1. Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by rapid onset of severe breathing difficulties, low oxygen levels in blood, and diffuse lung inflammation and fluid buildup leading to respiratory failure. 2. ARDS has many underlying causes and results from diffuse lung injury. While research has studied many potential treatments, ARDS remains untreatable and mortality remains high. 3. Ventilator management to prevent lung injury without compromising oxygen levels is the main supportive treatment for ARDS.

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2.  a clinical syndrome of severe dyspnea of rapid
onset, hypoxemia, and diffuse pulmonary infiltrates
leading to respiratory failure.
 caused by diffuse lung injury from many underlying
medical and surgical disorders.

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PATHOPHYSIOLOGY

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23.  Bedside flexible fiberoptic bronchoscope with BAL
 Protein (lavage/serum) <0.5 = Hydrostatic edema
 Protein (lavage/serum) >0.7 = Lung inflammation
 BAL cells 80% NeutrophilsARDS
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24.  Sensitive than CXR
 Earlier detection.
 Patchy abnormalities with increased density in dependent
lung zones.
 Also detects pneumothorax, effusions and
pneumomediastinum, cavitation, and mediastinal
lymphadenopathy.
 Potential benefit must be weighed against the risk
associated with transporting a critically ill patient.
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25.  Echocardiography.
 (Brain Natriuretic Peptide) BNP <100 pg/ml suggestive
of ARDS/ALI.
 Invasive Hemodynamic Monitoring
 A PCWP<18 mm Hg consistent with noncardiogenic
 Supporting evidence of Sepsis
 Fluid Management
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26.  Treatment of the underlying disorders
 Mechanical Ventilation
 Prophylaxis against
 DVT
 Stress Ulcer
 Aspiration
 CVP infections
 Prompt recognition of nosocomial infections
 Adequate nutrition.
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27.  Sometimes CPAP ventilation alone may be
sufficient to improve oxygenation.
 Less invasive, less complication.
 Lack of enough study and lack of definite
guidelines.
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28.  Goals
 Maintain oxygenation.
 Avoid oxygen toxicity.
 Avoid complications of mechanical ventilation.
 Target
 SpO2 @ 85-90% with FIO2< 65% within first 24-48
hours.
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31.  Conventional tidal volume12 mL/kg
 Low tidal volume6ml/kg
 was associated with a 9% (absolute) reduction in
mortality when the end inspiratory plateau pressure
was <30 cm H2O (18).
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33.  One of the consequences of low volume ventilation is
hypercapnia and respiratory acidosis.
 Data from clinical trials shows PCO2 60 -70 mm Hg
with pH-7.2- 7.25 safe for most patients.
 Brainstem respiratory stimulation with subsequent
hyperventilationventilator asynchrony.
 Hypercapneic acidosis may down-regulate
inflammatory cell activity, and may inhibit xanthine
oxidase, thus reducing oxidant stress. 33

34. 1. PEEP
 Collapse of terminal airways at
the end of expiration.
 PEEP act as a stent to keep
small airways open at the end
of expiration.
 Allows a reduction in theFiO2
to safer levels.
 Reduction of Cardiac Output.
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36. 2.“Inverse Ratio ventilation”
 Increasing Inspiration time such that I:E > 1:1
 Advantage of improving oxygenation allowing FI02
reduction.
 Diminished time to exhale, dynamic hyperinflation leading
to increased end-expiratory pressure, similar to ventilator
prescribed PEEP(Auto-PEEP generation)
 Sedation & Paralysis.
 No mortality benefit in ARDS has been demonstrated.
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37.  Partial liquid ventilation (PLV) with perfluorocarbon
 An inert, high-density liquid that easily solubilizes oxygen
and carbon dioxide
 Filling the lung with liquid removes the air-liquid interface
and supports alveoli thus preventing their collapse
 Promising preliminary tests
 Associated with increased incidence of pneumothorax,
mucus plugging and disruption of normal surfactant system
 Lung-replacement therapy with extracorporeal membrane
oxygenation (ECMO) - survival benefit in neonatal
respiratory distress syndrome, may also have utility in select
adult patients with ARDS.
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38.  Maintain a normal or low left atrial filling pressure
 Minimizes pulmonary edema
 prevents further decrements
 in arterial oxygenation
 lung compliance
 Shortens
 ICU stay
 duration of mechanical ventilation
 limited by
 Hypotension -- Add up to reduce venous return by PEEP
 “Diuretics don't reduce inflammation’’ 38

39.  Dobutamine is preferred ionotrope.
 Dopamine
 Avoided
 Constricts pulmonary veins
 Increase shunting
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40.  Despite nearly forty years of active research in
search of a cure, ARDS remains an untreatable
condition.
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41.  Anti-Inflammatory.
 Ability to promote collagen breakdown and inhibit
fibrosis.
 Methylprednisolone @ 2 to 3 mg/kg/day.
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43.  A randomized, clinical trial determined that
simvastatin, a hydroxymethylglutaryl-coenzyme A
reductase inhibitor,improved oxygenation and
respiratory mechanics in patients with ALI. Further
studies are needed, but treatment with simvastatin
appears safe and may be associated with improved
organ dysfunction in patients with ALI.
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45.  The medical literature is littered with failed
therapies in ARDS.
 Notable failures
 Nitric oxide
 Surfactant (in adults)
 Pentoxyphylline
 Ibuprofen, Prostaglandin E1
 Ketoconazole (inhibits thromboxane)
 N-acetylcysteine (an antioxidant)
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47.  Rationale for Use
 BAL from patients with ARDS have lower concentrations
of surfactant proteins.
 Successful trials in premature infants.
 Improve oxygenation acutely.
 Rapid weaning from mechanical ventilation.
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48. Basis for Recommendation
 More recruitment of atelectatic dorsal lung regions
 Decrease in abdominal compression of the thorax
 Mobilisation and removal of secretions
 Improve oxygenation in 70% of patients with ARDS
 Effect that persists in 50% after returning to the supine
position.
Repositioning critically ill patients can be
hazardous
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58.  Begin within 48-72 hours of mechanical ventilation.
 Tube feeding preferable to IV hyperalimentation.
 A low-carbohydrate high-fat formula.
 Include anti-inflammatory and vasodilating components
with antioxidants as supported by few studies.
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61.  Recent mortality estimates for ARDS range from 26 to 44%.
 Mortality in ARDS is largely attributable to nonpulmonary
causes, with sepsis and nonpulmonary organ failure accounting
for >80% of deaths.
 Advanced age ,Preexisting organ dysfunction are separate
predicotors of mortality.
 Little value in predicting mortality from lung severity index
 the PaO2/FIO2 ratio
 the level of PEEP used in mechanical ventilation,
 the respiratorycompliance,
 the extent of alveolar infiltrates on chest radiography,
 the lung injury score
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62.  Patients usually recover their maximum lung function
within 6 months.
 One year after endotracheal extubation, more than one-
third of ARDS survivors have normal spirometry values
and diffusion capacity.
 Severity Index & duration of mechanical ventilation are
associated with worse recovery of pulmonary function.
 Significant rates of depression and PTSD in ARDS 62