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14 Cards in this Set
- Front
- Back
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Definition |
Non cardiac pulmonary edema
Progressive refractory hypoxemia |
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Complication of hospitalized patients |
Serious medical-surgical problem
May not be lung related Mortality remains 50-60% |
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Characteristics |
Refractory Hypoxemia
Decreased Pulmonary Compliance Dyspnea Non cardiac bilateral pulmonary edema Dense pulmonary infiltrates with glass-ground appearance on CXR. |
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ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
Pathophysiology |
Injury or inflammation causes lung damage
Alveolar capillary membrane leaks Plasma and blood cells into interstitial space Interstitial pressure increases and fluid floods the alveoli Surfactant inactivated Coating forms over alveolar membrane |
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Etiology
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No single exogenous or endogenous precipitating factor multiple causes.
Exact causative mechanism is unknown Direct and Indirect Causes |
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Direct Lung Injury
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Aspiration of gastric contents
Severe thoracic trauma Pulmonary contusion Diffuse pulmonary infection Bacterial Viral Fungal: Pneumocystis carini Toxic gas (smoke inhalation) Near drowning |
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Indirect Lung Injury
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Severe sepsis
Shock Acute pancreatitis Severe nonthoracic trauma Multiple long bone fractures Drug overdose Hypertransfusion (multiple transfusions) Reperfusion injury After lung transplant After cardiopulmonary bypass |
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Phases of ARDS
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Phase I- Acute injury
Phase II- Latent period Phase III- Exudative phase Phase IV- Fibroproliferative phase |
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Clinical manifestations (Phase I)
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Change in personality, disorientation, anxiety
Initial dyspnea w/ hyperventilation Grunting respirations Cyanosis, pallor Retractions, use of accessory muscles Dry cough Diaphoresis Lungs sounds initially clear Crackles and rhonchi later Vitals Signs Fever Hypotension Tachycardia (dysrhythmias) Refractory hypoxia |
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Phase II-III (Diagnostic Studies)
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CXR -Diffuse, bilateral infiltrates
ABGs (Initial) Hypoxemia Respiratory alkalosis Later respiratory acidosis hypoxia, hypercapnia |
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Medical management (Phase III)
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Ventilator
FIO2 IMV PEEP Fluid control Swan Ganz catheter Measurement of pulmonary artery pressure (fluid) |
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Collaborative Management
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Drugs and Fluids
Corticosteroids (inflammation) Antibiotics (infection) Modify inflammatory response-Vit C and E, N-acetylcysteine, nitric oxide, surfactant replacement Optimal fluid therapy- titrate to maintain CO and tissue perfusion May need diuretics decrease lung edema but avoid hypotension and dehydration Red blood cells- transfusion if needed Positioning HOB elevated Rotation Prone Nutrition Enteral (tube feeding) nutrition or parenteral (TPN) nutrition started ASAP Electrolyte replacement |
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Interventions
Assess |
Sputum production
Oxygenation Heart sounds Lung sounds Hemodynamic status • Cardiac output • Urinary output Cardiac rhythm Monitor ABGs Pulse oximetry Ventilator settings Fluid maintenance Teach Ventilator Lines Psychosocial Support |
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Phase IV
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Multi-system failure
Heart failure Acute renal failure Acidosis Sepsis GI Bleed DIC Survival- vent dependent |
