Med-Surg · Respiratory

COPD & Asthma

Last reviewed October 15, 2026 by Kristina, RN

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On this page
  1. 1. Overview and Pathophysiology
  2. 2. Causes and Risk Factors
  3. 3. Signs and Symptoms
  4. 4. Diagnostics and Labs
  5. 5. Priority Nursing Assessments
  6. 6. Priority Nursing Interventions
  7. 7. Medications
  8. 8. Patient Education
  9. 9. Complications
  10. 10. Memory Aids
  11. 11. NCLEX-Style Practice Questions
  12. References

Prepared for Pass the Shift (owner: Kristina, RN). Always follow your facility’s protocols, provider orders, and current drug references.

1. Overview and Pathophysiology

is a progressive, mostly preventable lung disease with persistent airflow limitation, usually from long-term smoking or biomass exposure. Two overlapping phenotypes:

  • Chronic bronchitis: productive cough ≥ 3 months in 2 consecutive years; airway inflammation and mucus hypersecretion
  • Emphysema: alveolar wall destruction → loss of elastic recoil and air trapping (“pink puffer” stereotype is oversimplified)

is a chronic inflammatory airway disease with reversible airflow obstruction, bronchial hyperresponsiveness, and episodic wheezing, cough, and dyspnea. Triggers include allergens, infection, cold air, exercise, and irritants.

FeatureCOPDAsthma
OnsetMid-life, progressiveOften childhood; can start any age
ReversibilityMostly irreversibleLargely reversible with treatment
Smoking linkStrongVariable
InflammationNeutrophilic / mixedOften eosinophilic / allergic
Daily symptomsCommon, progressiveEpisodic between attacks

Exacerbations (worsening dyspnea, cough, sputum) drive hospitalizations and mortality. A “silent chest” during a severe asthma attack means airflow is so low you may not hear wheezes—an emergency.

2. Causes and Risk Factors

  • COPD: tobacco smoke, occupational dusts/chemicals, indoor biomass fuel, alpha-1 antitrypsin deficiency, aging, recurrent infections
  • Asthma: atopy/allergies, family history, viral infections, obesity, occupational exposures, GERD
  • Exacerbation triggers: respiratory infection, air pollution, nonadherence to inhalers, allergens

3. Signs and Symptoms

COPD: progressive dyspnea, chronic cough, sputum, barrel chest, prolonged expiration, pursed-lip breathing, accessory muscle use, , fatigue, weight loss in advanced disease. SpO₂ often chronically lower.

Asthma: episodic wheezing, chest tightness, nocturnal cough, dyspnea after exposure/exercise. Severe attack: accessory muscles, inability to speak full sentences, peak flow drop, agitation, then fatigue/silent chest/cyanosis.

Early hypoxia: restlessness, anxiety, tachycardia. Late: cyanosis, confusion, bradycardia.

4. Diagnostics and Labs

Lab reference ranges vary by laboratory. Always use your facility’s ranges.

TestTypical reference / targetNursing relevance
Spirometry FEV₁/FVC< 0.70 post-bronchodilator supports COPDConfirms obstruction; asthma shows reversibility
ABG: pH / PaCO₂ / HCO₃⁻ / PaO₂7.35–7.45 / 35–45 / 22–26 / 80–100COPD often chronic with compensated respiratory acidosis
SpO₂Many COPD targets 88–92%Avoid over-oxygenation in CO₂ retainers
Peak expiratory flow (asthma)Personal best–based zonesGreen/yellow/red action plan
WBC, sputum culturePer labInfection-driven exacerbations
Alpha-1 antitrypsinLab-dependentYoung nonsmokers with emphysema
Chest X-ray / CT—Hyperinflation, bullae, rule out pneumonia/pneumothorax

5. Priority Nursing Assessments

  1. RR, depth, effort, accessory muscles, positioning, ability to speak
  2. SpO₂ (know the client’s target), lung sounds, sputum color/amount
  3. Mental status (CO₂ narcosis, hypoxia)
  4. Peak flow / spirometry trends when ordered
  5. Medication technique and adherence; recent steroid or antibiotic use
  6. Hydration, nutrition, activity tolerance, anxiety

6. Priority Nursing Interventions

  • Position upright / high Fowler’s; allow tripod if helpful
  • Titrate O₂ to target (often 88–92% in COPD per order)—do not automatically crank to high flow
  • Teach pursed-lip and diaphragmatic breathing; paced activity; energy conservation
  • Hydration (if not contraindicated) to thin secretions; chest physiotherapy / flutter devices per order
  • Inhaler sequence: bronchodilator before inhaled corticosteroid; wait between puffs as instructed; rinse mouth after steroids
  • Vaccinations: influenza, pneumococcal, COVID-19 as indicated
  • Smoking cessation support (most important COPD intervention)
  • During severe exacerbation: nebulizers, systemic corticosteroids, antibiotics if bacterial, NIPPV for hypercapnic respiratory failure, prepare for intubation if tiring

7. Medications

Class / examplesHow it helpsKey nursing considerations
SABA (albuterol)Rescue bronchodilationTachycardia, tremor, hypokalemia with heavy use; spacer improves delivery
SAMA/LAMA (ipratropium, tiotropium)Anticholinergic bronchodilationDry mouth; tiotropium is maintenance, not rescue
LABA (salmeterol, formoterol)Long-acting bronchodilationNot for acute rescue alone; in asthma, combine with ICS
ICS (fluticasone, budesonide)Reduce airway inflammationOral thrush/hoarseness—rinse and spit; pneumonia risk in COPD
Systemic corticosteroidsExacerbation controlHyperglycemia, infection risk, mood changes; taper if prolonged
Leukotriene modifiers (montelukast)Asthma maintenanceNeuropsychiatric effects possible—teach to report
Methylxanthines (theophylline)Rarely used bronchodilatorNarrow therapeutic index; toxicity = nausea, seizures, arrhythmias
PDE-4 inhibitor (roflumilast)Severe COPD with chronic bronchitisWeight loss, diarrhea, mood changes
Oxygen (long-term)Survival benefit if severe resting hypoxemiaFire safety; no smoking near O₂; titrate carefully

8. Patient Education

  • Correct inhaler / spacer technique with teach-back; know rescue vs controller
  • Asthma action plan (green/yellow/red zones based on symptoms and peak flow)
  • Avoid triggers; get vaccines; quit smoking—counsel without shaming
  • Report increased sputum purulence, fever, or sudden dyspnea
  • Home O₂ safety and target SpO₂ if prescribed
  • Nutrition: small frequent meals for dyspneic clients; pulmonary rehab referral

9. Complications

  • Acute respiratory failure /
  • Cor pulmonale and right-sided HF
  • Pneumothorax (bullae rupture)
  • Pneumonia, pulmonary hypertension
  • Status asthmaticus; silent chest; intubation
  • Steroid-related hyperglycemia, osteoporosis, thrush

10. Memory Aids

  • “88–92 for many COPD clients” (when ordered)—don’t chase 100%
  • “Bronchodilator before steroid; rinse after steroid”
  • “Silent chest = scream for help”
  • COPD ≈ progressive & poorly reversible; asthma ≈ episodic & reversible
  • Pursed lips = “smell the roses, blow out the candle”

11. NCLEX-Style Practice Questions

1. A client with COPD on 2 L/min nasal cannula has SpO₂ 89%, RR 20, and is resting comfortably. What should the nurse do?

A. Increase O₂ to 6 L/min
B. Apply a non-rebreather mask
C. Continue current therapy and monitor
D. Call the rapid response team

Answer: C. Many COPD clients have a target of 88–92%. This client is stable within target; excess O₂ can worsen CO₂ retention in some clients.

2. When teaching inhaler use, which sequence is correct?

A. Inhaled steroid, then albuterol
B. Albuterol first, then inhaled steroid; rinse mouth afterward
C. Both inhalers at the same time
D. Steroid only during attacks

Answer: B. Open airways with the bronchodilator first so the steroid reaches deeper; rinsing prevents thrush.

3. Which finding during an asthma attack is most concerning?

A. Loud expiratory wheezes
B. Peak flow in the yellow zone
C. Sudden absence of wheezes with increasing lethargy
D. Mild tachycardia after albuterol

Answer: C. A silent chest with fatigue suggests critically low airflow—prepare for emergency airway support.

4. A client with COPD asks why smoking cessation still matters. Best response?

A. “It won’t help once you have COPD.”
B. “Quitting slows further lung damage and reduces exacerbations, even after diagnosis.”
C. “You only need to quit if you use oxygen.”
D. “Switching to menthol cigarettes is enough.”

Answer: B. Smoking cessation is the most effective intervention to slow COPD progression at any stage.

5. Why must the nurse teach mouth rinsing after fluticasone?

A. Prevents systemic hypertension
B. Reduces oral candidiasis and hoarseness
C. Improves albuterol absorption
D. Prevents hypokalemia

Answer: B. Local steroid residue causes thrush and dysphonia; rinse and spit after each use.

References

Global Initiative for Asthma. (2025). Global strategy for asthma management and prevention. https://ginasthma.org/

Global Initiative for Chronic Obstructive Lung Disease. (2025). GLOBAL strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. https://goldcopd.org/

MedlinePlus. (n.d.). COPD. National Library of Medicine. Retrieved October 15, 2026, from https://medlineplus.gov/copd.html

MedlinePlus. (n.d.). Asthma. National Library of Medicine. Retrieved October 15, 2026, from https://medlineplus.gov/asthma.html

National Council of State Boards of Nursing. (2026). 2026 NCLEX-RN test plan. https://www.nclex.com/test-plans.page