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30 Cards in this Set

  • Front
  • Back
Basement membranes of alveoli damaged
 Sudden, progressive form of acute respiratory failure
acute respiratory distress syndrome
 Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid
• Alveoli fill with fluid leading to:
• Severe dyspnea
• Hypoxemia
•  Lung compliance-lungs are very stiff-hard to oxygenate pateitns.
• Diffuse pulmonary infiltrates-any time have injury capillaries start to leak fluid leaks out of pulmonary capillaries.
 Develop from a variety of direct or indirect lung injuries
 Exact cause for damage to alveolar-capillary membrane not known
 Pathophysiologic changes of ARDS thought to be due to stimulation of inflammatory and immune systems
 Neutrophils are attracted and release mediators producing changes in lungs
•  Pulmonary capillary membrane permeability
• Destruction of elastin and collagen
• Formation of pulmonary microemboli
• Pulmonary artery vasoconstriction
etiology and patho of ARDS
: aspiration, inhallation injury, O2 toxicity, chest trauma, pancreatitis,pneumonia, near drowning
direct lung injury-ARDS
shock, multiple trauma, muliple organ failure, DIC, massive transfusion, burns, fat emboli, anaphylaxis
indirect lung injury-ARDS
beginning of interstitial space enlargement
• 1-7 days after direct lung injury or host insult
• Neutrophils adhere to pulmonary microcirculation
 Damage to vascular endothelium
 Increased capillary permeability
• Engorgement of peribronchial and perivascular interstitial space
• Fluid crosses into alveolar space
 Intrapulmonary shunt develops as alveoli fill with fluid and blood passing through cannot be oxygenated
• Alveolar cells type 1 and 2 are damaged
 Surfactant dysfunction  atelectasis-no protein makes stiff lungs filled with fluid
• Hyaline membranes line alveoli
 Contribute to atelectasis and fibrosis
• Severe V/Q mismatch and shunting of pulmonary capillary blood result in hypoxemia
 Unresponsive to increasing O2 concentrations-can increase O2 but O2 levels won’t go up
• Lungs become less compliant
•  Airway pressures must be generated-increased airway pressures to oxygenate patient
•  WOB
•  RR
•  Tidal volume
 Produces respiratory alkalosis from increase in CO2 removal
  CO and tissue perfusion-because increase pressures in lungs
 Injury or exudative phase-ARDS
• 1-2 weeks after initial lung injury
• Influx of neutrophils, monocytes, and lymphocytes
• Fibroblast proliferation
• Lung becomes dense and fibrous
• Lung compliance continues to decrease
• Hypoxemia worsens
 Thickened alveolar membrane
 Causes diffusion limitation and shunting
• If reparative phase persists, widespread fibrosis results-end up with wide spread fibrosis
• If phase is arrested, lesions resolve
 Reparative or proliferative phase-ARDS
• 2-3 weeks after initial lung injury
• Lung is completely remodeled by sparsely collagenous and fibrous tissues

  Lung compliance
 Reduced area for gas exchange
• Pulmonary hypertension –because increased pressures in lungs
 Results from pulmonary vascular destruction and fibrosis
 Fibrotic or chronic/late phase-ARDS
 Some persons survive acute phase of lung injury
• Pulmonary edema resolves
• Complete recovery

 Survival chances are poor for those who enter fibrotic phase
• Requires long-term mechanical ventilation
Clinical Progression-ARDS
 Initial presentation often insidious
 May only exhibit dyspnea, tachypnea, cough, and restlessness
 Auscultation may be normal or have fine, scattered crackles-from fluid
 Mild hypoxemia
 Chest x-ray may be normal or show minimal scattered interstitial infiltrates
• Edema may not show until 30% increase in lung fluid content
 Symptoms worsen with progression of fluid accumulation and decreased lung compliance
 Evident discomfort and WOB
 Pulmonary function tests reveal decreased compliance and lung volume
 Tachypnea
 Diaphoresis
 Cyanosis
 Pallor
 Decreases in sensorium
 As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation
 Chest x-ray termed whiteout or white lung due to consolidation and coalescing infiltrates widespread throughout lungs
 If prompt therapy not initiated, severe hypoxemia, hypercapnea, and metabolic acidosis may ensue
Clinical manifestations-ARDS
1. White out on chest xray (severe alveolar infiltrates)
2. Refractory hypoxemia
3. Predisposing condition
needed to have ARDS
nosocomial pneumonia, barotrauma, volu-pressure trauma, stress ulcers, renal failure
Complications of ARDS
d/t fluid in lungs
• Strategies for prevention
 Infection control measures
 Elevating HOB 45 degrees or more to prevent aspiration
Nosocomial pneumonia-complication of ARDS
if too much pressure can rupture alveoli
• Rupture of overdistended alveoli during mechanical ventilation
• To avoid, ventilate with smaller tidal volumes
 Results in higher PaCO2
 “Permissive hypercapnia”
Barotrauma-complication of ARDS
• Occurs when large tidal volumes used to ventilate noncompliant lungs
 Alveolar fractures and movement of fluids and proteins into alveolar spaces
• Avoid by using smaller tidal volumes or pressure ventilation
Valu-pressure trauma-comlication of ARDS
early use of tube feeding
• Bleeding from stress ulcer occurs in 30% of patients with ARDS on PPV
• Management strategies include correction of predisposing conditions, prophylactic antiulcer agents, and early initiation of enteral nutrition
stress ulcers-complcation of ARDS
d/t bodies increase stress
• Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or hypercapnia
• May also be caused by nephrotoxic drugs used for infections associated with ARDS
renal failure-complication of ARDS
 History of lung disease
 Exposures to lung toxins
 Smoking
 Related hospitalizations
 Spinal cord trauma
 Extreme obesity
 Use of O2, inhalers, nebulizers, immunosuppressant therapy
 Previous intubation
 Thoracic or abdominal surgery
 Exercise
 Immunizations
 Anorexia
 Weight gain/loss
 Diaphoresis
 Dizziness
 Dyspnea, wheezing, cough, sputum, palpitations, swollen feet
 Changes in sleep pattern
 Fatigue
Look for respiratory failure things that are not getting better

 Headache
 Chest pain
 Anxiety
 Restlessness
 Agitation
 Pale, cool, clammy or warm, flushed skin
 Shallow breathing with increased respiratory rate
 Use of accessory muscles
 Tachycardia progressing to bradycardia
 Extra heart sounds
 Abnormal breath sounds
 Hypertension progressing to hypotension
 Abdominal distention, ascites
 Somnolence, confusion, delirium
 Changes in pH, PaCO2, PaO2, SaO2
 Decreased tidal volume, FVC
 Abnormal x-ray, pulmonary artery and pulmonary artery wedge pressures
nursing assessment of ARDS
 Ineffective airway clearance
 Ineffective breathing pattern
 Risk for imbalanced fluid volume
 Anxiety
 Impaired gas exchange
 Imbalanced nutrition: less than body requirements
Nursing Diagnosis of ARDS
 Patient with PaO2 at least 60 mmHg and adequate lung ventilation to maintain normal pH following recovery will have
• PaO2 within normal limits
• SaO2 >90%
• Patent airway-#1
• Clear lungs on auscultation
If increased PEEP would need increased amount of O2 pressure to get air in.
 Oxygen
• High flow systems used to maximize O2 delivery
• SaO2 continuously monitored
• Give lowest concentration that results in PaO2 60 mmHg or greater
 Risk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hours-if on high flow O2 for long time
• ARDS patients commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels
 Mechanical ventilation
• May still be necessary to maintain FIO2 at 60% or greater to maintain PaO2 at 60 mmHg or greater
• PEEP (Positive end expiratory pressure) at 5 cm (usually 10-15) H2O to compensate for loss of glottic function-keeps alveoli inflated preventing collapse
 Opens collapsed alveoli
• Additional pressures from PEEP can compromise venous return to right side of the heart
 Decreases preload, CO, and BP
• Can cause hyperinflation of alveoli, compression of capillary bed, reduction in blood return to left side of heart, and reduction in blood pressure
• Can result in barotrauma and volu-pressure trauma
• Alternatives to PEEP used if hypoxemic failure persists

APRV-take big breath in then tiny small breaths in and out they breathe never breathe out all of the way out.
Respiratory therapy-ARDS
• Turn from prone to supine position
 May be sufficient to reduce inspired O2 or PEEP
• Fluid pools in dependent regions of lung
• Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone position
 Predisposes to atelectasis
• Prone position typically reserved for refractory hypoxemia not responding to other therapies
 Plan for immediate repositioning for cardiopulmonary resuscitation-fluid pools in depended region of lung.
• Lateral rotation therapy to provide continuous, slow, side-to-side turning
• Vibratory pack for chest PT
 Obtain baseline assessment prior to initiation
positioning strategies-ARDS
 Maintenance of cardiac output and tissue perfusion
• Continuous hemodynamic monitoring
• Arterial catheter
• Pulmonary artery catheter is normally inserted to allow monitoring of pulmonary artery pressure, pulmonary artery wedge pressures, and CO
 Administration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls
• Use of inotropic drugs may be necessary
• Hemoglobin usually kept at levels >9 or 10 with SaO2 >90%
• Packed RBCs
• Maintenance of fluid balance
• May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEP
• Monitor PAWP, daily weights, and I&Os, to assess fluid status
medical supportive therapy-ARDS
 No abnormal breath sounds
 Effective cough and expectoration
 Normal respiratory rate, rhythm, and depth
 Synchronous thoracoabdominal movement
 Appropriate use of accessory muscles
 Decreased or absent peripheral edema
 Normal pulmonary artery or pulmonary artery wedge pressures
 Decreased anxiety
 Verbalization of positive attitude toward outcome
 PaO2 and PaCO2 within normal ranges
 Maintenance of weight or weight gain
 Serum albumin and protein within normal ranges
air enters pleural space through chest wall
penetrating trauma
airway, ventilation, oxygen
clowe wound-careful not to cause tension pneumonthorax
tx: chest tube
Open pneumothorax (sucking chest wall)
compress heart so heart can't beat. increase accumulation of air and pressure
tx: needle in 2nd and 3rd intercostal space to release air out
tension pneumothorax
blood buildup in pleural space can happen from trauma and anticoagulants
section of ribs that are fractured
flail chest
use finger to feel pleura-widen spot and insert chest tube. chest tube is sutured down and have occlusive dressing to prevent air
chest tubes