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ACUTE RESPIRATORY DISTRESS SYNDROME

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Severe, acute lung injury involving diffuse alveolar damage, increased ... Dysfunction of surfactant. ARDS causes. Direct Lung Injury: ... – PowerPoint PPT presentation

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Title: ACUTE RESPIRATORY DISTRESS SYNDROME


1
ACUTE RESPIRATORY DISTRESS SYNDROME
  • Lyonel Carre PGY2
  • SICU conf
  • 10/02/06

2
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

3
ARDS Criteria
  • Acute onset of respiratory failure
  • Bilateral infiltrate on CXR(some cases do present
    unilaterally or with pleural effusion
  • PCWP lt18 or absence of left atrial htn,
  • PaO2/FiO2 lt 200

4
ARDS

5
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

6
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7
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

8
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

9
Stages of ARDS
  • 1. Exudative (acute) phase - 0- 4 days
  • 2. Proliferative phase - 4- 8 days
  • 3. Fibrotic phase - gt8 days
  • 4. Recovery

10
ARDS exudative and fibrotic phases
11
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.

12
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

13
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
14
ARDSnet protocol
  • Calculated predicted body weight(pbw)
  • male 502.3height(inches)-60
  • female 45.52.3height(inches)-60
  • Mode Volume assist-control
  • Change rate to adjust minute ventilation(notgt35/mi
    n)
  • PH goal 7.30-7.45
  • Plateau presslt30cmh20
  • PaO2 goal 55-80mmhg or SpO2 88-95
  • FiO2/PEEP combination to achieve oxygenation
    goal.

15
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

FIO2
PEEP
16
ARDSNetVentilator protocol
17
ARDS Ventilator setting
  • Greatest Lung strain PC IRV(IE 21), least w/ PC
    (IE 12) and intermediate w/ VC (IE 12)
  • No difference in gas exchanged, hemodynamics, and
    plateau pressure
  • No difference in outcome w/ ARDS pts randomized
    to pressure control vs volume cycled PC(n37),
    VC(n42).
  • Edibam et
    al Am J Resp Crit Care Med 2003

  • Esteban et al , Chest
    2000

18
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

19
HISTORY OF ALTERNATIVE VENTILATORY STRATEGIES FOR
ACUTE LUNG INJURYAND THE ACUTE RESPIRATORY
DISTRESS SYNDROME.
20
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.

21
When all else fails..
  • Recruitment maneuvers
  • Prone
  • Inhaled nitric oxide
  • High frequency oscillation

22
ARDSnet and Long-term outcome
  • 120pts randomized to low Vt or high Vt
  • a) 25mortality w/ low tidal volume
  • b) 45 mortality w/ high tidal volume
  • 20 had restricitve 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

  • Orme Am J respir Crit Care Med 2003
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