Page 1 of 14 Complex Alterations in Lower Respiratory Tract

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Page 1 of 14 Complex Alterations in Lower Respiratory Tract Powered By Docstoc
					Complex Alterations in Lower Respiratory Tract:
    Interstitial Pulmonary Diseases:
         Idiopathic Pulmonary Fibrosis
    Occupational Lung Disease
         Coal Miner’s Disease
             Farmer’s Lung
             Bird fancier’s lung
             Machine operator’s lung
    Chest Trauma
         Rib Fracture
         Flail Chest
         Tension Pneumothorax
         Tracheobronchial Trauma
         Pulmonary Contusion
    Adult Respiratory Distress Syndrome
    Pulmonary Embolism
Interstitial Pulmonary Diseases:
“Fibrotic Lung Disease”
         Restrictive disease
             Chronic inflammation causes thickening of lung tissue (fibrosis)
             Decreased elasticity or compliance of lung tissue
             (“stiff lung”)
             Decreases gas exchange
         Slow onset
         Most common manifestation: dyspnea

Sarcoidosis: (Interstitial Lung Disease/Fibrotic Lung Disease)
   Inflammatory disease that attacks organs in the body, most frequently the lung.
   Characterized by presences of granulomas that occur on walls of alveoli, bronchioles, and
   lymph nodes in the chest.
   No known cause.
        ? Disorder of the immune system.
        ? Viral syndrome.
        ? Exposure to environmental toxins or allergens.
   Signs and symptoms:
        Dry Cough
        Shortness of breath
        Mild chest pain
        Outside of lung, may have rash, fever, sore eyes,
          pain and edema of ankles.
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    Only 20-30% of pts with sarcoidosis are left with permanent lung damage. Small percentage
    of these have chronic sarcoidosis.
    Most common among African Americans and northern European Whites.
    In U.S., prevalence of Sarcoidosis is eight times greater in African-Americans than in whites.
    Affects young adults ages 20-40 and 45-65.
    Disease is self-limiting in most cases. In serious cases, manifestations include:
         Pumonary fibrosis( loss of elasticity).
         Interferes with breathing, esp. the ability to exchange O2 in the lungs.
Sarcoidosis: Assessment
    Staging of Sarcoidosis is done based on
    x-ray findings.
Stage 0: Normal Chest x-ray
Stage 1: Bilateral hilar adenopathy.
Stage 2: Bilater hilar adenopathy with diffuse                     parenchymal infiltrates.
Stage 3: Diffuse infiltrates with adenopathy
Stage 4: Lung Fibrosis
          abnormal chest x-ray
         R/O Lung infections and cancer
         Chest x-ray
         Indicators for treatment:
            Asymptomatic: no treatment
            Treatment of symptoms:
               Corticosteroids 40-60 mg/day with tapering dose over 6-8 wks. to 10-15 mg/day
               maintenance x 6 months.
               Monitoring includes:
                 Side effects of medication.
                 Pulmonary function studies.
                 Chest x-rays.
                 Serum Creatinine.
                 Serum Calcium
         Educate pt re: disease process and med. S/E.
Idiopathic Pulmonary Fibrosis:
    Common restrictive lung disease
            Elderly client
            Hx of cigarette smoking or exposure to inhaled irritants
            Survival less than 5 years after diagnosis

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          Chronic inflammation of lung tissue causing fibrosis and scarring of lung making gas
          exchange difficult.
            Dyspnea on exertion which worsens over time.
            Decreased forced vital capacity: maximum amt of air that can be exhaled quickly
            after maximum inspiration.
            Hypoxemia despite oxygen administration

        See drugs page 611
    Lung transplant
    Prevention of resp. infections
    Oxygen therapy
    Energy conservation: fatigue
    Encourage independence
    End stage disease: Morphine utilized to help control dyspnea (oral, parenteral, or nebulized)

Occupational Lung Disease:
See p. 612, Chart 33-12
  Occurs due to exposure to occupational or environmental fumes, dust, vapors, gases,
  bacterial or fungal antigens, and allergens that cause respiratory disorders.
  Most common form of Occupational Lung Disease is Occupational Asthma: Divided into 2
       Latency (allergic) asthma: Disease develops after a period of time with continued
         Causes airflow limitation, narrowing of airway
         Resolves with decreases/absent exposure
         Obstructive disease
       Type RADS ( reactive airways dysfunction) or Irritant-induced asthma: Onset of
       symptoms occurs within 24 hrs of exposure.
         Pathological changes that occur with exposure:
            Desquamation of epithelial layer.
            Thickening of basement membrane.
            Inflammation of bronchial mucosa.
            S/S: Cough, wheeze, dyspnea, and burning sensation in throat,        nose, and
            chest discomfort.
            Obstructive and restrictive disease

    Prevention in the workplace
    Remove worker from exposure to irritant
    Treatment for symptoms/asthma
    Refer to social worker
    Supplemental oxygen as required
    Other respiratory therapies as needed

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Occupational Lung Diseases: Byssinosis
    Byssinosis Cotton Worker’s Lung,Cotton Bract Disease, Monday Fever, and Brown Lung.
    An occupational disease of the lungs caused by inhalation of cotton dust or dusts from other
    vegetable fibers such as flax, hemp, or sisal.
         Symptoms are worse at the beginning of the work week and improve when away from
         the workplace.
         Repeated exposure can lead to chronic lung disease, SOB, and wheezing.
Pneumoconiosis: Silicosis
    Chronic lung disease characterized by fibrosis of lungs due to inhaled silica dust found in:
         Mining and quarrying
         Foundry work
         Pottery Making
         Stone Masonry
         Manufacture of tile and brick.
         Also in soaps, polishes, and filters.
    Chronic Silicosis results from > 20yrs exposure
    S/S: May be asymptomatic with mild ventilation restriction or may be severe with SOB,
    decreased lung volume, and fibrosis. Other symptoms: Fatigue, anorexia, and wt. loss.
Diffuse Interstitial Fibrosis: Asbestosis
    Diffuse interstitial fibrosis caused by exposure to asbestosis.
    Found in asbestos miners, millers, building trades, shipyards, carpenters, electricians,
    loggers, insulation workers, pipe fitters, steam fitters, sheet metal workers, and welders.
    Latency period of 10-20 years between initial exposure and fibrosis.
    Causes pleural thickening and calcification of diaphragm and pleural plaques.
    Pts have frequent resp. infections.
    May cause malignancies in bronchus, mesotheliomas of pleura and peritoneum.

Diffuse Interstitial Fibrosis: Talcosis
    Pulmonary fibrosis associated with talc dust found in:
        Roofing materials

Diffuse Interstitial Fibrosis: Berylliosis
    Chronic granulomatous disorder caused by inhalation of beryllium.
    Diffuse Interstitial Fibrosis
    Closely resembles Sarcoidosis.
    Restrictive disease

Extrinsic Allergic Alveolitis:
   Farmer’s lung
   Bird Fancier’s lung
   Machine operator’s lung

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Chest Trauma: Page 669
  Pumonary contusion
  Rib Fracture
  Flail Chest
  Tension Pneumothorax
  Tracheobronchial Trauma

Pulmonary Contusion:
Most common injury to chest.
   Progressive respiratory failure is characteristic d/t interstitial hemorrhage and alveolar
   Results in decreased compliance of lungs and impairment of gas exchange resulting in
   hypoxemia, dyspnea, and increased secretions.
Assessment and Interventions
       Decreased Breath Sounds
       Crackles, wheezes.
       Opacities on x-ray

        Maintain Oxygenation and ventilation
        Monitor CVP
        Fluid Restriction
        May need mechanical ventilation.
        May develop Flail chest
        May Develop ARDS
Rib Fracture:
   Frequently results from blunt chest trauma.
   Potential for punctured lung (pneumothorax) or pulmonary contusion.
   Assessment and Interventions:
           Pain with movement and defensive splinting of chest.
           Inadequate clearing of secretions.
           Prior pulmonary disease=increased risk for atelectasis and pneumonia
           Decrease pain to maintain ventilation.
           Intercostal nerve block for severe pain.
           Avoid respiratory depressing drugs.

Flail Chest: Paradoxic Respiration
    Inward movement of chest during inspiration and outward movement during expiration due to
    loose segment of chest wall from adjacent rib fractures. Usually on one side of chest.
    Results from multiple fractures of ribs from blunt chest trauma.
    High mortality rate (40%).
    Severely compromised gas exchange further reduced by patient splinting.
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   Inability to clear secretions adequately
Assessment and Interventions
   Assess for:
       Paradoxic movement of chest.

       Humidified O2
       Pain Mgmt.
       Deep breathing and proper position for adequate chest expansion.
       Promote clearing of secretions by pt or suction prn.
       Psychological support.
       Mechanical Vent. If needed.
       VS, CVP, fluid and electrolyte. balance as indicated.
Pneumothorax: (open or closed)
  Air in the pleural space.
  May be caused by blunt trauma.
  Often has hemothorax, as well.
  Assessment and Interventions:
          Decreased breath sounds.
          Hyperresonance with percussion
          Involved lung moves poorly with respirations.
          Deviation of trachea
             Away from if closed pneumothorax
             Towards if open pneumothorax.
             Subcutaneous emphysema
          Interventions: Chest tube placement to re-expand lungs after diagnosis with chest x-

Tension Pneumothorax:
   Results from blunt chest trauma:
        Air leak in the lung or chest wall.
        Forces air into the thoracic cavity and collapses lung.
        Air accumulates with increased pressure in thoracic cavity resulting in compressed
        mediastinal vessels and interferes with venous return.
        Compromised cardiac output d/t decreased diastolic filling of heart.
        Life threatening.
        Trauma where parenchyma fails to seal
        Mechanical ventilation with PEEP.
        Chest tube and drainage system.
        Placement of central venous catheters
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Assessment and Interventions
      Asymmetry of chest
      Tracheal deviation to unaffected side
      Resp. Distress
      Unilateral Absence of breath sounds
      Neck vein distention
      Hypertympanic sound over affected lung.
      Chest x-ray
      ABG’s: Hypoxia/resp. alkalosis.

       Insertion of large bore needle into 2nd intercostal space at midclavicular line.
       Chest tube insertion at between 4th intercostal space of midaxillary line and attaches to
       water seal drainage to reinflate lung.
  Simple: Blood loss of < 1500 ml.
  Massive: Blood loss > 1500 ml.
  Common injury associated with blunt trauma or penetrating injuries d/t rib/sternal fractures
  causing mild bleeding. Massive bleeding caused by trauma to heart, great vessels, and
  major systemic arteries.

Assessment and Interventions
        Simple: pt may be asymptomatic.
           Resp. Distress
           Decreased breath sounds.
           Percussion dull on affected side.
           Blood visible on chest x-ray.
           Diagnostic Thoracentesis confirms diagnosis.
        Evacuation of blood by insertion of chest tubes. (anterior and posterolateral.
        Assess drainage and serial x-rays.
        Thoracotomy if initial evacuation is 1500-2000 ml of blood or bleeding > 200cc/hr over 3
        Monitor VS, blood loss, I&O, Pt response to CT,.
        Administer IV fluids and blood as ordered. Consider Autotransfusion.
Tracheobronchial Trauma:
   Tears in tracheobronchial tree resulting from severe blunt trauma.
   Frequently occurs at junction of trachea and cricoid cartilage.
   Lacerations cause massive air leaks which in turn cause pneumomediastinum and
   subcutaneous emphysema.
   Pt may need tracheostomy or cricothyroidotomy below the level of injury for airway
   Assessment and Intervention:
        Assess hypoxemia via ABG results.
        Administer O2.
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        Mechanical Ventilation as required.
        Surgical Repair of injury may be needed
        Assess VS frequently
        Assess Subcutaneous Edema
        Auscultation of Lungs
          Decreased breath sounds
        Tracheostomy Care

Acute Respiratory Failure:
   Defined as:
       PaO2 < 60 mm Hg
       SaO2 < 90%
       Paco2 > 50 mm Hg
       pH < 7.30
       May be related to ventilation or oxygenation problems or both.

Ventilatory Failure:
       Normal perfusion/inadeqate ventilation
       Paco2 level > 45 mm Hg
  Causes: See Table 35-1, p. 656 (extrapulmonary and intrapulmonary causes)
       Mechanical abnormality
          Chest wall
       Injury to respiratory center in brain
       Impaired ventilatory muscle function

Oxygenation Failure:
      Ventilation normal/ perfusion decreased
  Causes: see Table 35-2, p. 657

Ventilation/Oxygenation Failure:
  Definition: Occurs in persons with abnormal lungs.
        Diseased alveoli
        Respiratory muscles unable to function d/t increasing work of breathing
        Chronic airflow limitation
           Chronic bronchitis
           Cardiac failure leading to respiratory failure

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   Assess for increasing dyspnea/orthopnea
      Changes in respiratory rate
      Changes in respiratory pattern
      Changes in lung sounds
      ABG’s (hypoxia, hypercarbia)
      Decreased O2 saturation

    O2 therapy (keep O2 level > 60 mm Hg
    Treat underlying cause of respiratory failure
    Position for comfort and for maximum expansion of lungs
    Drugs: Anxiolytics/bronchodialators/steroids
    Energy conservation measures

Acute Respiratory Distress Syndrome (ARDS):
   ARDS is a form of respiratory failure which exhibits:
       Refractory hypoxemia
       Decreased lung compliance (elasticity)
       Pulmonary edema (noncardiogenic)
       Pulmonary infiltrates
   Commonly precipitated by trauma, sepsis (systemic infection), diffuse pneumonia and shock.
   It may be associated with extensive surgery, and certain blood abnormalities. Less common
   causes include drowning and inhalation of toxic gases. In half the cases, onset occurs within
   24 hours of the original illness or injury;in nearly all, it occurs within three days.

   Systemic inflammatory response as a result of extrinsic/intrinsic injury (see Table 35-3, p.
   Damage occurs to alveolar/capillary membrane
   Increased in lung fluids/protein
   Decreased surfactant causing collapse of alveoli
   Decreased surface area for oxygenation
   Decreased elasticity of lungs
   Hypoxemia/respiratory failure

Prevention of ARDS:
   Early recognition of disease and risk factors
   Infection control to prevent infection

   Assessment: Physical/clinical symptoms
        Increased respirations and work of breathing (hyperpnea, grunting, cyanosis, pallor, and
        intercostal or substernal retractions).
        Initially there are no abnormal breath sounds. Occurs interstitially, not in airways.
        Changes in LOC
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       Poor response to increasing oxygen levels. Continues to have low PaO2.
       Sputum cultures via bronchoscopy or tracheobronchial aspiration. (R/O infection)
       Chest x-ray: White out of lungs (ground glass appearance of lungs).
       ECG (R/O cardiac problems)
       Hemodynamic monitoring (Swan Ganz); PCWP low to normal will differentiate between
       cardiogenic pulmonary edema and ARDS. Pulmonary edema of cardiac origin has high
       PCWP > 18.

Nursing diagnosis: ARDS
   Impaired Gas Exchange
   Disturbed Sleep Pattern r/t ICU environment
   Imbalanced Nutrition: Less than body requirements
   Risk for Injury r/t FIO2 or barotrauma
   Potential for Ventilator-Associated Pneumonia

         Endotracheal intubation and mechanical ventilation with PEEP or CPAP. (Possible
         complication of pneumothorax)
         Sedation and paralysis to reduce oxygen requirements.
         Assess lung sounds frequently. (potential for pneumothorax)
         Suction ETT
         Positioning for best oxygenation.
         Administer meds as ordered:
         Administer fluids to maintain adequate C.O. and tissue perfusion.
         Diuresis as ordered
         Monitor nutritional status
             administer tube feedings
            Administer parenteral feedings
         Focus on preventing complications according to phase of ARDS. SEE pg. 659
Interventions: ARDS
    Surfactant replacement
    Nitric Oxide
    Prone positioning
    High frequency Oscillatory Ventilation
    Phases of ARDS:
         Phase I: Dyspnea/Tachypnea
            Focus: support and oxygen
         Phase II: Patchy infiltrates/pulm. Edema
            Focus: Mech. Vent.; prevent complications
         Phase III: progressive hypoxemia over 2-10 days despite oxygenation at high levels.
            Focus: maintaining oxygen transport; prevent complications; support failing lung
            during healing time.
         Phase IV: Pulmonary fibrosis with progression after 10 days; Permanent damage to
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              Focus: prevention of sepsis, pneumonia, multiple organ failure; long term
              ventilation may occur.

Pulmonary Embolism:
   Solid, liquid, or gaseous substance that enters systemic circulation and lodges in the
   pulmonary vasculature causing obstruction, decreased oxygenation, tissue necrosis, and
   possibly death.
   Blood clot is the most common embolism evolving from a deep vein thrombosis (DVT).
   Most common (90%) acute pulmonary disease in hospitalized pts.
   Approx. 12% of pts with PE do not have hypoxemia.
   Approx. 10% of pts with PE die within 1 hour of onset of symptoms.

Pulmonary Embolus:
   Risk factors for PE include:
        Extended immobility
        Central venous catheters
        Advancing age
        Previous hx of thromboembolism
           Amniotic fluid embolus
        Estrogen Therapy
        Hx of CHF
        Hx of CVA
        Cancer, esp. lung or prostate.
        Trousseau’s Syndome (Cancer related thromboembolism)
        Major Trauma
           Fat emboli from fracture (DVT, PE)
        Foreign objects
        Infected fibrin clots or pus
        Air embolism
Assessment of PE:
        See Chart 35-1, p. 650
        Sudden onset of SOB
        Previous Hx of PE or DVT, Recent Surgery, or prolonged immobilization.
   Clinical Manifestations:
        See chart 35-2, Pg 651.
        Respiratory: dyspnea, tachypnea, pleuritic chest pain; Also, may have crackles, dry
        cough, hemoptysis.
        Cardiac: neck vein distention, syncope, cyanosis, hypotension; Abnormal heart sounds
        (S3 or S4); May have abnormal EKG;
        Other: low grade fever, petechiae (chest/axillae), N/V, malaise.
   Laboratory Assessment:
        ABG analysis indicates:
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          Respiratory Alkalosis initially, then resp. acidosis.
          Low PaCO2 initially, then rising.
          Metabolic Acidosis eventually occurs d/t increasing lactic acid from tissue hypoxia.

PE: Assessment
   Radiographic Assessment:
       CXR: alone is not diagnostic, may be normal.
   Other Diagnostic Assessment:
       V/Q scan: Ventilation/Perfusion Scan
       Pulmonary Angiography
       Spiral CT scans used increasingly to diagnose PE
       TEE: Transesophageal echocardiography
       Doppler studies for DVT
   Psychosocial Assessment:
       Pt is usually anxious and fearful.
       Explanation of procedures helpful.
   Prevention of PE
       See chart 35-1 pg. 650

Nursing Diagnosis: PE
   Problem: Hypoxemia
       Priority Nsg Dx:
          Decreased CO r/t acute pulmonary hypertension
          Anxiety r/t hypoxemia and life-threatening illness.
          Risk for injury (bleeding) r/t anticoagulation/ thrombolytic therapy.
       Additional Dx’s:
          Pg 651

Hypoxemia: PE
   Expected Outcome: Adequate Oxygenation
   Indicators of adequate perfusion:
        Normal ABG’s; SaO2 >95%; Normal LOC; Absent pallor/cyanosis
          Nonsurgical Mgmt:
             Oxygen therapy
               Mechanical ventilation, NC, FM
               Monitor ABG’s
               Pulse Oximetry
               Change in status
               Assess VS, Lung sounds, Cardiac and Respiratory status q 1-2 hrs. for dyspnea,
               dysrhythmias, distended neck veins, pedal or sacral edema, cyanosis, crackles,
               adventitious sounds..
             Anticoagulation/Thrombolytic Therapy: See pg.653.
               Heparin; Coumadin (warfarin); Lovenox; Alteplase;

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Anticoagulation/fibrinolytic therapy:
   Contraindicated in active bleeding, stroke, and recent trauma.
   For massive PE w/ hemodynamic instability:
        Fibrinolytics: alteplase/urokinase
           Adverse effect: bleeding
           Cautious use in clients using ASA, dipyridamole, heparin, or other anticoagulants.
   Heparin: Initial loading dose and adjustments made with PTT results for continuous
   infusion. LMWH used with coumadin to facilitate early discharge.
        Normal PTT = 20-30 seconds
        Therapeutic PTT for PE 1.5-2.5 x normal value
        Heparin therapy= 5-10 days; Coumadin started 3rd day of heparin until INR = 2.0-3.0.
   Coumadin continues 3-6 weeks; Monitor PT results;
        Normal PT = 11-12.5 seconds
        Therapeutic range = 1.5-2 x normal or control value.
        Therapeutic range for PE =2.5-3.0
        Therapeutic range for recurrent PE = 3.0-4.5

Preferred International Normalized Ratio (INR) according to indication for anticoagulation:
   DVT Prophylaxis               1.5-2.0
   Orthopedic Surgery            2.0-3.0
   DVT                                  2.0-3.0
   Prophylaxis for A.FIB         2.0-3.0
   Pulmonary embolism            3.0-4.0
   Prosthetic Valve Prophylaxis 2.5-3.5

Hypoxemia: PE
   Surgical Management:
       Embolectomy (removal of clots in pulm. Artery) when fibrinolytic therapy contraindicated
       Inferior Vena Cava Interruption: filter to catch clots for clients with:
           Anticoagulation contraindicated
          Bleeding with anticoagulants
          Septic PE
          Pulmonary embolectomy

Decreased C.O.: PE
  Expected Outcome: Adequate Circulation
  Indicators: normal pulse/BP; U.O.=30cc/hr; absent cyanosis;
       Interventions to manage hypoxemia
       IV fluid therapy to maintain adequate cardiac output, (crystaloids)
       Monitor EKG, PA/CVP pressures..
       Drug Therapy: Agents that increase myocardial contractility (positive inotropic drugs).
          Nitroprusside (vasodilators)

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Anxiety: PE
   Expected Outcome: Reduce level of anxiety.
   Indicators: Verbalizes reduced anxiety; absence of distress; effective use of coping
        Oxygen therapy
          Explain all procedures and rationales to patient.
        Drug Therapy:
          Antianxiety drugs.

Risk for Bleeding:
   Expected Outcome: Remain free of bleeding.
   Indicators: no bruising/petechiae; normal Hgb/Hct.
        Decrease situations that could lead to bleeding.
        Monitor pt. For bleeding.
        Educate pt re: s/s of bleeding and precautions.
           See chart 35-6, pg. 655.

Continuing Care:
  Teach pt.:
       Bleeding precautions
       Activities to decrease risk for PE and DVT.
       S/S of complications to report to MD.
       Importance of followup with MD.
       See client education guide-Chart 35-7, p. 655.
  Home Care Resources for:
       Assistance with ADLs
       O2 therapy
       Home Health Nursing

  Evaluation of outcomes:
      Adequate gas exchange and oxygenation
      No hypvolemia/shock
      No bleeding
      Decreased anxiety
      Uses effective coping

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