– Opening and closing of collapsed or atelectatic areas could cause “shear stress injury”
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Baby Lung Effect Shear Force Effect
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NEJM 1998;347
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• CT Scan and outcome study of patients with ARDS who had recruitable lung looked at
• Percentage of recruitable lung looked at as a predictor of outcomes
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• 13% of lung was recruitable
• Higher percentage of recruitable lung correlted with:
– Higher oxygenation requirments
– Heavier lungs
– Worse outcome
• BOTTOM LINE: THE JURY IS STILL OUT ON RECRUITMENT MANEUVERS
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• KCLIP DATA
• Survey of ALI and ARDS in King County
NEJM 2005;353:1685
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• KCLIP Cohort
NEJM 2005;353:1685
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NEJM 2005;353:1685
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ARDS
• Big Problem
• Small tidal volumes
• Small pressures
• PEEP around 10
• No recruitment maneuvers at this time.