Chapter 11: Respiratory Disorders

ACUTE DISORDERS

RESPIRATORY FAILURE

Respiratory failure is an alteration in the function of the respiratory system that causes the partial pressure of arterial oxygen (Pao₂) to fall below 50 mm Hg (hypoxemia) and/or the partial pressure of arterial carbon dioxide (Paco₂) to rise above 50 mm Hg (hypercapnia), as determined by arterial blood gas (ABG) analysis. Respiratory failure is classified as acute, chronic, or combined acute and chronic.

Classification

Acute Respiratory Failure

• Characterized by hypoxemia (Pao₂ less than 50 mm Hg) and/or hypercapnia (Paco₂ greater than 50 mm Hg) and acidemia (pH less than 7.35).
• Occurs rapidly, usually in minutes to hours or days.

Chronic Respiratory Failure

• Characterized by hypoxemia (decreased Pao₂) and/or hypercapnia (increased Paco₂) with a normal pH (7.35 to 7.45).
• Occurs over a period of months to years—allows for activation of compensatory mechanisms.

Acute and Chronic Respiratory Failure

• Characterized by an abrupt increase in the degree of hypoxemia or hypercapnia in patients with preexisting chronic respiratory failure.
• May occur after an acute upper respiratory infection or pneumonia, or without obvious cause.
• Extent of deterioration is best assessed by comparing the patient's present ABG levels with previous ABG levels (patient “normals”).

Pathophysiology and Etiology

Oxygenation Failure

Characterized by a decrease in Pao₂ and normal or decreased Paco₂.

• Primary problem is inability to adequately oxygenate the blood, resulting in hypoxemia.
• Hypoxemia occurs because damage to the alveolar-capillary membrane causes leakage of fluid into the interstitial space or into the alveoli and slows or prevents movement of oxygen from the alveoli to the pulmonary capillary blood.
  • Typically, this damage is widespread, resulting in many areas of the lung being poorly ventilated or nonventilated.
  • Consequences are severe ventilation-perfusion imbalance and shunt.
• Hypocapnia results from hypoxemia and decreased pulmonary compliance. Fluid within the lungs makes the lung less compliant or stiffer.
  • Change in compliance reflexively stimulates the increased ventilation.
  • Ventilation is also increased as a response to hypoxemia.
  • Ultimately, if treatment is unsuccessful, the Paco₂ will increase, and the patient will experience both an increase in Paco₂ and a decrease in Pao₂.
• Etiology includes:
  • Cardiogenic pulmonary edema (left ventricular failure; mitral stenosis).
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  • Acute respiratory distress syndrome (ARDS). Underlying causes of ARDS include shock of any etiology; infectious causes, such as gram-negative sepsis, viral pneumonia, bacterial pneumonia; trauma, such as fat emboli, head injury, lung contusion; aspiration of gastric fluid, near drowning; inhaled toxins, such as oxygen in high concentrations, smoke, corrosive chemicals; hematologic conditions, such as massive transfusions, post-cardiopulmonary bypass; and metabolic disorders, such as pancreatitis, uremia.

Ventilatory Failure with Normal Lungs

Characterized by a decrease in Pao₂, increase in Paco₂, and a decrease in pH.

• Primary problem is insufficient respiratory center stimulation or insufficient chest wall movement, resulting in alveolar hypoventilation.
• Hypercapnia occurs because impaired neuromuscular function or chest wall expansion limits the amount of carbon dioxide removed from the lungs.
  • Primary problem is not the lungs. The patient's minute ventilation (tidal volume times the number of breaths per minute) is insufficient to allow normal alveolar gas exchange.
• The carbon dioxide (CO₂) not excreted by the lungs combines with water (H₂O) to form carbonic acid (H₂CO₃). This predisposes to acidemia and a fall in pH.
• Hypoxemia occurs as a consequence of hypercapnia. When the Paco₂ rises, the Pao₂ must fall unless increased amounts of oxygen are added to the inspired air.
• Etiology includes:
  • Insufficient respiratory center activity (drug intoxication, such as opioid overdose, general anesthesia; vascular disorders, such as cerebral vascular insufficiency, brain tumor; trauma, such as head injury, increased intracranial pressure).
  • Insufficient chest wall function (neuromuscular disease, such as Guillain-Barré, myasthenia gravis, poliomyelitis; trauma to the chest wall resulting in multiple fractures; spinal cord trauma; kyphoscoliosis).

Ventilatory Failure with Intrinsic Lung Disease

Characterized by a decrease in Pao₂ and decreased pH.

• Primary problem is acute exacerbation or chronic progression of previously existing lung disease, resulting in CO₂ retention.
• Hypercapnia occurs because damage to the lung parenchyma and/or airway obstruction limits the amount of CO₂ removed by the lungs.
  • Primary problem is preexisting lung disease—usually chronic bronchitis, emphysema, or severe asthma. This limits CO₂ removal from the lungs.
• The CO₂ not excreted by the lungs combines with H₂O to form H₂CO₃. This predisposes to acidemia and a fall in pH.
• Hypoxemia occurs as a consequence of hypercapnia. In addition, damage to the lung parenchyma and/or airway obstruction limits the amount of oxygen that enters the pulmonary capillary blood.
• Etiology includes:
  • Chronic obstructive pulmonary disease (COPD) (chronic bronchitis, emphysema).
  • Severe asthma.
  • Cystic fibrosis.

Clinical Manifestations

• Hypoxemia—restlessness, agitation, dyspnea, disorientation, confusion, delirium, loss of consciousness.
• Hypercapnia—headache, somnolence, dizziness, confusion.
• Tachypnea initially; then when no longer able to compensate, bradypnea
• Accessory muscle use
• Asynchronous respirations

NURSING ALERT

Obtain ABG levels whenever the history or signs and symptoms suggest the patient is at risk for developing respiratory failure. Initial and subsequent values should be recorded so comparisons can be made over time. Need for ABG analysis can be decreased by using an oximeter to continuously monitor oxygen saturation (Sao₂). Correlate oximeter values with ABG values and then use oximeter for trending.

Diagnostic Evaluation

• ABG analysis—show changes in Pao₂, Paco₂, and pH from patient's normal; or Pao₂ less than 50 mm Hg, Paco₂ greater than 50 mm Hg, pH less than 7.35.
• Pulse oximetry—decreasing Sao₂.
• End tidal CO₂ monitoring—elevated.
• Complete blood count, serum electrolytes, chest X-ray, urinalysis, electrocardiogram (ECG), blood and sputum cultures—to determine underlying cause and patient's condition.

Management

• Oxygen therapy to correct the hypoxemia.
• Chest physical therapy and hydration to mobilize secretions.
• Bronchodilators and possibly corticosteroids to reduce bronchospasm and inflammation.
• Diuretics for pulmonary congestion.
• Mechanical ventilation as indicated. Noninvasive positive-pressure ventilation using a face mask may be a successful option for short-term support of ventilation.

NURSING ALERT

Avoid administration of oxygen at Fio₂ of 100% for COPD patients because you may depress the respiratory center drive. For COPD patients, the drive to breathe may be hypoxemia.

Complications

• Oxygen toxicity if prolonged high Fio₂ required.
• Barotrauma from mechanical ventilation intervention

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Nursing Assessment

See Standards of Care Guidelines.

• Note changes suggesting increased work of breathing (tachypnea, diaphoresis, intercostal muscle retraction, fatigue) or pulmonary edema (fine, coarse crackles or rales, frothy pink sputum).
• Assess breath sounds.
  • Diminished or absent sounds indicate inability to ventilate the lungs sufficiently to prevent atelectasis.
  • Crackles indicate ineffective airway clearance, fluid in the lungs.
  • Wheezing indicates narrowed airways and bronchospasm.
  • Rhonchi and crackles indicate ineffective secretion clearance.
• Assess level of consciousness (LOC) and ability to tolerate increased work of breathing.
  • Confusion, rapid shallow breathing, abdominal paradox (inward movement of abdominal wall during inspiration), and intercostal retractions suggest inability to maintain adequate minute ventilation.
• Assess for signs of hypoxemia and hypercapnia.
• Determine vital capacity (VC), respiratory rate, and negative inspiratory force (NIF) and compare with values indicating need for mechanical ventilation:
  • VC < 10 to 15 mL/kg.
  • Respiratory rate > 35 breaths/minute.
  • NIF <—15 to —25 cm H₂O.
• Analyze ABG and compare with previous values.
  • If the patient cannot maintain a minute ventilation sufficient to prevent CO₂ retention, pH will fall.
  • Mechanical ventilation or noninvasive ventilation may be needed if pH falls to 7.30 or below.
• Determine hemodynamic status (blood pressure, pulmonary wedge pressure, cardiac output, Svo₂) and compare with previous values. If patient is on mechanical ventilation and positive end-expiratory pressure (PEEP), venous return may be limited, resulting in decreased cardiac output.

Nursing Diagnoses

• Impaired Gas Exchange related to inadequate respiratory center activity or chest wall movement, airway obstruction, and/or fluid in lungs
• Ineffective Airway Clearance related to increased or tenacious secretions

Nursing Interventions

Improving Gas Exchange

• Administer antibiotics, cardiac medications, and diuretics as ordered for underlying disorder.
• Administer oxygen to maintain Pao₂ of 60 mm Hg or Sao₂ > 90% using devices that provide increased oxygen concentrations (aerosol mask, partial rebreathing mask, nonrebreathing mask).
• Monitor fluid balance by intake and output measurement, urine specific gravity, daily weight, and direct measurement of pulmonary capillary wedge pressure to detect presence of hypovolemia or hypervolemia.
• Provide measures to prevent atelectasis and promote chest expansion and secretion clearance, as ordered (incentive spirometer, nebulization, head of bed elevated 30 degrees, turn frequently, out of bed).
• Monitor adequacy of alveolar ventilation by frequent measurement of respiratory rate, VC, inspiratory force, and ABG levels.
• Compare monitored values with criteria indicating need for mechanical ventilation (see section titled “Nursing Assessment”). Report and prepare to assist with noninvasive ventilation or intubation and initiation of mechanical ventilation, if indicated.

STANDARDS OF CARE GUIDELINES

Respiratory Compromise

When caring for patients at risk for respiratory compromise, consider the following assessments and interventions:

• Be aware of the status of the patient when assuming care so comparison can be made with subsequent assessments.
• Perform thorough systematic assessment, including mental status, vital signs, respiratory status, and cardiovascular status.
• Document patient's condition to provide a record for continuity of care.
• Evaluate for signs of hypoxia when anxiety, restlessness, confusion, or aggression of new onset are noted. Do not administer sedatives unless hypoxia has been ruled out by performing respiratory assessment.
• Notify appropriate health care provider of significant findings of hypoxia—cyanosis, circumoral pallor, rapid and shallow respirations, abnormal breath sounds, change in behavior or level of consciousness. Request assessment and intervention by health care provider as indicated.
• Use extreme caution in administering sedatives and opioids to patients at risk for respiratory compromise.

Footnote

This information should serve as a general guideline only. Each patient situation presents a unique set of clinical factors and requires nursing judgment to guide care, which may include additional or alternative measures and approaches.

Maintaining Airway Clearance

• Administer medications to increase alveolar ventilation—bronchodilators to reduce bronchospasm, corticosteroids to reduce airway inflammation.
• Perform chest physiotherapy to remove mucus. Teach slow, pursed-lip breathing to reduce airway obstruction.
• Administer I.V. fluids and mucolytics to reduce sputum viscosity.
• Suction patient as needed to assist with removal of secretions.
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• If the patient becomes increasingly lethargic, cannot cough or expectorate secretions, cannot cooperate with therapy, or if pH falls below 7.30, despite use of the above therapy, report and prepare to assist with intubation and initiation of mechanical ventilation.

Patient Education and Health Maintenance

• Instruct patient with preexisting pulmonary disease to seek early intervention for infections to prevent acute respiratory failure.
• Teach patient about medication regimen.
  • Proper technique for inhaler use
  • Dosage and timing of medications
  • Monitoring for adverse effects of corticosteroids: weight gain due to fluid retention, polyuria and polydipsia due to hyperglycemia, mood changes; report to health care provider

Community and Home Care Considerations

• Encourage patients at risk, especially the elderly and those with preexisting lung disease, to get yearly influenza immunizations and pneumococcal pneumonia immunization.
  • Pneumococcal vaccine is 60% to 70% effective in preventing bacteremic pneumococcal infections in adults and children at least age 2 years.
  • If a person received their first pneumococcal vaccination before age 65, they should be revaccinated at age 65, if more than 5 years have elapsed since the previous dose.
• Vaccinate people over age 2 and with the following conditions for pneumococcal pneumonia, as recommended by the Centers for Disease Control and Prevention (CDC):
  • Chronic cardiovascular disease (including heart failure).
  • Chronic pulmonary disease (eg, emphysema).
  • Diabetes.
  • Alcoholism.
  • Chronic liver disease (including cirrhosis).
  • Cerebrospinal fluid leaks.
  • Asplenia (including functional asplenia such as sickle cell disease).
  • Immunocompromised people (including human immunodeficiency virus [HIV]).
  • People living in environments at higher risk for pneumococcal disease (Alaskan natives, certain American Indian populations, and residents of nursing homes and long-term care facilities).
• Immunize annually for influenza in the following groups, according to the CDC:
  • People age 50 and older
  • Immunocompromised patients
  • Residents of nursing homes or chronic care facilities
  • People with cardiovascular disease
  • People with diabetes mellitus
  • Patients receiving long-term aspirin therapy
  • Pregnant women who will be in the second or third trimester of pregnancy during flu season
  • Health care workers
  • Household contacts of people at risk

Evaluation: Expected Outcomes

• ABG values within patient's normal limits
• Decreased secretions; lungs clear

ACUTE RESPIRATORY DISTRESS SYNDROME

ARDS is a clinical syndrome also called noncardiogenic pulmonary edema in which there is severe hypoxemia and decreased compliance of the lungs, which leads to both oxygenation and ventilatory failure. Mortality is 50% to 60% but is improved with early intervention.

Pathophysiology and Etiology

• Pulmonary and/or nonpulmonary insult to the alveolar-capillary membrane causing fluid leakage into interstitial spaces.
• Ventilation-perfusion ([V with dot above]/[Q with dot above]) mismatch caused by shunting of blood (see Figure 11-1).

  FIGURE 11-1 Pathogenesis of ARDS.

• Etiologies are numerous and can be pulmonary or nonpulmonary. These include (but are not limited to):
  • Pneumonia, sepsis, aspiration.
  • Shock (any cause), trauma.
  • Metabolic, hematologic, and immunologic disorders.
  • Inhaled agents—smoke, high concentration of oxygen, corrosive substances.
  • Major surgery, fat or air embolism.

Clinical Manifestations

• Severe dyspnea, use of accessory muscles.
• Increasing requirements of oxygen therapy. Hypoxemia refractory to supplemental oxygen therapy.
• Severe crackles and rhonchi heard on auscultation.

Diagnostic Evaluation

• The hallmark sign for ARDS is a shunt; hypoxemia remains despite increasing oxygen therapy.
• Decreased lung compliance; increasing pressure required to ventilate patient on mechanical ventilation.
• Chest X-ray exhibits bilateral infiltrates.
• Pulmonary artery catheter readings: pulmonary artery wedge pressure >18 mm Hg.

Management

• The underlying cause for ARDS must be determined so appropriate treatment can be initiated.
• Ventilatory support with PEEP will be instituted. PEEP keeps the alveoli open, thereby improving gas exchange. Therefore, a lower oxygen concentration (Fio₂) can be used to maintain satisfactory oxygenation.
• Fluid management must be maintained. The patient may be hypovolemic due to the movement of fluid into the interstitium of the lung. Pulmonary artery catheter monitoring and inotropic medication can be helpful.
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• Medications are aimed at treating the underlying cause. Corticosteroids are used infrequently due to the controversy regarding benefits of usage.
• Adequate nutrition should be initiated early and maintained.

NURSING ALERT

The treatment for ARDS is aimed at symptom management, but the underlying cause must be treated or the ARDS will not resolve. Supportive measures will assist the patient while the underlying cause is being treated.

Complications

• Infections, such as pneumonia, sepsis.
• Respiratory complications, such as pulmonary emboli, barotrauma, oxygen toxicity, subcutaneous emphysema, or pulmonary fibrosis.
• GI complications, such as stress ulcer, ileus.
• Cardiac complications, such as decreased cardiac output and dysrhythmias.
• Renal failure, disseminated intravascular coagulation.

Nursing Interventions

Care is similar to patient with respiratory failure (page 281) and pulmonary edema (page 416). Also see “Mechanical Ventilation,” page 261.

ACUTE BRONCHITIS

Acute bronchitis is an infection of the lower respiratory tract that is generally an acute sequela to an upper respiratory tract infection.

Pathophysiology and Etiology

• Primarily viral etiology, but may also arise from bacterial agents.
• Airways become inflamed and irritated with increased mucous production.

Clinical Manifestations

• Dyspnea, fever, tachypnea.
• Productive cough, clear to purulent sputum.
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• Pleuritic chest pain, occasionally.
• Diffuse rhonchi and crackles heard on auscultation.

Diagnostic Evaluation

• Chest X-ray—no evidence of infiltrates or consolidation.
• Sputum for gram stain, culture, and sensitivity tests may be obtained to determine presence of bacterial infection.
• Spirometry to determine peak expiratory flow (may be decreased).

Management

• Antibiotic therapy for 7 to 10 days may be indicated for patients with underlying respiratory problems or chronic illness.
• Hydration and humidification.
• Secretion clearance interventions (controlled cough, positive expiratory pressure valve therapy, chest physical therapy).
• Bronchodilators for bronchospastic cough and bronchial irritation.
• Symptom management for fever, cough.

Nursing Assessment

• Obtain history of upper airway infection, course and length of symptoms.
• Assess severity of cough and characteristics of sputum production.
• Auscultate chest for diffuse rhonchi and crackles as opposed to localized crackles usually heard with pneumonia.

Nursing Diagnosis

• Ineffective Airway Clearance related to sputum production

Nursing Interventions

Establishing Effective Airway Clearance

• Administer or teach self-administration of antibiotics as ordered.
• Encourage mobilization of secretions, through hydration, chest physical therapy, and coughing. Educate patient that beverages with caffeine or alcohol do not promote hydration because of their diuretic effect.
• If ordered, administer or teach self-administration of inhaled bronchodilators to reduce bronchospasm and enhance secretion clearance.
• Caution patients on the use of over-the-counter cough suppressants, antihistamines, and decongestants that may cause drying and retention of secretions. Cough preparations containing the mucolytic guaifenesin may be appropriate.

Patient Education and Health Maintenance

• Instruct patient about medication regimen, including the completion of the full course of antibiotics prescribed and the effects of food on the absorption of the medications. If patient is not being treated with antibiotics, assure patient that the majority of cases of people recover from bronchitis without antibiotic treatment.
• Encourage patient to seek medical attention for shortness of breath and worsening condition.
• Advise patient that a dry cough may persist after bronchitis due to irritation of the airways. A bedside humidifier and avoidance of dry environments may help.
• Encourage patient to discuss alternative therapies with health care provider. Some people use garlic as an antimicrobial because it is believed to have antibacterial and antiviral activity due to the antiseptic oil, which is excreted through the lungs. It may also be helpful as part of a broader approach to bronchitic asthma. Other herbs believed to have antimicrobial activity for bronchitis are echinacea, eucalyptus, and thyme. The antiseptic volatile oils contained in eucalyptus and thyme can also be used in the form of inhalations or baths.

Evaluation:Expected Outcomes

• Coughs up clear secretions effectively

PNEUMONIA

Pneumonia is an inflammatory process, involving the terminal airways and alveoli of the lung, caused by infectious agents (see Table 11-1, pages 288 to 291). It is classified according to its causative agent.

TABLE 11-1 Commonly Encountered Pneumonias

TYPE ORGANISM RESPONSIBLE MANIFESTATIONS CLINICAL FEATURES TREATMENT COMPLICATIONS Bacterial Streptococcal pneumonia (pneumococcal pneumonia) (60% of community-acquired pneumonia) Streptococcus pneumoniae May be history of previous respiratory infection Sudden onset, with shaking and chills Rapidly rising fever; tachypnea Cough, with expectoration of rusty or green (purulent) sputum Pleuritic pain aggravated by cough Chest dull to percussion; crackles, bronchial breath sounds Confusion may be only presenting feature in elderly patient Usually involves one or more lobes Chest X-ray shows consolidation of affected areas Common community-acquired pneumonia as well as seen in nursing home residents, alcoholics, smokers, and those with chronic obstructive pulmonary disease (COPD) Macrolide antibiotics such as azithromycin (Zithromax) or clarithromycin (Biaxin); doxycycline (> age 8); oral beta lactams such as cefuroxime (Ceftin), amoxicillin, or amoxicillin clavulanate (Augmentin) Shock Pleural effusion Superinfections Pericarditis Otitis media Staphylococcal pneumonia Staphylococcus aureus Commonly, history of viral infection, especially influenza Insidious development of cough, with expectoration of yellow, blood-streaked mucus Onset may be sudden if patient is outside hospital Fever, pleuritic chest pain, progressive dyspnea Pulse varies; may be slow in proportion to temperature Commonly seen in hospital setting; during influenza epidemics; in I.V. drug abuse These infections commonly lead to necrosis and destruction of lung tissue Treatment must be vigorous and prolonged owing to disease's tendency to destroy the lungs Organism may develop rapid drug resistance Prolonged convalescence usual Cephalosporins; penicillinase-resistant extended-spectrum penicillins; vancomycin (Vancocin) for methicillin-resistant S. aureus Effusion/pneumothorax Lung abscess Empyema Meningitis Pneumonia due to gram-negative enteric bacilli Klebsiella species: Pseudomonas organisms, Escherichia coli, Serratia, Proteus species Sudden onset with fever, chills, dyspnea Pleuritic chest pain and production of purulent sputum Infection usually occurs from aspiration of pharyngeal flora into bronchioles Seen in persons with severe illness; among the more common causes of hospital-acquired pneumonia Usually multiple-drug regimens recommended: aminoglycosides; cephalosporins; and/or penicillinase-resistant extended-spectrum penicillin Early necrosis of lung tissue with rapid abscess formation High mortality Legionnaires' disease Legionella pneumophila High fever, chills, cough, chest pain, tachypnea Respiratory distress Peak incidence in people over age 50 who are cigarette smokers and have underlying diseases that increase susceptibility to infection Erythromycin (E-Mycin) or newer macrolide antibiotic such as clarithromycin (Biaxin) Respiratory failure Haemophilus influenza pneumonia H. influenzae Abrupt onset of coughing, fever, chills, tachypnea Common in smokers and former smokers May affect healthy young adults X-ray may show consolidation Erythromycin (E-Mycin), newer macrolide antibiotic, trimethoprim-sulfamethoxazole (Bactrim) High mortality in patients with underlying disease (cancer; COPD) Pleural effusion common Atypical and Non-bacterial Mycoplasma, chlamydial, or Legionella pneumonia Mycoplasma pneumoniae, Chlamydia trachomatis, or L. pneumophila Gradual onset; severe headache; irritating hacking cough producing scanty, mucoid sputum Anorexia; malaise Fever; nasal congestion; sore throat Occurs most commonly in children and young adults, as well as in older adults in community or hospital setting Rise in serum-complement-fixing antibodies to the organism Erythromycin (E-Mycin); newer macrolide antibiotic; tetracycline (Tetracyn); doxycycline (Vibramycin) Persisting cough, meningoencephalitis, polyneuritis, monoarticular arthritis, pericarditis, myocarditis Chlamydial pneumonia has been implicated in cardiac atheromatous lesions in some patients Viral pneumonia Influenza viruses Parainfluenza viruses Respiratory syncytial viruses Rhinoviruses Adenovirus Varicella, rubella, rubeola, herpes simplex, cytomegalovirus, Epstein-Barr virus Cough Constitutional symptoms may be pronounced (severe headache, anorexia, fever, and myalgia) In majority of patients, influenza begins as an acute coryza and myalgias; others have bronchitis and pleurisy, whereas still others develop GI symptoms Risk of developing influenza related to crowding and close contact with groups Treat symptomatically Amantadine (Symmetrel) relieves symptoms Prophylactic vaccination recommended for high-risk persons (over age 65; chronic cardiac or pulmonary disease, diabetes, and other metabolic disorders) Persons with underlying disease have increased risk of complications; primary influenzal pneumonia; secondary bacterial pneumonia Bacterial superinfection Pericarditis Endocarditis Atypical and Non-bacterial Pneumocystis pneumonia(PCP) P. carinii Insidious onset Increasing dyspnea and nonproductive cough Tachypnea; progresses rapidly to intercostal retraction, nasal flaring, and cyanosis Lowering of arterial oxygen tension Chest X-ray will reveal diffuse, bilateral interstitial pneumonia Usually seen in host whose resistance is compromised; most common opportunistic infection in acquired immunodeficiency syndrome (AIDS) in the United States Organism invades lungs of patients who have suppressed immune system (from AIDS, cancer, leukemia) or after immunosuppressive therapy for cancer, organ transplant, or collagen disease Frequently associated with concurrent infection by viruses (cytomegalovirus), bacteria, and fungi Co-trimoxazole (Bactrim); dapsone with trimethoprim (Trimpex); clindamycin (Cleocin) with primaquine Pentamidine methanesulfonate Patients are critically ill Prognosis guarded, because it is usually a complication of a severe underlying disorder Fungal pneumonia Aspergillus fumigatus Fever, productive cough, chest pain, hemoptysis Chest X-ray reveals broad range of abnormalities from infiltration to consolidation, cavitation, and empyema Neutropenic individual most susceptible May develop Aspergillus as a superinfection Amphotericin B (Fungizone); Itraconazole (Sporanox) High mortality rate Invades blood vessels and destroys lung tissue by direct invasion and vascular infarction

Pathophysiology and Etiology

• The organism gains access to the lungs through aspiration of oropharyngeal contents, by inhalation of respiratory secretions from infected individuals, by way of the bloodstream, or from direct spread to the lungs as a result of surgery or trauma.
• Patients with bacterial pneumonia may have an underlying disease that impairs host defense; pneumonia arises from endogenous flora of the person whose resistance has been altered, or from aspiration of oropharyngeal secretions.
  • Immunocompromised patients include those receiving corticosteroids or immunosuppressants, those with cancer, those being treated with chemotherapy or radiotherapy, those undergoing organ transplantation, alcoholics, I.V. drug abusers, and those with HIV disease and acquired immunodeficiency syndrome.
  • These people have an increased risk of developing overwhelming infection. Infectious agents include aerobic and anaerobic gram-negative bacilli; Staphylococcus; Nocardia; fungi; Candida; viruses, such as cytomegalovirus; Pneumocystis carinii (also known as P. jiroveci); reactivation of tuberculosis (TB); and others.
• When bacterial pneumonia occurs in a healthy person, there is usually a history of preceding viral illness.
• Other predisposing factors include conditions interfering with normal drainage of the lung, such as tumor, general anesthesia, and postoperative immobility; depression of the central nervous system (CNS) from drugs, neurologic disorders, or other conditions, such as alcoholism, and intubation or respiratory instrumentation.
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• Pneumonia may be divided into three groups:
  • Community acquired, due to a number of organisms, including Streptococcus pneumoniae
  • Hospital or nursing home acquired (nosocomial), due primarily to gram-negative bacilli and staphylococci
  • Pneumonia in the immunocompromised person
• People over age 65 have a high mortality, even with appropriate antimicrobial therapy.

NURSING ALERT

Recurring pneumonia commonly indicates underlying disease, such as cancer of the lung, multiple myeloma, or COPD.

Clinical Manifestations

For most common forms of bacterial pneumonia:

• Sudden onset; shaking chill; rapidly rising fever of 101° F to 105° F (38.3° C to 40.5° C).
• Cough productive of purulent sputum.
• Pleuritic chest pain aggravated by respiration/coughing
• Dyspnea, tachypnea accompanied by respiratory grunting, nasal flaring, use of accessory muscles of respiration, fatigue
• Rapid, bounding pulse

Diagnostic Evaluation

• Chest X-ray shows presence/extent of pulmonary disease, typically consolidation.
• Gram stain and culture and sensitivity tests of sputum—may indicate offending organism.
• Blood culture detects bacteremia (bloodstream invasion) occurring with bacterial pneumonia.
• Immunologic test detects microbial antigens in serum, sputum, and urine.

Management

• Antimicrobial therapy—depends on laboratory identification of causative organism and sensitivity to specific antimicrobials, or presumptive therapy with broad spectrum agent in milder cases.
• Oxygen therapy if patient has inadequate gas exchange

Complications

• Pleural effusion.
• Sustained hypotension and shock, especially in gram-negative bacterial disease, particularly in elderly patients.
• Superinfection: pericarditis, bacteremia, and meningitis.
• Delirium—this is considered a medical emergency.
• Atelectasis—due to mucous plugs.
• Delayed resolution.

Nursing Assessment

• Take a careful history to help establish etiologic diagnosis.
  • History of recent respiratory illness including mode of onset
  • Presence of purulent sputum, increased amount of sputum, fever, chills, chest pain, dyspnea, tachypnea
  • Any family illness
  • Medications, alcohol, tobacco, or I.V. drug use
• Observe for anxious, flushed appearance, shallow respirations, splinting of affected side, confusion, disorientation.
• Auscultate for crackles overlying affected region, and for bronchial breath sounds when consolidation (filling of airspaces with exudate) is present.

Nursing Diagnoses

• Impaired Gas Exchange related to decreased ventilation secondary to inflammation and infection involving distal airspaces
• Ineffective Airway Clearance related to excessive tracheobronchial secretions
• Acute Pain related to inflammatory process and dyspnea
• Risk for Injury secondary to complications

Nursing Interventions

Improving Gas Exchange

• Observe for cyanosis, dyspnea, hypoxia, and confusion, indicating worsening condition.
• Follow ABG levels/Sao₂ to determine oxygen need and response to oxygen therapy.
• Administer oxygen at concentration to maintain Pao₂ at acceptable level. Hypoxemia may be encountered because of abnormal ventilation-perfusion ratios in affected lung segments.
• Avoid high concentrations of oxygen in patients with COPD, particularly with evidence of CO₂ retention; use of high oxygen concentrations may worsen alveolar ventilation by depressing the patient's only remaining ventilatory drive. If high concentrations of oxygen are given, monitor alertness and Pao₂ and Paco₂ levels for signs of CO₂ retention.
• Place patient in an upright position to obtain greater lung expansion and improve aeration. Frequent turning and increased activity (up in chair, ambulate as tolerated) should be employed.

Enhancing Airway Clearance

• Obtain freshly expectorated sputum for gram stain and culture, preferably early morning specimen as directed. Instruct the patient as follows:
  • Rinse mouth with water to minimize contamination by normal flora.
  • Breathe deeply several times.
  • Cough deeply and expectorate raised sputum into sterile container.
• Encourage patient to cough; retained secretions interfere with gas exchange. Suction as necessary.
• Encourage increased fluid intake, unless contraindicated, to thin mucus and promote expectoration and replace fluid losses caused by fever, diaphoresis, dehydration, and dyspnea.
• Humidify air or oxygen therapy to loosen secretions and improve ventilation.
• Employ chest wall percussion and postural drainage when appropriate to loosen and mobilize secretions.
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• Auscultate the chest for crackles and rhonchi.
• Administer cough suppressants when coughing is nonproductive only if there is no evidence of retained secretions.
• Mobilize patient to improve secretion clearance and reduce risk of atelectasis and worsening pneumonia.

Relieving Pleuritic Pain

• Place in a comfortable position (semi-Fowler's) for resting and breathing; encourage frequent change of position to prevent pooling of secretions in lungs.
• Demonstrate how to splint the chest while coughing.
• Avoid suppressing a productive cough.
• Administer prescribed analgesic agent to relieve pain. Avoid opioids in patients with a history of COPD.
• Apply heat and/or cold to chest as prescribed.
• Assist with intercostal nerve block for pain relief.
• Encourage modified bed rest during febrile period.
• Watch for abdominal distention or ileus, which may be due to swallowing of air during intervals of severe dyspnea. Insert a nasogastric (NG) or rectal tube as directed.

GERONTOLOGIC ALERT

Sedatives, opioids, and cough suppressants should be used cautiously in elderly patients, because of their tendency to suppress cough and gag reflexes and respiratory drive. Also, provide or encourage frequent oral care for pneumonia prevention.

Monitoring for Complications

• Remember that fatal complications may develop during the early period of antimicrobial treatment.
• Monitor temperature, pulse, respiration, blood pressure, and oximetry at regular intervals to assess the patient's response to therapy.
• Auscultate lungs and heart. Heart murmurs or friction rub may indicate acute bacterial endocarditis, pericarditis, or myocarditis.
• Employ special nursing surveillance for patients with:
  • Alcoholism, COPD, immunosuppression—these people as well as elderly patients, may have little or no fever.
  • Chronic bronchitis—it is difficult to detect subtle changes in condition, because the patient may have seriously compromised pulmonary function.
  • Epilepsy—pneumonia may result from aspiration after a seizure.
  • Delirium—may be caused by hypoxia, meningitis, delirium tremens of alcoholism.
• Assess these patients for unusual behavior, alterations in mental status, stupor, and heart failure.
• Assess for resistant fever or return of fever, potentially indicating bacterial resistance to antibiotics.

NURSING ALERT

Delirium must be controlled to prevent exhaustion and cardiac failure. Prepare for lumbar puncture, if indicated, to rule out meningitis, which may be lethal. Mild sedation may be given.

Patient Education and Health Maintenance

• Advise patient that fatigue, weakness, and depression may be prolonged after pneumonia.
• Encourage chair rest after fever subsides; gradually increase activities to bring energy level back to preillness stage.
• Encourage breathing exercises to clear lungs and promote full expansion and function after the fever subsides.
• Explain that a chest X-ray is taken 4 to 6 weeks after recovery to evaluate lungs for clearing and detect any tumor or underlying cause.
• Advise smoking cessation. Cigarette smoke destroys tracheobronchial cilial action, which is the first line of defense of lungs; also irritates mucosa of bronchi and inhibits function of alveolar scavenger cells (macrophages).
• Advise the patient to keep up natural resistance with good nutrition, adequate rest. One episode of pneumonia may make the patient susceptible to recurring respiratory infections.
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• Instruct patient to avoid fatigue, sudden extremes in temperature, and excessive alcohol intake, which lower resistance to pneumonia.
• Encourage yearly immunization for influenza and S. pneumoniae, a major cause of bacterial pneumonia.
• Advise avoidance of contact with people who have upper respiratory infections for several months after pneumonia resolves.
• Practice frequent handwashing, especially after contact with others.

Evaluation: Expected Outcomes

• Cyanosis and dyspnea reduced; ABG levels and Sao₂ improved
• Coughs effectively; absence of crackles
• Appears more comfortable; free of pain
• Fever controlled, no signs of resistant infection

ASPIRATION PNEUMONIA

Aspiration is the inhalation of oropharyngeal secretions and/or stomach contents into the lungs. It may produce an acute form of pneumonia.

Pathophysiology and Etiology

• Patients at risk and factors associated with risk:
  • Loss of protective airway reflexes (swallowing, cough) caused by altered state of consciousness, alcohol or drug overdose, during resuscitation procedures, seriously ill or debilitated patients, abnormalities of gag and swallowing reflexes
  • NG tube feedings
  • Obstetric patients—from general anesthesia, lithotomy position, delayed emptying of stomach from enlarged uterus, labor contractions
  • GI conditions—hiatal hernia, intestinal obstruction, abdominal distention
• Effects of aspiration depend on volume and character of aspirated material
  • Particulate matter—mechanical blockage of airways and secondary infection
  • Anaerobic bacterial aspiration—from oropharyngeal secretions
  • Gastric juice—destructive to alveoli and capillaries; results in outpouring of protein-rich fluids into the interstitial and intra-alveolar spaces (Impairs exchange of oxygen and CO₂, producing hypoxemia, respiratory insufficiency, and respiratory failure.)

Clinical Manifestations

• Tachycardia, fever.
• Dyspnea, cough, tachypnea.
• Cyanosis
• Crackles, rhonchi, wheezing
• Pink, frothy sputum (may simulate acute pulmonary edema)

Diagnostic Evaluation

• Chest X-ray may be normal initially; with time, shows consolidation and other abnormalities.

Management

Depends on the material aspirated.

• Clearing the obstructed airway.
  • If foreign body is visible, it may be removed manually.
  • Place the patient in tilted head-down position on right side (right side more commonly affected if patient has aspirated solid particles).
  • Suction trachea/ET tube—to remove particulate matter.
• Laryngoscopy/bronchoscopy if patient has been asphyxiated by solid material.
• Fluid volume replacement for correction of hypotension.
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• Antimicrobial therapy if there is evidence of superimposed bacterial infection.
• Correction of acidosis; respiratory acidosis and metabolic acidosis indicate a severe reaction due to aspiration of gastric contents.
• Oxygen therapy and assisted ventilation if adequate ABG values cannot be maintained.

Complications

• Lung abscess; empyema.
• Necrotizing pneumonia

Nursing Assessment

• Assess for airway obstruction.
• Assess for risk factors for aspiration.
• Assess for development of fever, foul-smelling sputum, and development of congestion.

Nursing Diagnoses

(See pages 287 and 290 for nursing interventions.)

• Impaired Gas Exchange related to decreased ventilation secondary to inflammation and infection involving distal airspaces
• Ineffective Airway Clearance related to excessive tracheobronchial secretions
• Acute Pain related to inflammatory process and dyspnea
• Risk for Injury secondary to complications

Additional Nursing Interventions

• Be on guard constantly and monitor patients at risk as described above.
• Elevate head of bed for debilitated patients, for those receiving tube feedings, and for those with motor diseases of the esophagus.
• Place patients with impaired reflexes in a lateral position.
• Make sure NG tube is patent.
• Give tube feedings slowly, with patient sitting up in bed.
  • Check position of tube in stomach before feeding.
  • Check seal of cuff of tracheostomy or ET tube before feeding.
• Keep the patient in a fasting state before anesthesia (at least 8 hours).
• Feed patients with impaired swallowing slowly, and make sure that no food is retained in mouth after feeding.

NURSING ALERT

Morbidity and mortality rate of aspiration pneumonia remain high even with optimum treatment. Prevention is the key to the problem.

PULMONARY EMBOLISM

Pulmonary embolism refers to the obstruction of one or more pulmonary arteries by a thrombus (or thrombi) originating usually in the deep veins of the legs, the right side of the heart or, rarely, an upper extremity, which becomes dislodged and is carried to the pulmonary vasculature.

Pulmonary infarction refers to necrosis of lung tissue that can result from interference with blood supply.

Pathophysiology and Etiology

• Obstruction, either partial or full, of pulmonary arteries, which causes decrease or absent blood flow; therefore, there is ventilation but no perfusion ([V with dot above]/[Q with dot above] mismatch).
• Hemodynamic consequences:
  • Increased pulmonary vascular resistance
  • Increased pulmonary artery pressure (PAP)
  • Increased right ventricular workload to maintain pulmonary blood flow
  • Right ventricular failure
  • Decreased cardiac output
  • Decreased blood pressure
  • Shock
• Pulmonary emboli can vary in size and seriousness of consequences.
• Predisposing factors include:
  • Stasis, prolonged immobilization.
  • Concurrent phlebitis.
  • Previous heart (heart failure, myocardial infarction [MI]) or lung disease.
  • Injury to vessel wall.
  • Coagulation disorders.
  • Metabolic, endocrine, vascular, or collagen disorders.
  • Malignancy.
  • Advancing age, estrogen therapy.

NURSING ALERT

Be aware of high-risk patients for pulmonary embolism—immobilization, trauma to pelvis (especially surgical) and lower extremities (especially hip fracture), obesity, history of thromboembolic disease, varicose veins, pregnancy, heart failure, MI, malignant disease, postoperative patients, elderly patients.

Clinical Manifestations

• Dyspnea, pleuritic pain, tachypnea, apprehension.
• Chest pain with apprehension and a sense of impending doom occurs when most of the pulmonary artery is obstructed.
• Cyanosis, tachyarrhythmias, syncope, circulatory collapse and, possibly, death encountered in patients with massive pulmonary embolism
• Subtle deterioration in patient's condition with no explainable cause
• Pleural friction rub

NURSING ALERT

Have a high index of suspicion for pulmonary embolus if there is a subtle deterioration in the patient's condition and unexplained cardiovascular and pulmonary findings.

Diagnostic Evaluation

• ABG levels—decreased Pao₂ is usually found, due to perfusion abnormality of the lung.
• Chest X-ray—normal or possible wedge-shaped infiltrate.
• [V with dot above]/[Q with dot above] lung scans—perfusion scan investigates regional blood flow to determine presence of perfusion defects; ventilation scan may be done in patient with large perfusion defects.
• Pulmonary angiogram (most definitive)—emboli seen as “filling defects.”

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Management

Emergency Management

For massive pulmonary embolism, goal is to stabilize cardiorespiratory status

NURSING ALERT

Massive pulmonary embolism is a medical emergency; the patient's condition tends to deteriorate rapidly. There is a profound decrease in cardiac output, with an accompanying increase in right ventricular pressure.

• Oxygen is administered to relieve hypoxemia, respiratory distress, and cyanosis.
• An infusion is started to open an I.V. route for drugs and fluids.
• Vasopressors, inotropic agents such as dopamine (Intropin), and antidysrhythmic agents may be indicated to support circulation if the patient is unstable.
• ECG is monitored continuously for right-sided heart failure, which may have a rapid onset.
• Small doses of I.V. morphine are given to relieve anxiety, alleviate chest discomfort (which improves ventilation), and ease adaptation to mechanical ventilator, if this is necessary.
• Pulmonary angiography, hemodynamic measurements, ABG analysis, and other studies are carried out.

Subsequent Management—Anticoagulation and Thrombolysis

• I.V. heparin—stops further thrombus formation and extends the clotting time of the blood; it is an anticoagulant and antithrombotic.
  • I.V. loading dose usually followed by continuous pump or drip infusion or given intermittently every 4 to 6 hours.
  • Dosage adjusted to maintain the partial thromboplastin time (PTT) at 1½ to 2 times the pretreatment value (if the value was normal).
  • Protamine sulfate may be given to neutralize heparin in event of severe bleeding.
• Oral anticoagulation with warfarin (Coumadin) is usually used for follow-up anticoagulant therapy after heparin therapy has been established; interrupts the coagulation mechanism by interfering with the vitamin K-dependent synthesis of prothrombin and factors VII, IX, and X.
  • Dosage is controlled by monitoring serial tests of prothrombin time; desired prothrombin time (PT) is 2 to 3 times control value.
  • Reported as international normalized ratio (INR) of 2½by most laboratories.
  • Anticoagulation is used to prevent new clot formation but does not dissolve previously formed clots. Thrombolytics are used to dissolve clots.
• Thrombolytic agents, such as streptokinase (Streptase), may be used in patients with massive pulmonary embolism.
  • Effective in lysing recently formed thrombi.
  • Improve circulatory and hemodynamic status.
  • Administered I.V. in a loading dose followed by constant infusion.
• Newer clot-specific thrombolytics (tissue plasminogen activator, streptokinase activator complex, single-chain urokinase) are preferred.
  • Activate plasminogen only within thrombus itself rather than systematically.
  • Minimize occurrence of generalized fibrinolysis and subsequent bleeding.

GERONTOLOGIC ALERT

Consider the patient's age in dosing of anticoagulation therapy. Elderly patients will usually need a decreased dosing regimen.

Surgical Intervention

When anticoagulation is contraindicated or patient has recurrent embolization or develops serious complications from drug therapy.

• Interruption of vena cava—reduces channel size to prevent lower extremity emboli from reaching lungs. Accomplished by:
  • Ligation, plication, or clipping of the inferior vena cava.
  • Placement of transvenously inserted intraluminal filter in inferior vena cava to prevent migration of emboli (see Figure 11-2); inserted through femoral or jugular vein by way of catheter.

    FIGURE 11-2 Insertion of umbrella filter in inferior vena cava to prevent pulmonary embolism. Filter (compressed within an applicator catheter) is inserted through an incision in the right internal jugular vein. The applicator is withdrawn when the filter fixes itself to the wall of the inferior vena cava after ejection from the applicator.

• Embolectomy (removal of pulmonary embolic obstruction).

Complications

• Bleeding as a result of treatment.
• Respiratory failure

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Nursing Assessment

• Take nursing history with emphasis on onset and severity of dyspnea and nature of chest pain.
• Examine the patient's legs carefully. Assess for swelling of leg, duskiness, warmth, pain on pressure over gastrocnemius muscle, pain on dorsiflexion of the foot (positive Homans' sign), which indicate thrombophlebitis as source.
• Monitor respiratory rate—may be accelerated out of proportion to degree of fever and tachycardia.
  • Observe rate of inspiration to expiration.
  • Percuss for resonance, dullness, and flatness.
  • Auscultate for friction rub, crackles, rhonchi, and wheezing.
• Auscultate heart; listen for splitting of second heart sound.
• Evaluate results of PT/PTT tests for patients on anticoagulants and report results that are outside of therapeutic range; anticipate a dosage change.

Nursing Diagnoses

• Ineffective Breathing Pattern related to acute increase in alveolar dead airspace and possible changes in lung mechanics from embolism
• Ineffective Tissue Perfusion (Pulmonary) related to decreased blood circulation
• Acute Pain (pleuritic) related to congestion, possible pleural effusion, possible lung infarction
• Anxiety related to dyspnea, pain, and seriousness of condition
• Risk for Injury related to altered hemodynamic factors and anticoagulant therapy

Nursing Interventions

Correcting Breathing Pattern

• Assess for hypoxia, headache, restlessness, apprehension, pallor, cyanosis, behavioral changes.
• Monitor vital signs, ECG, oximetry, and ABG levels for adequacy of oxygenation.
• Monitor patient's response to I.V. fluids/vasopressors.
• Monitor oxygen therapy—used to relieve hypoxemia.
• Prepare patient for assisted ventilation when hypoxemia is due to local areas of pneumoconstriction and abnormalities of [V with dot above]/[Q with dot above] ratios.

Improving Tissue Perfusion

• Closely monitor for shock—decreasing blood pressure, tachycardia, cool, clammy skin.
• Monitor prescribed medications given to preserve right ventricular filling pressure and increase blood pressure.
• Maintain patient on bed rest to reduce oxygen demands and risk of bleeding.
• Monitor urinary output hourly, because there may be reduced renal perfusion and decreased glomerular filtration.

Relieving Pain

• Watch patient for signs of discomfort and pain.
• Ascertain if pain worsens with deep breathing and coughing; auscultate for friction rub.
• Give prescribed morphine (Duramorph), and monitor for pain relief and signs of respiratory depression.
• Position with head of bed slightly elevated (unless contraindicated by shock) and with chest splinted for deep breathing and coughing.
• Evaluate patient for signs of hypoxia thoroughly when anxiety, restlessness, and agitation of new onset are noted, before administering as needed sedatives. Consider physician evaluation when these signs are present, especially if accompanied by cyanotic nail beds, circumoral pallor, and increased respiratory rate.

Reducing Anxiety

• Correct dyspnea and relieve physical discomfort.
• Explain diagnostic procedures and the patient's role; correct misconceptions.
• Listen to the patient's concerns; attentive listening relieves anxiety and reduces emotional distress.
• Speak calmly and slowly.
• Do everything possible to enhance the patient's sense of control.

Intervening for Complications

• Be alert for shock from low cardiac output secondary to resistance to right ventricular outflow or to myocardial dysfunction due to ischemia.
  • Assess for skin color changes, particularly nail beds, lips, ear lobes, and mucous membranes.
  • Monitor blood pressure.
  • Measure urine output.
  • Monitor I.V. infusion of vasopressor or other prescribed agents.
• Bleeding—related to anticoagulant or thrombolytic therapy.
  • Assess patient for bleeding; major bleeding may occur from GI tract, brain, lungs, nose, and genitourinary (GU) tract.
  • Perform stool guaiac test to detect occult blood loss.
  • Monitor platelet count to detect heparin-induced thrombocytopenia.
  • Minimize risk of bleeding by performing essential ABG analysis on upper extremities; apply digital compression at puncture site for 30 minutes; apply pressure dressing to previously involved sites; check site for oozing.
  • Maintain patient on strict bed rest during thrombolytic therapy; avoid unnecessary handling.
  • Discontinue infusion in the event of uncontrolled bleeding.
  • Notify health care provider on call immediately for change in LOC, ability to follow commands, sensation, ability to move limbs, and respond to questions with clear articulation. Intracranial bleed may necessitate discontinuation of anticoagulation promptly to avert massive neurologic catastrophe.

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Patient Education and Health Maintenance

• Advise patient of the possible need to continue taking anticoagulant therapy for 6 weeks up to an indefinite period.
• Teach about signs of bleeding, especially of gums, nose, bruising, blood in urine and stools.
• For patients on anticoagulants, instruct to use soft toothbrush, avoid shaving with blade razor (use electric razor instead), and avoid aspirin-containing products. Notify health care provider of bleeding or increased bruising.
• Warn against taking medications unless approved by health care provider, because many drugs interact with anticoagulants.
• Instruct patient to tell dentist about taking an anticoagulant.
• Warn against inactivity for prolonged periods or sitting with legs crossed to prevent recurrence.
• Warn against sports/activities that may cause injury to legs and predispose to a thrombus.
• Encourage wearing a MedicAlert bracelet identifying patient as anticoagulant user.
• Instruct patient to lose weight if applicable; obesity is a risk factor for women.
• Discuss contraceptive methods with patient if applicable; females with history of pulmonary embolus are advised against taking hormonal contraceptives.

Evaluation: Expected Outcomes

• Verbalizes less shortness of breath
• Vital signs stable, adequate urinary output
• Reports freedom from pain
• Appears more relaxed; sleeping at long intervals
• Progresses without complications

TUBERCULOSIS

TB is an infectious disease caused by bacteria (Mycobacterium tuberculosis) that are usually spread from person to person through the air. It usually infects the lung but can occur at virtually any site in the body. HIV-infected patients are especially at risk. Drug-resistant TB is of particular concern in certain parts of the United States.

Pathophysiology and Etiology

Transmission

• The term Mycobacterium is descriptive of the organism, which is a bacterium that resembles a fungus. The organisms multiply at varying rates and are characterized as acid-fast aerobic organisms that can be killed by heat, sunshine, drying, and ultraviolet light.
• TB is an airborne disease transmitted by droplet nuclei, usually from within the respiratory tract of an infected person who exhales them during coughing, talking, sneezing, or singing.
• When an uninfected susceptible person inhales the droplet-containing air, the organism is carried into the lung to the pulmonary alveoli.
• Most people who become infected do not develop clinical illness, because the body's immune system brings the infection under control.

Pathology

• The bacilli of TB infect the lung, forming a tubercle (lesion).
• The tubercle:
  • May heal, leaving scar tissue.
  • May continue as a granuloma, then heal, or be reactivated.
  • May eventually proceed to necrosis, liquefaction, sloughing, and cavitation.
• The initial lesion may disseminate tubercle bacilli by extension to adjacent tissues, by way of the bloodstream, by way of the lymphatic system, or through the bronchi.
• Extrapulmonary TB occurs more commonly in children and immunocompromised individuals and can involve lymph nodes, bones, joints, pleural space, pericardium, CNS, GU tissue, and the peritoneum.

Clinical Manifestations

Patient may be asymptomatic or may have insidious symptoms that may be ignored.

• Constitutional symptoms
  • Fatigue, anorexia, weight loss, low-grade fever, night sweats, indigestion.
  • Some patients have acute febrile illness, chills, and flu-like symptoms.
• Pulmonary signs and symptoms
  • Cough (insidious onset) progressing in frequency and producing mucoid or mucopurulent sputum.
  • Hemoptysis; chest pain; dyspnea (indicates extensive involvement).
• Extrapulmonary TB: pain, inflammation, and dysfunction in any of the tissues infected.

Diagnostic Evaluation

• Sputum smear—detection of acid-fast bacilli in stained smears is the first bacteriologic clue of TB. Obtain first morning sputum on 3 consecutive days.
• Sputum culture—a positive culture for M. tuberculosis confirms a diagnosis of TB.
• Chest X-ray to determine presence and extent of disease.
• Tuberculin skin test (purified protein derivative [PPD] or Mantoux test)—inoculation of tubercle bacillus extract (tuberculin) into the intradermal layer of the inner aspect of the forearm (see Procedure Guidelines 11-1, pages 296 and 297). It is used to detect M. tuberculosis infection, past or present, active or inactive (latent).
• Nonspecific screening tests, such as multiple puncture tests (tine test), should not be used to determine if a person is infected.

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PROCEDURE GUIDELINES 11-1

Tuberculin Skin Test

EQUIPMENT

• Purified protein derivative (PPD) tuberculin antigen intermediate strength
• Tuberculin syringe
• Short ½″, 26G or 27G steel needle
• Alcohol pad
• Gloves

PROCEDURE

Nursing Action Rationale Preparatory phase 1. Determine if the patient has ever had bacille Calmette-Guérin (BCG) vaccine, recent viral disease, immunosuppression by disease, drugs, or steroids. 1. Any of these may cause false readings. Previous BCG vaccine or the other factors should not preclude PPD testing, but will be considered with the result. 2. Do not give PPD to person who has had a positive test or TB in the past. 2. Chest X-ray is indicated for testing. Performance phase 1. Draw up PPD-tuberculin into tuberculin syringe. 1. Follow the manufacturer's directions. Each 0.1-mL dose should contain 5 tuberculin units (TU) of PPD-tuberculin. Use the antigen immediately to avoid absorption onto the plastic/glass syringe. 2. Put on gloves. 2. Follow standard infection control precautions. 3. Clean the skin of the inner aspect of forearm with alcohol. Allow to dry. 3. Alcohol must dry for antisepsis. 4. Stretch the skin taut. 5. Hold the tuberculin syringe close to the skin so the hub of the needle touches it as the needle is introduced, bevel up. 5. This reduces the needle angle at the skin surface and facilitates the injection of tuberculin just beneath the surface of the skin. 6. Inject the tuberculin into the superficial layer of the skin to form a wheal 6 mm to 10 mm in diameter. 6. If no wheal appears (because the injection was made too deep), inject again at another site at least 2 inches (5cm) away. 7. Immediately place disposable needle and syringe into puncture-resistant sharps container. Follow-up phase To read the test 1. Read the test within 48 to 72 hours when the induration is most evident. 1. Tuberculin skin tests are tests of delayed hypersensitivity. 2. Have a good light available. Flex the patient's forearm slightly at the elbow. 3. Inspect for the presence of induration; inspect from a side view against the light; inspect by direct light. 3. Induration refers to hardening or thickening of tissues. 4. Palpate: Lightly rub the finger across the injection site from the area of normal skin to the area of induration. Outline the diameter of induration. 4. Erythema (redness) without induration is generally considered to be of no significance. 5. Measure the maximum transverse diameter of induration (not erythema) in millimeters with a flexible ruler. 5. The extent of induration is measured in two diameters and recorded. Interpretation 1. Induration of 5 mm or more in diameter 1. Considered positive in: a. People with human immunodeficiency virus (HIV). b. People who have had recent contact with active TB. c. People who have fibrotic changes on chest X-ray, consistent with healed TB. d. People with organ transplants or other causes of immunosuppression (including therapy with ≥15 mg/d prednisone × 1 month). 2. Induration of 10 mm or more in diameter 2. Considered positive in: a. People with medical conditions, such as substance abuse, TB within past 2 years, diabetes mellitus, silicosis, head and neck cancer, leukemia, end-stage renal disease, gastrectomy, intestinal bypass, prolonged corticosteroid therapy. b. Recent arrivals from areas of the world where TB is common (Asia, Africa, Latin America). c. Medically underserved, low-income populations. d. Residents of long-term care facilities. e. Children younger than age 4 years; adolescents exposed to adults in high-risk categories. f. I.V. drug users. g. Mycobaceteriology laboratory personnel. h. All people who do not meet above criteria but who have other risk factors for TB, such as homelessness, alcoholism, malnutrition, and health care work. 3. Induration of 15 mm or more in diameter 3. Considered positive in people who do not meet the above criteria. NURSINGALERT ALERT False-positive reaction may occur in people infected with mycobacteria other than M. tuberculosis and vaccination with BCG. False-negative reactions may occur in people with HIV infection, overwhelming miliary or pulmonary TB, severe or febrile illness, measles or other viral infections, Hodgkin's disease, sarcoidosis, live-virus vaccinations, and those receiving corticosteroids or immunosuppressive drugs.

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Management

See Table 11-2, page 298.

TABLE 11-2 Recommended Drugs for the Initial Treatment of Tuberculosis in Adults

DRUG DOSAGE FORMS DAILY DOSE TWICE WEEKLY DOSE THRICE WEEKLY DOSE MAJOR ADVERSE REACTIONS Isoniazid (INH) Tablets: 100 mg, 300 mg Syrup: 50 mg/5 mL Vials: 1 g 5 mg/kg PO or I.M. (maximum 300 mg) 15 mg/kg Maximum 900 mg (can also be given once a week) 15 mg/kg Maximum 900 mg Hepatic enzyme elevation, peripheral neuropathy, hepatitis, hypersensitivity Rifampin (Rifadin) Capsules: 150 mg, 300 mg Syrup: formulated from capsules, 10 mg/mL 10 mg/kg PO (maximum 600 mg) 10 mg/kg Maximum 600 mg 10 mg/kg Maximum 600 mg Orange discoloration of secretions and urine; nausea, vomiting, anorexia, hepatitis, febrile reaction, purpura (rare), pruritus and rash Pyrazinamide (PZA) Tablets: 500 mg 20-25 mg/kg PO 50-70 mg/kg 50-70 mg/kg Maximum 3 g Hepatotoxicity, hyperuricemia, arthralgias, skin rash, GI upset, Ethambutol (Myambutol) Tablets: 100 mg, 400 mg 15-20 mg/kg 50 mg/kg 25-30 mg/kg Optic neuritis (decreased red-green color discrimination, decreased visual acuity), skin rash

• A combination of drugs to which the organisms are susceptible is given to destroy viable bacilli as rapidly as possible and to protect against the emergence of drug-resistant organisms.
• Current recommended regimen of uncomplicated, previously untreated pulmonary TB is an initial phase of 2 months of bactericidal drugs, including isoniazid (INH), rifampin (Rifadin), pyrazinamide (PZA), and ethambutol (EMB). This regimen should be followed until the results of drug susceptibility studies are available, unless there is little possibility of drug resistance.
  • If drug susceptibility results are known and organism is fully susceptible, EMB does not need to be included.
  • For children whose visual acuity cannot be monitored, EMB is not normally recommended except with increased likelihood of INH resistance or if the child has upper lobe infiltration and/or cavity formation TB.
  • Due to increasing frequency of global streptomycin resistance, streptomycin is not considered interchangeable with EMB unless organism is known to be susceptible to streptomycin.
  • PZA may be withheld for severe liver disease, gout and, possibly, pregnancy.
  • Adverse effects including liver injury have been noted with rifampin and pyrazinamide in a once daily or twice weekly combination, therefore this combination is not recommended for the treatment of latent TB infection.
• Follow with 4 months of isoniazid and rifampin. Six months of therapy is usually effective for killing the three populations of bacilli: those rapidly dividing, those slowly dividing, and those only intermittently dividing.
• Sputum smears may be obtained every 2 weeks until they are negative; sputum cultures do not become negative for 3 to 5 months.
• Rifabutin (Mycobutin) is used as a substitute for rifampin if the organism is susceptible to rifabutin and for patients taking medications that may interact with rifampin.
• Second-line drugs, such as cycloserine (Seromycin), ethionamide (Trecator-SC), streptomycin, Amikacin (Amikin), kanamycin (Kantrex), capreomycin (Capastat),
  

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  para-aminosalicylic acid, and some fluoroquinolones, are used in patients with resistance, for retreatment, and in those with intolerance to other agents. Patients taking these drugs should be monitored by health providers experienced in their use.
• Alternative drug regimens for active TB have been recommended by the American Thoracic Society, 2003, See MMWR; 52 (No. RR-11), 1-78.
• For people suspected of having latent TB infection (LTBI), treatment should begin after active TB has been ruled out. See Table 11-3.

  TABLE 11-3 Drug Therapy for LTBI

  DRUGS DURATION(MONTHS) INTERVAL MINIMUM DOSES Isoniazid* 9 Daily 270 Twice 76 weekly Isoniazid 6 Daily 180 Twice 52 Weekly Rifampin 4 Daily 120 Rifampin/Pyrazinamide Generally should not be offered for treatment of LTBI because of severe liver injury and deaths — — * Preferred Adapted from Centers for Disease Control and Prevention, Treatment of Latent Tuberculosis Infection (LTBI), August 7, 2003, http://www.cdc.gov/nchstp/tb/pubs/tbfactssheet/250110.htm .

DRUG ALERT

Adverse reactions to anti-TB drugs may be significant. Most common adverse effects are rash, GI intolerance, and liver enzyme elevation, but neurotoxicity, hepatitis, hypersensitivity reactions, and optic neuritis may occur. Liver toxicity is the most worrisome adverse reaction because toxic hepatitis may occur in patients receiving INH, RIF, or PZA. Instruct patients to seek immediate medical attention if symptoms or signs of hepatitis occur (nausea, emesis, anorexia, jaundice, and/or abdominal pain). The CDC is collecting reports of severe liver injury (ie, leading to hospital admission or death) in patients receiving any treatment regimen for LTBI. Report possible cases to the Division of Tuberculosis Elimination at (404) 639-8442.

Complications

• Pleural effusion.
• TB pneumonia.
• Other organ involvement with TB
• Serious reactions to drug therapy
  • INH may produce asymptomatic elevation in liver enzymes, rare peripheral neurotoxicity, hepatitis that may, rarely, be fatal, CNS effects (dysarthria, irritability, seizures, dysphoria, diminished concentration), lupus-like syndrome, hypersensitivity reactions, and monoamine poisoning (rarely occurring with consumption of some wines and cheeses). Patients with pre-existing liver disease should be monitored closely.
  • Ethambutol may cause retrobulbar optic neuritis with decreased visual acuity and decreased red-green discrimination in one or both eyes, although this occurs rarely with daily doses of 15 mg/kg/day. EMB may also cause peripheral neuritis and cutaneous reactions. Patients should have baseline visual acuity and color discrimination (Ishihara test) testing as well as monthly monitoring.
  • Pyrazinamide may cause hepatotoxicity, GI symptoms, nongouty polyarthralgia, asymptomatic hyperuricemia, and acute gouty arthritis.
  • Any anti-TB drug may cause rash. If rash occurs, withhold all medications until rash subsides. Rechallenge drugs sequentially every 3 to 4 days to find cause. Usual sequence is INH, rifampin, PZA, EMB, using the first line (most important) drug first.
  • Rifampin may cause pruritus with or without rash, GI adverse effects, flu-like symptoms, hepatotoxicity, rare severe immunologic reactions, orange discoloration of body fluids, and drug interactions with hormonal contraceptives, methadone, and warfarin.

Nursing Assessment

• Obtain history of exposure to TB.
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• Assess for symptoms of active disease—productive cough, night sweats, afternoon temperature elevation, unintentional weight loss, pleuritic chest pain.
• Auscultate lungs for crackles.
• During drug therapy, assess for liver dysfunction.
  • Question the patient about loss of appetite, fatigue, joint pain, fever, tenderness in liver region, clay-colored stools, and dark urine.
  • Monitor for fever, right upper quadrant abdominal tenderness, nausea, vomiting, rash, and persistent paresthesia of hands and feet.
  • Monitor results of periodic liver function studies.

Nursing Diagnoses

• Ineffective Breathing Pattern related to pulmonary infection and potential for long-term scarring with decreased lung capacity
• Risk for Infection related to nature of the disease and patient's symptoms
• Imbalanced Nutrition: Less Than Body Requirements related to poor appetite, fatigue, and productive cough
• Noncompliance related to lack of motivation and long-term treatment

Nursing Interventions

Improving Breathing Pattern

• Administer and teach self-administration of medications as ordered.
• Encourage rest and avoidance of exertion.
• Monitor breath sounds, respiratory rate, sputum production, and dyspnea.
• Provide supplemental oxygen as ordered.

Preventing Transmission of Infection

• Be aware that TB is transmitted by respiratory droplets or secretions.
• Provide care for hospitalized patient in a negative-pressure room to prevent respiratory droplets from escaping when door is opened.
• Enforce rule that all staff and visitors use well-fitted standard dust/mist/fume masks (Class C) for contact with patient.
• Use high-efficiency particulate masks, such as HEPA filter masks, for high-risk procedures, including suctioning, bronchoscopy, or pentamidine treatments.
• Use standard precautions for additional protection: gowns and gloves for direct contact with patient, linens or articles in room, meticulous handwashing.
• Educate the patient to control spread of infection through secretions.
  • Cover mouth and nose with double-ply tissue when coughing or sneezing. Do not sneeze into bare hand.
  • Wash hands after coughing or sneezing.
  • Dispose of tissues promptly into closed plastic bag.

Improving Nutritional Status

• Explain the importance of eating a nutritious diet to promote healing and improve defense against infection.
• Provide small, frequent meals and liquid supplements during symptomatic period.
• Monitor weight.
• Administer vitamin supplements, as ordered, particularly pyridoxine (vitamin B₆) to prevent peripheral neuropathy in patients taking isoniazid.

Improving Compliance

• Educate the patient about the etiology, transmission, and effects of TB. Stress the importance of continuing to take medicine for the prescribed time because bacilli multiply slowly and thus can only be eradicated over a long period.
• Review adverse effects of the drug therapy (see Table 11-2). Question the patient specifically about common toxicities of drugs being used, and emphasize immediate reporting should these occur.
• Participate in observation of medication taking, weekly pill counts, or other programs designed to increase compliance with treatment for TB.

NURSING ALERT

Patient compliance remains a major problem in eradicating TB. Therefore, it may be helpful and necessary to have patient take medication in observed setting.

Community and Home Care Considerations

• Improve ventilation in the home by opening windows in room of affected person, and keeping bedroom door closed as much as possible.
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• Instruct patient to cover mouth with fresh tissue when coughing or sneezing and to dispose of tissues promptly in plastic bags.
• Discuss TB testing of people residing with patient.
• Investigate living conditions, availability of transportation, financial status, alcohol and drug abuse, and motivation, which may affect compliance with follow-up and treatment. Initiate referrals to a social worker for interventions in these areas.
• Report new cases of TB to public heath department for screening of close contacts and monitoring.

Patient Education and Health Maintenance

• Review possible complications: hemorrhage, pleurisy, symptoms of recurrence (persistent cough, fever, or hemoptysis).
• Instruct patient on avoidance of job-related exposure to excessive amounts of silicone (working in foundry, rock quarry, sand blasting), which increases risk of reactivation.
• Encourage patient to report at specified intervals for bacteriologic (smear) examination of sputum to monitor therapeutic response and compliance.
• Instruct patient in basic hygiene practices and investigate living conditions. Crowded, poorly ventilated conditions contribute to development and spread of TB.
• Encourage regular symptom screening and follow-up chest X-rays for rest of life to evaluate for recurrence.
• Instruct patient on prophylaxis with isoniazid for people infected with the tubercle bacillus without active disease to prevent disease from occurring, or to people at high risk of becoming infected.
• Educate asymptomatic people about PPD testing and treatment of latent TB for positive results, based on risk grouping.

Evaluation: Expected Outcomes

• Afebrile; dyspnea relieved
• Standard precautions observed; disposes of respiratory secretions properly
• Maintains body weight
• Takes medications as prescribed

PLEURISY

Pleurisy is a clinical term to describe pleuritis (inflammation of the pleura, both parietal and visceral).

Pathophysiology and Etiology

• Inflammation of the pleura stimulates nerve endings, causing pain.
• May occur in the course of many pulmonary diseases:
  • Pneumonia (bacterial, viral).
  • TB.
  • Pulmonary infarction, embolism.
  • Pulmonary abscess.
  • Upper respiratory tract infection.
  • Pulmonary neoplasm.

Clinical Manifestations

• Chest pain—becomes severe, sharp, and knifelike on inspiration (pleuritic pain)
  • May become minimal or absent when breath is held
  • May be localized or radiate to shoulder or abdomen
• Intercostal tenderness on palpation.
• Pleural friction rub—grating or leathery sounds heard in both phases of respiration; heard low in the axilla or over the lung base posteriorly; may be heard for only a day or so
• Evidence of infection; fever, malaise, increased white cell count

Diagnostic Evaluation

• Chest X-ray may show pleural thickening.
• Sputum examination may indicate infectious organism.
• Examination of pleural fluid obtained by thoracentesis for smear and culture.
• Pleural biopsy may be necessary to rule out other conditions.

Management

• Treatment for the underlying primary disease (pneumonia, infarction); inflammation usually resolves when the primary disease subsides.
• Pain relief, using pharmacologic and nonpharmacologic methods.
• Intercostal nerve block may be necessary when pain causes hypoventilation (see Procedure Guidelines 11-2).

Complications

• Severe pleural effusion.
• Atelectasis due to shallow breathing to avoid pain

Nursing Assessment

• Assess patient's level of pain.
• Observe for signs and symptoms of pleural effusion (dyspnea, pain, decreased diaphragmatic excursion on affected side).
• Auscultate lungs for pleural friction rub.

Nursing Diagnosis

• Ineffective Breathing Pattern related to stabbing chest pain

Nursing Interventions

Easing Painful Respiration

• Assist patient to find comfortable position that will promote aeration; lying on affected side decreases stretching of the pleura and, therefore, the pain decreases.
• Instruct patient in splinting chest while taking a deep breath or coughing.
• Administer or teach self-administration of pain medications as ordered.
• Employ nonpharmacologic interventions for pain relief, such as application of heat, muscle relaxation, and imagery.
• Assist with intercostal nerve block if indicated.
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• Evaluate patient for signs of hypoxia thoroughly when anxiety, restlessness, and agitation of new onset are noted, before administering as needed sedatives. Consider evaluation by a health care provider when these signs are present, especially if accompanied by cyanotic nail beds, circumoral pallor, and increased respiratory rate.

PROCEDURE GUIDELINES 11-2

Assisting with an Intercostal Nerve Block

EQUIPMENT

• Syringes, 10-mL luer-lock
• Needles
• Anesthetic solution (lidocaine, bupivacaine, procaine)
• Skin germicide; sterile gloves

PROCEDURE

Nursing Action Rationale Preparatory phase 1. Inform the patient that he will experience the prick of the needle and a slight sensation of pressure. 2. Position the patient as directed: 2. a. Have the patient sit up, bend forward, and hug a pillow a. This posture moves the scapulae forward and out of the way. or b. Place the patient prone with pillow under chest b. The prone position helps immobilize the patient. or c. Have the patient lie on unaffected side with upper arm hanging over the side of the table c. This pulls the scapula out of the way. 3. Ask the patient to identify the site of pain. 3. To determine which intercostal nerves are to be injected. Performance phase (By the physician) 1. After the skin is prepared, the lower margin of the rib is palpated and a small skin wheal is raised, using a 25G to 30G needle. 1. This is infiltration anesthesia. 2. Usually nerve blocks are done at the posterior angle of the ribs between the posterior axillary line and the spine. 2. The posterior angle is the most prominent and accessible, and an injection at this area produces a block of the entire distal nerve. 3. A fine needle is advanced through the wheal and directed downward so it slips under the edge of the rib into the upper portion of the interspace. 3. The intercostal nerve runs in a groove along the undersurface of the above rib. 4. The syringe (needle in place) is aspirated. 4. To make sure the needle has not punctured the lung or that an intercostal vessel has been entered. 5. The local anesthetic (usually 3 to 5 mL) is injected into the area. 5. Usually the local anesthetic is injected above and below the painful rib to obtain complete relief of pain, as the sensory fields of intercostal nerves overlap. Intercostal nerve block Follow-up phase 1. Assess for relief of pain and less painful coughing. 1. This is the expected outcome. 2. Obtain a chest X-ray. 2. To make sure that pneumothorax has not occurred. 3. Complications include: a. Intravascular injection. b. Puncture of the lung with pneumothorax. c. Hypotension.

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Patient Education and Health Maintenance

• Instruct patient to seek early intervention for pulmonary diseases so pleurisy can be avoided.
• Reassure and encourage patience because pain will subside.
• Advise patient on reporting shortness of breath, which could indicate pleural effusion.

Evaluation: Expected Outcomes

• Respirations deep without pain

PLEURAL EFFUSION

Pleural effusion refers to a collection of fluid in the pleural space. It is almost always secondary to other diseases.

Pathophysiology and Etiology

• May be either transudative or exudative.
• Transudative effusions occur primarily in noninflammatory conditions; is an accumulation of low-protein, low cell count fluid.
• Exudative effusions occur in an area of inflammation; is an accumulation of high-protein fluid.
• Occurs as a complication of:
  • Disseminated cancer (particularly lung and breast), lymphoma.
  • Pleuropulmonary infections (pneumonia).
  • Heart failure, cirrhosis, nephrosis.
  • Other conditions—sarcoidosis, systemic lupus erythematosus (SLE), peritoneal dialysis.

Clinical Manifestations

• Dyspnea, pleuritic chest pain, cough.
• Dullness or flatness to percussion (over areas of fluid) with decreased or absent breath sounds

Diagnostic Evaluation

• Chest X-ray or ultrasound detects presence of fluid.
• Thoracentesis—biochemical, bacteriologic, and cytologic studies of pleural fluid indicates cause.

Management

General

• Treatment is aimed at underlying cause (heart disease, infection).
• Thoracentesis is done to remove fluid, collect a specimen, and relieve dyspnea.

For Malignant Effusions

• Chest tube drainage, radiation, chemotherapy, surgical pleurectomy, pleuroperitoneal shunt, or pleurodesis.
• In malignant conditions, thoracentesis may provide only transient benefits, because effusion may reaccumulate within a few days.
• Pleurodesis—production of adhesions between the parietal and visceral pleura accomplished by tube thoracostomy, pleural space drainage, and intrapleural instillation of a sclerosing agent (tetracycline, doxycycline, or minocycline).
  • Drug introduced through tube into pleural space; tube clamped.
  • Patient is assisted into various positions for 3 to 5 minutes each to allow drug to spread to all pleural surfaces.
  • Tube is unclamped as prescribed.
  • Chest drainage continued for 24 hours or longer.
  • Resulting pleural irritation, inflammation, and fibrosis cause adhesion of the visceral and parietal surfaces when they are brought together by the negative pressure caused by chest suction.

Complications

• Large effusion could lead to respiratory failure.

Nursing Assessment

• Obtain history of previous pulmonary condition.
• Assess patient for dyspnea and tachypnea.
• Auscultate and percuss lungs for abnormalities.

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Nursing Diagnosis

• Ineffective Breathing Pattern related to collection of fluid in pleural space

Nursing Interventions

Maintaining Normal Breathing Pattern

• Institute treatments to resolve the underlying cause as ordered.
• Assist with thoracentesis if indicated (see page 209).
• Maintain chest drainage as needed (see page 278).
• Provide care after pleurodesis.
  • Monitor for excessive pain from the sclerosing agent, which may cause hypoventilation.
  • Administer prescribed analgesic.
  • Assist patient undergoing instillation of intrapleural lidocaine if pain relief is not forthcoming.
  • Administer oxygen as indicated by dyspnea and hypoxemia.
  • Observe patient's breathing pattern, oxygen saturation, and other vital signs, for evidence of improvement or deterioration.

Patient Education and Health Maintenance

• Instruct patient to seek early intervention for unusual shortness of breath, especially if he has underlying chronic lung disease.

Evaluation: Expected Outcomes

• Reports absence of shortness of breath

LUNG ABSCESS

A lung abscess is a localized, pus-containing, necrotic lesion in the lung characterized by cavity formation.

Pathophysiology and Etiology

• Most commonly occurs due to aspiration of vomitus or infected material from upper respiratory tract.
• Secondary causes include:
  • Aspiration of foreign body into lung.
  • Pulmonary embolus.
  • Trauma.
  • TB, necrotizing pneumonia.
  • Bronchial obstruction (usually a tumor) causes obstruction to bronchus, leading to infection distal to the growth.
• The right lung is involved more frequently than the left because of dependent position of the right bronchus, the less acute angle that the right main bronchus forms within the trachea, and its larger size.
• In the initial stages, the cavity in the lung may communicate with the bronchus.
• Eventually, the cavity becomes surrounded or encapsulated by a wall of fibrous tissue, except at one or two points where the necrotic process extends until it reaches the lumen of some bronchus or pleural space and establishes a communication with the respiratory tract, the pleural cavity (bronchopleural fistula), or both.
• The organisms typically seen are Klebsiella pneumoniae and Staphylococcus aureus.

Clinical Manifestations

• Cough, fever, and malaise from segmental pneumonitis and atelectasis.
• Headache, anemia, weight loss, dyspnea, weakness.
• Pleuritic chest pain from extension of suppurative pneumonitis to pleural surface.
• Production of mucopurulent sputum, usually foul-smelling; blood streaking common; may become profuse after abscess ruptures into bronchial tree.
• Chest may be dull to percussion, decreased or absent breath sounds, intermittent pleural friction rub.

Diagnostic Evaluation

• Chest X-ray helps diagnose and locate lesion.
• Direct bronchoscopic visualization to exclude possibility of tumor or foreign body; bronchial washings and brush biopsy may be done for cytopathologic study.
• Sputum culture and sensitivity tests to determine causative organisms and antimicrobial sensitivity.

Management

• Administration of appropriate antimicrobial agent, usually by I.V. route, until clinical condition improves; then oral administration.
• Chest postural drainage to drain cavity.
• Bronchoscopy to drain abscess is controversial.
• Surgical intervention only if patient fails to respond to medical management, sustains a hemorrhage, or has a suspected tumor.
• Nutritional management is usually a high-calorie, high-protein diet.

Complications

• Hemoptysis from erosion of a vessel.
• Empyema, bronchopleural fistula

Nursing Assessment

• Examine oral cavity, because poor condition of teeth and gums increases number of anaerobes in oral cavity and could be source for infection.
• Perform chest examination for abnormalities.
• Monitor for foul-smelling sputum, which may indicate an anaerobic pulmonary infection.
• Review results of laboratory and X-ray findings for location of abscess and identification of causative organism.

Nursing Diagnoses

• Ineffective Breathing Pattern related to presence of suppurative lung disease
• Acute or Chronic Pain related to infection
• Imbalanced Nutrition: Less Than Body Requirements related to catabolic state from chronic infection

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Nursing Interventions

Minimizing Respiratory Dysfunction

• Monitor patient's response to antimicrobial therapy; take temperature at prescribed intervals.
• Carry out drainage procedures to hasten resolution.
  • Postural drainage positions to be assumed depend on location of abscess.
  • Carry out percussion, coughing, and breathing exercises.
  • Measure and record the volume of sputum to follow patient's clinical course (may be of limited use due to patient swallowing of sputum).
  • Give adequate fluids to enhance liquefying of secretions.

Attaining Comfort

• Use nursing measures to combat generalized discomfort; oral hygiene, positions of comfort, relaxing massage.
• Take temperature, pulse, and respirations at regular intervals to determine type of fever and monitor the severity and duration of the infectious process.
• Encourage rest and limitation of physical activity during febrile periods.
• Monitor chest tube functioning.
• Evaluate patient for signs of hypoxia thoroughly when anxiety, restlessness, and agitation of new onset are noted, before administering as needed sedatives. Consider physician evaluation when these signs are present, especially if accompanied by cyanotic nail beds, circumoral pallor, increased respiratory rate.
• Administer analgesics as directed but avoid opioids that might depress respirations.

Improving Nutritional Status

• Provide a high-protein and high-calorie diet.
• Offer liquid supplements for additional nutritional support when anorexia limits patient's intake.
• Monitor weight weekly.

Patient Education and Health Maintenance

• Teach the patient that an extended course of antimicrobial therapy (4 to 8 weeks) is usually necessary; mixed infections are common and may require multiple antibiotics.
• Encourage patient to have periodontal care, especially in presence of gingival lesions.
• Stress importance of follow-up X-rays to monitor abscess cavity closure.
• Remind family that patient may aspirate if weakness, confusion, alcoholism, seizures, and swallowing difficulties are present.
• Encourage patient to assume responsibility for attaining and maintaining an optimal state of health through a planned program of nutrition, rest, and exercise.

Evaluation: Expected Outcomes

• Respirations unlabored; temperature in normal range; less purulent sputum expectorated
• Appears more comfortable; verbalizes less pain
• Eats better; weight stable

CANCER OF THE LUNG (BRONCHOGENIC CANCER)

Bronchogenic cancer refers to a malignant tumor of the lung arising within the wall or epithelial lining of the bronchus. The lung is also a common site of metastasis by way of venous circulation or lymphatic spread. Bronchogenic cancer is classified according to cell type:

• Epidermoid (squamous cell)—most common
• Adenocarcinoma
• Small cell (oat cell) carcinoma
• Large cell (undifferentiated) carcinoma

Pathophysiology and Etiology

Predisposing Factors

• Cigarette smoking—amount, frequency, and duration of smoking have positive relationship to cancer of the lung.
• Occupational exposure to asbestos, arsenic, chromium, nickel, iron, radioactive substances, isopropyl oil, coal tar products, petroleum oil mists alone or in combination with tobacco smoke.

NURSING ALERT

Suspect lung cancer in patients who belong to a susceptible, high-risk group and who have repeated unresolved respiratory infections.

Staging

• Refers to anatomic extent of tumor, lymph node involvement, and metastatic spread.
• Staging done by:
  • Tissue diagnosis
  • Lymph node biopsy
  • Mediastinoscopy

Clinical Manifestations

Usually occur late and are related to size and location of tumor, extent of spread, and involvement of other structures

• Cough, especially a new type or changing cough, results from bronchial irritation.
• Dyspnea, wheezing (suggests partial bronchial obstruction).
• Chest pain (poorly localized and aching)
• Excessive sputum production, repeated upper respiratory infections
• Hemoptysis
• Malaise, fever, weight loss, fatigue, anorexia
• Paraneoplastic syndrome—metabolic or neurologic disturbances related to the secretion of substances by the neoplasm
• Symptoms of metastasis—bone pain; abdominal discomfort, nausea and vomiting from liver involvement; pancytopenia from bone marrow involvement; headache from CNS metastasis
• Usual sites of metastasis—lymph nodes, bones, liver

Diagnostic Evaluation

• Computed tomography (CT) scan and positron-emission tomography (PET) scan are indicated because lung cancers
  

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  may be partly or completely hidden by other structures on chest X-ray.
• Cytologic examination of sputum/chest fluids for malignant cells.
• Fiber-optic bronchoscopy for observation of location and extent of tumor; for biopsy.
• PET scan—sensitive in detecting small nodules and metastatic lesions.
• Lymph node biopsy; mediastinoscopy to establish lymphatic spread; to plan treatment.
• Pulmonary function tests (PFTs) combined with split-function perfusion scan to determine if patient will have adequate pulmonary reserve to withstand surgical procedure.

Management

• The treatment depends on the cell type, stage of disease, and the physiologic status of the patient. It includes a multidisciplinary approach that may be used separately or in combination, including:
  • Surgical resection.
  • Radiation therapy.
  • Chemotherapy.
  • Immunotherapy.
• Refer to the American College of Chest Physicians Diagnosis and Management of Lung Cancer: Evidence-Based Guidelines, 2003 for further information. (Chest, 123 [1 Supp] January, 2003).

Complications

• Superior vena cava syndrome—oncologic complication caused by obstruction of major blood vessels draining the head, neck, and upper torso.
• Hypercalcemia—commonly from bone metastasis.
• Syndrome of inappropriate antidiuretic hormone with hyponatremia and abnormal water retention
• Pleural effusion
• Infectious complications, especially upper respiratory infections
• Brain metastasis, spinal cord compression, pulmonary scarring

Nursing Assessment

• Determine onset and duration of coughing, sputum production, and the degree of dyspnea. Auscultate for breath sounds. Observe symmetry of chest during respirations.
• Take anthropometric measurements: weigh patient, review laboratory biochemical tests, and conduct appraisal of 24-hour food intake.
• Ask about pain, including location, intensity, and factors influencing pain.

Nursing Diagnoses

• Ineffective Breathing Pattern related to obstructive and restrictive respiratory processes associated with lung cancer
• Imbalanced Nutrition: Less Than Body Requirements related to hypermetabolic state, taste aversion, anorexia secondary to radiotherapy/chemotherapy
• Acute or Chronic Pain related to tumor effects, invasion of adjacent structures, toxicities associated with radiotherapy/chemotherapy
• Anxiety related to uncertain outcome and fear of recurrence

Nursing Interventions

See also Chapter 8, page 135, for interventions related to specific cancer treatment.

Improving Breathing Patterns

• Prepare patient physically, emotionally, and intellectually for prescribed therapeutic program.
• Elevate head of bed to promote gravity drainage and prevent fluid collection in upper body (from superior vena cava syndrome).
• Teach breathing retraining exercises to increase diaphragmatic excursion with resultant reduction in work of breathing.
• Give prescribed treatment for productive cough (expectorant, antimicrobial agent) to prevent thickened or retained secretions and subsequent dyspnea.
• Augment the patient's ability to cough effectively.
  • Splint chest manually with hands.
  • Instruct patient to inspire fully and cough two to three times in one breath.
  • Provide humidifier/vaporizer to provide moisture to loosen secretions.
• Support patient undergoing removal of pleural fluid (by thoracentesis or tube thoracostomy) and instillation of sclerosing agent to obliterate pleural space and prevent fluid recurrence.
• Administer oxygen by way of nasal cannula as prescribed.
• Encourage energy conservation through decreasing activities.
• Allow patient to sleep in a reclining chair or with head of bed elevated if severely dyspneic.
• Recognize the anxiety associated with dyspnea; teach relaxation techniques.

Improving Nutritional Status

• Emphasize that nutrition is an important part of the treatment of lung cancer.
  • Encourage small amounts of high-calorie and high-protein foods frequently, rather than three daily meals.
  • Suggest eating major meal in the morning if rapidly becoming satiated and feeling full are problems.
  • Ensure adequate protein intake—milk, eggs, chicken, fowl, fish, cheese, and oral nutritional supplements if patient cannot tolerate meats or other protein sources.
• Administer or encourage prescribed vitamin supplement to avoid deficiency states, glossitis, and cheilosis.
• Change consistency of diet to soft or liquid if patient has esophagitis from radiation therapy.
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• Give enteral or total parenteral nutrition for malnourished patient who is unable or unwilling to eat.

Controlling Pain

• Take a history of pain complaint; assess presence/absence of support system.
• Administer prescribed drug, usually starting with nonsteroidal anti-inflammatory drugs (NSAIDs) and progressing to adjuvant analgesic and opioid agents.
  • Administer regularly to maintain pain at tolerable level.
  • Titrate to achieve pain control.
• Consider alternative methods, such as cognitive and behavioral training, biofeedback, relaxation, to increase patient's sense of control.
• Evaluate problems of insomnia, depression, anxiety, and so forth that may be contributing to patient's pain.
• Initiate bowel training program, because constipation is a adverse effect of some analgesic/opioid agents.
• Facilitate referral to pain clinic/specialist if pain becomes refractory (unyielding) to usual methods of control.

Minimizing Anxiety

• Realize that shock, disbelief, denial, anger, and depression are all normal reactions to the diagnosis of lung cancer.
• Try to have the patient express concerns; share these concerns with health professionals.
• Encourage the patient to communicate feelings to significant people in his life.
• Expect some feelings of anxiety and depression to recur during illness.
• Encourage the patient to keep active and remain in the mainstream. Continue with usual activities (work, recreation, sexual) as much as possible.

Patient Education and Health Maintenance

• Teach patient to use NSAID or other prescribed medication as necessary for pain without being overly concerned about addiction.
• Help the patient realize that not every ache and pain is caused by lung cancer; some patients do not experience pain.
• Tell the patient that radiation therapy may be used for pain control if tumor has spread to bone.
• Advise the patient to report new or persistent pain; it may be due to some other cause such as arthritis.
• Suggest talking to a social worker about financial assistance, or other services that may be needed.
• For additional information, contact the American Cancer Society, 1-800-ACS-2345; http://www.cancer.org.

Evaluation: Expected Outcomes

• Performs self-care without dyspnea
• Eats small meals four to five times per day; weight stable
• Reports pain decreased from level 6 to level 2 with medication
• Verbalizes anger; practices relaxation techniques

CHRONIC DISORDERS

BRONCHIECTASIS

Bronchiectasis is a chronic dilatation of the bronchi and bronchioles due to inflammation and destruction of their walls.

Pathophysiology and Etiology

• There is damage to the bronchial wall, which leads to the buildup of thick sputum, causing obstruction.
• Severe coughing results in the permanent dilation of the bronchial walls.
• Usually involves the lower lobes.
• As the process progresses, there is atelectasis and fibrosis, which lead to respiratory insufficiency.
• Pulmonary infections, obstruction of bronchi, aspiration of foreign bodies, vomitus, or material from upper respiratory tract, and immunodeficiency are common causes.

Clinical Manifestations

• Persistent cough with production of copious amounts of purulent sputum.
• Intermittent hemoptysis; breathlessness.
• Recurrent fever and bouts of pulmonary infection
• Crackles and rhonchi heard over involved lobes
• Finger clubbing

Diagnostic Evaluation

• Chest X-ray may reveal areas of atelectasis with widespread dilatation of bronchi.
• Sputum examination may detect offending pathogens.
• High-resolution CT scan is useful in diagnosis of bronchiectasis.

Management

Goal: prevent progression of disease.

• Infection controlled by:
  • Smoking cessation.
  • Prompt antimicrobial treatment of exacerbations of infection.
  • Immunization against potential pulmonary pathogens (influenza and pneumococcal vaccine).
• Secretion clearance techniques, such as postural drainage, positive expiratory pressure (PEP) valve, flutter valve, Acapella device, Vest therapy and, possibly, percussion and vibration or other methods.
• Bronchodilators for bronchodilatation and improved secretion clearance.
• Surgical resection (segmental resection) when conservative management fails.

Complications

• Progressive suppuration.
• Hemoptysis, major pulmonary hemorrhage.
• COPD, emphysema, chronic respiratory insufficiency

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Nursing Assessment

• Obtain history regarding amount and characteristics of sputum produced, including hemoptysis.
• Auscultate lungs for diffuse rhonchi and crackles.

Nursing Diagnosis

• Ineffective Airway Clearance related to tenacious and copious secretions

Nursing Interventions

Maintaining Airway Clearance

• Encourage use of chest physical therapy techniques to empty the bronchi of accumulated secretions.
  • Assist with postural drainage positioning for involved lung segments to drain the bronchiectatic areas by gravity, thus reducing degree of infection and symptoms.
  • Use percussion and vibration to assist in mobilizing secretions.
  • Encourage productive coughing to help clear secretions.
  • Consider PEP valve, flutter valve, Acapella device, or Vest therapy for enhanced secretion clearance.
• Encourage increased intake of fluids to reduce viscosity of sputum and make expectoration easier.
• Consider vaporizer to provide humidification and keep secretions thin.

Patient Education and Health Maintenance

• Instruct the patient to avoid noxious fumes, dusts, smoke, and other pulmonary irritants.
• Teach the patient to monitor sputum. Report if change in quantity or character occurs.
• Instruct the patient and family about importance of pulmonary drainage.
  • Teach drainage exercises and chest physical therapy techniques.
  • Encourage postural drainage before rising in the morning, because sputum accumulates during night.
  • Encourage patient to engage in physical activity throughout day to help mobilize mucus.
• Encourage regular dental care because copious sputum production may affect dentition.
• Emphasize the importance of influenza and pneumococcal immunizations and prompt treatment of respiratory infections.

Evaluation: Expected Outcomes

• Decreased sputum; lungs clear after chest physical therapy

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

COPD refers to a disease characterized by airflow limitation that is not fully reversible. The airflow limitation is generally progressive and is normally associated with an inflammatory response of the lungs due to irritants. COPD includes chronic bronchitis and pulmonary emphysema. Some clinicians consider asthma as part of COPD, but due to its reversibility, it is considered by most to be a separate entity (see Chapter 28).

Chronic bronchitis is a chronic inflammation of the lower respiratory tract characterized by excessive mucous secretion, cough, and dyspnea associated with recurring infections of the lower respiratory tract.

Pulmonary emphysema is a complex lung disease characterized by destruction of the alveoli, enlargement of distal airspaces, and a breakdown of alveolar walls. There is a slowly progressive deterioration of lung function for many years before the development of illness.

Pathophysiology and Etiology

• The person with COPD may have (see Figure 11-3, page 308):

  FIGURE 11-3 Airway changes in COPD compared with normal.

  • Excessive secretion of mucus and chronic infection within the airways (bronchitis)—infection, irritation, hypersensitivity→local hyperemia→hypertrophy of mucous glands→increase in size and number of mucus-producing elements in bronchi (mucous glands and goblet cells)→inflammation and edema→narrowing and obstruction of airflow.
  • Increase in size of airspaces distal to the terminal bronchioles, with loss of alveolar walls and elastic recoil of the lungs (emphysema).
  • There may be an overlap of these conditions.
• As a result of these conditions, there is a subsequent derangement of airway dynamics (eg, obstruction to airflow).
• The etiology of COPD includes:
  • Cigarette smoking.
  • Air pollution, occupational exposure.
  • Allergy, autoimmunity.
  • Infection.
  • Genetic predisposition, aging.
• Alpha₁-antitrypsin deficiency is a genetically determined cause of emphysema and occasionally liver disease. Alpha₁-antitrypsin serves primarily as an inhibitor of neutrophil elastase, an elastin-degrading protease released by neutrophils. When alveolar structures are left unprotected from exposure to elastase, progressive destruction of elastin tissues results in the development of emphysema.

Clinical Manifestations

Chronic Bronchitis

Usually insidious, developing over a period of years

• Presence of a productive cough lasting at least 3 months a year for 2 successive years.
• Production of thick, gelatinous sputum; greater amounts produced during superimposed infections.
• Wheezing and dyspnea as disease progresses

Emphysema

Gradual in onset and steadily progressive

• Dyspnea, decreased exercise tolerance.
• Cough may be minimal, except with respiratory infection.
• Sputum expectoration—mild.
• Increased anteroposterior diameter of chest (barrel chest) due to air trapping with diaphragmatic flattening.

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Diagnostic Evaluation

• PFTs demonstrate airflow obstruction—reduced forced vital capacity (FVC), FEV₁, FEV₁ to FVC ratio; increased residual volume to total lung capacity (TLC) ratio, possibly increased TLC (see page 212).
• ABG levels—decreased Pao₂, pH, and increased CO₂.
• Chest X-ray—in late stages, hyperinflation, flattened diaphragm, increased retrosternal space, decreased vascular markings, possible bullae
• Alpha₁-antitrypsin assay useful in identifying genetically determined deficiency in emphysema

Management

The goal is to reverse airflow obstruction. For treatment regimens based on severity, see: Global Initiative for Chronic Lung Disease, Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease (GOLD Guidelines) 2003, National Institutes of Health, Executive Summary, NHLBI, http://www.goldcopd.com/.

• Smoking cessation.
• Inhaled bronchodilators (see Table 11-4, pages 310 to 313) reduce dyspnea and bronchospasm; delivered by metered dose inhalers (MDI) or handheld or mask nebulizer devices.

  TABLE 11-4 Commonly Used Pulmonary Drugs

  DRUGS/ADMINISTRATION PHARMACOLOGIC EFFECTS INDICATIONS ADVERSE EFFECTS NURSING CONSIDERATIONS Bronchodilators Aminophylline(Amoline)(intravenous injection) Methylxanthine compound—relaxes smooth muscle by increasing level of cyclic adenosine monophosphate Acute exacerbation of asthma or bronchitis CNS: irritability, restlessness, insomnia CV: palpitations, tachycardia, hypotension GI: nausea, vomiting, diarrhea Too rapid administration can cause hypotension, extra systoles, muscle tremors. Administer at prescribed rate with an I.V. infusion pump. Theophylline preparations(Theo-Dur)(oral) Methylxanthine compound—relaxes muscle by increasing cyclic adenosine monophosphate Mild bronchodilator, maintenance therapy for bronchospasm CNS: irritability, restlessness, insomnia, seizures in toxic ranges CV: palpitations, tachycardia, hypotension GI: nausea, vomiting, diarrhea Teach patients to take at equal intervals throughout the day. To decrease GI irritation, take with milk or crackers. Monitor theophylline blood level periodically as directed to ensure therapeutic range and prevent toxicity. Albuterol (Proventil, Ventolin)(oral, metered dose inhaler [MDI], nebulized liquid) Sympathomimetic (beta2-adrenergic agonist) with highly selective beta2 activity Oral: Maintenance therapy for bronchospasm, works within 30 minutes Nervousness, tachycardia, headache, nausea, tremors Continuous nebulization may cause hypokalemia. Observe inhalation by patient to be certain that correct technique is used. Caution patient not to exceed prescribed dose. Adverse effects often associated with excessive use. Does not reduce inflammation. Terbutaline (Brethine)(oral, MDI, subcutaneous injection) Sympathomimetic with selective beta2 activity Acute exacerbation of asthma or bronchitis (subcutaneous preparation) Maintenance therapy for bronchospams (inhaled and oral preparation) Nervousness, tachycardia, headache, nausea (subcutaneous preparation) Hand tremors (subcutaneous and oral preparations) Caution patients that hand tremors may occur. Tremors decrease with prolonged oral use. Observe inhalation by patient to be certain that correct technique is used. Metaproterenol (Alupent) (oral, MDI, inhalant solution Sympathomimetic with selective beta2 activity Maintenance therapy for bronchospasm MDI onset of action 5 to 30 minutes Nervousness, tachycardia, headache, nausea Observe inhalation by patient to make sure that correct technique is used. Pirbuterol acetate(Maxair)(MDI) Sympathomimetic with selective beta2 activity Maintenance therapy for bronchospasm Nervousness, tachycardia, headache, nausea Observe inhalation by patient to make sure that correct technique is used. Salmeterol xinafoate(Serevent)(MDI) Sympathomimetic with selective beta2 activity Maintenance therapy for bronchospasm, long-acting (12 h) Nervousness, tachycardia, headache, nausea Observe inhalation by patient to make sure that correct technique is used. Instruct patient that not for immediate relief of bronchospasm, dyspnea. Maximum dose two puffs every 12 h Ipratropium bromide(Atrovent)(MDI, nebulized liquid) Anticholinergic Maintenance therapy for bronchospasm Acts within 15 minutes Rare: Can cause blurring of vision if sprayed into the eyes(atropine derivative) Voice hoarseness Instruct patient to use spacer device with MDI or close lips around inhaler mouthpiece, close eyes during inhalation. Combivent (albuterol with ipratropium combination MDI) Sympathomimetic with selective beta2 and anticholinergic activity Fast acting and maintenance therapy for bronchospasm See albuterol and ipratropium See albuterol and ipratropium One puff of Combivent equals one puff of albuterol and one puff of ipratropium Levalbuterol (Xopenex) Sympathomimetic with selective beta-2 activity Treatment and prevention of bronchospasm Tachycardia, hypertension, nervousness Administered by nebulization every 6-8 hours Formoterol (Foradil)-DPI Sympathomimetic with long-acting selective beta2 activity Treatment and prevention of bronchospasm Headaches, tremor, throat irritation, possible palpitations Train patient proper use of aerolizer Administer twice daily or 15 minutes before exercise Corticosteroids Hydrocortisone/prednisone (Deltasone) (intravenous injection, oral preparation) Potent anti-inflammatory activity Acute exacerbation of asthma or bronchitis (I.V. preparation) Acute exacerbation or maintenance therapy (oral preparation) CNS: depression, euphoria, mood changes GI: gastric irritation, peptic ulcer Metabolic: hypernatremia, hypokalemia, hyperglycemia, water retention, and weight gain Long term, high dose: adrenal insufficiency, osteoporosis, muscle weakness, cataracts, glaucoma, fragile and easily bruised skin, immunosuppression Long-term use: Do not stop abruptly due to adrenal suppression Take oral form with food. Usually given as taper from higher dose to lowest possible dose that achieves desired effect Beclomethasone(Vanceril, Beclovent)(MDI) Synthetic corticosteroid with potent anti-inflammatory activity; effective only by inhalation Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Asthma (alternative to use of oral steroids) COPD Oral candidiasis, dysphonia Systemic adverse effects associated with oral steroids do not occur May experience skin bruising in high doses Inhaled as a aerosol. May precipitate bronchospasm in acute exacerbation. Not used with status asthmaticus or acute asthma episodes. Use a spacer device with MDI, and use water gargle, rinse and spit after use to prevent oral candidiasis Triamcinolone acetonide(Azmacort)(MDI) Anti-inflammatory steroid; effective only by inhalation Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Asthma COPD Oral candidiasis, dysphonia Systemic adverse effects associated with oral steroids do not occur May experience skin bruising in high doses Packaged with a spacer. Decreases oral deposition and oral candidiasis. Use water gargle, rinse and spit after use to prevent oral yeast growth. Flunisolide(AeroBid)(MDI) Anti-inflammatory steroid; effective only by inhalation Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Asthma COPD Oral candidiasis, dysphonia Systemic adverse effects associated with oral steroids do not occur May experience skin bruising in high doses Longer acting. May be prescribed twice a day, rather than four times per day. Use a spacer device with MDI, and use water gargle, rinse and spit after use to prevent oral candidiasis. Fluticasone (Flovent) Anti-inflammatory steroid; effective only by inhalation Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Asthma COPD Oral candidiasis, dysphonia Systemic adverse effects associated with oral steroids do not occur May experience skin bruising in high doses Longer acting. May be prescribed twice a day, rather than four times per day. Use a spacer device with MDI, and use water gargle, rinse and spit after use to prevent oral candidiasis. Pulmocort (Budesonide Dry Powder Inhaler) Anti-inflammatory steroid; effective only by inhalation Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Asthma COPD Oral candidiasis Systemic adverse effects associated with oral steroids do not occur May experience skin bruising in high doses Longer acting. May be prescribed twice a day, rather than four times per day. Use water gargle, rinse and spit after use to prevent oral candidiasis. Advair discus (fluticasone and salmeterol)-DPI Combination inhaled corticosteroid and long-acting beta agonist bronchodilator Asthma COPD Maintenance therapy for controlled bronchospasm Oral candidiasis, dysphonia, possible bruising in high doses Long acting. Use once or twice daily. Rinse and spit after use to prevent candidiasis. Mast Cell Stabilizers Cromolyn (Intal)(solution for inhalation, powder used with special inhaler) Inhibits activation of a variety of inflammatory cells associated with asthma, prevents bronchospasm Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Maintenance therapy for asthma Cough, bronchospasm Should not be used with status asthmaticus or acute asthma episodes. May be given in combination with bronchodilator if administration causes bronchospasm. Nedocromil (Tilade) (MDI) Inhibits activation of a variety of inflammatory cells associated with asthma, prevents bronchospasm Not effective in acute attack; must be used for 2 to 4 weeks to show effectiveness Maintenance therapy for asthma Cough, bronchospasm GI: nausea, vomiting Should not be used with status asthmaticus or acute asthma episodes. May be given in combination with bronchodilator if administration causes bronchospasm. Leukotriene Receptor Antagonists Zafirlukast (Accolate) Blocks leukotriene receptors Prophylaxis and chronic treatment of mild to moderate asthma for persons older than age 12 Potential drug interactions, particularly warfarin Will not reverse acute bronchospasm. Zileuton (Zyflo) Blocks leukotriene receptors Prophylaxis and chronic treatment of mild to moderate asthma for persons older than age 12 Potential drug interactions Will not reverse acute bronchospasm. Montelukast (Singulair) Blocks leukotriene receptors Prophylaxis and chronic treatment of mild to moderate asthma for persons older than age 5 Potential drug interactions, particularly phenobarbital Will not reverse acute bronchospasm.

  • Anticholinergics such as ipratropium (Atrovent)
  • Short-acting beta-adrenergic agonists such as albuterol (Proventil, Ventolin)
  • Long-acting beta-adrenergic agonists such as salmeterol (Serevent)
• Methylxanthines, such as theophylline (Theo-Dur), given orally as sustained-release formulation for chronic maintenance therapy (less commonly used).
• Inhaled corticosteroids are recommended for patients with symptomatic COPD with documented spirometric improvement from glucocorticosteroids, or in those with an FEV₁ that is less than 50% of the predicted value and repeated exacerbations requiring treatment with antibiotics and/or oral glucocorticosteroids.
• Oral corticosteroids are used in acute exacerbations for anti-inflammatory effect; may also be given I.V. in severe cases.
• Chest physical therapy, including postural drainage for secretion clearance and breathing retraining for improved ventilation and control of dyspnea.
• Supplemental oxygen therapy for patients with hypoxemia. CO₂ must be monitored to determine increased CO₂ retention.
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• Pulmonary rehabilitation to improve function, strength, symptom control, disease self-management techniques, independence, and quality of life.
  • Studies on pulmonary rehabilitation demonstrate increased strength, function, and independence, activities of daily living (ADLs) management, and improved symptom control, coping, well-being, and quality of life as well as decreased hospital admissions and decreased length of stay.
  • Improved survival in COPD is associated with supplemental O₂ use and smoking cessation.
• Antimicrobial agents for episodes of respiratory infection.
• Lung volume reduction surgery is under investigation for treatment of heterogeneous emphysema.
• Treatment for alpha₁-antitrypsin deficiency:
  • Regular I.V. infusions (every 1 to 2 weeks) of human alpha₁-antitrypsin (Prolastin) as replacement therapy to correct the antiprotease imbalance in the lungs.
  • Prevent damage to lungs by quitting smoking.
  • Lung transplantation may be considered for people with severely disabling alpha₁-antitrypsin disease.

DRUG ALERT

Inhaled bronchodilators have become the mainstay of therapy because of the systemic adverse effects, multiple drug interactions, need for therapeutic drug level monitoring, and potential toxicity of theophylline.

Complications

• Respiratory failure.
• Pneumonia, overwhelming respiratory infection.
• Right-sided heart failure, dysrhythmias
• Depression
• Skeletal muscle dysfunction

Nursing Assessment

• Determine smoking history, exposure history, positive family history of respiratory disease, onset of dyspnea.
• Note amount, color, and consistency of sputum.
• Inspect for use of accessory muscles of respiration and use of abdominal muscles during expiration; note increase of anteroposterior diameter of chest.
• Auscultate for decreased/absent breath sounds, crackles, decreased heart sounds.
• Determine level of dyspnea, how it compares to patient's baseline.
• Determine oxygen saturation at rest and with activity.

Nursing Diagnoses

• Ineffective Airway Clearance related to bronchoconstriction, increased mucus production, ineffective cough, possible bronchopulmonary infection
• Ineffective Breathing Pattern related to chronic airflow limitation
• Risk for Infection related to compromised pulmonary function, retained secretions, and compromised defense mechanisms
• Impaired Gas Exchange related to chronic pulmonary obstruction, [V with dot above]/[Q with dot above] abnormalities due to destruction of alveolar capillary membrane
• Imbalanced Nutrition: Less Than Body Requirements related to increased work of breathing, air swallowing, drug effects with resultant wasting of respiratory and skeletal muscles
• Activity Intolerance related to compromised pulmonary function, resulting in shortness of breath and fatigue
• Disturbed Sleep Pattern related to hypoxemia and hypercapnia
• Ineffective Coping related to the stress of living with chronic disease, loss of independence

NURSING ALERT

Early in the patient's course, issues of a living will, advance directive, and resuscitation status need to be addressed. It is better to have these discussions with the patient before crisis situations.

Nursing Interventions

Improving Airway Clearance

• Eliminate pulmonary irritants, particularly cigarette smoking.
  • Cessation of smoking usually results in less pulmonary irritation, sputum production, and cough, and may slow progression of COPD.
  • Keep patient's room as dust-free as possible.
  • Add moisture (humidifier, vaporizer) to indoor environment, if appropriate.
• Administer bronchodilators to control bronchospasm and dyspnea and assist with raising sputum.
  • Assess for adverse effects—tremulousness, tachycardia, cardiac dysrhythmias, CNS stimulation, hypertension.
  • Auscultate the chest after administration of aerosol bronchodilators to assess for improvement of aeration and reduction of adventitious breath sounds.
  • Observe if patient has reduction in dyspnea.
  • Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent toxicity.
• Use postural drainage positions to aid in clearance of secretions, if mucopurulent secretions are responsible for airway obstruction (see page 230).
• Use controlled coughing (see page 231).
• Keep secretions liquid.
  • Encourage high level of fluid intake (8 to 10 glasses; 2 to 2½qt [2 to 2.5 L] daily) within level of cardiac reserve.
  • Give continuous aerolized sterile water or nebulized normal saline to humidify bronchial tree and liquefy sputum if appropriate.
  • Avoid dairy products if these increase sputum production.

Improving Breathing Pattern

• Teach and supervise breathing retraining exercises to strengthen diaphragm and muscles of expiration to decrease work of breathing (see page 237).
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  • Teach diaphragmatic, lower costal, and abdominal breathing, using a slow and relaxed breathing pattern to reduce respiratory rate and decrease energy cost of breathing.
  • Use pursed-lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination. Diaphragmatic and pursed-lip breathing should be practiced for 10 breaths four times daily before meals and before sleep. Inspiratory to expiratory ratio should be 1:2.
• Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.
• Encourage patient to assume position of comfort to decrease dyspnea. Positions might include leaning trunk forward with arms supported on a fixed object.

Controlling Infection

• Recognize early manifestations of respiratory infection—increased dyspnea, fatigue; change in color, amount, and character of sputum; nervousness; irritability; low-grade fever.
• Obtain sputum for Gram stain and culture and sensitivity.
• Administer prescribed antimicrobials to control secondary bacterial infections in the bronchial tree, thus clearing the airways.

Improving Gas Exchange

• Watch for and report excessive somnolence, restlessness, aggressiveness, anxiety, or confusion; central cyanosis; and shortness of breath at rest, which is commonly caused by acute respiratory insufficiency and may signal respiratory failure.
• Review ABG levels; record values on a flow sheet so comparisons can be made over time.
• Monitor oxygen saturation and give supplemental oxygen as ordered to correct hypoxemia in a controlled manner. Monitor and minimize CO₂ retention. Patients that experience CO₂ retention may need lower oxygen flow rates.
• Be prepared to assist with noninvasive ventilation or intubation and mechanical ventilation if acute respiratory failure and rapid CO₂ retention occur.

NURSING ALERT

Normally, CO₂ levels in the blood provide a stimulus for respiration. However, in patients with COPD, chronically elevated CO₂ impairs this mechanism and low oxygen levels act as stimulus for respiration. Giving a high concentration of supplemental oxygen to people who retain CO₂ may suppress the hypoxic drive, leading to worsening hypoventilation, respiratory decompensation, and the development of a worsening respiratory acidosis.

Improving Nutrition

• Take nutritional history, weight, and anthropometric measurements.
• Encourage frequent small meals if patient is dyspneic; even a small increase in abdominal contents may press on diaphragm and impede breathing. Encourage snacking on high-calorie, high-protein snacks, such as cheese, nuts.
• Offer liquid nutritional supplements to improve caloric intake and counteract weight loss.
• Avoid foods producing gas and abdominal discomfort.
• Employ good oral hygiene before meals to sharpen taste sensations.
• Encourage pursed-lip breathing between bites if patient is short of breath; rest after meals.
• Give supplemental oxygen while patient is eating to relieve dyspnea as directed.
• Monitor body weight.

Increasing Activity Tolerance

• Reemphasize the importance of graded exercise and physical conditioning programs (enhances delivery of oxygen to tissues; allows a higher level of functioning with greater comfort). This may be part of a formalized pulmonary rehabilitation program or a referral to physical or occupational therapy.
  • Discuss walking, stationary bicycling, swimming.
  • Encourage use of portable oxygen system for ambulation for patients with hypoxemia.
• Encourage patient to carry out regular exercise program 3 to 7 days per week to increase physical endurance.
• Train patient in energy conservation techniques.

Improving Sleep Patterns

• Maintain a balanced schedule of activity and rest.
• Use nocturnal oxygen therapy when appropriate.
• Avoid use of sedatives that may cause respiratory depression.

Enhancing Coping

• Understand that the constant shortness of breath and fatigue make the patient irritable, apprehensive, anxious, and depressed, with feelings of helplessness and hopelessness.
• Assess the patient for reactive behaviors (anger, depression, acceptance).
• Demonstrate a positive and interested approach to the patient.
  • Be a good listener and show that you care.
  • Be sensitive to patient's fears, anxiety, and depression; may provide emotional relief and insight.
  • Provide patient with control of as many aspects of care as possible.
• Strengthen the patient's self-image.
• Allow the patient to express feelings. Be aware that (within a controlled degree) the mechanisms of denial and repression may be useful defense mechanisms.
• Be aware that sexual dysfunction is common in patients with COPD. Encourage discussion of concerns and fears, and clarify misunderstandings. Encourage patient to use a bronchodilator and secretion clearance techniques before sexual activity, plan for sexual relations at time of day when patient has highest level of energy, use supplemental oxygen if needed, and consider alternative displays of affection to loved one.
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• Support spouse/family members. Refer to local or national support groups (American Lung Association 1-800-LUNG USA; http://www.lungusa.org).

Community and Home Care Considerations

• Encourage patient to live within the limitations that emphysema imposes.
• Help to relax and work at a slower pace. Obtain occupational therapy consult to help employ work simplification techniques such as sitting for tasks, pacing activities, using dressing aids (grabber, sock aid, long-handled shoe horn), shower bench, and handheld shower head.
• Encourage enrollment in a pulmonary rehabilitation program where available and Better Breathers club or other support group found through the American Lung Association or the American Association for Cardiovascular and Pulmonary Rehabilitation at 312-321-5146 or http://www.aacvpr.org/. Components include breathing retraining techniques, proper use of medications and inhalers, secretion clearance techniques, prevention and management of respiratory infection, panic control, controlling dyspnea with ADLs and stair climbing, control of pulmonary irritants, monitored and supervised exercise, proper use of oxygen systems, and group support.
• Suggest vocational counseling to help patient maintain gainful employment within his physical limits for as long as possible.
• Warn patient to avoid excessive fatigue, which is a factor in producing respiratory distress.
• Advise to adjust activities per individual fatigue patterns.
• Advise to try to cope with emotional stress as positively as possible. Such stress triggers attacks of dyspnea. Teach coping strategies, such as relaxation techniques, meditation, guided imagery.
• Stress that progression of worsening lung function may be slowed through close medical follow-up for rest of life.

Patient Education and Health Maintenance

General Education

• Give the patient a clear explanation of the disease, what to expect, how to treat and live with it. Reinforce by frequent explanations, reading material, demonstrations, and question and answer sessions. (See Patient Education Guidelines, page 316.).
• Review with the patient the objectives of treatment and nursing management.
• Work with the patient to set goals (eg, stair climbing, return to work).
• Encourage patient involvement in disease self-management techniques, such as identification and prompt reporting of respiratory infection or respiratory deterioration. Encourage patient to have open communication and partnership with primary care provider.

Avoid Exposure to Respiratory Irritants

• Advise patient to stop smoking and avoid exposure to second-hand smoke.
• Advise patient to avoid sweeping, dusting, and exposure to paint, aerosols, bleaches, ammonia, and other respiratory irritants.
• Advise patient to keep entire house well-ventilated.
• Warn patient to stay out of extremely hot/cold weather to avoid bronchospasm and dyspnea.
  • Keep a warm mask or scarf over nose and mouth, and drink a warm beverage to warm inspired air in cold weather.
  • Stay indoors with air conditioning when air pollution level is high.
  • Try to avoid abrupt environmental changes.
  • Shower in warm water.
• Instruct patient to humidify indoor air in winter; maintain 30% to 50% humidity for optimal mucociliary function.
• Suggest the use of a HEPA air cleaner to remove dust, pollen, and other particulates; this is controversial as to the benefit to the patient.

Prevent and Treat Respiratory Infections

• Warn against exposure to people with respiratory infections; a respiratory infection makes symptoms worse and can produce further irreversible damage.
• Advise patient to avoid crowds and areas with poor ventilation.
• Stress the importance of obtaining influenza vaccine (annual) and pneumococcal vaccine to decrease likelihood of developing these infections.
• Teach patient how to recognize and report evidence of respiratory infection promptly—changes in character of sputum (amount, color, or consistency—becoming purulent), increasing cough, wheezing, increasing shortness of breath, fever, chills, increasing difficulty in raising sputum, chest pain.
• Instruct patient to discuss with health care provider taking prescribed antimicrobial at first sign of infection and adding oral corticosteroids for exacerbation of COPD.

Reduce Bronchial Secretions

• Advise patient to maintain an adequate fluid intake (8 to 10 glasses daily); mark down the amount of liquid consumed daily.
• Encourage use of bronchodilators as directed.
• Teach postural drainage exercises as prescribed.
  • Stay in each position 5 to 15 minutes as tolerated.
  • Use controlled cough after each position.
• Use other secretion clearance techniques, such as PEP valve, flutter valve, huff cough and, possibly, chest percussion if needed for enhanced secretion clearance.

Improve Airflow

• Teach the proper technique for inhalation of medication to maximize aerosol deposition in the bronchial tree.
  • Use spacer device, breathe out normally; place MDI (attached to spacer device) in mouth, make tight seal around mouthpiece (if not using spacer device: place inhaler 1 inch [2.5 cm] in front of open mouth).
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  • Actuate cartridge to release spray and inhale slowly over 5 seconds.
  • Pause, holding breath for about 10 seconds; exhale slowly.
• Encourage routine use of a spacer device or holding chamber to allow easier inhalation of bronchodilator medication and enhanced medication deposition. Follow manufacturer's instructions for use of holding chambers.
• If using a dried powder inhaler, instruct in proper use according to manufacturer's instructions. Spacer devices are not necessary.

PATIENT EDUCATION GUIDELINES

Chronic Obstructive Pulmonary Disease

There are two types of chronic obstructive pulmonary disease, chronic bronchitis and emphysema, which may occur together or separately. Chronic bronchitis is diagnosed when there is a chronic cough with phlegm (sputum) for at least 3 months over a period of 2 years. With emphysema, there is a loss of elasticity of the lung tissue. Both result in inflammation and blockage of the airways. Smoking is the leading cause.

CONTROLLING SYMPTOMS

To control cough and phlegm

• Drink plenty of water (8 to 10 glasses per day) to keep phlegm thin.
• Use inhalers on a regular basis as prescribed:
  • Bronchodilators, such as Proventil, to open up the airways.
  • Atrovent to decrease cough and mucous production.
  • Corticosteroids to reduced swelling.
• Avoid irritants to the lungs, such as cigarette smoke, dust, smog, perfume, cold air, and very hot air.
• Report change in color, amount, or thickness of phlegm that could indicate an infection.
• Try to avoid respiratory infections by limiting contact with people during cold and flu season. Get the influenza and pneumonia vaccines and wash hands frequently.

To control shortness of breath

• Practice “pursed-lip breathing” by breathing in through the nose and out through pursed lips (like you are whistling), with a long, slow expiration.
• Position yourself for better breathing by leaning forward while sitting with elbows on table or resting on knees.
• Use relaxation techniques, such as listening to soft music, imagining you are in a quiet peaceful place, or having someone give you a massage.
• If prescribed, use oxygen as directed, especially while performing such activities as bathing, dressing, eating, and walking.

To control fatigue

• Do not stop doing physical activity; instead, learn how to manage by planning activities to conserve energy.
• Start with an exercise program that is easy, and progress slowly to increase your activity.
• Talk to your health care provider about joining a pulmonary rehabilitation program.
• Eat a well-balanced diet.
• Sleep with head elevated using several pillows or in a reclining chair to reduce shortness of breath and increase rest.
• If awakened by cough, sit up, sip fluid, and use inhaler to try to clear lungs of phlegm.
• Avoid overuse of inhalers, which may cause shakiness and insomnia.

To compensate for poor appetite

• Eat six or more small meals and snacks per day rather than two or three large meals.
• Eat slowly; plan at least 30 minutes per meal. Sit forward with elbows propped on table.
• Unless otherwise directed, try a high-protein, moderate-fat, and lower-carbohydrate diet of sufficient calories to cover the increased work of breathing.
• Consider a high-calorie, high-protein drink if you do not feel like eating.

Footnote

Adapted from Wright, L. (1998). Learning to cope with chronic obstructive pulmonary disease. Lippincott's Primary Care Practice, 2(6), 647-649.

DRUG ALERT

Instruct patient in proper sequence of medications, using bronchodilator first, followed by inhaled corticosteroid. Instruct patient to use a spacer device with inhaled corticosteroids, and rinse and spit after using inhaled corticosteroid to prevent oral candidiasis. To determine how long (how many days) MDI will last, divide puffs used per day into total puffs in inhaler. Write down date MDI will run out on canister and/or calendar. (See page 999 for patient education on MDI use.)

Breathing Exercises

• Explain that goal is to strengthen and coordinate muscles of breathing to lessen work of breathing and help lung empty more completely.
• Stress the importance of controlled breathing.
• Teach diaphragmatic breathing and pursed-lip breathing for episodes of dyspnea and stress.
• Encourage muscle toning by regular exercise.

General Health

• Teach good habits of well-balanced, nutritious intake.
• Encourage high-protein diet with adequate mineral, vitamin, and fluid intake.
• Advise against excessive hot or cold fluids and foods, which may provoke an irritating cough.
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• Advise to avoid hard-to-chew foods (causes tiring) and gas-forming foods, which cause distention and restrict diaphragmatic movement.
• Encourage five to six small meals daily to ease shortness of breath during and after meals.
• Suggest rest periods before and after meals if eating produces shortness of breath.
• Warn against potassium depletion. Patients with COPD tend to have low potassium levels; also, patient may be taking diuretics.
  • Watch for weakness, numbness, tingling of fingers, leg cramps.
  • Encourage foods high in potassium include bananas, dried fruits, dates, figs, orange juice, grape juice, milk, peaches, potatoes, tomatoes.
• Advise patient on restricting sodium as directed.
• Limit carbohydrates if CO₂ is retained by patient, because they increase CO₂.
• Use community resources, such as Meals On Wheels or a home care aide if energy level is low.

Evaluation: Expected Outcomes

• Coughs up secretions easily; decreased wheezing and crackles
• Reports less dyspnea; effectively using pursed-lip breathing
• No fever or change in sputum
• ABG levels and/or Spo₂ improved on low-flow oxygen
• Tolerates small, frequent meals; weight stable
• Reports walking longer distances without tiring
• Sleeping in 4- to 6-hour intervals; uses low-flow oxygen at night
• Demonstrates more effective coping; expresses feelings; seeks support group

COR PULMONALE

Pulmonary heart disease (cor pulmonale) is an alteration in the structure or function of the right ventricle resulting from disease of lung structure or function or its vasculature (except when this alteration results from disease of the left side of the heart or from congenital heart disease). It is heart disease caused by lung disease.

Pathophysiology and Etiology

• Condition that deprives lungs of oxygen: hypoxemia, hypercapnia, acidosis, circulatory complications, pulmonary hypertension, right heart enlargement, right-sided heart failure.
• Etiology includes:
  • Pulmonary vascular disease.
  • Pulmonary embolism.
  • COPD.

Clinical Manifestations

• Increasing dyspnea and fatigue; progressive dyspnea (orthopnea, paroxysmal nocturnal dyspnea), chronic cough.
• Distended jugular veins, peripheral edema, hepatomegaly.
• Bibasilar crackles and split second heart sound on auscultation of chest
• Manifestations of CO₂ narcosis—headache, confusion, somnolence, coma

Diagnostic Evaluation

• ABG levels—decreased Pao₂ and pH, increased Paco₂.
• PFTs may show airway obstruction.
• ECG changes are consistent with right ventricular hypertrophy.
• Chest X-ray shows right heart enlargement.
• Echocardiogram shows right heart enlargement.

Management

Goal: treatment of underlying lung disease and management of heart disease.

• Long-term, low-flow oxygen to improve oxygen delivery to peripheral tissues, thus decreasing cardiac work and lessening sympathetic vasoconstriction. Liter flow individualized during activities, rest, and sleep.
• Diuretics to lower PAP by reducing total blood volume and excess fluid in lungs.
• Pulmonary vasodilators such as nitroprusside (Nitropress); hydralazine (Apresoline); calcium channel blockers to dilate pulmonary vascular bed and reduce pulmonary vascular resistance; use is controversial.
• Bronchodilators to improve lung function.
• Mechanical ventilation, if patient in respiratory failure.
• Sodium restriction to reduce edema.

Complications

• Respiratory failure.
• Dysrhythmias

Nursing Assessment

• Determine if patient has longstanding history of lung disease.
• Assess degree of dyspnea, fatigue, hypoxemia.
• Inspect for jugular vein distention and peripheral edema.

Nursing Diagnoses

• Impaired Gas Exchange related to excess fluid in lungs; increased pulmonary vascular resistance
• Excess Fluid Volume related to right-sided heart failure

Nursing Interventions

Improving Gas Exchange

• Monitor ABG values and/or oxygen saturation as a guide in assessing adequacy of ventilation.
• Use continuous low-flow oxygen as directed to reduce PAP.
• Avoid CNS depressants (opioids, hypnotics). They have depressant action on respiratory centers and mask symptoms of hypercapnia.
• Monitor for signs of respiratory infection, because infection causes CO₂ retention and hypoxemia.

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Attaining Fluid Balance

• Watch alterations in electrolyte levels, especially potassium, which can lead to disturbances of cardiac rhythm.
• Employ ECG monitoring when necessary, and monitor closely for dysrhythmias.
• Limit physical activity until improvement is seen.
• Restrict sodium intake based on evidence of fluid retention.

Patient Education and Health Maintenance

• Emphasize importance of stopping cigarette smoking; cigarette smoking is a major cause of pulmonary heart disease.
  • Ask patient about smoking habits.
  • Inform patient of risks of smoking and benefits to be gained when smoking is stopped.
• Teach patient to recognize and treat infections immediately.
• Inform patient of interrelationship among infection, air pollution, and cardiopulmonary disease.
• Explain to patient and family that restlessness, depression, and poor sleeping as well as irritable and angry behavior, may be characteristic; patient should improve with rise in oxygen and fall in CO₂ levels in ABG values.
• Treat hypoxemia with supplemental oxygen, which will reduce further work load on the right side of heart.
• Explain that if patient has chronic lung disease, it may be necessary to have continuous low-flow oxygen therapy at home.

Evaluation: Expected Outcomes

• Less dyspneic; ABG levels improved, oxygen saturation = 90%
• Edema reduced; no dysrhythmias

INTERSTITIAL LUNG DISEASE (PULMONARY FIBROSIS)

Pulmonary fibrosis is a general term that refers to a variety of chronic lung disorders, such as asbestosis, silicosis, coal worker's pneumoconiosis (CWP), and sarcoidosis. There are estimated to be 130 types of interstitial lung disease; only about one-third have known causes. Causes include occupational exposure, environmental exposure, drugs and poisons, radiation, infections as well as connective tissue disease. Pulmonary fibrosis may also be idiopathic.

PATHOPHYSIOLOGY AND ETIOLOGY

• May be related to occupational exposure:
  • Asbestosis (increased risk for lung cancer)
  • Silicosis
  • CWP
• May be related to environmental exposure:
  • Hard metal disease (cobalt, tungsten, carbide)
  • Gas, fumes, vapors, aerosols
  • Drug and poison exposure
  • Cancer drugs (nitrofurantoin, methotrexate, busulfan, bleomycin)
  • Anti-inflammatory drugs (aspirin, gold, penicillamine)
  • Cardiac drugs (amiodarone)
  • Abused substances: heroin, methadone, propoxyphene (Darvon), talc used in I.V. drug abuse
  • Exposure to radiation
  • Exposure to infections
  • Connective tissue disease
• Chronic changes include lung tissue damage, inflammation of alveoli with scarring, and fibrosis and stiffening of the interstitium (tissue between the alveoli)
• The damage limits oxygen transport through scarred alveolar capillary membranes into the bloodstream

CLINICAL MANIFESTATIONS

• The most prevalent symptom is dyspnea, particularly with exercise.
• Dry cough.
• Symptoms may vary in severity, and the course of the disease may be unpredictable.

Additional information follows on idiopathic pulmonary fibrosis, interstitial lung disease due to sarcoidosis and other connective tissue diseases, and occupational lung diseases. A generalized nursing process appears on page 320.

IDIOPATHIC PULMONARY FIBROSIS

Incidence and Etiology

• Idiopathic pulmonary fibrosis has no identifiable cause.
• Incidence is approximately five cases per 100,000 people.
• It is generally diagnosed between ages 40 and 70.

Clinical Manifestations

• Slow onset of dyspnea and dry cough are present.
• Hypoxia with exercise.
• Rarely, patients may have weight loss, fever, myalgias.
• Breath sounds commonly include crackles.
• Finger clubbing is common.

Diagnostic Evaluation

• PFTs show decreased TLC and VC, with decreased diffusion capacity.
• ABG levels show low arterial oxygen level.
• Chest X-ray may demonstrate patchy, nonuniform infiltrates, ground glass pattern, reticular nodular pattern, honeycomb pattern, and small lung volumes.
• Exercise test shows hypoxia with exercise.

Management

• Corticosteroids: About one-third of patients respond to corticosteroids within 4 to 6 weeks. Patients may be started on prednisone 60 to 100 mg/day for 6 weeks then tapered over 3 months to a maintenance dose of 20 mg/day.
• Azathioprine (Imuran) 1 to 3 mg/kg/day.
• Cyclophosphamide (Cytoxan) 2 mg/kg/day; may have toxic adverse effects.
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• Lung transplantation may offer improved symptoms, function, and survival for some patients.
• Oxygen for hypoxemia.

DRUG ALERT

Long-term use of oral steroids may cause osteoporosis, decreased immune function, muscle wasting, glaucoma, cataracts, friable skin, mood changes, weight gain, hyperglycemia, gastric upset, and ulcers. Adverse effects are commonly related to higher doses of steroids used over an extended period. Review potential adverse effects with the patient when therapy is begun. Instruct the patient not to abruptly cease therapy. If unable to continue oral steroids, patient should notify the health care provider immediately.

SARCOIDOSIS AND OTHER CONNECTIVE TISSUE DISEASES

Causes

• Rheumatoid arthritis (RA): Twenty percent of patients with RA develop interstitial lung disease due to pleural inflammation between ages 50 and 60. Pulmonary involvement is most common in females.
• Systemic lupus erythematosus (SLE).
• Scleroderma: CREST syndrome (calcinosis, Raynaud's syndrome, esophageal dysmotility, sclerodactyly, telangiectasia).
• Ankylosing spondylitis.
• Sarcoidosis:
  • Granulomatous disease in which clumps of inflammatory epithelial cells occur in many organs, primarily in lungs.
  • Lymph node enlargement seen on chest X-ray.
  • Sarcoidosis usually occurs between ages 20 and 40.

Management

Comprehensive management of the inflammatory process and multisystem effects. (See Chapter 30.)

OCCUPATIONAL LUNG DISEASES

Types

• Asbestosis is a diffuse interstitial fibrosis of the lung caused by inhalation of asbestos dust and particles.
  • Found in workers involved in manufacture, cutting, and demolition of asbestos-containing materials; there are more than 4,000 known sources of asbestos fiber (asbestos mining and manufacturing, construction, roofing, demolition work, brake linings, floor tiles, paints, plastics, shipyards, insulation).
  • Asbestos fibers are inhaled and enter alveoli, which, in time, are obliterated by fibrous tissue that surrounds the asbestos particles.
  • Fibrous pleural thickening and pleural plaque formation produce restrictive lung disease, decrease in lung volume, diminished gas transfer, and hypoxemia with subsequent development of cor pulmonale.
• Silicosis is a chronic pulmonary fibrosis caused by inhalation of silica dust.
  • Exposure to silica dust is encountered in almost any form of mining because the earth's crust is composed of silica and silicates (gold, coal, tin, copper mining); also stone cutting, quarrying, manufacture of abrasives, ceramics, pottery, and foundry work.
  • When silica particles (which have fibrogenic properties) are inhaled, nodular lesions are produced throughout the lungs. These nodules undergo fibrosis, enlarge, and fuse.
  • Dense masses form in the upper portion of the lungs; restrictive and obstructive lung disease results.
• CWP (“black lung”) is a variety of respiratory disease found in coal workers in which there is an accumulation of coal dust in the lungs, causing a tissue reaction in its presence.
  • Dusts (coal, kaolin, mica, silica) are inhaled and deposited in the alveoli and respiratory bronchioles.
  • There is an increase of macrophages that engulf the particles and transport them to terminal bronchioles.
  • When normal clearance mechanisms can no longer handle the excessive dust load, the respiratory bronchioles and alveoli become clogged with coal dust, dying macrophages, and fibroblasts, which lead to the formation of the coal macule, the primary lesion of CWP.
  • As macules enlarge, there is dilation of the weakening bronchiole, with subsequent development of focal or centrilobular emphysema.

Pathophysiology

• Effects of inhaling organic dust (moldy hay, mushroom compost, malt, moldy maple bark, pigeon or parrot droppings, feathers, or contaminated grain), noxious particles, gases, or fumes. Development of disease depends on composition of inhaled substance, its antigenic (precipitating an immune response) or irritating properties, the dose inhaled, the length of time inhaled, and the host's response.
• Exposure to inorganic dusts stimulates pulmonary interstitial fibroblasts, resulting in pulmonary interstitial fibrosis.
• Acute symptoms of fever, cough, and chills may occur 4 to 12 hours after exposure and reoccur with repeated exposure. Chronic disease develops years later.
• Noxious fumes may cause acute injury to alveolar wall with increasing capillary permeability and pulmonary edema.
• Occupational lung diseases usually develop slowly (over 20 to 30 years) and are usually asymptomatic in the early stages.

NURSING ALERT

Asbestosis is strongly associated with bronchogenic cancer and mesotheliomas of the pleura and peritoneal surfaces. Smoking increases the risk of lung cancer 50 to 100 times.

Clinical Manifestations

• Chronic cough; productive in silicosis and CWP.
• Dyspnea on exertion; progressive and irreversible in asbestosis and CWP.
• Susceptibility to lower respiratory tract infections
• Bibasilar crackles in asbestosis
• Expectoration of varying amounts of black fluid in CWP

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Diagnostic Evaluation

• Chest X-ray—nodules of upper lobes in silicosis and CWP; diffuse parenchymal fibrosis, especially of lower lobes, in asbestosis.
• PFTs primarily show restrictive pattern.
• Bronchoscopy with lavage to identify specific exposure.
• CT scan, sputum examination, and lung biopsy may be needed to rule out other disorders.

Management

• There is no specific treatment; exposure is eliminated, and the patient is treated symptomatically.
• Give prophylactic isoniazid (INH) to patient with positive tuberculin test, because silicosis is associated with high risk of TB.
• Persuade people who have been exposed to asbestos fibers to stop smoking to decrease risk of lung cancer.
• Keep asbestos worker under cancer surveillance; watch for changing cough, hemoptysis, weight loss, melena.
• Bronchodilators may be of some benefit if any degree of airway obstruction is present.

Complications

• Respiratory failure.
• Lung cancer

NURSING CARE OF THE PATIENT WITH INTERSTITIAL LUNG DISEASE

Nursing Assessment

• Obtain occupational and environmental exposure history. Determine length and degree of exposure.
• Obtain full medical history and family history for connective tissue disorders.
• Obtain medication history.
• Obtain history of smoking, respiratory infections, and other chronic lung disease.
• Evaluate symptoms, functional capacity, and auscultate lungs for crackles.

Nursing Diagnoses

• Ineffective Breathing Pattern related to fibrotic lung tissue causing restriction
• Impaired Gas Exchange related to fibrotic lung tissue and secretions

Nursing Interventions

Improving Breathing Pattern

• Administer oxygen therapy as required.
• Administer or teach self-administration of bronchodilators as ordered.
• Encourage smoking cessation.

Promoting Gas Exchange

• Encourage mobilization of secretions through hydration and breathing and coughing exercises.
• Advise patient on pacing activities to prevent fatigue.

Patient Education and Health Maintenance

• Provide information about the importance of smoking cessation as well as methods of smoking cessation.
• Instruct patient in methods of health maintenance, such as adequate nutrition and exercise, so additional medical problems can be avoided.
• Advise patient that compensation may be obtained for impairment related to occupational lung disease through the Worker's Compensation Act.
• Provide information to healthy workers on prevention of occupational lung disease.
  • Enclose toxic substances to reduce their concentration in the air.
  • Employ engineering controls to reduce exposure.
  • Monitor air samples.
  • Ventilate the environment properly to reduce dust content of work atmosphere.
  • Use protective devices, such as face masks, respirators, hoods.

Evaluation: Expected Outcomes

• Reports less dyspnea
• Effectively mobilizes secretions

TRAUMATIC DISORDERS

PNEUMOTHORAX

Air in the pleural space occurring spontaneously or from trauma (see Figure 11-4). In patients with chest trauma, it is usually the result of a laceration to the lung parenchyma, tracheobronchial tree, or esophagus. The patient's clinical status depends on the rate of air leakage and size of wound. Pneumothorax is classified as:

FIGURE 11-4 Open pneumothorax and tension pneumothorax. In open pneumothorax, air enters the chest during inspiration and exits during expiration. There may be slight inflation of the affected lung due to a decrease in pressure as air moves out of the chest. In tension pneumothorax, air can enter but not leave the chest. As the pressure in the chest increases, the heart and great vessels are compressed and the mediastinal structures are shifted toward the opposite side of the chest. The trachea is pushed from its normal midline position toward the opposite side of the chest, and the unaffected lung is compressed.

Spontaneous pneumothorax—sudden onset of air in the pleural space with deflation of the affected lung in the absence of trauma.

Open pneumothorax (sucking wound of chest)—implies an opening in the chest wall large enough to allow air to pass freely in and out of thoracic cavity with each attempted respiration.

Tension pneumothorax—buildup of air under pressure in the pleural space resulting in interference with filling of both the heart and lungs.

Pathophysiology and Etiology

• When there is a large open hole in the chest wall, the patient will have a “steal” in ventilation of other lung.
• A portion of the tidal volume will move back and forth through the hole in the chest wall, rather than the trachea as it normally does.
• Spontaneous pneumothorax is usually due to rupture of a subpleural bleb.
  • May occur secondary to chronic respiratory diseases or idiopathically.
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  • May occur in healthy people, particularly in thin, white males and those with family history of pneumothorax.

Clinical Manifestations

• Hyperresonance; diminished breath sounds.
• Reduced mobility of affected half of thorax.
• Tracheal deviation away from affected side in tension pneumothorax
• Clinical picture of open or tension pneumothorax is one of air hunger, agitation, hypotension, and cyanosis
• Mild to moderate dyspnea and chest discomfort may be present with spontaneous pneumothorax

Diagnostic Evaluation

• Chest X-ray confirms presence of air in pleural space.

Management

Spontaneous Pneumothorax

• Treatment is generally nonoperative if pneumothorax is not too extensive.
  • Observe and allow for spontaneous resolution for less than 50% pneumothorax in otherwise healthy person.
  • Needle aspiration or chest tube drainage may be necessary to achieve reexpansion of collapsed lung if greater than 50% pneumothorax.
• Surgical intervention by pleurodesis (see page 269) or thoracotomy with resection of apical blebs is advised for patients with recurrent spontaneous pneumothorax.

Tension Pneumothorax

• Immediate decompression to prevent cardiovascular collapse by thoracentesis or chest tube insertion to let air escape.
• Chest tube drainage with underwater-seal suction to allow for full lung expansion and healing

Open Pneumothorax

• Close the chest wound immediately to restore adequate ventilation and respiration.
  • Patient is instructed to inhale and exhale gently against a closed glottis (Valsalva maneuver) as a pressure dressing (petroleum gauze secured with elastic adhesive) is applied. This maneuver helps to expand collapsed lung.
• Chest tube is inserted and water-seal drainage set up to permit evacuation of fluid/air and produce reexpansion of the lung.
• Surgical intervention may be necessary to repair trauma.

Complications

• Acute respiratory failure.
• Cardiovascular collapse with tension pneumothorax

Nursing Assessment

• Obtain history for chronic respiratory disease, trauma, and onset of symptoms.
• Inspect chest for reduced mobility and tracheal deviation.
• Auscultate chest for diminished breath sounds and percuss for hyperresonance.

Nursing Diagnoses

• Ineffective Breathing Pattern related to air in the pleural space
• Impaired Gas Exchange related to atelectasis and collapse of lung

Nursing Interventions

Achieving Effective Breathing Pattern

• Provide emergency care as indicated.
  • Apply petroleum gauze to sucking chest wound (see “Management”)
  • Assist with emergency thoracentesis or thoracostomy.
  • Be prepared to perform cardiopulmonary resuscitation or administer medications if cardiovascular collapse occurs.
• Maintain patent airway; suction as needed.
• Position patient upright if condition permits to allow greater chest expansion.
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• Maintain patency of chest tubes.
• Assist patient to splint chest while turning or coughing and administer pain medications as needed.

Resolving Impaired Gas Exchange

• Encourage patient in the use of incentive spirometer.
• Monitor oximetry and ABG levels to determine oxygenation.
• Provide oxygen as needed.

Patient Education and Health Maintenance

• Instruct patient to continue use of the incentive spirometer at home.
• For patients with spontaneous pneumothorax, there is an increased risk for repeat occurrence; therefore, encourage these patients to report sudden dyspnea immediately.

Evaluation: Expected Outcomes

• Breath sounds equal bilaterally; less dyspneic
• ABG levels improved

CHEST INJURIES

Chest injuries are potentially life-threatening because of immediate disturbances of cardiorespiratory physiology and hemorrhage and later developments of infection, damaged lung and thoracic cage. Traumatic chest injuries include rib fracture, hemothorax, flail chest, pulmonary contusion, and cardiac tamponade. Patients with chest trauma may have injuries to multiple organ systems. The patient should be examined for intra-abdominal injuries, which must be treated aggressively.

Pathophysiology and Clinical Manifestations

Rib Fracture

• Most common chest injury.
• May interfere with ventilation and may lacerate underlying lung.
• Causes pain at fracture site; painful, shallow respirations; localized tenderness and crepitus (crackling) over fracture site

Hemothorax

• Blood in pleural space as a result of penetrating or blunt chest trauma.
• Accompanies a high percentage of chest injuries.
• Can result in hidden blood loss
• Patient may be asymptomatic, dyspneic, apprehensive, or in shock

Flail Chest

• Loss of stability of chest wall as a result of multiple rib fractures, or combined rib and sternum fractures.
• When this occurs, one portion of the chest has lost its bony connection to the rest of the rib cage.
• During respiration, the detached part of the chest will be pulled in on inspiration and blown out on expiration (paradoxical movement)
• Normal mechanics of breathing are impaired to a degree that seriously jeopardizes ventilation, causing dyspnea and cyanosis
• Generally associated with other serious chest injuries; lung contusion, lung laceration, diffuse alveolar damage

Pulmonary Contusion

• Bruise of the lung parenchyma that results in leakage of blood and edema fluid into the alveolar and interstitial spaces of the lung.
• May not be fully developed for 24 to 72 hours.
• Signs and symptoms include:
  • Tachypnea, tachycardia
  • Crackles on auscultation
  • Pleuritic chest pain
  • Copious secretions
  • Cough—constant, loose, rattling

Cardiac Tamponade

• Compression of the heart as a result of accumulation of fluid within the pericardial space.
• Caused by penetrating injuries, metastasis, other disorders.
• Signs and symptoms include:
  • Falling blood pressure
  • Distended jugular veins, elevated central venous pressure (CVP)
  • Muffled heart sounds
  • Pulsus paradoxus (audible blood pressure fluctuation with respiration)
  • Dyspnea, cyanosis, shock

NURSING ALERT

A rapidly developing tamponade interferes with ventricular filling and causes impairment of circulation. Thus, there is a reduced cardiac output and poor venous return to the heart. Cardiac collapse can result. In the patient with hypovolemia caused by associated injuries, the CVP may not rise, thus masking the signs of cardiac tamponade.

Management and Nursing Interventions

The goal is to restore normal cardiorespiratory function as quickly a possible. This is accomplished by performing effective resuscitation while simultaneously assessing the patient, restoring chest wall integrity, and reexpanding the lung. The order of priority is determined by the clinical status of the patient.

Rib Fracture

• Give analgesics (usually nonopioid) to assist in effective coughing and deep breathing.
• Encourage deep breathing with strong inspiration; give local support to injured area by splinting with hands.
• Assist with intercostal nerve block (see Procedure Guidelines 11-2, pages 301 and 302) to relieve pain so coughing and deep breathing may be accomplished. An intercostal nerve block is the injection of a local anesthetic into the area around the intercostal nerves to relieve pain temporarily after rib fractures, chest wall injury, or thoracotomy.
• For multiple rib fractures, epidural anesthesia may be used.

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Hemothorax

• Assist with thoracentesis to aspirate blood from pleural space, if being done before a chest tube insertion.
• Assist with chest tube insertion and set up drainage system for complete and continuous removal of blood and air.
  • Auscultate lungs and monitor for relief of dyspnea.
  • Monitor amount of blood loss in drainage.
• Replace volume with I.V. fluids or blood products.

Flail Chest

• Stabilize the flail portion of the chest with hands; apply a pressure dressing and turn the patient on injured side, or place 10-lb sandbag at site of flail.
• Thoracic epidural analgesia may be used for some patients to relieve pain and improve ventilation.
• If respiratory failure is present, prepare for immediate ET intubation and mechanical ventilation—treats underlying pulmonary contusion and serves to stabilize the thoracic cage for healing of fractures, improves alveolar ventilation, and restores thoracic cage stability and intrathoracic volume by decreasing work of breathing.
• Prepare for operative stabilization of chest wall in select patients.

Pulmonary Contusion

For moderate lung contusion

• Employ mechanical ventilation to keep lungs inflated.
• Administer diuretics to reduce edema.
• Correct metabolic acidosis with I.V. sodium bicarbonate.
• Use PAP monitoring.
• Monitor for development of pneumonia.

Cardiac Tamponade

For penetrating injuries

• Assist with pericardiocentesis (see page 363) to provide emergency relief and improve hemodynamic function until surgery can be undertaken.
• Prepare for emergency thoracotomy to control bleeding and to repair cardiac injury.

Additional Responsibilities

• Secure and support the airway as indicated.
• Prepare for tracheostomy if indicated.
  • Tracheostomy helps to clear tracheobronchial tree, helps the patient breathe with less effort, decreases the amount of dead airspace in the respiratory tree, and helps reduce paradoxical motion.
  • When used with mechanical ventilation, provides a closed system and stabilizes the chest.
• Secure one or more I.V. lines for fluid replacement, and obtain blood for baseline studies, such as hemoglobin level and hematocrit.
• Monitor serial CVP readings to prevent hypovolemia and circulatory overload.
• Monitor ABG/Spo₂ results to determine need for supplemental oxygen, mechanical ventilation.
• Obtain urinary output hourly to evaluate tissue perfusion.
• Continue to monitor thoracic drainage to provide information about rate of blood loss, whether bleeding has stopped, whether surgical intervention is necessary.
• Institute ECG monitoring for early detection and treatment of cardiac dysrhythmias (dysrhythmias are a frequent cause of death in chest trauma).
• Maintain ongoing surveillance for complications:
  • Aspiration
  • Atelectasis
  • Pneumonia
  • Mediastinal/subcutaneous emphysema
  • Respiratory failure

Patient Education and Health Maintenance

• Instruct patient in splinting techniques.
• Make sure patient is aware of importance of automobile seat belt use to reduce serious chest injuries caused by automobile accidents.
• Teach patient to report signs of complications—increasing dyspnea, fever, cough.