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Acute Respiratory Distress Syndrome ARDS Dr. Ghodrati S. Internist & Pulmonologist Prevention of alveolar edema: Retained intravascular protien maintains an osmotic gradient favoring reabsorption. The interstitial lymphatics can return large quantities of fluid to the circulation Tight junction between alveolar epithelium prevent leakage into the air spaces Inflammatory injury to the alveoli producing diffuse alveolar damage. Normal barriers to alveolar edema are lost, protien escapes from the vascular space, and the osmotic gradient favoring resorption of fluid is lost. Air spaces fill with bloody, protienaceous edema fluid and debris from degenerating cells Functional surfactant is lost, resulting alveolar collapse Definition • Acute lung injury (ALI) : • is defined as a syndrome of acute and persistent lung inflammation with increased vascular permeability. • ALI is characterized by 3 clinical features: - Bilateral radiographic infiltrates. - A ratio of the PaO2/FiO2 between 201 and 300 mmHg, - No clinical evidence for an elevated left atrial pressure. (the pulmonary capillary wedge pressure is 18 mmHg or less) • Acute respiratory distress syndrome(ARDS): - The definition of ARDS is the same as ALI except that the hypoxia is worse, requiring a PaO2/FiO2 ratio of 200 mmHg or less and 10-15% of patients admitted to ICU and up 20% of mechanically ventilated patients meet criteria for ARDS. Clinical Disorders Commonly Associated with ARDS Direct Lung Injury Indirect Lung Injury Pneumonia Sepsis Aspiration of gastric contents Severe trauma Pulmonary contusion Multiple bone fractures Near-drowning Flail chest Toxic inhalation injury Head trauma Burns Multiple transfusions Drug overdose Pancreatitis Post-cardiopulmonary bypass ARDS stages • Exudative stage: diffuse alveolar damage • Proliferative stage: resolution of pulmonary edema, proliferation of type II pneumocyte, squamous metaplasia, interstitial infiltration and collagen deposition. • Fibrotic stage: obliteration of normal lung architecture, diffuse fibrosis and cyst formation. Early finding • Pulmonary dysfunction typically develops within 24 – 48 hrs of the inciting event. • Patients develop rapidly worsening tachypnea, dyspnea, tachycardia , cyanosis, hypoxemia requiring high concentration O2, dry cough , chest pain and diffuse rales in the chest. • Most patients follow a fairly stereotypical course : severe initial hypoxemia , followed by a prolonged need for mechanical ventilation Laboratory finding • Nonspecific : leukocytosis , DIC , lactic acidosis. • ABG: acute respiratory alkalosis, ↑ (A – a )O2 gradient , severe hypoxemia. • CXR typically shows diffuse, fluffy alveolar infiltrates in multiple lung zones with prominent air bronchograms. Subsequent course • Oxygenation improve over the first few days as pulmonary edema resolves. • but most patients remain ventilator – dependent due to continued hypoxemia, high minute ventilation , poor lung compliance. • Radiographic densities become less opaque. • Clinical course become dominated by complication ( barotrauma, nosocomial infection, or the development of the multiple organ dysfunction syndrom). Prognosis • Mortality currently is 41 – 65% • Death during the first three days usually resulted from the underlying cause of ARDS. • Later in the course, nosocomial infection and sepsis accounted for most deaths. • Only 16% of fatalities were due to irreversible respiratory failure. • May show only mild abnormalities in pulmonary function and are often asymptomatic. • Persistent symptoms one year after recovery correlate with the duration of mechanical ventilation, requirement of an FIO2 > 0.6 for more than 24 hour. Benefits of mechanical ventilation • Reliable oxygen supplementation • Decreased work of breathing • Decrease venous return to the heart, decrease transvascular hydrostatic pressures and edema formation ( early in ARDS) • Recruitment of atelectatic lung units, decrease intrapulmonary shunts. Treatment • Most patient with ARDS require mechanical ventilation during their illness. • low tidal volume ventilation • The use of PEEP to improve hypoxemia and limit cyclical or tidal atelectasis. • Open lung ventilation. • Modes: CMV / ACMV , SIMV → PCV / PCV ₊ IRV • VT: 4-6 cc/kg f: 20-28 Fio2: 100% → taper PEEP: 10-15 cmH2O or high OXYGEN THERAPY MODES OF OXYGEN DELIVERY APPARATUS Low Flow Nasal canula Oronasal mask Partial non-rebreathable mask Total non-rebreathable mask O2 FLOW (L / MIN) 1–6 5 - 10 6 – 15 6 – 15 CONC. % 25 – 40 35 - 60 40 – 70 40 – 95 HIGH FLOW VENTURI MASK VENTILATORS CPAP CIRCUITS 6 – 12 VARYING VARYING 24 - 60 21 – 100 21 – 100 LOW FLOW SYSTEM HIGH FLOW SYSTEM