Pathophysiology
P-II-15. Respiratory disease, Case 2
呼吸器疾患 症例2
Case II — 69-year-old male; main complaints are dyspnea, high fever, chest pain (COPD)
Medical history:
50 pack years smoking, hyperlipidemia, hypertension, acute myocardial infarction, coronaria bypass surgery, chronic obstructive pulmonary disease (COPD), many hospital stays because of acute exacerbation, need for non-invasive respiratory support (acute but reversible global respiratory insufficiency).
Permanent medication:
Aspirin, ACE inhibitor, Betaloc (nonselective β-blocker), inhaled long-acting β2-agonist (LABA) and inhaled long-acting muscarinic antagonist (LAMA).
Complaints:
Fever (39.0 °C), chest pain, dyspnea.
Physical examination:
- Blood pressure: 145/82 mmHg, pulse: 90/min
- Wheezing (rather deep sound) over the lungs; over the left lateral zone of the chest above the diaphragm faint crackles can be heard
Pulmonary function test:
Irreversible obstruction of the large and small airways; FVC 1.35 L (34%), FEV1 0.58 L/s (19%), FEV1/FVC 0.5 (below 0.7 might be COPD), Rairway 405%. Body plethysmography: hyperinflation, dynamic compression of the small airways; total airway resistance 4-fold.
Blood gas, acid-base:
- pO2: 66 mmHg (with 2 L/min O2 inhalation - FiO2 27%)
- pH: 7.40
- pCO2: 43 mmHg
Chemistry:
- CRP: 88 mg/L
- Electrolytes in reference range
- GGT and LDH increased
- Troponin T negative, BNP in reference range
ECG: no new alterations.
Chest X-rays: Diaphragm is elevated on the left, left costodiaphragmatic angle is rounded, configuration of the heart is abnormal (pulm. hypertension?). Sutures of sternotomy (coronaria bypass).
Treatment and blood gas results:
Antibiotics, systemic steroid, inhaled bronchodilator (like in the acute exacerbation of COPD).
| before | after | |
|---|---|---|
| PaO2 | 66 mmHg (+2 l/min O2, FiO2 27%) | 60 (without O2) |
| PaO2/FiO2 | 244 | 286 |
| pH | 7.40 | 7.43 |
| pCO2 | 43 | 47 |
| BE | +1.0 mmol/l | +6.1 mmol/l |
Diagnoses upon discharge:
- J4490 Chronic obstructive pulmonary disease, unspecified
- J1890 Pneumonia, unspecified
- I2500 Atherosclerotic cardiovascular disease, so described
- I10H0 Essential (primary) hypertension
- E7850 Hyperlipidemia, unspecified
- J4390 Emphysema, unspecified
After a few days the complaints improved. Supposedly there was a mild acute exacerbation. It is not certain based on the findings.
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “50 pack years smoking” + known COPD/emphysema | Heavy smoking → the principal cause of chronic obstructive pulmonary disease |
| FEV1/FVC 0.5, FEV1 0.58 L (19%), “Irreversible obstruction” | Fixed airflow obstruction (ratio < 0.7, very low FEV1) → confirms COPD, not asthma |
| Body plethysmography: “hyperinflation … total airway resistance 4-fold” | Air trapping and high airway resistance from small-airway disease/emphysema |
| Fever 39 °C, CRP 88, left basal crackles, X-ray changes | Superimposed infection/pneumonia precipitating an acute exacerbation |
| pCO2 43→47 mmHg + “global respiratory insufficiency” | Tendency to CO2 retention (type 2 respiratory failure) during exacerbation |
| Troponin negative, BNP normal, ECG unchanged | Excludes acute cardiac causes of the dyspnoea/chest pain |
| “Betaloc (nonselective β-blocker)” | Non-selective β-blockade can worsen bronchospasm — a relevant medication caution in COPD |
Key Points
- Diagnosis: Chronic obstructive pulmonary disease with an acute exacerbation (and likely pneumonia).
- Spirometry: Irreversible obstruction (FEV1/FVC < 0.7) with very low FEV1 and hyperinflation — distinguishes COPD from asthma.
- Pathophysiology: Smoking-induced small-airway inflammation + emphysema → air trapping, dynamic compression, and impaired gas exchange.
- Respiratory failure: Prone to type 2 (hypercapnic) failure — controlled O2 needed to avoid worsening CO2 retention.
- Comorbidity: Significant cardiovascular disease (prior MI, bypass, hypertension) and a medication caution (non-selective β-blocker).
一問一答
▶What is the diagnosis in a heavy smoker with irreversible airflow obstruction, hyperinflation, fever, and CRP 88?
COPD with an acute exacerbation (likely with superimposed pneumonia).
▶What spirometric criterion defines COPD?
A post-bronchodilator FEV1/FVC ratio below 0.7 (fixed airflow obstruction).
▶How does COPD's airflow obstruction differ from asthma?
COPD obstruction is largely fixed/irreversible, whereas asthma obstruction is reversible with bronchodilators.
▶What is the principal cause of COPD?
Long-term cigarette smoking (here 50 pack-years).
▶Why does hyperinflation occur in COPD?
Air trapping from small-airway collapse/loss of elastic recoil leaves excess air in the lungs at end-expiration.
▶What is dynamic airway compression in COPD?
During expiration, loss of structural support lets small airways collapse, trapping air distally.
▶Why is airway resistance markedly increased (4-fold) in this patient?
Small-airway inflammation, narrowing, and dynamic compression raise resistance to airflow.
▶Why is this patient prone to type 2 (hypercapnic) respiratory failure?
Severe airflow obstruction impairs CO2 elimination, causing CO2 retention during exacerbations.
▶What typically triggers an acute exacerbation of COPD?
Respiratory infections (viral or bacterial) or environmental pollutants.
▶Why must oxygen be given in a controlled (titrated) manner in COPD?
Excessive O2 can worsen CO2 retention (reduced hypoxic drive and V/Q effects), risking hypercapnic acidosis.
▶What is the standard treatment of an acute COPD exacerbation?
Inhaled bronchodilators, systemic corticosteroids, controlled oxygen, and antibiotics if infection is present.
▶Why is a non-selective β-blocker (Betaloc) a concern in this COPD patient?
Non-selective β-blockade can cause bronchoconstriction, worsening airflow obstruction.
▶How do negative troponin, normal BNP, and unchanged ECG help here?
They exclude acute cardiac causes (MI, heart failure) of the dyspnoea and chest pain.
▶What is emphysema and how does it impair gas exchange?
Destruction of alveolar walls reduces surface area and elastic recoil, impairing gas exchange and causing air trapping.
▶Why may COPD lead to pulmonary hypertension and cor pulmonale?
Chronic hypoxia causes pulmonary vasoconstriction and vascular remodelling, raising pulmonary pressures and straining the right heart.
▶Why does the patient have wheezing on auscultation?
Airflow through narrowed, obstructed airways produces the wheeze.
▶Why do localized basal crackles and raised CRP point to pneumonia in this patient?
Focal crackles plus a high inflammatory marker and fever indicate a superimposed lung infection.
▶What single intervention most slows COPD progression?
Smoking cessation.
▶What is the role of inhaled LABA and LAMA maintenance therapy in COPD?
Long-acting bronchodilators relax airway smooth muscle, reducing symptoms and exacerbation frequency.
▶Why is an elevated bicarbonate/base excess often seen in chronic COPD?
Renal compensation for chronic CO2 retention raises bicarbonate to buffer the respiratory acidosis.