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44 Cards in this Set
- Front
- Back
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Introduction - ARDS
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A form of respiratory failure that results in hypoxia, reduced lung compliance, diffuse pulmonary infiltrates and hyaline membrane formation
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Historical Perspective
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-First described in 1967 and named Adult Respiratory Distress Syndrome
-Also known as shock lung -Renamed Acute Respiratory Distress Syndrome in 1994 by the American European Consensus Committee -Second disorder identified at this time named acute lung injury |
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Incidence and Mortality
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-15-18% of all ventilated patients in the US have ARDS
-150,000 cases identified annually -32-45% mortality rate -Death is usually from multiorgan systems failure not from respiratory failure -Patients who recover can suffer permanent lung damage |
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Defining Criteria
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-onset acute
-Partial pressure of arterial oxygen to fractional inspired oxygen to fractional inspired oxygen concentration ratio <200 mmHg -<300 mmHg acute lung injury -bilateral pulmonary infiltrates on chest xray -pulmonary artery wedge pressure ,18 mmHg or no clinical evidence of left atrial hypertension |
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Clinical Causes (Direct)
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DIRECT:
-aspiration -pneumonia -near drowning -chest trauma -inhalation of toxic substances |
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Clinical Causes (Indirect)
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INDIRECT:
-sepsis -burns -trauma -multiple blood transfusions -CABG -pancreatitis -fat emboli |
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Pathophysiology
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-injury to alveolar capillary membrane
-activation of inflammation reponse -intrapulmonary shunt develops -surfactant dysfunction -hyaline membrane formation |
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Injury of the Alveolar Capillary Membrane
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-Alveolar capillary membrane damaged from direct or indirect injury.
-Alveolar Capillary membrane becomes more permeable to fluids. -Intravascular fluid enters the interstitial space and the alveolus. -Ventilation is reduced as a result of pulmonary edema. -Noncardiac pulmonary edema without left ventricular failure or elevated PCWP. |
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Activation of the Inflammatory Response
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-Mediators like interleukins, tumor necrosis factor, and platelet activating factor are released.
-Mediators cause constriction in small airways increasing airway resistance. -Inflammatory process causes pulmonary vasoconstriction, decreased pulmonary perfusion and pulmonary hypertension. -Pulmonary hypertension stresses right ventricle of the heart. -Right ventricular hypertrophy decreases left ventricular filling and cardiac output. |
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Intrapulmonary Shunt
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-Ventilation perfusion (V/Q) mismatch occurs where some alveoli are under ventilated and some are under perfused.
-Patient develops a significant shunt where blood flows by under ventilated alveoli without participating in gas exchange. |
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Surfactant Dysfunction
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-Pulmonary edema causes dysfunction of type II alveolar cells, decreasing surfactant production and reducing lung compliance.
-Surface tension of water in the alveolus creates atelectasis, making alveoli difficult to inflate. This increases the work of breathing. |
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Hyaline Membrane Production
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-Type I alveolar cells are damaged by the influx of protein rich fluid, fibrin, and cellular debris producing hyaline membranes.
-Hyaline membranes are scar tissue forming across the alveoli making them less functional. -Formation of hyaline membrane is highly variable. |
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Clinical Manifestations
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-Early signs
-Progressive -Late signs |
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Early Signs
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-Within 1-2 days of a precipitating event the patient will exhibit tachypnea, hypoxia, fine scattered crackles, decreased lung compliance, confusion, anxiety, increase in accessory muscle use, diffuse patchy infiltrates on chest x-ray.
-The patient with ARDS has pulmonary edema with normal heart size on chest x-ray, and absence of left ventricular failure and fluid overload. -PCWP <18mmHg -Costophrenic angles are often spared. -ABGs respiratory alkalosis with low PO2, normal or low PCO2, elevated pH. |
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Progressive Symptoms
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-Symptoms worsen as fluid accumulates and lung compliance decreases.
-Work of breathing increases, tachypnea and hypoxia increase with increase use of accessory muscles, tachycardia, diaphoresis, and tripod position. -Decreased mental status, cyanosis, pallor, diffuse crackles to coarse rhonchi. -Widespread infiltrates on chest x-ray. Patient requires mechanical ventilation with high FIO2 and PEEP. |
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Late Signs
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-Profound respiratory distress requiring mechanical ventilation.
-Chest x-ray progresses to white out -Severe hypoxia, hypercapnea -Coarse crackles unless breath sounds are diminished by consolidation or pneumonia. -Hallmark signs hypoxia refractory to oxygen therapy and requiring increasing ventilator pressures. |
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Treatment of ARDS
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-Mechanical Ventilation
-Fluid management -Nutrition -Medications -Ventilator modalities -Nursing care |
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Mechanical Ventilation
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-Respiratory failure requiring mechanical ventilation.
-Patient requires high FIO2 and will exhibit high peak inspiratory pressures. -Positive end expiratory pressure (PEEP) is used to improve oxygenation, allowing FIO2 to be reduced. -Goal is FIO2 below 60% to reduce damage from oxygen toxicity. -Goals of ventilation are to use the lowest FIO2 that will maintain PO2 80-100 and SAO2 90%. |
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Oxyhemoglobin Curve
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-Relation exist between PAO2 and SAO2.
-Sharp decline in PO2 when patient’s SAO2 decreases below 90%. |
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Mechanical Ventilation
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-PEEP should begin at a low level and increased in increments of 3 cms until optimal oxygenation is achieved.
-PEEP has some undesirable side effects so be cautious particularly with high levels > 12cm. -Can be used at high levels such as 18cm for severe hypoxia in order to keep FIO2 below 60%. -PEEP can cause barotrauma, pneumothorax, and decreased cardiac output. |
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Protective Ventilation
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-Small tidal volumes <6ml/kg body weight may be effective in decreasing airway resistance and preventing barotrauma.
-Repeated alveolar trauma from high tidal volumes can increase the inflammatory response and worsen ARDS. -In the ARDS Network Study protective ventilation with low tidal volumes, low plateau pressures and PEEP demonstrated decreased mortality, and decreased ventilator days. Applying PEEP was associated with a 16-33% improvement in mortality and ventilator days -Hypercapnea that may result has been shown to be well tolerated at the level of 60-100 if it occurs gradually. |
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Fluid Balance
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-Careful assessment critical to promote optimal cardiac output and lung perfusion, but reduce any additional pulmonary edema.
-Patient is maintained on the dry side. -Monitor fluid balance with central venous pressure (CVP) or swan ganz catheter. -Death is usually from multiorgan systems failure, goal of fluid therapy is to support other organ systems. |
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Nutrition
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-In research adequate nutrition has been associated with positive outcomes in the critically ill patient.
-Tube feeding can also help to prevent stress ulcers. -Nutrition needs should be assessed by a dietician, and supplied by the most natural route possible. -Nutrition needs 35-45kcal/kg/day of a balanced formula of CHO, fats and proteins. -Using a low CHO formula will help prevent overproduction of CO2. -The patient may have an ileus in the early stages of illness and residuals should be carefully monitored. -HOB elevated while tube feeding is in progress. |
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Medications
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-Steroids are used to stabilize cell membranes and reduce inflammation.
-Research on effectiveness of steroids in ARDS indicate steroids given in low doses in the 7-10th day of ARDS are most effective. -Remember to monitor blood glucose -Always taper steroids to avoid adrenal crisis. -Antibiotics are not used prophylactically, but are indicated for positive cultures. Patients with ARDS who develop sepsis have a very poor prognosis. |
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Medications (con't)
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-H2 blockers are used with caution. Could neutralize acid environment of GI system allowing increase bacterial count and promoting pneumonia.
-Sedatives and neuroparalytics are often used for ventilator control and to improve oxygenation. -Bronchodilators may be helpful in maintaining airway patency in cases of bronchospasm. May increase surfactant production and have an anti-inflammatory effect. |
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Modes of Ventilation
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-Inverse ratio ventilation – reversal of the normal inspiratory expiratory ratio to 1:1 or 2:1, prolongs inspiration allowing more alveoli to be inflated and overcome airway resistance.
-High frequency oscillatory ventilation – very low tidal volumes delivered at rates of 60-100 breaths per minute decreasing airway resistance and decreasing the risk of barotrauma. |
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Prone Positioning
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-Prone positioning – CT scanning has demonstrated greater alveolar involvement in dependent areas of lungs. Increases perfusion to the anterior lobes which may be relatively unaffected.
-Prone positioning has been shown to improve oxygenation but only for the first four hours. There was no improvement in outcomes or ventilator days with prone positioning. -In the same study applying PEEP to recruit alveoli showed a 16-33% improvement by CT scan. -Complications of prone positioning include accidental extubation, aspiration, loss of vascular access, facial edema, delays in CPR in case of cardiac arrest. |
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Nursing Care
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-Assess breath sounds for pneumothorax.
-Palpate for subcutaneous emphysema. -Chest tube maintenance. -Prevent complications of immobility. -DVT prophylactics. -Skin care and oral care. -Emotional support for family. |
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Experimental Treatments
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-Vasodilators such as nipride or nitroglycerin to improve alveolar perfusion and decrease pulmonary hypertension. Results show a brief initial improvement in oxygenation but no improvement in outcomes.
-Nitric oxide is an inhaled gas administered through the ventilator causing selective pulmonary vasodilatation, improving pulmonary perfusion and decreasing pulmonary hypertension. Demonstrated improved oxygenation in the first 24 hours, but also did not improve outcomes. Effects were better in neonates and children. |
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Experimental Treatments (con't)
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Surfactant replacement used for years with neonates with hyaline membrane disease has shown no effectiveness in adults. It demonstrated no adverse effects.
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Morbidity and Mortality
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-Patients recover within two weeks of onset.
-Death is usually from multiorgan system failure not respiratory failure. -Studies demonstrated that cognitive and psychological changes persisted in some patients for years. -Reasoning, judgment, and memory were impaired at 3 years. -Patients reported hallucinations, paranoia, depression, and personality changes after ARDS. -Patients older than 70 had increased ventilator days and significant higher mortality. |
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Conclusion
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-ARDS results from direct or indirect injury
-Hallmark signs are hypoxia refractory to oxygen, with increasing ventilator pressures. -Hypoxia requires mechanical ventilation with high concentrations of oxygen. -PEEP should be used to improve oxygenation and reduce FIO2to 60%. -Protective ventilation with low tidal volumes and permissive hypercapnea should be considered. -Never forget to treat the patient among the tubes |
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Case Study
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Gladys Weber is a 54 year old African American female admitted to the hospital with uterine fibroids and elective hysterectomy. She has chronic bronchitis and frequent colds in the winter. General health is good with no known drug allergies.
Social history – married for 30 years to a high school principal. She works as a chef in a local restaurant. She is a nonsmoker, does not drink alcohol. She has a high school education. She has two grown children who are present. |
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Case Study (con't)
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Her recovery from surgery has been complicated by a paralytic ileus with abdominal distention. Frequent vomiting made insertion of a nasogastric tube necessary. She has resisted efforts by the nurses to cough or ambulate. She has an IV D5W at 75cc/hr.
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Case Study (con't)
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You arrive on postoperative day 2 and are assigned to Ms. Weber. Initial assessment finds her alert and oriented, anxious, short of breath and diaphoretic. Auscultation reveals wheezing in upper airways and crackles in the right lower lung.
What other assessment measures would be helpful here? |
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Case Study Assessment
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SAO2 is 88%
Urine output 100cc/hr CVP 8cm H2O, No JVD No peripheral edema, negative calf swelling or tenderness BP 140/96 Heart rate 106 Respirations 24 Temp 102 Chest x-ray right lower lobe pneumonia |
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Physician orders for Case Study
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O2 nasal cannula 3l/min with SAO2 improving to 93 %.
Sputum culture taken with antibiotics started. Wall nebs every 4 hrs and PRN Up in chair without fail. |
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Case Study (con't)
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Post operative day three you are again assigned to Ms. Webre. Initial assessment reveals dyspnea and diaphoresis. O2 at 3l/min with SAO2 86%. Nasal cannula is changed to 100% nonrebreather with no improvement.
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Case Study (con't)
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She is transferred to ICU for intubation and mechanical ventilation.
Ventilator settings are 70% FIO2, control mode ventilation 12, TV 700ml, 5cm PEEP. ABG 7.32, PCO2 50, PO2 89, HCO3 24. Chest xray shows clearing pneumonia with diffuse patchy infiltrates in both lungs. Diagnosis ARDS |
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Case Study (con't)
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Protective ventilation is initiated with TV decreased to 600, FIO2 lowered to 60% with the addition of 10 cm PEEP. ABGs improve.
Pt recovers and is extubated on day 9. She has residual fibrosis from hyaline membranes but is able to return to activities of daily living. She remains permanently disabled from work. |
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A nurse gets the report on a patient who is showing hypoxia, reduced lung compliance, diffuse pulmonary infiltrates, and hyaline formation. The FIOC is <200 mmHg and the pulmonry arterial wedge pressure is 18 mm Hg. She supects?
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ARDS
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The nurse knows that ARDS can be caused directly by?
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aspiration
pneumonia near drowing chest trauma inhalation of toxic substances |
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The nurse knows that ARDS can be indirectly caused by?
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sepsis
burns trauma multiple bl. transfusions CABG pancreatitis fat emboli |
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A nurse overhears the doctor telling interns that the pt in room 4 has hyaline membrane formation. She knows that this means?
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the pt probably has ARDS- this is when the aveoli collaspe and become atelectic-scarring
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