ACUTE RESPIRATORY DISTRESS SYNDROME

 ARDS Definition

•         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 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) 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

 

•         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

St        Ages of ARDS

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

•         2. Proliferative phase - 4- 8 days

•         3. Fibrotic phase - >8 days

•         4. Recovery

             

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/kg

PaCO2                        43 ± 12             36 ±9

Respiratory rate           30 ± 7              17 ± 7

PaO2/F /FIO2             160 ± 68           177 ± 81

Plateau pressure          26 ± 7               34 ± 9

PEEP                          9.2 ± 3.6           8.6 ± 4.2

 

ARDS net protocol

•         Calculated predicted body weight(pbw)

       male: 50+2.3[height(inches)-60]

       female: 45.5+2.3[height(inches)-60]

Mode: Volume assist-control

Change rate to adjust minute ventilation(not>35/min)

PH goal 7.30-7.45

Plateau press<30cmh20

PaO2 goal: 55-80mmhg or SpO2 88-95%

FiO2/PEEP combination to achieve oxygenation goal.

 

ARDS net How 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

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).

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

ARDS Treatment

•         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 (ARDS Net 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.

ARDS net 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 restrictive defect and 20% had obstructive defect 1 yr after recovery

      About 80% had DLCO reduction 1 yr after recovery

      Standardized tested showed health-related quality of life lower than normal

     No difference in long-term outcomes between tidal volume group