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