Obstructive Pulmonary Diseases PDF

31 Obstructive Pulmonary Diseases Eugene E. Mondor http://evolve.elsevier.com/Lewis/medsurg/ CONCEPTUAL FOCUS Fatigue Infection Functional Ability Self-Management Gas Exchange LE...

31 Obstructive Pulmonary Diseases Eugene E. Mondor http://evolve.elsevier.com/Lewis/medsurg/ CONCEPTUAL FOCUS Fatigue Infection Functional Ability Self-Management Gas Exchange LEARNING OUTCOMES 1. Describe the pathophysiology, clinical manifestations, and 5. Describe the interprofessional care and nursing interprofessional and nursing management of the patient management of the patient with asthma. with bronchiectasis. 6. Identify the classes of drugs used in the treatment of asthma 2. Describe the pathophysiology, clinical manifestations, and and chronic obstructive pulmonary disease (COPD). interprofessional and nursing management of the patient 7. Describe the etiology, pathophysiology, clinical with cystic fibrosis. manifestations, and interprofessional care of the patient 3. Describe the etiology, pathophysiology, and clinical with COPD. manifestations of asthma. 8. Explain the nursing management of the patient with COPD. 4. Explain the difference between an acute asthma exacerbation and status asthmaticus. KEY TERMS α1-antitrypsin deficiency (AATD) cor pulmonale asthma cystic fibrosis (CF) bronchiectasis emphysema chronic bronchitis peak expiratory flow rate chronic obstructive pulmonary disease (COPD) status asthmaticus Imagine needing to consciously think about every breath that factors. Bronchiectasis affects more than 500,000 people in the you take each minute, each hour, and every day of your life. US.1 It is more common in women. It affects 1 in every 150 peo- Many people with obstructive lung disease have this experience. ple over age 75.2 Obstructive pulmonary diseases are the most common chronic lung diseases. They have in common increased resistance to air- Etiology and Pathophysiology flow because of airway obstruction or airway narrowing. The hallmark characteristic of bronchiectasis is permanent, The 4 obstructive lung diseases discussed in this chapter abnormal dilation of medium-sized bronchi. It results from are bronchiectasis, cystic fibrosis (CF), asthma, and chronic inflammatory changes that destroy elastic and muscular struc- obstructive pulmonary disease (COPD). Drug therapy plays tures supporting the bronchial wall. There is a continuing cycle a key role in managing these conditions. Knowing common of inflammation, airway damage, and remodeling, enhanced by terms used in discussing respiratory care will help you better the accumulation of neutrophils in the airways. Airways can understand this content (Table 31.1). become colonized with microorganisms (e.g., Pseudomonas), causing the bronchial walls to weaken and pockets of infection to form (Fig. 31.1). BRONCHIECTASIS When the walls of the bronchial system are injured, the In bronchiectasis, the bronchioles are dilated, making it hard mucociliary mechanism is damaged. This allows bacteria and to clear secretions. It most often results from poorly treated or mucus to accumulate within the pockets. Bacteria attract neu- untreated lung infections, immune system problems, or genetic trophils, which enhances inflammation and causes edema. 632  CHAPTER 31 Obstructive Pulmonary Diseases 633 TABLE 31.1 Common Terms Used in Impaired clearance of mucus by the cilia leads to stasis of thick Respiratory Care mucus. This results in a reduced ability to clear mucus from the lungs and decreased expiratory airflow. Respiratory Terms Around 40% of cases have no known cause.1 CF is the main FeNO Fractional concentration of exhaled nitric oxide (NO) cause of bronchiectasis in children. Bacterial infection of the FEV1 Forced expired volume in 1 second lungs is the main cause in adults. It can follow a single episode FEV1/FVC Volume of air exhaled during the 1st second of a forced of severe pneumonia or infection that was either not treated or exhalation, expressed as a percentage (%) of FVC received inadequate or delayed treatment. Other risk factors FVC Forced vital capacity include airway obstruction with mucus plugs, impaired pulmo- Pharmacologic Terms nary defenses, and repeated aspiration. Several systemic prob- ICS Inhaled corticosteroid lems, such as diabetes, inflammatory bowel disease, rheumatoid LABA Long-acting B2 agonist arthritis, immune disorders (e.g., acquired immunodeficiency LAMA Long-acting muscarinic antagonist syndrome [AIDS]), and α-1 antitrypsin deficiency (AATD), are SABA Short-acting B2 agonist risk factors.3 SAMA Short-acting muscarinic antagonist Clinical Manifestations The key sign is a persistent cough with consistent production of thick, tenacious, purulent sputum. In rare situations, some patients with severe disease and upper lobe involvement may have no sputum production and little cough. Recurrent infec- Mucus and pus tions injure blood vessels. Large connections (anastomoses) may develop between blood vessels in the lungs, and hemop- tysis may occur. In severe cases, bleeding can be life-threaten- ing. Other manifestations include pleuritic chest pain, dyspnea, wheezing, clubbing, weight loss, and anemia. Adventitious A sounds are heard (e.g., crackles, wheezes) over the lung fields. Cylindric Complications Complications include pulmonary hypertension and repeated exacerbations of the condition, often accompanied by chronic inflammation and hypoxemia. Colonization with multi-drug resistant organisms can occur, especially if the patient has received antibiotic therapy over long periods of time. Mucus Neovascularization (development of new blood vessels after B Saccular injury) of the bronchial arteries is a significant complication.4 This can lead to hemoptysis and in some situations hemorrhage. Massive hemoptysis is a life-threatening emergency. Diagnostic Studies A person who presents with a chronic productive cough with copious purulent sputum (which may be blood streaked) should be suspected of having bronchiectasis. A CT scan is the gold standard for diagnosing bronchiectasis. Chest x-rays may show nonspecific abnormalities. Spirometry usually shows an obstructive pattern, including decreases in FEV1 and FEV1/FVC (see Table 27.18). Sputum cul- tures may confirm the presence of infection. Patients often have Hemophilus influenzae, Staphylococcus aureus, or Pseudomonas aeruginosa.4 P. aeruginosa leads to frequent exacerbations and C rapid decline in lung function. A complete blood cell count and Fig. 31.1 Pathologic changes in bronchiectasis. (A) Longitudinal section AAT level may be done. of bronchial wall where chronic infection has caused damage. (B) Col- lection of purulent material in dilated bronchioles, leading to persistent infection. (C) Bronchiectasis in a patient with CF who underwent lung INTERPROFESSIONAL CARE transplantation. Cut surfaces of the lung show markedly distended peripheral bronchi filled with mucopurulent secretions. (C, From Kumar There is no cure for bronchiectasis. Most patients are safely V, Abbas AK, Aster JC: Robbins and Cotran pathologic basis of disease, managed on an outpatient basis. Contact with the health care ed 10, Philadelphia, 2021, Saunders.) system is often related to an exacerbation. When the patient is 634 SECTION 6 Problems of Oxygenation: Ventilation not responding to care, hospitalization may be needed for mon- of fluid daily. To achieve this, tell the patient to increase intake itoring and further treatment. by 1 glass per day until they reach that goal. Have the patient use Therapy is aimed at treating acute flare-ups and preventing a low-sodium fluids to avoid fluid retention. Rest is important to decline in lung function. Antibiotics are the mainstay of treat- prevent overexertion. ment. They are often given for a minimum of 14 days. Antibiotics Teach the patient and caregiver signs and symptoms to may be given orally, IV, or inhaled (nebulizer). Choice of antibi- report to the HCP. These include increased work of breathing otic mainly depends on culture results or the most likely organ- (WOB), sputum production, or dyspnea. Fever, chills, and chest ism. Long-term antibiotic therapy is given to patients who have pain may or may not occur with an exacerbation. Teach patients symptoms that recur a few days after stopping antibiotics. when to contact the HCP if hemoptysis occurs. Some patients Bronchodilator therapy with short-acting β-2 agonists expectorate a “spot” of blood at times. This is usual for them (SABAs), long-acting β-2 agonists (LABAs), or anticholin- and does not require urgent attention. However, if the patient ergics can prevent bronchospasm and stimulate mucus clear- expectorates a moderate to large amount of blood, they should ance. Patients may receive oral or inhaled corticosteroids (ICS) contact the HCP at once. depending on the severity of the condition. Surgical resection of parts of the lungs was common in the Acute Care past. It has largely been replaced by more effective supportive In the acute care setting, elevate the head of the bed to at least therapy and antibiotic treatment. For select patients who are 30 degrees. Monitor vital signs and respiratory status, includ- disabled despite maximal therapy, a lung transplant may be an ing rate, rhythm, and SpO2. Apply O2 therapy via a low-flow option. delivery device (e.g., nasal cannula) if O2 saturation is less than 90% on room air. If you suspect that the patient may be bleeding NURSING MANAGEMENT: BRONCHIECTASIS from the airways, place the patient in a side-lying position with the suspected bleeding side down. Have oral suction available. Assessment Ensure there is a valid type and crossmatch. When the patient in immediate distress, priorities include One important goal is to promote drainage and removal of maintaining a patent airway, ensuring an adequate route for mucus. Various ACTs can help with secretion removal. Chest ventilation, and stable vital signs. Notify the HCP, especially if physiotherapy (CPT) with postural drainage is widely used. the patient is expectorating large amounts of blood. Direct hydration of the respiratory system may help with the For the patient not in immediate distress, obtain a patient expectoration of secretions. Hyperosmolar agents (e.g., hyper- and family history. If possible, identify onset, risk factors, and tonic saline) given by nebulizer can liquefy secretions. At home, any past complications. Review the current drug therapy and a steamy shower can be effective. Active bleeding is a contrain- treatments the patient is receiving. dication to CPT. Good nutrition is important. It may be hard to maintain Clinical Problems because the patient is often anorexic. Oral hygiene to cleanse Clinical problems for the patient with bronchiectasis may the mouth and remove dried sputum crusts may improve include: the patient’s appetite. Foods that are appealing, provided in Impaired respiratory function smaller quantities, and offered more often may increase the Activity intolerance desire to eat. e cient nowledge Evaluation Planning The expected outcomes of a patient with bronchiectasis include: The overall goals for the patient with bronchiectasis include (1) Maintain a patent airway maintain a patent airway; (2) have slow, steady, and unlabored Have a normal respiratory rate and rhythm breathing; and (3) develop a routine that permits as much func- emonstrate a health balance between activity and rest with tional independence as possible with activities of daily living ADLs (ADLs). Perform optimal self management Implementation Health Promotion CYSTIC FIBROSIS Patient teaching is important. Encourage them to follow as Cystic fibrosis (CF) is an inherited, autosomal recessive healthy a lifestyle as possible. Stress the need to quit smoking genetic disorder, characterized by altered transport of sodium or, at minimum, reduce the amount smoked. Stress the need to and chloride ions in and out of epithelial cells. Airway obstruc- follow a healthy diet. Encourage the patient to engage in some tion occurs because of changes in exocrine glandular secre- type of regular exercise (within the comfort and safety of their tions, resulting in increased mucus production. This defect also condition). Discuss how to prevent exacerbations and review affects the gastrointestinal (GI) system (pancreas and biliary airway clearance techniques (ACTs). tract) and reproductive organs. There are about 30,000 people Maintaining hydration is important to liquefy secretions. in the US living with CF. More than 50% of the CF population Unless contraindicated, the patient should drink at least 2 to 3 L are adults.5  CHAPTER 31 Obstructive Pulmonary Diseases 635 Mutant CFTR channel BOX 31.1 GENETICS IN CLINICAL Normal CFTR channel does not move sodium and moves the sodium and PRACTICE chloride ions to the chloride ions, causing sticky outside of the cell. mucus to build up on the Cystic Fibrosis outside of the cell. Genetic Basis Outside cell Mucus Autosomal recessive disorder Caused by mutations in CF transmembrane regulator (CFTR) gene CFTR gene provides the instructions for making the protein that controls the channel that transports sodium and chloride Inside There are more than 1,700 different mutations of the CFTR gene cell Mutations in the CFTR gene disrupt the function of the channels, preventing them from regulating the flow of sodium, chloride, and water across cell membranes Sodium The most common mutation is 2 copies (homozygous) of the F508 mutation and in the CFTR gene chloride ions Incidence In the US, 1 in 2500–3000 White births Fig. 31.2 Cystic fibrosis transmembrane conductance regulator (CFTR) is a protein of the cell membrane that normally helps sodium and chlo- One in 25–30 Whites are carriers of the gene ride move in and out of cells. People with CF inherit a defective gene. 10,000 new cases diagnosed each year, most before 1 year of age As a result, movement of sodium and chloride is blocked. Abnormally thick sticky mucus is produced on the outside of the cell. Clinical Implications Most people who have a child with CF are not aware of a family history of CF. We should offer CF screening to all people of reproductive age regardless (Fig. 31.2). The thick secretions plug up the ducts in these of family history. organs. This causes scarring in the organs and results in organ failure. The high concentrations of sodium and chloride in the Genetic Testing sweat of the patient with CF result from decreased chloride Can identify if a person is a carrier of the mutation for the CFTR gene reabsorption in the sweat duct. Blood-based DNA testing is available for disease and carrier states All 50 states require newborn CF screening Pathophysiology Testing is usually done in children if CF is suspected or if parents are possi- ble carriers CF has a significant effect on the airways. It can affect both the In parents who are known carriers, amniocentesis between 15 and 20 upper and lower respiratory tracts. CF progresses from being a weeks or chorionic villus sampling between 10 and 13 weeks of pregnancy disease of the small airways to involving the larger airways with can be done (although testing can also occur in pregnant women beyond these destruction of lung tissue. The mucus lining the airways becomes dates) dehydrated and tenacious due to defects in chloride secretion and sodium absorption. Cilia become overwhelmed with thick secre- tions. As a result, cilia motility is decreased, allowing mucus to The median age at diagnosis is 6 to 8 months of age. Two- adhere to the airways. At the same time, the bronchioles become thirds of patients are diagnosed in the first year of life.5 Some obstructed with the thick mucus, leading to scarring of the air- are not diagnosed until they are adults. The severity and pro- ways, air trapping, and hyperinflation of the lungs. gression of CF vary. With early diagnosis and improvements With CF, there is a persistent, chronic airway infection that in therapy, the prognosis of patients with CF has significantly cannot be cured. Pseudomonas is the most common organ- improved. The median predicted survival in 1970 was 16 years ism in adults.7 Antibiotic resistance can develop after multiple of age. Today it has increased to more than 46 years.6 There are exposures to antibiotics. Lung inflammation is associated with many persons with CF who have lived beyond this age. chronic infection. It can narrow airways and cause a decrease in lung function. An increase in inflammatory mediators (e.g., Genetic Link interleukins, oxidants, proteases released by neutrophils) con- CF is an autosomal recessive disorder (Box 31.1). The CF gene tributes to disease progression. is found on chromosome 7, which makes a protein called CF Lung disorders that initially occur are chronic bronchiolitis transmembrane conductance regulator (CFTR).7 The CFTR pro- and bronchiectasis. Over a long period, pulmonary vascular tein localizes to the epithelial surface of the airways, GI tract, remodeling occurs because of local hypoxia and arteriolar vaso- and ducts of the liver, pancreas, and sweat glands. Under normal constriction. Enlarged pulmonary arteries, pulmonary hyper- conditions, CFTR regulates sodium and chloride movement in tension, and cor pulmonale occur in the later phases of the and out of epithelial cells. disease. Blebs and large cysts are severe manifestations of lung Mutations in the CFTR gene change this protein so that the destruction. Pneumothorax may occur. There is a proliferation channels are blocked. As a result, cells that line the passage- of capillaries in response to chronic infection. During exacerba- ways of the lungs, pancreas, intestines, and other organs make tions, there may be erosion of these capillaries and hemoptysis secretions that are low in sodium chloride content (thus low can occur. Hemoptysis may range from scant streaking to major in water content), making them abnormally thick and sticky bleeding, which can be fatal. 636 SECTION 6 Problems of Oxygenation: Ventilation Mucous plugging of the pancreatic exocrine ducts causes Patients with DIOS may have right lower quadrant pain (the pancreatic insufficiency. This results in atrophy and progres- area of the ileocecal valve), nausea, vomiting, and a palpable sive fibrotic cyst formation. The pancreas’s exocrine function mass. Insufficient pancreatic enzyme release causes the typical may be completely lost. Because of this, the pancreas does not pattern of protein and fat malabsorption. Many persons are thin make enough pancreatic enzymes, such as lipase, amylase, and with a low body mass index (BMI). They may have frequent proteases (trypsin, chymotrypsin), to allow for the absorption bulky, foul-smelling stools. of nutrients. Malabsorption of fat, protein, and fat-soluble Both males and females have delayed puberty. Some women vitamins (A, D, E, and K) occurs. Fat malabsorption results in have difficulty conceiving. The cervical mucus may be thick. steatorrhea (large, oily, frequent bowel movements). Protein During exacerbations, menstrual irregularities and secondary malabsorption results in the failure to grow and gain weight. amenorrhea are common. Most women with CF can become Osteopenia and osteoporosis are common. They are related to pregnant. Most pregnancies result in viable infants. malnutrition, malabsorption of vitamin D, low testosterone lev- Nearly all men with CF have reproductive issues. Because the els, and chronic infections. Pancreatitis may occur. vas deferens fails to develop in utero, there is no transport of CF-related diabetes (CFRD) is caused by the underdevelop- sperm from storage in the testes to the penile urethra. However, ment of pancreatic islet cells (in utero) and destruction of islet they make sperm normally and can father a child with assisted cells over the person’s lifetime. CFRD is unique because it has reproductive technology. characteristics of both type 1 and type 2 diabetes. The pancreas in people with CF makes insulin, but they make it too late to Complications fully respond to carbohydrate intake. Complications include CFRD and bone, sinus, and liver dis- Persons with CF often have other GI problems, including gas- ease. Respiratory failure and cor pulmonale caused by pulmo- troesophageal reflux disease GERD, gallstones, and cirrhosis. nary hypertension are late complications of CF. Pneumothorax, Mucus deposits in the ducts can damage the liver and gall blad- a rare but serious complication, is caused by the formation of der. Liver enzymes may become chronically increased. Cirrhosis bullae and blebs on the surface of the lung. A small amount of develops over time. Portal hypertension can occur. Distal intestinal blood in sputum is common because of chronic lung infection. obstruction syndrome (DIOS) results from an intermittent obstruc- Massive hemoptysis, though rare, can be life-threatening. Liver tion, often in the terminal ileum at the point of the ileocecal junc- failure and bowel obstruction may occur in severe CF. tion. It is caused by thickened, dehydrated stool and mucus. DIOS develops because of chronic malabsorption related to exocrine dys- Diagnostic Studies function, under- or over-dosing of pancreatic replacement enzyme The diagnostic criteria for CF include a combination of clinical supplements, dehydration, and swallowing of mucus. The patient presentation, family history, and laboratory and genetic testing. may appear to have a small bowel obstruction. The sweat glands of patients with CF secrete normal volumes of sweat. They do not absorb sodium chloride from their sweat Clinical Manifestations as it moves through the sweat duct. As a result, they excrete 4 The manifestations vary depending on the severity of the dis- times the normal amount of sodium and chloride in sweat. This ease. Severity may vary greatly, both within families and among problem usually does not directly affect the person’s health but different families. Carriers do not have symptoms. helps confirm a diagnosis of CF. Meconium ileus in a newborn prompts the diagnosis in 20% The sweat chloride test is the gold standard for diagnosing CF. of people. Other signs that suggest a CF diagnosis in childhood It is done with the pilocarpine iontophoresis method.8 Pilocarpine are acute or persistent respiratory symptoms (wheezing, cough- is placed on the skin and carried by a small electric current to ing, frequent pneumonia), failure to thrive, malnutrition, ste- stimulate sweat production. This part of the process takes about 5 atorrhea, bronchiectasis, and family history. Without treatment, minutes. Explain to the patient they may feel a slight tingling or a large, protuberant abdomen may develop with an emaciated warmth. Next, the area (usually an arm) is wrapped in plastic to appearance of the extremities. promote sweating. The sweat is collected on filter paper or gauze In adults, patients often present with atypical symptoms, such and then analyzed for sweat chloride concentrations. The test takes as new-onset diabetes or infertility problems. A common symp- about 1 hour. Sweat chloride values above 60 mmol/L are consid- tom of CF in the adult is a frequent cough. With time, the cough ered positive for the diagnosis of CF.8 A second sweat chloride test is becomes persistent and produces thick, purulent sputum. URI done at the same time (1 test in each arm) to confirm the diagnosis. manifestations may include chronic sinusitis and nasal polypo- Genetic testing is often done if the results from a sweat chlo- sis. Other lung problems include recurring lung infections, such ride test are uncertain. We can send a blood or cell sample to as bronchiolitis, bronchitis, and pneumonia. With advanced a laboratory that specializes in genetic testing. Most laborato- lung disease, clubbing occurs. As the disease progresses, peri- ries test for only the most common mutations of the CF gene. ods of clinical stability are interspersed by exacerbations char- Because more than 1700 mutations cause CF, screening for all acterized by increased cough, weight loss, increased sputum mutations is difficult and done only at specialized laboratories. production, and decreased lung function. Over time, exacerba- tions become more frequent, bronchiectasis worsens, and the Interprofessional Care recovery of lost lung function is less complete. These changes An interprofessional team should be involved in the care of a may lead to respiratory failure. patient with CF. The Cystic Fibrosis Foundation funds more  CHAPTER 31 Obstructive Pulmonary Diseases 637 than 120 CF care centers nationwide. The high quality of special- The patient with cor pulmonale or hypoxemia may need ized care from the care center network has led to the improved home O2 therapy. Those with a large pneumothorax need chest length and quality of life for people with CF. These care centers tube drainage, sometimes repeatedly. Sclerosing of the pleural offer the best care, treatments, and support for those with CF. space or partial pleural stripping and pleural abrasion may be The teams at these care centers include a nurse, physician, respi- done for recurrent episodes of pneumothorax. With massive ratory therapist, physical therapist, dietitian, social worker, and hemoptysis, bronchial artery embolization is done. CF has often a nurse practitioner. become a leading reason for lung transplantation. Management of lung problems aims at relieving airway The management of pancreatic insufficiency includes pan- obstruction and controlling infection. Aerosol and nebulizer creatic enzyme replacement of lipase, protease, and amylase treatments promote drainage of thick bronchial mucus. The drugs (e.g., pancrelipase [Pancreaze, Creon, Zenpep]) taken before we use dilate the airways, liquefy mucus, and promote clearance. each meal and snack. Adequate intake of fat, calories, protein, The abnormal viscosity of secretions is increased by con- and vitamins is important. Fat-soluble vitamins (A, D, E, and centrated DNA from neutrophils involved in chronic infection. K) must be supplemented since they are malabsorbed. Caloric Drugs that degrade the DNA in CF sputum (e.g., inhaled dor- supplements improve nutrition status. Extra salt is needed when nase alfa [Pulmozyme]) increase airflow and reduce the number sweating is increased, such as during hot weather, with a fever, of acute exacerbations. Inhaled hypertonic saline (7%) increases or from intense physical activity. Hyperglycemia may need osmolality, allowing water to collect on airway surfaces. It is insulin treatment. effective in clearing mucus and decreases the frequency of If the patient develops DIOS with partial or complete bowel exacerbations. Some patients need bronchodilators (e.g., β2-ad- obstruction, we make every attempt to manage the condition renergic agonists) to control bronchospasm, but the long-term medically. Options include prokinetic agents (e.g., macrolide benefit is not known. antibiotics, metoclopramide), mucolytics (oral N-acetylcysteine ACTs are critical since the normal ciliary motion in CF [NAC]), stimulant laxatives, lactulose, and polyethylene glycol airways is impaired. CPT (including postural drainage with (PEG) electrolyte solution.9 Careful monitoring of bowel hab- percussion and vibration) and high-frequency chest wall oscil- its and patterns is essential for CF patients. If DIOS does not lation loosen mucus. Specialized expiratory techniques that use resolve with medical treatment, surgery may be done to prevent airflow to remove the loosened secretions help clear secretions. ischemic bowel. Examples include breathing exercises, pursed-lip breathing, and All patients with CF should have CFTR genotyping. This will huff coughing (see Chapter 28). Patients may prefer a certain help see if they carry a mutation that is a target of CFTR mod- technique or device that works well for them in their daily rou- ulator therapy. Drugs, such as ivacaftor/lumacaftor (Orkambi) tine. No ACT is better than the others. and Ivacaftor (Kalydeco), are used to treat patients with specific Most patients with CF die of complications from lung infec- CFTR gene mutations.10 tion. Thus, early intervention with antibiotics is key when infec- tion is present. Antibiotic choice should be based on sputum NURSING MANAGEMENT: CYSTIC FIBROSIS culture results. The usual treatment is 2 antibiotics with differ- ent mechanisms of action (e.g., cephalosporin and an amino- Assessment glycoside). They may be given for 10 days to 3 weeks or longer. Subjective and objective data you should obtain from the patient Prolonged high-dose therapy (larger doses, more frequent dos- with CF are shown in Table 31.2. ing) may be needed because many drugs are abnormally metab- olized and rapidly excreted in the patient with CF. Some need Clinical Problems chronic suppressive therapy. If home support and resources are Clinical problems for the patient with CF may include: adequate, the patient and caregiver may be able to administer Impaired respiratory function IV antibiotic therapy at home independently. Nutritionally compromised Oral agents used for mild exacerbations (e.g., increased cough e cient nowledge and sputum) include a semisynthetic penicillin, trimethoprim/ sulfamethoxazole (to treat S. aureus), or oral quinolones, espe- Planning cially ciprofloxacin (to treat Pseudomonas). Quinolones are The overall goals are that the patient with CF will have (1) ade- used with caution because of the rapid development of resistant quate airway clearance, (2) absence of respiratory infection, (3) strains. adequate nutrition to maintain appropriate weight, (4) ability to Most patients have Pseudomonas infection, which can be independently (or with assist) perform ADLs, (5) recognize and hard to treat over time because the organism develops resis- treat complications related to CF, and (6) actively take part in tance to antibiotics. Pseudomonas can form a biofilm that pro- planning and implementing the treatment plan. tects the organism from antibiotics. A common antibiotic used to treat patients with chronic Pseudomonas infection is aerosol- Implementation ized tobramycin. It is given twice a day, every day, every other Acute Care month. Azithromycin used longer than 6 months decreases the Acute care for the patient with CF includes relief of bron- frequency of exacerbations, especially in those infected with choconstriction, airway obstruction, and airflow limitation. Pseudomonas. We also think it acts as an antiinflammatory. Interventions include aggressive CPT, antibiotics, and O2 638 SECTION 6 Problems of Oxygenation: Ventilation TABLE 31.2 NURSING ASSESSMENT responsibility for their care and life goals. One issue to discuss with the patient is sexuality. Delayed development of second- Cystic Fibrosis ary sex characteristics and irregular menses are common. The Subjective Data Objective Data issue of marrying and having children is complicated. Genetic Important Health Information Cardiovascular counseling is appropriate when the patient is considering hav- Health history: Recurrent respira- ↑ Heart rate ing children. Another concern is uncertainty surrounding the tory and sinus infections, persistent shortened life span of the parent with CF. cough with excess sputum produc- Eyes Other crises and life transitions that must be dealt with in the tion Scleral icterus young adult include identifying employment goals, developing Medications: Use of and compli- motivation, learning to cope with the treatment, and adjusting ance with bronchodilators, antibiot- General to the need for dependence if health fails. Disclosing the CF ics Restlessness, failure to thrive diagnosis to friends, potential spouses, and/or employers may pose significant emotional, social, and financial challenges. Functional Health Patterns GI Referral to counseling may help depending on the patient’s Health perception–health mainte- Protuberant abdomen; abdominal nance: Family history of CF, when distention; foul, fatty stools ability to cope with the condition and availability of support diagnosed, genetic testing networks. Nutritional-metabolic: Diet intoler- Respiratory CF imposes a significant emotional and financial burden on ances, voracious appetite, weight Sinus congestion, postnasal drip, the patient and family. In many situations, the cost of drugs, loss, heartburn persistent runny nose special equipment, and health care poses financial hardship. The Elimination: Intestinal gas. Large, Decreased breath sounds, adven- burden of living with a chronic disease at a young age can be frequent bowel movements, consti- titious breath sounds (crackles, emotionally overwhelming. There is a higher incidence of anx- pation wheezes) iety and depression among persons with CF than their unaf- Activity-exercise: Fatigue, ↓ exer- Sputum (thick, tenacious) fected peers.11 Issues related to costs of health care, burden of cise tolerance, amount and type of ↑ WOB, accessory muscle use, barrel self-care, career choices, fertility, and decreased life expectancy exercise. Dyspnea, cough, excess chest may lead to depression. Community resources are available to mucus or sputum production, cough- ing up blood, ACTs Skin help patients and caregivers. The Cystic Fibrosis Foundation Cognitive-perceptual: Abdominal Salty skin; clubbing; cyanosis (cir- can be a source of information and support. pain cumoral, nail bed) Sexuality-reproductive: Delayed men- arche, menstrual problem, infertility Possible Diagnostic Findings ASTHMA Coping–stress tolerance: Anxiety, Abnormal sweat chloride test, Asthma is a diverse disease characterized by bronchial hyper- depression, difficulty coping abnormal ABGs and pulmonary reactivity with reversible expiratory airflow limitation, either function tests spontaneously or with treatment. Signs and symptoms can be Abnormal chest x-ray, fecal fat variable. For example, there may be mild shortness of breath analysis and chest tightness with a minor asthma attack. A major asthma attack may include severe shortness of breath, accessory muscle therapy in severe disease. Measures to optimize nutrition are use, stridor, and severe hypoxemia. If left untreated, respiratory important. and/or cardiac arrest can occur. In severe cases, patients may be cared for in the intensive Asthma affects around 25 million adult Americans.12 It is care unit (ICU). Reasons for ICU admission include acute respi- a major public health concern. There are more than 2 million ratory insufficiency or failure and hemoptysis. The patient may emergency department (ED) visits, 10 million outpatient vis- need mechanical ventilation and hemodynamic monitoring. its, and 500,000 hospitalizations each year.13 The clinical course of asthma is unpredictable. It ranges from periods of adequate Ambulatory Care control to frequent attacks with poor control of symptoms. A focus on ACTs, treatment of infection with antibiotic ther- The mortality for asthma has decreased over the past 10 years. apy, nutrition support (including pancreatic enzymes), and psy- Unfortunately, more than 4000 people still die each year from chosocial support are important components of care. This may asthma.13 involve many members of the health care team, including phy- sician, nursing, dietary, pharmacy, physiotherapy, occupational Risk Factors and Triggers therapy, and psychology. Risk factors for asthma and triggers of asthma attacks are related We should encourage the patient to take part in aerobic exer- to the patient (e.g., genetic factors) or the environment (e.g., cise. It is effective in clearing the airways. Considerations when pollen) (Table 31.3 and Box 31.2). We discuss the most import- planning an exercise program include (1) meeting increased ant risk factors and triggers of asthma attacks here. nutrition demands of exercise, (2) observing for dehydration, (3) drinking large amounts of fluid, and (4) replacing salt Nose and Sinus Problems losses. Most patients have a history of allergic rhinitis. Treatment of As these persons continue into adulthood, you can help them allergic rhinitis usually improves asthma symptoms. Acute and achieve greater independence by allowing them to assume more chronic sinusitis, especially bacterial rhinosinusitis, may worsen  CHAPTER 31 Obstructive Pulmonary Diseases 639 Cigarette Smoke TABLE 31.3 Triggers of Asthma Attacks The Centers for Disease Control and Prevention (CDC) esti- Air Pollutants Aerosol sprays mates that 21% of persons with asthma smoke.14 In a person Cigarette smoke Exhaust fumes with asthma, smoking is associated with a faster decline of lung Oxidants function, increased severity, more frequent HCP visits, and a Perfumes decreased response to treatment. Passive smoking is the expo- Sulfur dioxides sure of non-smokers to cigarette smoke. It is also known as envi- Allergen Animal dander (e.g., dogs, cats, mice, guinea pigs) ronmental tobacco smoke (ETS) or secondhand smoke. It is also Inhalation Cockroaches a risk factor. House dust mite Molds Air Pollutants Pollens Various air pollutants, such as wood smoke or vehicle exhaust, Drugs Aspirin can trigger asthma attacks. In heavily industrialized or densely β-Adrenergic blockers populated areas, climate conditions often lead to concentrated NSAIDs Food Additives Beer, wine, dried fruit, shrimp, processed potatoes pollution in the atmosphere, especially with thermal inversions Monosodium glutamate and stagnant air masses. News sources often report ozone alert Sulfites (bisulfites and metabisulfites) days. Patients with breathing problems should minimize out- Tartrazine door activity during these times. Occupational Agriculture, farming Exposure Industrial chemicals and plastics Respiratory Tract Infections Laundry detergents Respiratory tract infections are often a major trigger of an acute Metal salts asthma attack. Acute URIs can decrease the diameter of the air- Paints, solvents ways and induce airway hyperresponsiveness. Viral-induced Wood and vegetable dusts changes in epithelial cells, the accumulation of cells that enhance Pulmonary Sinusitis, allergic rhinitis inflammation, and edema of airway walls contribute to altered Viral URI Other Factors Exercise and cold, dry air respiratory function. These changes may worsen asthma. GERD Hormones, menses Immune Response Stress People who have a lower incidence of asthma were exposed to certain infections early in life. They received fewer antibi- otics, were around other children (e.g., siblings, day care), or BOX 31.2 BIOLOGIC SEX CONSIDERATIONS lived in rural settings or with pets. The hygiene hypothesis sug- Asthma gests that in extremely clean environments, a newborn and child’s immune system will not fully mature and develop. In Men other words, exposure to different germs and various infec- Before puberty, asthma affects more boys. tions during infancy and childhood helps strengthen your Boys most likely to have less severe symptoms by late teen years. immune system. However, we know that this view does not tell Women the full story. The link between respiratory problems and the In adulthood, asthma affects more women. predisposition to develop certain conditions, like asthma, is Between 40 and 60 years of age, have a higher incidence and severity. complicated. Women who present to the emergency department are more likely to need hospitalization. Genetics Have a higher overall mortality. The genetics of asthma are complex. Many genes may be involved. They are likely responsible for different responses to triggers and asthma drugs. Atopy, the genetic predisposition asthma. Patients often have chronic sinus problems that cause to develop an allergic (immunoglobulin E [IgE]–mediated) inflammation of the mucous membranes and can trigger an response to common allergens, is a major risk factor. asthma attack. Sinusitis must be treated and large nasal polyps removed for the patient to have good control of their asthma. Gastroesophageal Reflux Disease GERD is more common in people with asthma. GERD can Allergens worsen asthma symptoms because reflux may trigger bronchoc- Allergens cause varying degrees of allergic reactions in suscepti- onstriction and cause aspiration. Asthma drugs can also worsen ble persons. Indoor and outdoor allergens, such as cockroaches, GERD symptoms. β2-Agonists used to treat asthma (especially furry animals, fungi, pollen, and molds, can trigger asthma when given orally) relax the lower esophageal sphincter. This attacks. However, we are not clear about their role in the devel- allows stomach contents to reflux into the esophagus and poten- opment of asthma. tially be aspirated. GERD treatment can improve nocturnal 640 SECTION 6 Problems of Oxygenation: Ventilation asthma control, improve quality of life, and prevent asthma anxiety. These emotions, and other psychologic factors, can lead symptoms in some patients. GERD is discussed in Chapter 46. to bronchoconstriction through stimulation of the cholinergic reflex pathways. Extreme behavioral expressions (e.g., crying, Drugs and Food Additives laughing, anger, fear) can lead to hyperventilation and hypocap- Some people with asthma have what we call the asthma triad: nia, which can cause airway narrowing and an asthma attack. nasal polyps, asthma, and sensitivity to aspirin and nonsteroi- dal antiinflammatory drugs (NSAIDs).15 Some persons with Pathophysiology asthma who use salicylic acid (e.g., aspirin) or NSAIDs can The main pathophysiologic process in asthma is persistent but develop wheezing within 2 hours. In addition, there is usually variable inflammation of the airways. Airflow is limited because profound rhinorrhea, congestion, and tearing. Angioedema can inflammation results in bronchoconstriction, airway hyper- occur. These patients must avoid salicylic acid and NSAIDs. responsiveness (hyperreactivity), and edema of the airways. Teach the patient the importance of reading labels. Salicylic acid Exposure to allergens or irritants starts the inflammatory cas- is in many OTC drugs and some foods, beverages, and flavor- cade (Fig. 31.3). A variety of inflammatory cells are involved, ings. Under the care of an allergist, daily administration of the including mast cells, macrophages, eosinophils, neutrophils, T drug can desensitize some patients. and B lymphocytes, and epithelial cells of the airways. β-Adrenergic blockers in oral form (e.g., metoprolol) or topi- As the inflammatory process begins, mast cells (found cal eye drops (e.g., timolol) may trigger an asthma attack because beneath the basement membrane of the bronchial wall) degran- they can cause bronchospasm. ACE inhibitors (e.g., lisinopril) ulate and release multiple inflammatory mediators. IgE anti- may cause a dry, hacking cough, making asthma symptoms bodies are linked to mast cells, and the allergen cross-links worse. Asthma attacks can occur after the use of sulfite-contain- the IgE. As a result, inflammatory mediators, such as leukot- ing preservatives found in topical ophthalmic solutions, IV corti- rienes, histamine, cytokines, prostaglandins, and nitric oxide, costeroids, and some inhaled bronchodilator solutions. are released (Fig. 31.4). Inflammatory mediators have effects on Food and drug additives that may trigger asthma include tar- the (1) blood vessels, causing vasodilation and increasing capil- trazine (yellow dye no. 5) and sulfiting agents. They are common lary permeability (runny nose); (2) nerve cells, causing itching; preservatives and sanitizing agents. Sulfiting agents are in fruits, (3) smooth muscle cells, causing bronchial spasms and airway beer, and wine. They are used in salad bars to protect vegetables narrowing; and (4) goblet cells, causing mucus production. As from oxidation. Food allergies triggering asthma reactions in a result, edema of airway mucosa, muscle spasm, and accumula- adults are rare. tion of secretions produce varying degrees of expiratory airflow obstruction (Fig. 31.5). Exercise This process is the early-phase response of asthma. Clinically, We call asthma that is induced or becomes worse during physi- it occurs within minutes after exposure to an allergen or irri- cal exertion exercise-induced asthma (EIA) or exercise-induced tant. It generally resolves within 1 to 2 hours. Symptoms can bronchoconstriction (EIB).16 Typically, symptoms of EIA or EIB recur 4 to 6 hours after the early response because of the influx are worse during activities in which there is exposure to cold, of inflammatory cells, which are set in motion by the initial dry air. For example, swimming in an indoor heated pool is less response. At this later time, the patient may develop symptoms likely to cause symptoms than skiing. again or worsening of symptoms. Varying degrees of airway obstruction may occur due to We call this the late-phase response. It occurs in about 50% changes in airway mucosa caused by hyperventilation during of people with asthma. In the late-phase response, the body exercise. Inhaling either cool or re-warmed air and airway activates more inflammatory cells, with continuing airway edema from capillary leakage in the airway wall contributes to inflammation. Bronchoconstriction with symptoms can last for this condition. EIB often occurs after less than 10 minutes of 24 hours or more. Corticosteroids are often effective in treat- vigorous exercise. It most often resolves within 60 minutes.16 ing inflammation in this late phase. Chronic inflammation may cause structural changes in the bronchial wall, known as remod- Occupational Factors eling. Over time, a progressive loss of lung function occurs that Occupational asthma is the most common job-related respi- therapy cannot fully reverse. Structural changes include fibrosis ratory problem. Occupational irritants cause a change in the of the subepithelium, hypertrophy of the smooth muscle of the responsiveness of the airways. The development of symptoms airways, mucus hypersecretion, continued inflammation, and may not occur until the patient has had months to years of angiogenesis. Remodeling and genetic factors may explain why exposure. These agents are diverse and include wood dusts, some persons have persistent asthma and limited response to laundry detergents, metal salts, chemicals, paints, solvents, and therapy. plastics. Often, people with occupational asthma give a history of arriving at work feeling well but gradually develop symptoms, Clinical Manifestations which may become progressively worse, by the end of the day. The characteristic manifestations of an asthma attack are wheez- ing, cough, dyspnea, and chest tightness after exposure to a risk Psychologic Factors factor or trigger. Normally, the bronchioles constrict during Many people report that symptoms worsen with stress. An expiration. However, in asthma, the airways become narrower asthma attack caused by any trigger can cause panic, stress, and than usual because of bronchospasm, edema, and mucus. As a  CHAPTER 31 Obstructive Pulmonary Diseases 641 PATHOPHYSIOLOGY MAP Triggers Infection Allergens Exercise Irritants Immune activation Mast cell degranulation (IL-4, IgE production) Inflammatory mediators Vasodilation Cellular infiltration Increased capillary permeability (neutrophils, lymphocytes, eosinophils) Bronchospasm Vascular congestion Edema formation Neuropeptides released Mucus secretion with autonomic Impaired mucociliary function nervous system effects Thickening of airway walls Bronchial hyperresponsiveness Airway Airway obstruction remodeling Fig. 31.3 Pathophysiology of asthma. IL, Interleukin; IgE, immunoglobulin E. (Adapted from McCance KL, Huether SE: Pathophysiology: the biologic basis for disease in adults and children, ed 7, St. Louis, 2015, Elsevier.) Allergens B lymphocyte Mast cell IgE Smooth muscle antibodies Plasma cells Swollen mucosa Allergens Muscle Mucus in spasm Histamine Inflammatory mediators Mast cell Mucus A Mucus B Fig. 31.4 Allergic asthma is triggered when an allergen cross-links Fig. 31.5 Factors causing expiratory obstruction in asthma. (A) Cross immunoglobulin E (IgE) receptors on mast cells, which are then acti- section of a bronchiole occluded by muscle spasm, edema of mucosa, vated to release histamine and other inflammatory mediators (early- and mucus in the lumen. (B) Longitudinal section of a bronchiole. phase response). A late-phase response may occur due to further (Redrawn from Price SA, Wilson SM: Pathophysiology: clinical concepts inflammation and edema. of disease processes, ed 6, St. Louis, 2003, Mosby.) 642 SECTION 6 Problems of Oxygenation: Ventilation result, it takes longer for the air to move out of the bronchioles Asthma Classifications (airflow obstruction). This causes the characteristic wheezing, Several sets of national and international guidelines exist for air trapping, and hyperinflation of the lungs. As a result, expira- classifying asthma. Each guideline has a slightly different per- tion may be prolonged. spective about asthma and how to classify the severity of an The most common finding during an acute asthma event is asthma attack. The severity of an asthma attack is used to guide wheezing. For wheezing to occur, the patient must be able to treatment decisions. All the guidelines focus on assessing the move enough air to make the sound. Wheezing usually occurs severity of the disease at diagnosis and initial treatment and first on exhalation. As asthma progresses, the patient may periodic monitoring to control the disease. All groups endorse wheeze during inspiration and expiration. the use of “stepping up” or “stepping down” medications during However, wheezing is an unreliable sign to gauge the severity and after an acute asthma attack and having an “action plan” to of an attack. Many patients with minor attacks wheeze loudly. help prevent future attacks. They promote patient teaching and Others with severe attacks do not wheeze. The patient with a adherence to the treatment plan. severe asthma attack may wheeze only during forced expiration The Global Initiative for Asthma (GINA) guidelines are the or have no audible wheezing because of the marked reduction most widely recognized evidence-based strategies for addressing in airflow. asthma worldwide.17 Many HCPs use the 2012 National Heart, Decreased or absent breath sounds may signal a significant Lung, and Blood Institute (NIH) guidelines for classifying asthma decrease in air movement resulting from exhaustion and an severity (Table 31.4). They describe asthma as intermittent, mild inability to generate enough muscle force to breathe. Severely persistent, moderate persistent, or severe persistent.18 decreased breath sounds, often referred to as the “silent chest,” are an ominous sign. This often means severe airway obstruc- Complications tion and impending acute respiratory failure (ARF). Asthma attacks range from minor interferences in breathing to life-threatening episodes. Depending on a person’s physiologic response, asthma can rapidly progress from normal breathing SAFETY ALERT to an acute, severe attack or a life-threatening medical emer- Silent Chest gency within a few minutes. In some people, airway remodeling predisposes them to If the patient with asthma has been wheezing, followed by a sudden respiratory-related issues. As bronchi become thicker and less absence of a wheeze (e.g., silent chest) and the patient struggling to elastic and airways become narrower, this may increase WOB. breathe, this is a life-threatening emergency. Compromised lung function may lead to a state of continuous Call for help immediately. symptoms and chronic debilitation, including fatigue, head- The patient may need mechanical ventilation. aches, and lack of activity. Asthma predisposes patients to pneu- monia, worse episodes of the flu, and in rare situations, tension Hyperventilation occurs during an asthma attack as lung pneumothorax. ARF and status asthmaticus are the most severe receptors respond to the increase in lung volume from trapped complications of an asthma attack. air and airflow limitation. Decreased alveolar perfusion and ventilation and increased alveolar gas pressure lead to V/Q Status Asthmaticus mismatch. The patient may be hypoxemic early with decreased A life-threatening medical emergency, status asthmaticus is the PaCO2 and increased pH (respiratory alkalosis) because they are most extreme form of an acute asthma attack. It is characterized hyperventilating. As the airflow limitation worsens with subse- by hypoxia, hypercapnia, and ARF. The patient is unresponsive quent air trapping, the patient works much harder to breathe. to treatment with bronchodilators and corticosteroids. They The PaCO2 normalizes as the patient tires but then increases to may have chest tightness, a severely marked increase in short- produce respiratory acidosis. A rising PaCO2 level and decreas- ness of breath, or suddenly be unable to speak. Hypotension, ing pH is an ominous sign of ARF. bradycardia, and respiratory and/or cardiac arrest may occur if In some patients with asthma, cough is the only symptom. we do not recognize that the patient is getting worse. This is termed cough variant asthma. Bronchospasm is not pres- IV magnesium sulfate has a bronchodilator effect. It may be ent or may not be severe enough to cause airflow obstruction or given to patients with a very low FEV1 or peak flow (less than wheezing, but it can increase bronchial tone and cause irritation 40% of predicted or personal best) or those who do not respond with stimulation of the cough receptors. The cough may be non- to initial treatment. IV magnesium should not delay the need productive or with secretions. Sputum may be thick, tenacious, for intubation of the patient who is with status asthmaticus. and gelatinous, making removal difficult. The patient needs immediate mechanical ventilation. Hemodynamic monitoring is critical. Continuous analgesic infu- CHECK YOUR PRACTICE sions (e.g., ketamine, morphine) and sedation with drugs such as propofol help decrease WOB and promote synchrony with A patient with asthma is in the ED with acute respiratory distress. He has been the ventilator. In some circumstances, neuromuscular blocking receiving therapy and seems to be responding. You suddenly notice he is no agents (e.g., rocuronium) may be used. Inhaled anesthetics, such longer wheezing. as isoflurane, are an option for those not responding to conven- Should you consider this finding a sign that he is doing better? tional treatment. These patients are cared for in the ICU.  CHAPTER 31 Obstructive Pulmonary Diseases 643 TABLE 31.4 Diagnostic Criteria Asthma Severity Classification ASTHMA SEVERITY PERSISTENT Components of Severity Intermittent Mild Moderate Severe Impairment Symptoms >2 days/week >2 days/week, not daily Daily Continuous Flare-ups Brief, vary in intensity Noticeable More frequent Daily Interference with ADLs Usually none May affect ADLs Some limitations, may affect ADLs Often restricts ADLs Nighttime awakenings >2/month 3–4/month >1/week, but not nightly Every night (7/week) FEV1 >80% FEV1 >80% predicted; FEV1 60%–80% predicted; FEV1 5% attacks); FEV1/FVC normal Risk Consider severity and interval since last attack. Frequency and severity may fluctuate over time. Relative annual risk for exacerbation may be related to FEV1. Recommended Step for Initiating Treatment Step 1 Step 2 Step 3 Step 4 or 5 Reevaluate asthma control in 2–6 weeks and adjust therapy as needed Guidelines for Using Table This stepwise approach is meant to help guide the HCP. It is not a substitute for patient assessment and clinical decision making. Assign patients to the most severe step in which any feature occurs. Clinical features may overlap across steps. Determine level of severity by assessing impairment and risk. Assess impairment by recall of previous 2 to 4 weeks spirometry results. A person’s classification should change over time with treatment. After treatment, the focus switches to the level of control, not the classification of severity. aPercent predicted values for FEV or ratio of FEV /FVC. Normal FEV /FVC: 8–19 years, 85%; 20–39 years, 80%; 40–59 years, 75%; 60–80 years, 70%. 1 1 1 Source: Adapted from National Asthma Education and Prevention Program, National Heart, Lung, and Blood Institute: Expert Panel report 3: guide- lines for the diagnosis and management of asthma, NIH pub no 08-4051, Bethesda, MD, 2007, National Institutes of Health. show an obstructive pattern including a decrease in forced vital Diagnostic Studies capacity (FVC), PEFR, FEV1, and FEV1/FVC ratio. Tests used to diagnose asthma are shown in Table 31.5. In gen- When a spirometry test is scheduled, the patient must stop eral, the HCP should consider a diagnosis of asthma if various taking any bronchodilator drugs for 6 to 12 hours before the indicators (e.g., manifestations, health history, peak flow vari- test. Spirometry can be done before and after the administra- ability, spirometry) are positive. tion of a bronchodilator to assess the degree of the response. Under-diagnosis of asthma is common. The history is This helps determine the reversibility of airway obstruction, important to determine if a person has had similar attacks, which is important in diagnosing asthma. A positive (favorable) which are often precipitated by a known trigger. Because wheez- response to the bronchodilator is an increase of more than 200 ing and cough occur with a variety of disorders (e.g., COPD, mL and an increase of more than 12% between pre-administra- GERD, vocal cord problems, heart failure [HF]), it is important tion and post-administration values.19 to determine if asthma or another disease is causing these prob- A hand-held, point-of-care device to measure fractional lems. Table 31.6 shows a comparison of asthma and COPD. exhaled nitric oxide (FeNO) can help determine asthma The peak expiratory flow rate (PEFR) measured by the peak severity. FeNO levels are increased in people with asthma flow meter (at home or in a health care setting) is a test of lung from eosinophilic-induced airway inflammation. FeNO can function. PEFR measures the maximum rate of airflow after a gauge loss of asthma control and attacks, adherence to ther- forceful exhalation. When monitored routinely, PEFR measure- apy, or if more inhaled or oral antiinflammatory medication ments can provide a baseline of the patient’s health status. PEFR is needed.20 can help predict an asthma attack or monitor the severity of dis- Increased serum eosinophil counts and IgE levels suggest an ease. Test results depend on the patient’s age, gender, and height. allergen or genetic link with asthma. Allergy skin testing can Since peak flow meters vary, PEFR should be compared with the assess sensitivity to specific allergens. A positive skin test does patient’s previous best measurements using their meter. not necessarily mean that the allergen is causing the asthma Spirometry is usually normal between asthma attacks if the attack. On the other hand, a negative allergy test does not mean patient has no other underlying lung disease. The patient may that the asthma event is not allergy related. 644 SECTION 6 Problems of Oxygenation: Ventilation TABLE 31.5 Interprofessional Care TABLE 31.6 Comparison of Asthma and Asthma COPDa Diagnostic Assessment Asthma COPD History and physical assessment Clinical Features Spirometry, including response to bronchodilator therapy Age Usually 10–20 pack-years) Pulse oximetry Health and Presence of allergy, Infrequent allergies. May have Allergy skin testing (if indicated) family rhinitis, eczema. Family exposure to environment Blood level of eosinophils and IgE (if indicated) history history of asthma pollutants. With AATD, family history of lung or liver disease Management without smoking Identify and avoid or eliminate triggers Clinical Intermittent, vary day to Slowly progressive, persistent. Patient and caregiver teaching symptoms day. May be worse at Worsening of condition over Drug therapy (Tables 31.8 and 31.9 and Figs. 31.6 and 31.7) night or early morning time Asthma action plan (Fig. 31.11) Dyspnea Absent except in attacks or Dyspnea during exercise and/ Desensitization (immunotherapy) if indicated poor control or ADL’s Assess for control (e.g., Asthma Control Test [ACT]) Sputum Infrequent Often Disease Often stable (with varying Progressive worsening (with Acute Attacks course number and severity of increasingly more frequent Inhaled corticosteroids (alternatives: IV or oral corticosteroids) attacks each year) exacerbations) Inhaled β2-adrenergic agonists Inhaled anticholinergics Diagnostic Study Results Position upright (semi to high-Fowler’s) ABGs Normal between or during Between exacerbations in O2 by nasal cannula or mask attacks advanced COPD SpO2 monitoring Often low-normal pH and ABGs PaO2 IV fluids High-normal PaCO2 with IV magnesium normal to high HCO3− (may As required: Mechanical ventilation be fully or partially compen- sated respiratory acidosis) pH ↑ Early in attack, then ↓ Normal →↓ A chest x-ray in an asymptomatic patient with asthma is if prolonged or severe usually normal. Chest x-rays are usually not done unless other attack manifestations, such as fever or chills, are present. It can show if PaO2 ↓ N→↓ something else is causing symptoms similar to those of asthma PaCO2 ↓ Early in attack, then ↑ if N→↑ (e.g., pneumonia, foreign body in the airway). A sputum spec- prolonged or severe attack Chest x-ray May be normal or Hyperinflation, flattened imen for culture may be done to rule out bacterial infection, show some degree of diaphragm. May have cardiac especially if the patient has purulent sputum, a history of URI, a hyperinflation enlargement fever, or an increased white blood cell (WBC) count. Lung volumes Often normal Usually not normal as disease progresses Interprofessional Care Total lung ↑ ↑ The goal of care is to achieve and maintain control of the capacity asthma. Guidelines provide direction about medications (based Residual ↑ ↑ on steps) the patient needs (Figs. 31.6 and 31.7). The HCP will volume step up medication therapy as asthma symptoms worsen and FEV1 ↓→ N ↓ step down the medication as the patient achieves control (Table FEV1/FVC N→↓ ↓ (2 days/week Throughout the day Nighttime awakenings ≤2/months 1–3/weeks ≥4/weeks Interference with normal activity None Some limitation Extremely limited FEV1 or PEFR >80% predicted/personal best 60%–80% predicted/personal best