Pathophysiology

Respiratory

Case Study

Patient Profile

Name: Mrs. Eleanor Thompson

Age: 90 years old

Gender: female

History of Present Illness

E.T. is a 90-year-old woman who presents to urgent care with worsening shortness of breath, increased cough with greenish sputum, and fever for the past three days.

Past Medical History

  • Chronic Obstructive Pulmonary Disease (COPD) – diagnosed 15 years ago.
  • Hypertension
  • Osteoarthritis
  • History of two COPD exacerbations in the past year requiring hospitalization, no history of mechanical ventilation.
  • Previous pneumonia episode 6 months ago.

Social History

  • Widowed, lives alone in a second-floor apartment over daughter’s garage, has a chair lift on stairs.
  • Former smoker (40 pack-year history, quit 10 years ago).
  • Has a daughter who assists with medications and activities of daily living.
  • Limited mobility due to arthritis, uses a walker.
  • No occupational exposures.
  • Up to date on vaccinations (influenza, pneumococcal, COVID-19).

Current Medications

  • Maintenance Medications:
    • Tiotropium (Spiriva) 18 mcg inhaler daily
    • Fluticasone/Salmeterol (Advair) 250/50 mcg twice daily
    • Albuterol MDI 90 mcg as needed
    • Lisinopril 10 mg daily for hypertension
    • Acetaminophen 650 mg as needed for arthritis pain
  • Recent Additions:
    • Has been using an albuterol inhaler more frequently over the past three days.
    • Started on over-the-counter Mucinex two days ago.

Physical Assessment

Vitals

  • Temperature: 38.5°C (101.3°F)
  • Blood pressure: 148/88 mm Hg
  • Heart rate: 102 bpm
  • Respiratory rate: 26 bpm
  • SpO2: 87% on room air

General Survey

  • General Appearance:
    • Alert and oriented x3
    • Mild confusion compared to baseline per daughter
  • Respiratory Examination:
    • Elderly female in moderate respiratory distress, sitting upright in tripod position, speaking in short phrases
    • Using accessory muscles for breathing with intercostal retractions, no cyanosis of lips or nail beds
    • Diffuse wheezing throughout all lung fields, decreased breath sounds throughout, and crackles in the right lower lobe
    • Using pursed-lip breathing, prolonged expiratory phase
    • Productive cough with greenish sputum
  • Cardiovascular Examination:
    • Tachycardia with regular rhythm
    • No murmurs
    • Mild peripheral edema bilateral lower extremities
    • Jugular venous distension present

Diagnostic Testing

  • Complete Blood Count (CBC):
    • White blood cell (WBC): 14,500/μL (elevated)
    • Hemoglobin: 11.2 g/dL
    • Hematocrit: 34%
    • Platelets: 245,000/μL
  • Basic Metabolic Panel:
    • Sodium: 138 mEq/L
    • Potassium: 3.8 mEq/L
    • Creatinine: 1.1 mg/dL
    • Blood urea nitrogen (BUN): 22 mg/dL
  • Other Studies:
    • C-reactive protein: 12 mg/dL (elevated)
    • Procalcitonin: 0.8 ng/mL (elevated)
    • Sputum culture and Gram stain obtained
    • COVID-19 and Influenza testing negative
  • Imaging
    • Chest X-ray: Right lower lobe infiltrate consistent with pneumonia, hyperinflation consistent with COPD, no pneumothorax or pleural effusion
    • Electrocardiogram (ECG): Sinus tachycardia, no acute ischemic changes

Diagnosis

  • Acute COPD exacerbation (moderate to severe) evidenced by:
    • Increased dyspnea and work of breathing
    • Increased sputum production and purulence
  • Community-acquired pneumonia evidenced by:
    • Fever
    • Right lower lobe infiltrate on chest X-ray
    • Elevated inflammatory markers
    • Leukocytosis

Mrs. Thompson is placed on continuous monitoring of oxygen saturation and given supplemental oxygen via a low-flow nasal cannula titrated to maintain her oxygen saturation between 88% and 92%. She is transferred to the Emergency Room for further evaluation and management.

Activity: Pathophysiology of COPD Exacerbation and Pneumonia

Fill in the blanks with the correct term: Streptococcus pneumoniae, Clostridium difficile, cytokines, neutrophils, eosinophils, acidosis, alkalosis.

The pathophysiology of a COPD exacerbation caused by pneumonia involves a combination of underlying chronic airway inflammation and acute infection. COPD is characterized by chronic inflammation of the airways, alveolar destruction/loss of surface area, and excessive mucus production.  This produces airflow limitations and impaired gas exchange, leading to symptoms such as dyspnea, chronic cough, and sputum production. During an exacerbation triggered by a bacterial or viral infection, these processes intensify. The invasion of the lung parenchyma, leading to pneumonia, is most likely due to pathogens such as _____________________, Haemophilus influenzae, and Moraxella catarrhalis. This leads to an acute inflammatory response in the alveoli, characterized by the release of pro-inflammatory cytokines, infiltration of neutrophils, and increased capillary permeability, resulting in alveolar filling with fluid, inflammatory cells, and exudates, which further narrows the airways and increases airflow obstruction. These changes exacerbate the pre-existing lung damage in COPD, worsen ventilation-perfusion mismatch, reduce oxygenation, and increase breathing effort.

Additionally pneumonia further intensifies systemic inflammation, leading to _____________________ and hypercapnia due to impaired gas exchange and reduced respiratory reserve. The increased mucus production and airway narrowing in COPD patients, compounded by pneumonia, result in worsened airway obstruction and sputum retention, further decreasing airflow. This exacerbation can lead to respiratory _____________________ and acute respiratory failure, particularly in severe cases. The combination of these mechanisms explains the rapid deterioration seen during a COPD exacerbation triggered by pneumonia and highlights the need for timely intervention with antibiotics, bronchodilators, corticosteroids, and oxygen therapy.

Review Questions

Click the arrow to expand the section and view the correct answers.

  1. What is the primary pathophysiological feature of COPD?
    1. Hyperresponsiveness of airways leading to bronchoconstriction.
    2. Progressive and irreversible airflow limitation due to airway inflammation and alveolar destruction.
    3. Accumulation of fluid in the alveoli causes reduced oxygen exchange.
    4. Increased pulmonary vascular resistance leading to right heart failure.
Answer:

B). Progressive and irreversible airflow limitation due to airway inflammation and alveolar destruction.. Feedback: COPD is defined by persistent respiratory symptoms and airflow limitation that is progressive and not fully reversible. This is due to chronic inflammation causing narrowing of the airways, destruction of alveolar walls (emphysema), and excessive mucus production, as described in the pathophysiology section of the case. The other options describe features more typical of asthma, pulmonary edema, or pulmonary hypertension, respectively.

  1. Which of the following is a hallmark symptom of a COPD exacerbation?
    1. Persistent cough without sputum production.
    2. Sudden onset of chest pain.
    3. C). Worsened dyspnea, increased sputum production, and purulent sputum.
    4. Non-productive cough with fever.
Answer:

C) Worsened dyspnea, increased sputum production, and purulent sputum.. Feedback: A hallmark of COPD exacerbation is an increase in baseline symptoms: increased breathlessness (dyspnea), and increased sputum, especially a change in sputum color or purulence (indicating infection).

  1. In the case of Mrs. Thompson, what was the most likely trigger for her COPD exacerbation?
    1. Pulmonary embolism
    2. Viral or bacterial pneumonia
    3. Heart failure
    4. Air pollution
Answer:

B) Viral or bacterial pneumonia. Feedback: The case notes that she has a fever, a new infiltrate on chest X-ray, and purulent sputum, all classic signs of pneumonia, which is a common trigger for COPD exacerbations. The other choices are possible but less supported by the clinical evidence presented.

  1. Which diagnostic test confirmed the presence of pneumonia in Mrs. Thompson?
    1. Arterial blood gas (ABG) analysis.
    2. Chest X-ray showing right lower lobe infiltrate.
    3. Sputum culture revealing purulent sputum.
    4. Elevated C-reactive protein (CRP).
Answer:

B) Chest X-ray showing right lower lobe infiltrate.. Feedback: The chest X-ray, showing a right lower lobe infiltrate, is the definitive imaging test used to confirm pneumonia in this case. While CRP and sputum culture are supportive tests, they are not diagnostic on their own. Arterial blood gas provides information on gas exchange but does not diagnose pneumonia.

  1. Why is it important to target oxygen saturation (SpO2) levels between 88% and 92% in COPD patients during exacerbations?
    1. To prevent hypoxia and maintain high oxygen delivery.
    2. To avoid hypercapnia and worsening of respiratory acidosis.
    3. To optimize oxygen delivery to peripheral tissues.
    4. To prevent oxygen toxicity.
Answer:

B) To avoid hypercapnia and worsening of respiratory acidosis.. Feedback: COPD patients often have chronic hypercapnia (elevated CO2 levels) due to impaired gas exchange. Administering excessive oxygen can suppress their hypoxic drive for respiration, leading to worsened CO2 retention and respiratory acidosis. Therefore, maintaining SpO2 levels between 88% and 92% ensures adequate oxygenation while minimizing the risk of hypercapnia.

  1. Which of the following medications is typically used to decrease airway inflammation during a COPD exacerbation?
    1. Tiotropium
    2. Albuterol
    3. Prednisone
    4. Ceftriaxone
Answer:

C) Prednisone. Feedback: Systemic corticosteroids like prednisone are commonly used during COPD exacerbations to reduce airway inflammation and improve symptoms. Tiotropium and albuterol are bronchodilators, while ceftriaxone is an antibiotic used to treat infections, not inflammation.

  1. What ABG finding in Mrs. Thompson confirms the presence of respiratory acidosis?
    1. pH: 7.45, PaCO2: 35 mmHg
    2. pH: 7.32, PaCO2: 48 mmHg
    3. pH: 7.50, PaCO2: 25 mmHg
    4. pH: 7.38, PaCO2: 40 mmHg
Answer:

B) pH: 7.32, PaCO2: 48 mmHg. Feedback: A low pH (<7.35) with an elevated PaCO2 (>45 mmHg) indicates respiratory acidosis, a common finding in COPD exacerbations due to impaired gas exchange and CO2 retention. The other ABG values either indicate normal acid-base balance, respiratory alkalosis, or are inconsistent with acidosis.

  1. Which of the following is the most likely bacterial pathogen triggering pneumonia in a COPD exacerbation?
    1. Pseudomonas aeruginosa
    2. Mycobacterium tuberculosis
    3. Streptococcus pneumoniae
    4. Staphylococcus aureus
Answer:

C) Streptococcus pneumoniae. Feedback: Streptococcus pneumoniae is one of the most common bacterial pathogens causing pneumonia in COPD patients, along with Haemophilus influenzae and Moraxella catarrhalis. Pseudomonas aeruginosa is more common in advanced COPD with frequent exacerbations or prior hospitalizations, while tuberculosis and Staphylococcus aureus are less likely in this context.

  1. Why was Mrs. Thompson’s elevated CRP significant in this case?
    1. It helps differentiate bacterial from viral pneumonia.
    2. It confirms the presence of systemic inflammation caused by infection.
    3. It indicates irreversible lung damage.
    4. It predicts the need for non-invasive ventilation.
Answer:

B) It confirms the presence of systemic inflammation caused by infection.. Feedback: CRP is a marker of systemic inflammation, commonly elevated in infections like pneumonia. It cannot differentiate bacterial from viral pneumonia, nor does it indicate irreversible lung damage or predict ventilation needs.

  1. A 72-year-old female with COPD is being managed in your office for an exacerbation. She has a history of frequent exacerbations and is currently on long-term inhaled corticosteroids (ICS) and a long-acting muscarinic antagonist (LAMA). What additional treatment would you consider during this exacerbation?
    1. Add a short course of systemic corticosteroids.
    2. Discontinue her maintenance inhalers.
    3. Prescribe a leukotriene receptor antagonist.
    4. Initiate long-term oxygen therapy.
Answer:

B) It confirms the presence of systemic inflammation caused by infection.

Feedback: During exacerbations, a short course of systemic corticosteroids is typically added to reduce inflammation and improve symptoms. Maintenance inhalers should not be discontinued, and leukotriene receptor antagonists are not standard for COPD. Long-term oxygen therapy is reserved for chronic hypoxemia, not acute exacerbations.

References

Fuehrer, M. (2024).  Lecture on the respiratory system. [Transcript].

Stoller, J. & Hatipoglu, U. (2025). Up to Date. COPD exacerbations. Available at: https://www.uptodate.com/contents/copd-exacerbations-management

Tkacs, N. (Ed.). (2020). Advanced physiology and pathophysiology: Essentials for clinical practice. Springer Publishing Company.

You.com. (n.d.). ARI. You.com. Retrieved March 1, 2025, from https://www.you.com

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Be Prepared for Your Nurse Practitioner Clinical Readiness Exam Copyright © 2026 by Elizabeth Heavey, Renee Biedlingmaier, Colleen Burgoyne and Carnel C. Jackson is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.

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