Pathophysiology
II-11. Pulmonary ventilation disorders & respiratory failure
換気障害と呼吸機能検査；呼吸不全
Obstructive vs Restrictive Lung Disease
- Obstructive (COPD, asthma): initially hypoxemic (type 1) → long-term hypercapnic/global (type 2) failure, with comorbidities (cardiac failure).
- Restrictive (pulmonary/idiopathic fibrosis, autoimmune — RA/scleroderma, sarcoidosis): continuous partial (type 1) failure, hypercapnia only before death. Progresses faster (earlier lethal), with impaired diffusion (hypoxemia under stress).
Oxygen Transport (Normoxia)
- Pulmonary blood flow ~2.4 L/min/lung, with alveolar pO₂ ~100 mmHg.
- V/Q ratio ~0.8 (physiological) — more than enough time for gas exchange. Alveolar and capillary pO₂ nearly equal.
Arterial Blood Gas (ABG)
- Indicates ventilation, gas exchange, acid-base status (radial artery).
- Components: pH (7.35–7.45), pO₂ (83–108 mmHg), pCO₂ (35–48 mmHg), O₂ saturation, Hb, standard bicarbonate (21–28 mmol/L), base excess (0±3), lactate (0.5–2.2).
- Interpretation: pH (↑ alkalosis / ↓ acidosis), pCO₂ (↑ respiratory acidosis / ↓ respiratory alkalosis), HCO₃⁻ (↑ metabolic alkalosis / ↓ metabolic acidosis).
Mechanisms of Hypoxemia
- V/Q mismatch (asthma, COPD, pneumonia): responds well to O₂ — parts under-ventilated.
- Diffusion impairment (COPD, fibrosis, pulmonary edema, ARDS): responds well to O₂.
- Right-to-left shunt (ARDS, severe COVID pneumonia): no alveolar ventilation but perfusion continues — most severe, O₂-refractory, with 25–50% of lung unventilated.
V/Q Mismatch Details
- Hb already nearly saturated at physiological pO₂ → hyperventilation cannot increase blood oxygenation (but removes CO₂ → no hypercapnia).
- V/Q <1 → ↓pO₂, barely ↑pCO₂. V/Q >1 → ↑pO₂, ↓pCO₂ but no ↑transported O₂ (Hb saturated).
- CO₂ content linearly proportional to pCO₂ → hyperventilation removes retained CO₂.
一問一答
▶What are the three mechanisms of hypoxemia and their response to oxygen?
V/Q mismatch (responds well to O₂), diffusion impairment (responds well to O₂), and right-to-left shunt (O₂-refractory, most severe).
▶How do obstructive and restrictive lung diseases differ in their pattern of respiratory failure?
Obstructive (COPD, asthma) starts as hypoxemic (type 1) then becomes hypercapnic/global (type 2). Restrictive (fibrosis, autoimmune, sarcoidosis) causes continuous partial (type 1) failure, with hypercapnia only before death, and progresses faster.
▶How do you interpret pCO₂ and HCO₃⁻ on an ABG?
↑pCO₂ = respiratory acidosis, ↓pCO₂ = respiratory alkalosis; ↑HCO₃⁻ = metabolic alkalosis, ↓HCO₃⁻ = metabolic acidosis.
▶What does an arterial blood gas measure and what are the normal values?
Ventilation, gas exchange, and acid-base status: pH 7.35–7.45, pO₂ 83–108 mmHg, pCO₂ 35–48 mmHg, standard bicarbonate 21–28 mmol/L, base excess 0±3, lactate 0.5–2.2.
▶What is the physiological V/Q ratio and its significance?
~0.8 — it provides more than enough time for gas exchange, so alveolar and capillary pO₂ are nearly equal.
▶Why is a right-to-left shunt the most severe cause of hypoxemia?
Blood perfuses lung that has no alveolar ventilation (25–50% unventilated), so giving oxygen cannot correct it (O₂-refractory) — e.g. ARDS, severe COVID pneumonia.
▶Why does hyperventilation effectively remove CO₂ but not raise O₂?
CO₂ content is linearly proportional to pCO₂ (so hyperventilation removes retained CO₂), whereas O₂ content follows the sigmoid Hb saturation curve, which is already near maximal.
▶Why can't hyperventilation increase blood oxygenation in V/Q mismatch?
Hemoglobin is already nearly saturated at physiological pO₂, so increasing ventilation cannot raise transported O₂ — but it does remove CO₂ (no hypercapnia).
▶Give examples of obstructive and restrictive lung diseases.
Obstructive: COPD, asthma. Restrictive: pulmonary/idiopathic fibrosis, autoimmune (RA, scleroderma), and sarcoidosis.
▶How does V/Q affect pO₂ and pCO₂ in different lung regions?
V/Q <1 → ↓pO₂, barely ↑pCO₂; V/Q >1 → ↑pO₂ and ↓pCO₂ but no increase in transported O₂ (Hb already saturated).
▶Why does restrictive lung disease cause hypoxemia mainly under stress?
Impaired diffusion is compensated at rest but the limited gas-exchange reserve fails under increased demand (exercise/stress).
▶From which artery is an ABG sample typically drawn?
The radial artery.
▶What conditions cause diffusion impairment as a mechanism of hypoxemia?
COPD, pulmonary fibrosis, pulmonary edema, and ARDS — these respond well to supplemental oxygen.
▶How is pH interpreted on an ABG?
↑pH = alkalosis, ↓pH = acidosis (normal 7.35–7.45).
▶What conditions cause V/Q mismatch?
Asthma, COPD, and pneumonia — parts of the lung are under-ventilated relative to perfusion; responds well to oxygen.
▶Why does obstructive disease eventually progress to hypercapnia, unlike restrictive disease early on?
In obstruction, chronically impaired ventilation leads to long-term CO₂ retention (type 2); restrictive disease keeps CO₂ clearance until very late because CO₂ diffuses readily and hyperventilation compensates.
▶What comorbidity commonly accompanies long-standing obstructive lung disease?
Cardiac (heart) failure.
▶What is base excess and its normal range?
A measure of the metabolic component of acid-base balance; normal is 0 ± 3.
▶Why does restrictive lung disease tend to be lethal earlier than obstructive disease?
It progresses faster, with impaired diffusion causing hypoxemia under stress and continuous type 1 failure.
▶What is the normal alveolar pO₂ and approximate pulmonary blood flow per lung?
Alveolar pO₂ ~100 mmHg with pulmonary blood flow ~2.4 L/min per lung.