Pathophysiology

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.