ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Timothy G. Janz, MD Department of Emergency Medicine Pulmonary/Critical Care Division Department of Internal Medicine

ARDS
Definitions
Acute Lung Injury
150 200 mmHg < PaO2/FIO2 < 250 300 mmHg

ARDS
PaO2/FIO2 < 150 200 mmHg

ARDS
Epidemiology
Incidence:
5 71 per 100,000

Financial cost:
$5,000,000,000 per annum

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Pathophysiology
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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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

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Acute Exudative Phase

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Acute Exudative Phase

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Acute Exudative Phase

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Proliferative Phase
Type II pneumocyte
proliferate differentiate into Type I cells reline alveolar walls

Fibroblast proliferation
interstitial/alveolar fibrosis

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Proliferative Phase

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Fibrotic Phase
Characterized by:
local fibrosis vascular obliteration

Repair process:
resolution vs fibrosis

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Pathophysiology
Interstitial/alveolar edema Severe hypoxemia
due to intra-pulmonary shunt (V/Q = 0) shunt ~ 25% - 50%

Increased airway resistance

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Pathophysiology
High ventilatory demands
high metabolic state increased VD/VT decreased lung compliance

Pulmonary HTN
neurohumoral factors, hypoxia, edema

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Etiology

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Etiology
Hospital-acquired
infection/sepsis massive blood transfusions gastric aspiration

Community-acquired
trauma pneumonia drugs/aspiration/inhalations

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Clinical Phases
I. Injury Phase II. Latent/Lag Phase III. ARF Phase IV. Recuperative/Terminal Phase

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Clinical 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)

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Clinical Features: CXR

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Clinical Features: CXR

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Differential Diagnosis
CARDIOGENIC PULMONARY EDEMA
Bronchopneumonia Hypersensitivity pneumonitis Pulmonary hemorrhage Acute interstitial pneumonia (Hamman-Rich Syndrome)

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Diagnosis
Resistant hypoxemia
PaO2/FIO2 < 150 200 mmHg

CXR
diffuse, bilateral infiltrates

No evidence of LV failure
(PAWP < 18 mmHg)

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Diagnosis

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Diagnosis
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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Treatment: 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

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Open-Lung Approach to PEEP

Amato, Am J Respir Crit Care Med 1995; 152:1835

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Treatment: PEEP
Open-lung approach
Not practical Does not improve outcomes

Optimal PEEP
??? Most cases: PEEP ~ 15 20 cmH2O

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Optimal 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

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Optimal PEEP
ARDS Network protocol

FIO2 - 0.3 PEEP - 5

0.4
5-8

0.5
8-10

0.6
10

0.7

0.8

0.9
14-18

1.0
18-22

10-14 14

www.ardsnet.org

ARDS Network, N Engl J Med 2000; 342:1301

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Ventilator-Induced Lung Injury

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Treatment:Lung-Protective Ventilation

ardsnet.org

ARDS Network, N Engl J Med 2000; 342:1301

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Treatment: 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
Treatment: Lung-Protective Ventilation
VT = 6 mL/kg

Limit peak airway pressures < 40 cmH2O

Limit plateau pressures < 30 cmH2O

ARDS
Treatment: Lung-Protective Ventilation
Complications: (derecruitement)
Elevated PaCO2
Limit: pH > 7.20 7.25

Worsening hypoxemia
Correction:
Recruitement maneuver increasing PEEP

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Treatment: Mechanical Ventilation (MV)
Pressure controlled ventilation
Controlled airway pressures Controlled inspiratory times Patient comfort

Effectiveness:
PCV = VCV

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Treatment: 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

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Treatment: Prone Positioning

Chatte, Am J Respir Crit Care Med 1997; 25:1539

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Treatment: Prone Positioning

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Treatment: Prone Positioning
65% responders Multiple proposed mechanisms
Improved oxygenation

Difficult to implement No improvement in outcomes

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Treatment: 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

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Treatment: Partial Liquid Ventilation
Used as lavage + conventional MV

Multiple proposed mechanisms

Improves oxygenation

No improvement in outcomes

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Treatment: Vasodilators

Gerlach, Eur J Clin Invest 1993; 23:499

ARDS
Treatment: Vasodilators
NO has 83% response rate Problems:
Special equipment Rebound phenomenon No improvements in outcomes

Prostacyclin may be better agent

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Treatment: Other Modalities
Antiinflammatory agents
Steroids may have a role

Antioxidants Surfactant replacement Increased alveolar fluid removal

Effect sodium channels Activate Na+-K+-ATPase pump

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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

The End