ACUTE RESPIRATORY DISTRESS SYNDROME

Lyonel Carre PGY2

SICU conf

10/02/06

ARDSDefinition

• Severe, acute lung injury involving diffuse alveolar damage, increased microvascular permeability and non cardiogenic pulmonary edema

• Acute refractory hypoxemia• Annual incidence 75/100,000 in the US• High mortality- 40%-60%• First described in 1967

ARDS Criteria

• Acute onset of respiratory failure

• Bilateral infiltrate on CXR(some cases do present unilaterally or with pleural effusion

• PCWP <18 or absence of left atrial htn,

• PaO2/FiO2 < 200

ARDS

•

ARDS mechanism of lung injury

• Activation of inflammatory mediators and cellular components resulting in damage to capillary endothelial and alveolar epithelial cells

• Increased permeability of alveolar capillary membrane

• Influx of protein rich edema fluid and inflammatory cells into air spaces

• Dysfunction of surfactant

ARDS causes

• Direct Lung Injury: a) PNA and aspiration of gastric contents or other causes of chemical pneumonitis b) pulmonary contusion, penetrating lung injury c) fat emboli d) near drowning e) inhalation injury f) reperfusion pulm edema after lung transplant

ARDS causes

• Indirect lung injury a) sepsis

b) severe trauma w/ shock hypoperfusion

c) drug over dose

d) cardiopulmonary bypass

e) acute pancreatitis

f) transfusion of multp blood products

Stages of ARDS

• 1. Exudative (acute) phase - 0- 4 days

• 2. Proliferative phase - 4- 8 days• 3. Fibrotic phase - >8 days• 4. Recovery

ARDS exudative and fibrotic phases

Predictors of outcome

• Factors whose presence can be used to predict the risk of death at the time of diagnosis of acute lung injury and the acute respiratory distress syndrome include

a)chronic liver disease b)non-pulmonary organ dysfunction, c)sepsis, d)advanced age.

ARDS network study

• patients with ALI/ARDS at 10 centers, 861 patients

• Patients randomized to tidal volumes of 12 mL /kg or 6 ml/kg(volume control, assist control, plat Press = 30 cm H2O)

• 22% reduction in mortality in patients receiving smaller tidal volume

• Number-needed to treat: 12 patients

ARDS Network Study 

6ml/kg 12m/kgPaCO2 43 ± 12 36 ±9 Respiratory rate 30 ± 7 17 ± 7PaO2/F /FIO2 160 ± 68 177 ± 81Plateau pressure 26 ± 7 34 ± 9PEEP 9.2 ± 3.6 8.6 ± 4.2

ARDSnet protocol• Calculated predicted body weight(pbw) male: 50+2.3[height(inches)-60] female: 45.5+2.3[height(inches)-60]Mode: Volume assist-controlChange rate to adjust minute ventilation(not>35/min)PH goal 7.30-7.45Plateau press<30cmh20PaO2 goal: 55-80mmhg or SpO2 88-95%FiO2/PEEP combination to achieve oxygenation goal.

ARDSnetHow to select PEEP

• PEEP/FiO2 relationship to maintain adequate PaO2/SpO2

• PaO2 goal: 55-80mmHg or SpO2 88-95% use FiO2/PEEP combination to achieve oxygenation goal

0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0

5 5 8 8 10 10 10 12 14 14 14 16 18 20-24

FIO2

PEEP

ARDSNetVentilator protocol

ARDS Ventilator setting

• Greatest Lung strain PC IRV(I:E 2:1), least w/ PC (I:E 1:2) and intermediate w/ VC (I:E 1:2)

• No difference in gas exchanged, hemodynamics, and plateau pressure

• No difference in outcome w/ ARDS pts randomized to pressure control vs volume cycled PC(n=37), VC(n=42).

Edibam et al Am J Resp Crit Care Med 2003

Esteban et al , Chest 2000

Permissive Hypercapnia

• Low Vt (6ml/kg) to prevent over-distention• increase respiratory rate to avoid very high level

of hypercapnia• PaCO2 allowed to rise• Usually well tolerated• May be beneficial• Potential Problems: tissue acidosis, autonomic

dysregulation, CNS effect, and circulatory effects

HISTORY OF ALTERNATIVE VENTILATORY STRATEGIES FOR ACUTE LUNG INJURY

AND THE ACUTE RESPIRATORY DISTRESS SYNDROME.

ARDSTreatment

• Ventilator-induced lung injury: it was previously thought that oxygen toxicity was one of the most important factors in the progression of ARDS and resultant mortality. Recently, it was found that high volume(volutrauma) and high press(barotrauma) are equally if not more detrimental to these pts

• Treatment strategy is one of low volume and high frequency ventilation(ARDSNet protocol)

• Search for and treat the underlying cause• Treat abdominal infx promptly w/ abx and surgery• Ensure adequate nutrition and place on GI/DVT prophylaxis• Prevent and treat nosocomial infx

• Consider short course of high dose steroids in pts w/ severe dz that is

not resolving.

When all else fails..

• Recruitment maneuvers

• Prone

• Inhaled nitric oxide

• High frequency oscillation

ARDSnet and Long-term outcome

120pts randomized to low Vt or high Vt a) 25%mortality w/ low tidal volume b) 45% mortality w/ high tidal volume 20% had restricitve defect and 20% had obstructive defect 1

yr after recoveryAbout 80% had DLCO reduction 1 yr after recoveryStandardized tested showed health-related quality of life

lower than normalNo difference in long-term outcomes between tidal volume

group Orme Am J respir Crit Care Med 2003