NSG210 Hinkle Ch. 20: Management of Patients With Chronic Pulmonary Disease

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 20, pp. 602-646 (textbooks/HINKLE_MS_CH20.pdf, also in textbooks/exam01/). Week 02 reading; on Exam 1 (COPD 6 and asthma 5 of 34 med-surg questions). Also reassigned in Week 09 for chest tubes and lung cancer, but that content is in Ch. 19. See also nsg210-week-02-summary.

Learning Outcomes

1. Describe pathophysiology, manifestations, and management of COPD, bronchiectasis, asthma, and cystic fibrosis.
2. Discuss COPD risk factors and nursing interventions to minimize them.
3. Use the nursing process for the patient with COPD.
4. Develop an education plan for COPD.
5. Discuss nursing management and teaching for oxygen therapy.
6. Describe asthma self-management.

Key terms:

• Air trapping: incomplete emptying of alveoli on expiration
• Alpha1-antitrypsin deficiency: genetic lack of a lung-protective enzyme; panacinar emphysema even without smoking
• Chronic bronchitis: cough and sputum for at least 3 months in each of 2 consecutive years
• Emphysema: destruction of walls of overdistended alveoli
• Bronchiectasis: chronic irreversible dilation of bronchi and bronchioles
• Polycythemia: increased RBCs to raise oxygen-carrying capacity
• Desaturate: sudden drop in hemoglobin oxygen saturation
• FiO2: fraction of inspired oxygen (1.0 = 100%)
• pMDI, DPI, SVN: pressurized metered-dose inhaler, dry-powder inhaler, small-volume nebulizer

I. Chronic Obstructive Pulmonary Disease (COPD)

A. Definition and epidemiology

• Preventable, treatable, slowly progressive airflow obstruction that is not fully reversible
• Includes emphysema and chronic bronchitis (most patients have features of both)
• Asthma is a separate disorder (reversible inflammation) but can coexist
• Fourth leading cause of death overall; third for age 65 and older
• Over 16 million Americans diagnosed

B. Pathophysiology

• Chronic inflammation from noxious particles or gases throughout airways, parenchyma, pulmonary vessels
• Proximal airways: more goblet cells, enlarged submucosal glands leads to mucus hypersecretion
• Peripheral airways: wall thickening, peribronchial fibrosis, exudate, narrowing (scarring over time)
• Parenchyma: alveolar wall destruction, loss of elastic recoil
• Vessels: thickening and smooth muscle hypertrophy leads to pulmonary hypertension
• Proteinase-antiproteinase imbalance (alpha1-antitrypsin deficiency)

Chronic bronchitis:

• Irritants cause inflammation and mucus hypersecretion; more goblet cells; mucus plugging reduces ciliary function; thick bronchial walls
• Damaged alveolar macrophages leads to infection susceptibility; exacerbations most common in winter

Emphysema:

• Alveolar wall destruction reduces surface area leads to increased dead space, hypoxemia; later hypercapnia and respiratory acidosis
• Reduced capillary bed increases pulmonary resistance leads to pulmonary hypertension leads to cor pulmonale (right-sided HF: dependent edema, JVD, liver pain)
• Panlobular (panacinar): whole lobule destroyed; hyperinflated chest, marked dyspnea on exertion, weight loss; expiration becomes active
• Centrilobular (centroacinar): center of lobule; V/Q mismatch, chronic hypoxemia, hypercapnia, polycythemia, right HF, central cyanosis, edema

C. Risk factors (Chart 20-1)

• Tobacco smoke causes 80-90% of COPD; dose-response with pack-years; also pipes, cigars, marijuana, secondhand smoke
• Smoking depresses scavenger cells and cilia, irritates goblet cells; carbon monoxide forms carboxyhemoglobin
• E-cigarettes and vaping (ENDS) may cause similar lung changes
• Occupational dusts and chemicals, indoor and outdoor air pollution
• Alpha1-antitrypsin deficiency: about 2% of COPD; rapid emphysema in young people even without smoking; screen symptomatic adults, especially under 45 or with family history; augmentation therapy available (costly, ongoing)
• Age; low socioeconomic status (exposures)

D. Clinical manifestations

• Three primary symptoms: chronic cough, sputum production, dyspnea (progressive, worse with exercise, later at rest)
• Cough and sputum often precede airflow limitation by years
• Weight loss (dyspnea interferes with eating; work of breathing burns energy)
• Accessory muscle use
• Barrel chest (emphysema): ribs fixed in inspiratory position, increased AP diameter
• Leans forward, supraclavicular retraction, shoulders heave on inspiration
• Systemic: muscle wasting, metabolic disturbance, depression, diabetes

E. Assessment and diagnostics (Chart 20-2)

• History: exposures, smoking and vaping, family history, symptom pattern, exercise tolerance, triggers, exacerbations, comorbidities, support
• Physical: position, RR and HR, can patient finish a sentence, abdominal muscle use, accessory muscles, prolonged expiration, central cyanosis, JVD, edema, cough and sputum, clubbing, breath sounds, cognition
• Spirometry confirms obstruction: FEV1/FVC under 70%; repeat after bronchodilator to test reversibility
• ABG baseline in advanced COPD; chest x-ray to exclude other diagnoses
• Differential: asthma (main), HF, bronchiectasis, TB

GOLD grades (Table 20-1), all with FEV1/FVC under 70%:

• Grade I mild: FEV1 80% predicted or more
• Grade II moderate: FEV1 50-79%
• Grade III severe: FEV1 30-49%
• Grade IV very severe: FEV1 under 30%

F. Complications

• Respiratory insufficiency and failure (chronic or acute with bronchospasm or pneumonia)
• Pneumonia, chronic atelectasis, pneumothorax (bullae rupture), pulmonary arterial hypertension (cor pulmonale)

II. COPD Medical Management

A. Risk reduction - smoking cessation

• Single most cost-effective intervention to prevent COPD and stop progression
• Personalize the risk, set a quit date, refer to a program, follow up within 3-5 days of quit date, analyze relapses, emphasize successes
• Nicotine replacement (gum, inhaler, nasal spray, patch, lozenge) is first-line; bupropion SR, nortriptyline, varenicline; clonidine (side effects limit)
• Pharmacotherapy not appropriate for light smokers (under 10 cigarettes/day), pregnant women, adolescents, or with contraindications

B. Oxygen therapy - general principles

• Room air 21% oxygen; oxygen is a medication requiring a prescription except in emergencies
• Indicators of need: change in respiratory rate or pattern
• Hypoxemia signs: mental status changes (impaired judgment, agitation, confusion, lethargy, coma), dyspnea, increased BP, HR changes, arrhythmias, central cyanosis (late), diaphoresis, cool extremities
• Rapid hypoxia resembles alcohol intoxication; chronic hypoxia causes fatigue, drowsiness, apathy, delayed reactions
• Goal: return PaO2 to the patient’s baseline (60-95 mm Hg); SaO2 80-98%; more oxygen adds little and can be toxic
• Oxygen toxicity: high concentration for more than 24 hours; free radicals damage alveolar-capillary membrane, ARDS-like picture; signs - substernal discomfort, paresthesias, dyspnea, restlessness, fatigue, refractory hypoxemia, atelectasis, infiltrates; prevent with lowest effective FiO2
• Absorption atelectasis: FiO2 over 50% in sedated patients with small tidal volumes washes out nitrogen and alveoli collapse
• Fire hazard: “No Smoking” signs; change tubing per policy (infection)
• Older adults: weaker muscles, fewer cilia, stiffer chest wall; aspiration and infection risk

C. Oxygen delivery devices (Table 20-2)

Low-flow (variable FiO2; patient also breathes room air):

• Nasal cannula: 1-2 L = 24-28%; 3-5 L = 32-40%; 6 L = 44%; can eat and talk; over 4 L/min dries mucosa and causes air swallowing
• Reservoir cannula: stores oxygen; must exhale through the nose
• Nasal (oropharyngeal) catheter: 1-6 L = 24-44%; change every 8 hours, alternate nostrils
• Simple mask: 5-8 L = 40-60%; must remove to eat
• Partial rebreather: 8-11 L = 50-75%; reservoir bag must stay inflated
• Nonrebreather: 10-15 L = 80-95%; one-way valves; keep bag from collapsing on inspiration

High-flow (fixed FiO2, independent of breathing pattern):

• Venturi mask: 4-6 L = 24-28%; 6-8 L = 30-40%; most reliable and precise noninvasive method; used primarily in COPD to avoid suppressing hypoxic drive; use nasal cannula while eating
• Aerosol mask, tracheostomy collar, T-piece, face tent: 8-10 L, 28-100%, good humidity
• Transtracheal catheter: surgically placed; lower flows needed; less visible
• Oxygen-conserving (pulse dose) devices save 50-75% of oxygen
• Concept Mastery Alert: low-flow systems can give high but imprecise concentrations (nonrebreather); the Venturi mask is high flow but delivers precise low concentrations
• Humidify at high flow rates; concentrators deliver 1-10 L/min, about 40% FiO2

D. Oxygen therapy in COPD

• Goal: resting PaO2 at least 60 mm Hg, SaO2 at least 90%
• Long-term oxygen (more than 15 hours/day) improves survival, quality of life, pulmonary pressures, dyspnea
• Indications for long-term oxygen: PaO2 55 mm Hg or less or SaO2 88% or less; or evidence of tissue hypoxia (cor pulmonale, secondary polycythemia, right HF edema, impaired mentation)
• Hypoxemic while awake usually means hypoxemic in sleep: prescribe continuous 24-hour use
• Intermittent oxygen for desaturation only with activity, exercise, or sleep
• Too much oxygen causes CO2 retention (depressed drive and V/Q mismatch); pulse oximetry does not measure PaCO2; SaO2 88% or less warrants ABG
• Usually low flow 1-2 L/min; titrate to lowest flow that keeps SpO2 at 90%
• Watch for other drive depressants: neurologic impairment, electrolyte problems, opioids, sedatives
• Smoking may make pulse oximetry falsely high (carbon monoxide)
• Quality and Safety Nursing Alert: goal is acceptable oxygenation without a fall in pH (worsening hypercapnia)

E. Pharmacologic therapy

By GOLD grade:

• Grade I: short-acting bronchodilator
• Grade II-III: short-acting plus one or more long-acting bronchodilators
• Grade III-IV: long-acting bronchodilators and/or inhaled corticosteroids for repeated exacerbations

Bronchodilators:

• Central to symptom management; do not change disease decline
• Relieve bronchospasm, widen airways, improve emptying; can be used before activity (eating, walking)
• Classes: SABA (albuterol, levalbuterol; 4-6 hours), LABA (salmeterol, formoterol, arformoterol, indacaterol, olodaterol; 12+ hours), SAMA (ipratropium), LAMA (tiotropium, umeclidinium), SABA/SAMA combination (albuterol/ipratropium)
• Fixed-dose LABA/LAMA combinations are now the foundation of COPD treatment: synergy, lower doses, fewer devices
• Side effects: tachycardia, arrhythmias, CNS excitation, nausea, vomiting

Inhaler devices (Table 20-3):

• pMDI: slow deep inhalation (3-5 seconds) with actuation, then 10-second breath-hold; requires coordination; 50-80% deposits in oropharynx
• Breath-actuated pMDI: for poor coordination
• Spacer or valved holding chamber: actuate once per inhalation; improves lung delivery; rinse monthly with mild detergent
• DPI: rapid deep inhalation (1-2 seconds); no coordination needed but requires strong inspiratory flow (may fail in severe COPD); do not exhale into device
• SVN (nebulizer): slow tidal breathing; easiest to use, needs power; mask reduces delivery by 50%; clean to prevent infection

Corticosteroids:

• Improve symptoms but do not slow lung function decline
• Short oral trial possible; long-term oral steroids not recommended (steroid myopathy)
• ICS often combined with LABA: budesonide/formoterol, fluticasone/salmeterol, fluticasone furoate/vilanterol, mometasone/formoterol

Other: alpha1-antitrypsin augmentation, antibiotics, mucolytics, antitussives, vasodilators, opioids; influenza and pneumococcal vaccines.

F. Exacerbations

• Acute worsening beyond daily variation requiring medication change; increased dyspnea from hyperinflation and air trapping
• Most often viral (rhinovirus); also bacterial and environmental
• Roflumilast (oral PDE4 inhibitor, once daily) reduces exacerbations in severe COPD with chronic bronchitis
• Treatment: optimize bronchodilators (first line), corticosteroids (oral or IV), antibiotics if all three cardinal symptoms - increased dyspnea, increased sputum volume, purulent sputum; oxygen; ventilatory support
• ED: oxygen first, assess for life threat, short-acting bronchodilator
• Hospitalize for: marked increase in symptoms, severe underlying COPD, new signs (accessory muscles, paradoxical chest movement, new cyanosis, edema, right HF, decreased alertness), failure to respond, older age, poor home support
• Outcome worse with respiratory acidosis, comorbidities, need for ventilation

G. Surgical management

• Bullectomy: removes large bullae compressing lung
• Lung volume reduction surgery: palliative for grade IV emphysema; reduces hyperinflation, improves recoil and diaphragm mechanics
• Bronchoscopic valves and coils (investigational)
• Lung transplantation for select patients

H. Pulmonary rehabilitation

• Holistic, cost-effective; improves exercise capacity, breathlessness, quality of life; fewer hospitalizations; less anxiety and depression
• Assessment, education, smoking cessation, reconditioning, nutrition, skills training, psychological support, breathing exercises
• Best for moderate or severe COPD; optimal programs 6-8 weeks

I. Nutrition and palliative care

• Weight loss is common; assess caloric needs, meal planning, supplements, monitor weight
• Palliative care for advanced COPD: dyspnea, anxiety, panic, depression, spiritual support, end-of-life planning

III. COPD Nursing Management

A. Plan of care highlights (Chart 20-4)

• Smoking cessation: evaluate habits, educate, refer
• Avoid occupational and environmental pollutants; monitor air quality alerts
• Bronchodilators: inhalation preferred; give treatments before meals; check technique
• Oxygen: low flow 1-2 L/min; report restlessness, anxiety, somnolence, cyanosis, tachycardia; hold ABG site 5 minutes; no smoking
• Airway clearance: hydration (caution with HF), diaphragmatic breathing and coughing, postural drainage, avoid irritants (smoke, aerosols, temperature extremes, fumes)
• Report early infection: increased sputum, change in color or thickness, increased dyspnea or chest tightness or fatigue, increased cough, fever or chills
• Vaccines: influenza and pneumococcal; avoid crowds in flu season
• Breathing pattern: diaphragmatic and pursed-lip breathing; inspiratory muscle trainer; alternate activity and rest
• Self-care: coordinate breathing with walking and bending; energy conservation
• Activity: graded exercise (treadmill, bicycle, walking); portable oxygen during exercise; upper and lower body
• Coping: realistic goals, relaxation, pulmonary rehab
• Complications: atelectasis (tachypnea, diminished breath sounds), pneumothorax (sudden dyspnea, tachycardia, pleuritic pain, tracheal deviation away from affected side, absent breath sounds, decreased fremitus - prepare for chest tube), respiratory failure, pulmonary hypertension (right HF signs)

B. Airway clearance techniques

• Directed cough: slow maximal inspiration, hold several seconds, 2-3 coughs
• Huff cough: 1-2 forced exhalations from low to medium lung volume with glottis open
• Postural drainage: gravity drains secretions; lower lobes drain head down, upper lobes head up; 2-4 times daily before meals and at bedtime; bronchodilator or mucolytic first; lower lobes first, then upper; 10-15 minutes per position; inhale through nose, exhale through pursed lips; auscultate before and after; may need oxygen
• Chest percussion: cupped hands over a towel; with vibration 3-5 minutes per position; avoid tubes, sternum, spine, liver, kidneys, spleen, breasts; caution in older adults (osteoporosis, rib fracture)
• Vibration: compression and tremor during exhalation; cough after 3-4 vibrations
• HFCWO vest: compresses chest 8-18 times per second; any position; as effective as manual CPT
• Flutter valve: oscillating steel ball; useful in CF
• Stop CPT for increased pain, dyspnea, weakness, lightheadedness, or hemoptysis

C. Breathing retraining (Chart 20-5)

• Diaphragmatic breathing: hand on abdomen and chest; inhale through nose letting abdomen protrude; exhale through pursed lips tightening abdomen; 1 minute then rest 2 minutes; build to 5 minutes several times a day
• Pursed-lip breathing: inhale through nose to count of 3 (“smell a rose”); exhale through pursed lips to count of 7 (“blow out the candle”); prolongs exhalation, prevents small airway collapse, reduces air trapping and panic
• Walking: inhale for 2 steps, exhale for 4-5 steps

D. Activity, coping, complications

• Tolerance worst in the morning (secretions pooled overnight); arms above chest level cause fatigue; plan care after patient has been up an hour
• Exercise training benefits all grades
• Anxiety, depression, role change, sexual dysfunction; support caregivers
• Monitor for cognitive changes, increasing dyspnea, tachypnea, tachycardia (impending respiratory failure)
• Minor infections can be life threatening; viral infections often followed by bacterial pneumonia (S. pneumoniae, M. catarrhalis, H. influenzae)
• Sudden dyspnea: assess for pneumothorax (chest symmetry, breath sounds, SpO2)

E. Teaching and home care

• Avoid heat (raises oxygen demand) and cold (bronchospasm); avoid pollutants, aerosol sprays, talcum; high altitude worsens hypoxemia
• Moderate activity, rest, sleep; avoid emotional stress
• pMDI technique (Chart 20-6): shake, exhale fully, open-mouth (2 finger widths away) or closed-mouth technique, actuate and inhale slowly, hold 10 seconds, wait 1 minute between puffs, rinse mouth after steroid inhalers
• Home oxygen safety (Chart 20-7): no smoking; “No Smoking - Oxygen in Use” signs; notify fire department and electric company; no flammables; keep 15 feet from open flame and 5 feet from TV, radio, appliances; out of direct sunlight; tank on floor behind front seat in car; notify airline at least 2 weeks ahead; humidify (except portable)
• Oxygen is not addictive; do not change flow arbitrarily
• Follow-up with provider every 6 months; ABG at least yearly
• End-of-life discussions

IV. Bronchiectasis

• Chronic irreversible dilation of bronchi and bronchioles from destroyed muscle and elastic tissue
• Causes: recurrent infections, CF, rheumatic disease, ciliary dysfunction, TB, immune deficiency; often comorbid with COPD
• Pathophysiology: damaged walls, thick sputum obstructs bronchi; saccular dilations act like abscesses; usually localized, most often lower lobes; atelectasis, fibrosis, V/Q mismatch, hypoxemia
• Manifestations: chronic cough with copious purulent sputum, hemoptysis, clubbing, repeated infections
• Diagnosis: chronic productive cough with sputum negative for TB; CT shows bronchial dilation
• Treatment: CPT and postural drainage essential; bronchoscopy to remove secretions; smoking cessation; antibiotics (cornerstone; pathogens H. influenzae, M. catarrhalis, S. aureus, P. aeruginosa); low-dose macrolide if 2 or more exacerbations a year; vaccines; mucolytics, hypertonic saline, bronchodilators before treatments; hydration
• Surgery (segmental resection, lobectomy) if localized; preop goal is a dry tracheobronchial tree
• Nursing: secretion clearance, postural drainage teaching, avoid infected people, energy conservation, nutrition (copious mucus decreases appetite)

V. Asthma

A. Definition and epidemiology

• Heterogeneous disease of chronic airway inflammation causing hyperresponsiveness, mucosal edema, mucus production
• Symptoms: cough, chest tightness, wheezing, dyspnea; vary over time
• About 19 million US adults; nearly 10% of ED visits
• Largely reversible, unlike COPD; disparities in African American and Hispanic urban populations
• Asthma-COPD overlap in smokers

B. Triggers

• Allergy is the strongest predisposing factor
• Allergens: seasonal (grass, tree, weed pollens) or perennial (mold, dust, roaches, animal dander)
• Triggers: irritants (pollution, cold, heat, weather changes, strong odors, perfume, smoke, occupational exposures), foods (shellfish, nuts), exercise, stress, hormones, medications (aspirin, beta-blockers, NSAIDs), viral infections, GERD, latex

C. Pathophysiology

• Reversible diffuse airway inflammation; bronchoconstriction, airway edema, hyperresponsiveness, remodeling
• Mast cells, macrophages, T lymphocytes, neutrophils, eosinophils
• Mast cell mediators: histamine, bradykinin, prostanoids, cytokines, leukotrienes
• Acute bronchoconstriction from IgE-dependent mediator release
• Beta-2 stimulation raises cyclic AMP, inhibiting mediators and causing bronchodilation
• Persistent asthma: edema, mucus hypersecretion, mucus plugs, remodeling (may become irreversible)

D. Clinical manifestations

• Cough (may be the only symptom), dyspnea, wheezing
• Often at night or early morning
• Wheezing first on expiration, then inspiration; chest tightness; prolonged effortful expiration
• Progression: diaphoresis, tachycardia, widened pulse pressure, hypoxemia, central cyanosis (late)
• Exercise-induced: symptoms during exercise, none at night, “choking” sensation

E. Assessment and diagnosis

• Episodic obstruction that is at least partially reversible; other causes excluded
• Control questions: night or early-morning symptoms; needing rescue inhaler more than usual; unscheduled care; activity limitation
• Eosinophilia in sputum and blood; elevated IgE with allergy
• Early ABG: hypoxemia with hypocapnia and respiratory alkalosis; PaCO2 rises as patient tires
• Quality and Safety Nursing Alert: a normal PaCO2 during an asthma attack may signal impending respiratory failure
• FEV1 and FVC drop during exacerbation and improve with bronchodilator; normal between attacks
• Occupational asthma: 5-20% of new adult cases; remove exposure
• Severity: impairment (night awakenings, SABA use, missed work or school, activity, quality of life, spirometry) and risk (exacerbations, ED visits and hospitalizations in past year, not using ICS, smoking, psychosocial factors)

F. Prevention and complications

• Allergy testing; avoid identified triggers
• Complications: status asthmaticus, respiratory failure, pneumonia, atelectasis
• Patients often dehydrated (diaphoresis, hyperventilation) - give fluids

G. Pharmacologic therapy

Quick-relief (Table 20-5):

• SABAs (albuterol, levalbuterol): drug of choice for acute symptoms and prevention of exercise-induced bronchospasm; side effects tachycardia, tremor, hypokalemia, headache, hyperglycemia; needing it regularly means poor control
• Anticholinergic (ipratropium): if SABA not tolerated; dry mouth; check for allergy to atropine, soy, peanuts, glaucoma, BPH; not for long-term control
• Ipratropium-albuterol by nebulizer for acute symptoms
• Systemic corticosteroids: 3-10 day burst for moderate or severe exacerbations; hyperglycemia, fluid retention, mood changes, insomnia; give last dose before 2 PM

Long-term control (Table 20-6):

• Inhaled corticosteroids (beclomethasone, budesonide, fluticasone, mometasone): most potent anti-inflammatories; rinse mouth and spit to prevent thrush; spacer if poor coordination
• Systemic corticosteroids for severe persistent asthma: single morning dose or alternate-day; long-term risks (adrenal suppression, Cushing’s, diabetes, cataracts, osteoporosis)
• LABAs (salmeterol, formoterol): added to ICS; at least 12 hours; prevent nocturnal and exercise symptoms; never for acute symptoms; never alone (risk of severe exacerbation)
• ICS/LABA combinations: fluticasone/salmeterol, budesonide/formoterol, fluticasone furoate/vilanterol, mometasone/formoterol
• Leukotriene modifiers: montelukast, zafirlukast (take 1 hour before or 2 hours after meals; inhibits warfarin metabolism - monitor INR; liver dysfunction), zileuton (liver enzymes; interacts with warfarin, theophylline)
• Theophylline: add-on only; therapeutic serum level 5-15 mcg/mL; toxicity - tachycardia, nausea, vomiting, arrhythmias, seizures; many drug interactions; mandatory level monitoring
• Biologics for severe asthma: omalizumab (anti-IgE; anaphylaxis in 0.2% - monitor after injection; refrigerate), mepolizumab, reslizumab, benralizumab (anti-IL-5, eosinophilic), dupilumab (IL-4 receptor)

H. Exacerbations and action plans

• Early treatment and written asthma action plan
• ICS to prevent exacerbations; SABA for relief; systemic steroids if no response; oxygen for hypoxemia
• Antibiotics only with signs of bacterial infection

Peak flow monitoring:

• For moderate or severe persistent asthma, poor symptom perception
• Establish personal best after 2-3 weeks of optimal therapy
• Green 80-100% of personal best: continue controller medications
• Yellow 60-80% (action plan shows 50-79%): add quick-relief medication, call provider if not back to green
• Red under 60% (action plan: under 50%): quick-relief medication and seek emergency care
• Technique (Chart 20-8): indicator to bottom, stand, deep breath, lips around mouthpiece (tongue out), blow hard and fast, record, repeat 3 times and record highest

I. Nursing management

• Calm approach; monitor symptoms, breath sounds, peak flow, SpO2, VS
• Ask about medication allergies; identify current medications; give medications and monitor response; fluids if dehydrated; assist with intubation if needed
• Teaching: asthma is chronic inflammation; inflammation vs bronchoconstriction; purpose of each medication; trigger avoidance; inhaler technique; peak flow; action plan; when and how to seek help

VI. Status Asthmaticus

• Severe, persistent asthma not responding to conventional therapy; can progress to asphyxia
• Contributors: infection, anxiety, inhaler overuse, dehydration, adrenergic blockade, irritants; aspirin, beta-blockers, NSAIDs
• Severe bronchospasm with mucus plugging; V/Q mismatch, hypoxemia; initially respiratory alkalosis, then rising PaCO2 and respiratory acidosis
• Labored breathing, prolonged exhalation, JVD, wheezing
• Disappearance of wheezing as obstruction worsens may signal impending respiratory failure (“silent chest”)
• Rising PaCO2 (to normal or above) is a danger sign
• Assess: breathlessness, ability to talk, position, alertness, RR, accessory muscles, cyanosis, pulsus paradoxus, peak flow, ABG
• Treatment: inhaled SABA (often continuous nebulizer), systemic corticosteroids, oxygen (partial or non-rebreather), IV fluids; sedatives contraindicated; IV magnesium sulfate 2 g over 20 minutes for severe cases (flushing, warmth, hypotension, respiratory depression); mechanical ventilation if fatigued or failing; bronchial thermoplasty for select severe uncontrolled asthma
• Risk factors for asthma death: prior intubation or ICU, ED visit or hospitalization in past year, current or recent oral steroids, not using ICS, SABA overuse, psychiatric or psychosocial problems, poor adherence, food allergy
• Nursing: monitor closely for 12-24 hours; skin turgor; IV fluids up to 3-4 L/day unless contraindicated; continuous BP and cardiac monitoring; quiet room free of irritants (flowers, smoke, perfume, cleaners); nonallergenic pillows; latex-free products if allergic; identify triggers afterward

VII. Cystic Fibrosis (CF)

• Most common fatal autosomal recessive disease in Caucasians; two defective CFTR genes needed
• Carriers (heterozygous) are unaffected; two carrier parents have 25% risk per pregnancy; offer genetic testing
• Over 75% diagnosed by age 2; median survival about 37
• CFTR protein dysfunction impairs chloride transport: thick secretions in lungs, pancreas, liver, intestine, reproductive tract; salty sweat; most common mutation F508del
• Pulmonary: productive cough, wheezing, hyperinflation, obstructive PFTs; mucus plugging, inflammation, bronchiectasis (starts in upper lobes); colonization with S. aureus and H. influenzae early, then P. aeruginosa; sinusitis, nasal polyps; lung disease is the main cause of death
• Nonpulmonary: pancreatic insufficiency, abdominal pain, biliary cirrhosis, vitamin deficiencies, pancreatitis, weight loss, CF-related diabetes, infertility (absent vas deferens)
• Treatment: multimodal antibiotics (IV, oral, inhaled), airway clearance, bronchodilators, CFTR modulators, nutrition, exercise
• Influenza vaccine essential; may use oseltamivir or zanamivir prophylaxis
• P. aeruginosa exacerbation: two IV antibiotics (tobramycin plus piperacillin-tazobactam, ceftazidime, or meropenem); add vancomycin for MRSA
• Inhaled tobramycin (first line) or aztreonam, often 28 days on and 28 days off
• B. cepacia complex: resistant, poor outcomes, may exclude transplant
• Airway clearance: CPT, HFCWO, autogenic drainage, PEP masks, flutter valve; dornase alfa (breaks down DNA in mucus); inhaled hypertonic saline
• Pancreatic enzymes with meals; fat-soluble vitamins A, D, E, K; high-calorie nutrition
• CFTR modulators: potentiators (ivacaftor) and correctors (lumacaftor, tezacaftor, elexacaftor) used in combination; target the cause
• Oxygen for progressive hypoxemia; double-lung transplant for end stage
• Nursing: secretion removal, CPT, breathing exercises, avoid crowds and sick contacts, early infection signs, fluids and nutrition, home reassessment, end-of-life planning

High-Yield Numbers

• Chronic bronchitis: cough and sputum 3 months a year for 2 consecutive years
• Smoking causes 80-90% of COPD
• COPD diagnosis: FEV1/FVC under 70%; GOLD I at least 80%, II 50-79%, III 30-49%, IV under 30%
• COPD oxygen goal: PaO2 at least 60 mm Hg, SaO2 at least 90%; long-term oxygen if PaO2 55 or less or SaO2 88% or less; more than 15 hours/day; usual flow 1-2 L/min
• Room air 21%; FiO2 over 50% risks absorption atelectasis; toxicity after more than 24 hours at high FiO2
• Nasal cannula 1-6 L (24-44%), over 4 L dries mucosa; simple mask 5-8 L (40-60%); partial rebreather 8-11 L (50-75%); nonrebreather 10-15 L (80-95%); Venturi 24-40% precise
• Smoking cessation follow-up 3-5 days after quit date
• Pulmonary rehab 6-8 weeks
• Antibiotics in COPD exacerbation if increased dyspnea, sputum volume, and purulence
• Postural drainage 2-4 times daily, 10-15 minutes per position; percussion 3-5 minutes; HFCWO 8-18 per second
• Pursed-lip: in 3, out 7; diaphragmatic 1 minute on, 2 minutes rest
• pMDI: inhale 3-5 seconds, hold 10 seconds, 1 minute between puffs; DPI: rapid 1-2 second inhalation
• Home oxygen: 15 feet from flame, 5 feet from appliances; airline 2 weeks notice
• Peak flow zones: green 80-100%, yellow 60-80%, red under 60%
• Theophylline level 5-15 mcg/mL
• Magnesium for status asthmaticus 2 g over 20 minutes; IV fluids up to 3-4 L/day
• CF: 25% risk with two carrier parents; inhaled antibiotics 28 days on/off

Priority Nursing Actions and Red Flags

• COPD on oxygen: watch for rising PaCO2 (somnolence, confusion, headache); give lowest flow for SpO2 about 90%; Venturi mask for precise delivery
• Signs of hypoxemia: restlessness, confusion, tachycardia, tachypnea, cyanosis (late)
• Sudden dyspnea in emphysema: suspect pneumothorax (absent breath sounds, tracheal shift, asymmetric chest)
• Asthma: normal or rising PaCO2 and a “silent chest” mean impending respiratory failure
• Status asthmaticus: no sedatives; continuous bronchodilator, steroids, oxygen, fluids
• LABAs never for acute symptoms or as monotherapy in asthma
• Rinse mouth after inhaled corticosteroids
• Avoid aspirin, NSAIDs, nonselective beta-blockers in asthma
• Report early infection signs (sputum change, fever, increased dyspnea)
• Oxygen fire safety at home
• Omalizumab: observe for anaphylaxis
• Theophylline: monitor levels and drug interactions

Medications

Related

• nsg210-hinkle-ch17-respiratory-assessment
• nsg210-hinkle-ch25-heart-failure-complications - cor pulmonale and right-sided HF
• nsg210-week-02-summary
• INDEX