CHAPTER 2 Respiratory Disorders

Section One Acute Respiratory Disorders

Acute respiratory disorders are short-term diseases or acute complications of chronic conditions. They can occur once and respond to treatment or recur to further complicate an underlying disease process.

Atelectasis

Overview/Pathophysiology

Atelectasis is a spontaneous collapse of alveolar lung tissue secondary to persistent hypoinflation. It is most common following major abdominal or thoracic surgery and results from hypoventilation of dependent portions of the lungs or inadequate clearing of secretions. Atelectasis can be an acute or a chronic condition and occurs most often in individuals with COPD. Postoperatively, atelectasis can be precipitated by the effects of anesthesia, sedation, and decreased mobility. Other precipitating factors include mucus plugs, foreign objects in the airways, pleural effusion, bronchogenic carcinoma, history of smoking, and obesity. Atelectasis can lead to pulmonary infection.

Assessment

The clinical picture is determined by the site of collapse, rate of development, and size of the affected area.

Signs and symptoms/physical findings

Pleuritic chest pain, tachypnea, shortness of breath, fever, dyspnea, decreased chest wall movement on affected side, dullness to percussion, decreased or absent breath sounds, crackles (rales) persisting after deep inspiration or cough, restlessness, agitation, change in level of consciousness (LOC), cyanosis.

Collaborative Management

Management is aimed at preventing this condition in all patients. If atelectasis occurs and is left untreated, the affected lung area eventually may become infected, fibrotic, and functionless.

Nursing Diagnoses and Interventions

For Patients at Risk for Atelectasis

Ineffective breathing pattern

related to decreased lung expansion secondary to inactivity or omission of deep breathing

Desired outcomes

Patient demonstrates deep breathing and effective coughing at least hourly and is eupneic (respiratory rate [RR] 12-20 breaths/min with normal depth and pattern) at all other times. Auscultation of patient’s lungs reveals no adventitious sounds.

Nursing Interventions

♦ Auscultate breath sounds at least q2-4h (or as indicated by patient’s condition) and during hyperinflation therapy. Report any decrease in breath sounds or presence of/increase in adventitious breath sounds.

♦ Instruct patient in use of hyperinflation device (e.g., incentive spirometer) to expand the lungs maximally.

• Inhale slowly and deeply 2 × normal tidal volume.

• Hold breath at least 5 sec at the end of inspiration.

• Do this 10 × per hr to maintain adequate alveolar inflation.

Deep breathing expands the alveoli and aids in mobilizing secretions to the airways, and coughing further mobilizes and clears the secretions. Monitor patient’s progress and document in nurses’ notes.

♦ Administer analgesics as prescribed to reduce pain and thereby facilitate coughing and deep-breathing exercises.

♦ When appropriate, teach methods of splinting wounds or painful areas to enable coughing and deep breathing.

♦ Instruct patients who are unable to cough effectively in technique of cascade cough (i.e., succession of short and more forceful exhalations).

♦ Encourage frequent position changes and other activity as prescribed to help mobilize secretions and promote effective airway clearance. Use upright sitting position if permitted to promote good chest expansion.

♦ When not contraindicated, instruct patient to increase fluid intake (to more than 2.5 L/day) to decrease viscosity of pulmonary secretions and facilitate their mobilization.

♦ When appropriate, coordinate deep-breathing and coughing exercises with peak effectiveness of bronchodilator therapy to maximize potential for mobilization of secretions.

Patient-Family Teaching and Discharge Planning

Provide verbal and written information about the following:

♦ Use of hyperinflation device if patient is to continue this therapy at home. Conduct a predischarge check of patient’s technique and document assessment in progress notes.

♦ Importance of maintaining activity level as prescribed.

♦ Importance of maintaining fluid intake of more than 2.5 L/day.

♦ Medications, including drug name, purpose, dosage, schedule, precautions, and potential side effects. Also discuss drug/drug, herb/drug, and food/drug interactions.

♦ Pain management techniques, such as medications and splinting.

♦ Precipitating factors in the development of atelectasis.

♦ Importance of notifying health care provider if signs and symptoms recur.

♦ Importance of medical follow-up. Review date and time of next appointment.

Pneumonia

Overview/Pathophysiology

Pneumonia is an acute bacterial or viral infection that causes inflammation of the lung parenchyma (alveolar spaces and interstitial tissue). As a result of the inflammation, involved lung tissue becomes edematous and air spaces fill with exudate (consolidation), gas exchange cannot occur, and nonoxygenated blood is shunted into the vascular system, with resulting hypoxemia. Bacterial pneumonias involve all or part of a lobe, whereas viral pneumonias appear diffusely throughout the lungs.

Influenza, which can cause pneumonia, is the most serious viral airway infection for adults. Patients more than 65 yr old, residents of extended care facilities, and individuals with chronic health conditions have the highest mortality from influenza.

Pneumonias usually are classified into two general types: community acquired and hospital associated (nosocomial). A third type now recognized is pneumonia in the immunocompromised individual.

Community acquired

Individuals with community-acquired pneumonia, the most common type, generally do not require hospitalization unless an underlying medical condition, such as chronic obstructive pulmonary disease (COPD), cardiac disease, or diabetes mellitus, or an immunocompromised state complicates the illness.

Hospital associated (nosocomial)

Nosocomial pneumonias usually occur following aspiration of oropharyngeal flora or stomach contents in an individual whose resistance is altered or whose coughing mechanisms are impaired (e.g., a patient who has decreased level of consciousness (LOC), dysphagia, diminished gag reflex, or a nasogastric tube or who has undergone thoracoabdominal surgery or is on mechanical ventilation). Bacteria invade the lower respiratory tract via three routes: (1) gastric acid aspiration (the most common route), which causes toxic injury to the lung and makes it susceptible to bacterial growth; (2) partial obstruction of airway by a foreign body or fluids contaminated with bacteria; and (3) outright infection (rare occurrence). Gram-negative pneumonias are associated with a high mortality rate, even with appropriate antibiotic therapy. If the alveolar-capillary membrane is affected, acute respiratory distress syndrome (ARDS) (formerly known as adult respiratory distress syndrome) may develop.

Pneumonia in the immunocompromised individual

Immunosuppression and neutropenia are predisposing factors in the development of nosocomial pneumonias from both common and unusual pathogens. Severely immunocompromised patients are affected not only by bacteria but also by fungi (Candida, Aspergillus), viruses (cytomegalovirus), and protozoa (Pneumocystis jiroveci, formerly known as P. carinii). Most commonly, P. jiroveci is seen in persons with human immunodeficiency virus (HIV) disease or in persons who are immunosuppressed therapeutically following organ transplants.

Assessment

Findings are influenced by patient’s age, extent of the disease process, underlying medical condition, and pathogen involved. Generally, any factor that alters integrity of the lower airways, thereby inhibiting ciliary activity, increases the likelihood of developing pneumonia (TABLE 2-1).

TABLE 2-1 ASSESSMENT GUIDELINES BY PNEUMONIA TYPE

Signs and symptoms/physical findings

Cough (productive and nonproductive), increased sputum production (rust colored, discolored, purulent, bloody, or mucoid), fever, pleuritic chest pain (more common in community-acquired bacterial pneumonias), dyspnea, chills, headache, myalgia, restlessness; anxiety; decreased skin turgor and dry mucous membranes secondary to dehydration; presence of nasal flaring and expiratory grunt; use of accessory muscles of respiration (scalene, sternocleidomastoid, external intercostals); decreased chest expansion caused by pleuritic pain; dullness on percussion over affected (consolidated) areas; tachypnea (respiratory rate [RR] more than 20 breaths/min); tachycardia (heart rate [HR] more than 90 beats per minute [bpm]); increased vocal fremitus; egophony (“e” to “a” change) over area of consolidation; decreased breath sounds; high-pitched and inspiratory crackles (rales) (increased by or heard only after coughing); low-pitched inspiratory crackles (rales) caused by airway secretions; and circumoral cyanosis (a late finding). Older adults may be confused or disoriented and have low-grade fevers but may present with few other signs and symptoms.

Diagnostic Tests

Chest x-ray examination

Confirms presence of pneumonia (i.e., infiltrate appearing on the film).

Sputum for Gram stain and culture and sensitivity tests

Sputum is obtained from lower respiratory tract by endotracheal aspiration, protected catheter brush, or bronchoalveolar lavage (BAL) before initiation or change of antibiotic therapy to identify causative organism in cases of hospital-acquired pneumonia. For community-acquired pneumonias, this approach is recommended only if organism resistant to usual antibiotic therapy is suspected.

WBC count

Increased (more than 12,000/mm³) in the presence of bacterial pneumonias. Normal or low WBC (less than 4000/mm³) count may be seen with viral or mycoplasma pneumonias.

Chemistry panel

Detects presence of hypernatremia and/or hyperglycemia.

Blood culture and sensitivity

Determine presence of bacteremia and aid in identification of causative organism. Used in cases of hospital-acquired pneumonia and in seriously ill patients with community-acquired pneumonia.

Oximetry

May reveal decreased O₂ saturation (92% or less).

Arterial blood gas (ABG) values

May vary, depending on presence of underlying pulmonary or other debilitating disease. May demonstrate hypoxemia (PaO₂ less than 80 mm Hg) and hypocarbia (PaCO₂ less than 32-35 mm Hg), with resultant respiratory alkalosis (pH more than 7.45), in the absence of underlying pulmonary disease.

Serologic studies

Acute and convalescent antibody titers drawn to diagnose viral pneumonia. A relative rise in antibody titers suggests viral infection.

Acid-fast stains and cultures

Rule out tuberculosis (TB).

Collaborative Management

O₂ therapy

Administered when O₂ saturation or ABG results demonstrate hypoxemia. Goal is to maintain PaO₂ at 60 mm Hg or higher. Special consideration must be given to patients with chronic CO₂ retention because their respiratory drive is stimulated by low/decreasing PaO₂ levels and not by increasing PaCO₂ levels as is normal. Therefore high concentrations of O₂ can depress respiration in these patients so O₂ is delivered in low concentrations initially, and O₂ saturations or ABG levels are monitored closely. If O₂ saturation or PaO₂ does not rise to acceptable levels (greater than 92% or 60 mm Hg or more, respectively), fraction of inspired O₂ (FIO₂) is increased in small increments, with concomitant checks of ABG values or O₂ saturations.

Antibiotic agents

Prescribed empirically based on presenting signs and symptoms, clinical findings, and chest x-ray results until sputum or blood culture results are available. Many organisms responsible for nosocomial pneumonias are resistant to multiple antibiotics. Proper identification of the organism and determination of sensitivity to specific antibiotics are critical for determining appropriate therapy.

A macrolide or levofloxacin is used for empirical out-patient treatment of community-acquired pneumonia; cephalosporins plus a macrolide and doxycycline are used for patients who are not in the ICU; IV beta-lactam and an IV quinolone or IV azithromycin are used for ICU patients.

Hospital-acquired pneumonia is empirically treated with IV ceftriaxone, or levofloxacin, or ampicillin/sulbactam or ertapenem if it is early onset and the patient has no risk factors for multidrug-resistant (MDR) disease; all other cases are treated initially with multiagent regimens. Vancomycin is added if risk of methicillin-resistant Staphylococcus aureus (MRSA) exists.

Hydration

IV fluids may be necessary to replace fluids lost from insensible sources (e.g., tachypnea, diaphoresis, fever) and decreased oral intake.

Percussion and postural drainage

Indicated if deep breathing and coughing are ineffective in mobilizing secretions.

Hyperinflation therapy

Prescribed for patients with inadequate inspiratory effort. (See p. 58)

Antitussives

Given in the absence of sputum production if coughing is continuous and exhausting to the patient.

Antipyretics and analgesics

Prescribed to reduce fever and provide relief from pleuritic pain or pain from coughing.

Vaccines

Pneumococcal vaccine

Administered to patients who have chronic health conditions and to those who are more than 65 yr old and/or are residents of an extended care facility and who have not received the vaccine within the last 5 yr. Vaccine history should be assessed on admission, and vaccine should be given to patients who meet criteria without contraindications (allergy).

Influenza vaccine

Administered to patients with chronic health conditions and to those who are more than 50 yr old and/or are residents of an extended care facility and who have not received the vaccine within the year. Influenza vaccines are routinely administered from October through March. Vaccine history should be assessed on admission, and vaccine should be given to patients who meet criteria without contraindications (e.g., allergy, history of Guillain-Barré syndrome).

Infection control

See discussion in Appendix 1, p. 743.

Nursing Diagnoses and Interventions

For Patients with Pneumonia

Impaired gas exchange

related to altered O₂ supply and alveolar-capillary membrane changes secondary to inflammatory process in the lungs

Desired outcomes

Hospital discharge based on patient exhibiting at least five of the following indicators: temperature 37.8° C or less, HR 100 bpm or less, RR 24 breaths/min or less, SBP 90 mm Hg or more, O₂ saturation 90% or more, and ability to maintain oral intake.

Nursing Interventions

♦ Administer antibiotics within 4 hr of hospital admission to reduce risk of death.

♦ Observe for restlessness, anxiety, mental status changes, shortness of breath, tachypnea, and use of accessory muscles of respiration, all of which are indicators of respiratory distress. Remember that cyanosis of the lips and nail beds may be a late indicator of hypoxia.

♦ Monitor and document VS q2-4h. Be alert to a rising temperature and other changes in VS that may indicate infection (e.g., increased HR, increased RR).

♦ Auscultate breath sounds at least q2-4h or as indicated by patient’s condition. Monitor for decreased or adventitious sounds (e.g., crackles, wheezes).

♦ Monitor oximetry readings; report O₂ saturation 92% or less because this can indicate a need for O₂ therapy.

♦ Monitor ABG results. A decreasing PaO₂ often indicates need for O₂ therapy.

♦ Position patient for comfort (usually semi-Fowler’s position) to promote diaphragmatic descent, maximize inhalation, and decrease work of breathing (WOB). In patients with unilateral pneumonia, positioning on unaffected side (i.e., “good side down”) promotes ventilation/perfusion matching.

♦ Deliver O₂ with humidity as prescribed; monitor oximetry or inspired concentration of oxygen (FIO₂) to ensure that oxygen is within prescribed concentrations. Be aware that patients with COPD may not tolerate O₂ at a delivery greater than 2 L/min, which can suppress the centrally mediated respiratory drive.

♦ Facilitate coordination among health care providers to provide rest periods between care activities to decrease O₂ demand. Allow 90 min for undisturbed rest.

Ineffective airway clearance

related to presence of tracheobronchial secretions secondary to infection or related to pain and fatigue secondary to lung consolidation

Desired outcomes

Patient demonstrates effective cough. Following intervention, patient’s airway is free of adventitious breath sounds.

Nursing Interventions

♦ Maintain a patent airway and ensure that secretions are removed. Suction as indicated/prescribed.

♦ Auscultate breath sounds q2-4h (or as indicated by patient’s condition), and report changes in patient’s ability to clear pulmonary secretions.

♦ Inspect sputum for quantity, odor, color, and consistency; document findings. As patient’s condition worsens, sputum can change in color from clear → white → yellow → green, or it may show other discoloration characteristic of underlying bacterial infection (e.g., rust colored, “currant jelly”).

♦ Ensure that patient performs deep-breathing with coughing exercises at least q2h. Assist patient into position of comfort, usually semi-Fowler’s position, to facilitate effectiveness and ease of these exercises.

♦ Assess need for hyperinflation therapy (i.e., patient’s inability to take deep breaths). Report complications of hyperinflation therapy to health care provider, including hyperventilation, gastric distention, headache, hypotension, and signs and symptoms of pneumothorax (shortness of breath, sharp chest pain, unilateral diminished breath sounds, dyspnea, cough).

♦ Teach patient to splint chest with pillow, folded blanket, or crossed arms when coughing, to reduce pain.

♦ Ensure that patient receives prescribed chest physiotherapy. Document patient’s response to treatment.

♦ Assist patient with position changes q2h to help mobilize secretions. If the patient is ambulatory, encourage ambulation to patient’s tolerance.

♦ When not contraindicated, encourage fluid intake (2.5 L/day or more) to decrease sputum viscosity.

♦ For other interventions, see “Atelectasis” for Ineffective breathing pattern, p. 58.

Deficient fluid volume

related to increased insensible loss secondary to tachypnea, fever, or diaphoresis

Desired outcomes

At least 24 hr before hospital discharge, patient is normovolemic as evidenced by urine output 30 mL/hr or more, stable weight, HR less than 100 bpm, SBP greater than 90 mm Hg, fluid intake approximating fluid output, moist mucous membranes, and normal skin turgor.

For Patients at Risk for Developing Pneumonia

Risk for infection (nosocomial pneumonia)

related to inadequate primary defenses (e.g., decreased ciliary action), invasive procedures (e.g., intubation), and/or chronic disease

Desired outcome

Patient is free of infection as evidenced by normothermia, WBC count 12,000/mm³ or less, and sputum clear to whitish.

Nursing Interventions

♦ Perform good handwashing technique before and after contact with patient (even though gloves are worn).

♦ Identify presurgical candidate who is at increased risk for nosocomial pneumonia because of the following: older adult (more than 70 yr), obesity, COPD, other chronic pulmonary conditions (e.g., asthma), history of smoking, abnormal pulmonary function tests (PFTs; especially decreased forced expiratory flow rate), intubation, and upper abdominal/thoracic surgery.

♦ Provide preoperative teaching; explain and demonstrate the following pulmonary activities that will be used postoperatively to prevent respiratory infection: deep breathing, coughing, turning in bed, splinting wounds, ambulating, maintaining adequate oral fluid intake, and using hyperinflation device. Make sure that patient verbalizes knowledge of the exercises and their rationale and returns demonstrations appropriately.

♦ Advise patients who smoke to discontinue smoking, especially during preoperative and postoperative periods. Refer to a community-based smoking cessation program as needed. When appropriate, discuss possibility of health care provider’s prescription of transdermal nicotine patches to facilitate smoking cessation.

♦ Administer analgesics

hr before deep-breathing exercises to control pain, which interferes with lung expansion. Scheduled analgesics also promote pain control. Support (splint) surgical wound with hands, pillows, or folded blanket placed firmly across site of incision.

♦ Identify patients who are at increased risk for aspiration: individuals with depressed LOC, dysphagia, or nasogastric (NG) or enteral tube in place. Maintain head of bead (HOB) at 30-45-degree elevation, and turn patient onto side rather than back. When patient receives enteral alimentation, recommend continuous rather than bolus feedings. Hold feedings when patient is lying flat.

♦ Recognize risk factors for patients with tracheostomy: presence of underlying lung disease or other serious illness, increased colonization of oropharynx or trachea by aerobic gram-negative bacteria, greater access of bacteria to lower respiratory tract, and cross-contamination caused by manipulation of tracheostomy tube.

• Wear gloves on both hands until tracheostomy wound has healed or formed granulation tissue around the tube or when handling mechanical ventilation tubing.

• Suction prn rather than on a routine basis because frequent suctioning increases risk of trauma and cross-contamination.

• Use sterile catheter for each suctioning procedure. Consider use of closed suction system to further minimize risk of contamination; replace closed suction system if soiled, for mechanical failure, or per agency policy. Always avoid reusing a suction system for subsequent patients. Avoid saline instillation during suctioning. If patient has tenacious secretions, increase heat and humidity to loosen them.

• Always wear gloves on both hands to suction.

• Recognize the ways in which nebulizer reservoirs can contaminate patient: introduction of nonsterile fluids or air, manipulation of nebulizer cup, or backflow of condensate from delivery tubing into reservoir or into patient when tubing is manipulated.

• Use only sterile fluids and dispense them using sterile technique.

• Replace (rather than replenish) solutions and equipment at frequent intervals. For example, empty reservoir completely and refill with sterile solution q8-24h, per agency protocol.

• Change breathing circuits every week unless circuits are soiled, mechanical failure occurs, or agency policy states otherwise.

• Fill fluid reservoirs immediately before use (not far in advance).

• Discard any fluid that has condensed in tubing; do not allow fluid to drain back into reservoir or into patient.

Patient-Family Teaching and Discharge Planning

Provide verbal and written information about the following:

♦ Techniques that mobilize secretions and promote gas.

♦ Medications, including drug names, purpose, dosage, frequency or schedule, precautions, and potential side effects, particularly of antibiotics. Also discuss drug/drug, herb/drug, and food/drug interactions. Instruct patient to complete full regimen of antibiotics to prevent reinfection and subsequent readmission.

♦ Signs and symptoms of pneumonia and importance of reporting them promptly if they recur. Teach patient’s significant others that changes in mental status may be the only indicator of pneumonia if patient is elderly.

♦ Importance of preventing fatigue by pacing activities and allowing frequent rest periods.

♦ Importance of avoiding exposure to individuals known to have flu and colds. Recommend that patient receive pneumococcal vaccination and annual influenza vaccination.

♦ Minimizing factors that can cause reinfection, including close living conditions, poor nutrition, and poorly ventilated living quarters or work environment.

♦ Importance of smoking cessation education and community resources to assist in cessation.

♦ Phone numbers to call if questions or concerns arise about therapy or disease after discharge. Additional general information can be obtained from the American Lung Association at www.lungusa.org.

♦ Information about the free brochures that discuss ways to stop smoking such as the following:

How to Help Your Patients Stop Using Tobacco: A National Cancer Institute Manual for the Oral Health Team, from the Smoking and Tobacco Control Program of the National Cancer Institute; call (800) 4-CANCER.

Pleural Effusion

Overview/Pathophysiology

A pleural effusion is an accumulation of fluid (blood, pus, chyle, serous fluid) in the pleural space. Generally, fluid gravitates to the most dependent area of the thorax, and the adjacent lung becomes compressed. Pleural effusion is rarely a disease in itself, but rather it is caused by a number of inflammatory, circulatory, or neoplastic diseases. Transudate effusion results from changes in hydrodynamic forces in the circulation and usually is caused by heart failure (increased hydrostatic pressure) or cirrhosis (decreased colloidal osmotic pressure). Exudate effusion results from irritation of the pleural membranes secondary to inflammatory, infective, or malignant processes. More exact nomenclature can be used once the nature of the fluid in the pleural effusion has been identified, that is, hydrothorax (a transudate or exudate of serous fluid), pyothorax or empyema (collection of purulent material), hemothorax (bloody fluid), or chylothorax (effused chyle).

Assessment

Clinical indicators of pleural effusion are related to the underlying disease. Patients with a small effusion (less than 300 mL) may be asymptomatic.

Signs and symptoms/physical findings

Pleuritic chest or shoulder pain, diaphoresis, cough, fever, dyspnea, orthopnea, decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophony (“e” to “a” change) over effusion site, tracheal deviation away from affected side, and pleural friction rub.

Nursing Diagnoses and Interventions

Ineffective breathing pattern

related to decreased lung expansion secondary to fluid accumulation in the pleural space

Desired outcome

Following intervention, patient’s breathing pattern moves toward eupnea.

Nursing Interventions

♦ Auscultate breath sounds q2-4h (or as indicated by patient’s condition), and monitor for decreasing breath sounds or presence of pleural friction rub.

♦ Monitor oximetry readings; report O₂ saturation 92% or less because this can indicate need for O₂ therapy.

♦ Ensure patency of chest drainage system (see guidelines, p. 79, in “Pneumothorax/Hemothorax”).

♦ Position patient for maximum chest expansion, generally semi-Fowler’s position.

♦ If hyperinflation therapy is prescribed, instruct patient in its use and document patient’s progress.

Patient-Family Teaching and Discharge Planning

Provide verbal and written information about the following:

♦ Importance of smoking cessation. Provide patient with resources related to community smoking cessation programs. When appropriate, discuss possibility of health care provider’s prescription of transdermal nicotine patches to facilitate smoking cessation.

♦ Signs of respiratory distress, such as restlessness, mental status changes, agitation, changes in behavior, and complaints of shortness of breath or dyspnea, and importance of rapidly notifying health care provider if these signs occur.

♦ Use of equipment at home (e.g., hyperinflation device, nebulizer, O₂).

♦ Medications, including drug names, dosage, purpose, schedule, precautions, and potential side effects. Also discuss drug/drug, herb/drug, and food/drug interactions.

Pulmonary Embolism

Overview/Pathophysiology

The most common pulmonary perfusion abnormality is pulmonary embolism (PE). PE is caused by passage of a foreign substance (blood clot, fat, air, or amniotic fluid) into the pulmonary artery or its branches, with resulting obstruction of the blood supply to lung tissue and subsequent collapse. The most common source is a dislodged blood clot from the systemic circulation, typically the deep veins of the legs or pelvis. Thrombus formation is the result of the following factors: blood stasis, alterations in clotting factors, and injury to vessel walls. A fat embolus is the most common nonthrombotic cause of pulmonary perfusion disorders (see p. 74).

Total obstruction leading to pulmonary infarction is rare because the pulmonary circulation has multiple sources of blood supply. Early diagnosis and appropriate treatment reduce mortality to less than 10%. Although most cases of PE resolve completely with no residual deficits, some patients may be left with chronic pulmonary hypertension.

Assessment

Signs and symptoms/physical findings

Often nonspecific and variable, depending on extent of obstruction and whether patient has infarction as a result of the obstruction.

Sudden onset of dyspnea and sharp chest pain, restlessness, anxiety, nonproductive cough or hemoptysis, palpitations, nausea, syncope, tachypnea, tachycardia, hypotension, crackles (rales), decreased chest wall excursion secondary to splinting, S₃ and S₄ gallop rhythms, transient pleural friction rub, jugular venous distention, diaphoresis, edema, and cyanosis.

If infarction has occurred, fever, pleuritic chest pain, and hemoptysis are common.

Varicose veins or prior thromboembolic disease

Age

Risk of thromboembolism is greatest for patients 55-65 yr of age.

Diagnostic Tests

Arterial blood gas (ABG) values

Hypoxemia (PaO₂ less than 80 mm Hg), hypocarbia (PaCO₂ less than 35 mm Hg), and respiratory alkalosis (pH more than 7.45) usually are present. Normal values do not rule out PE.

D-dimer

A degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin and measured by enzyme-linked immunosorbent assay (ELISA). The higher the result (with less than 250 ng/mL considered negative in most laboratories), the more likely it is patient has PE. This test is not sensitive or specific enough to diagnose PE, but it may be used in conjunction with other diagnostic tests.

Cardiac troponin level

Elevated in PE as a result of right ventricular dilation and myocardial injury.

Chest x-ray examination

Initially findings are usually normal, or elevated hemidiaphragm may be present. After 24 hr, x-ray examination may reveal small infiltrates secondary to atelectasis that result from the decrease in surfactant. If pulmonary infarction is present, infiltrates and pleural effusions may be seen within 12-36 hr.

ECG results

Abnormal in 85% of patients with PE.

Spiral or helical computed tomography (CT)

Images pulmonary arteries (PAs) during a single breath. Spiral CT is rapidly becoming the test of choice in diagnosing PE because of its higher specificity and sensitivity.

Pulmonary ventilation/perfusion scan

Used to detect abnormalities of ventilation or perfusion in the pulmonary system. Radiopaque agents are inhaled and injected peripherally. Images of distribution of both agents throughout the lung are scanned. If the scan shows a mismatch of ventilation and perfusion (i.e., pattern of normal ventilation with decreased perfusion), vascular obstruction is suggested.

Pulmonary angiography

Definitive study for PE: An invasive procedure that involves catheterization of right side of the heart and injection of dye into the PA to visualize pulmonary vessels. Abrupt vessel “cutoff” may be seen at the site of embolization. Usually, filling defects are seen. More specific findings are abnormal blood vessel diameters (i.e., obstruction of right PA would cause dilation of left PA) and abnormal blood vessel shapes (i.e., affected blood vessel may taper to a sharp point and disappear).

Collaborative Management

The three goals of therapy are (1) prophylaxis for individuals at risk for development of PE, (2) treatment during acute embolic event, and (3) prevention of future embolic events in individuals who have experienced PE.

O₂ therapy

Delivered at appropriate concentration to maintain a PaO₂ of more than 60 mm Hg or O₂ saturation greater than 90%.

Anticoagulation

Low molecular weight heparin (LMWH) or unfractionated heparin (UFH) therapy

Started immediately in patients without bleeding or clotting disorders and in whom PE is strongly suspected with the aim of inhibiting further thrombus growth, promoting resolution of the formed thrombus, and preventing further embolus formation. Continued for at least 5 days to allow for depletion of thrombin.

LMWH

Preferred to UFH because of more predictable dosing, fewer side effects, once- or twice-daily subcutaneous administration, and lack of need to monitor activated partial thromboplastin time. Dose is weight based and differs for various LMWH preparations. Dose must be adjusted for individuals with renal impairment because most LMWH is excreted by the kidneys. LMWH has been shown to be safe if given during pregnancy.

UFH

Has shorter half-life than LMWH and effect is completely reversible with protamine. Ideally, dosage is weight based (e.g., IV bolus of 80 units/kg followed by a maintenance dose of 18 units/kg/hr). Alternatively, an initial IV bolus of 5000-10,000 units followed by continuous infusion of 1000 units/hr may be given. Effect is monitored by activated partial thromboplastin time (aPTT) measurements every 6 hr after initial dose until the goal of 1.5 to 2.5 × control value is consistently established.

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Respiratory Disorders

Section One Acute Respiratory Disorders

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