ventilation-perfusion ratio

**Definition and normal values** - V/Q = alveolar ventilation / pulmonary blood flow. Normal whole-lung value ≈ 0.8 (4 L/min ÷ 5 L/min). - Regional variation in the upright lung: both V and Q are greater at the base, but Q increases more steeply (gravity). So V/Q is highest at the apex (~3) and lowest at the base (~0.6). - Apex: V/Q ~3, with higher PAO2 (~132 mmHg), lower PACO2, and a higher pH. This is a favorable site for *M. tuberculosis* (an aerobe), so secondary TB is apical. - Base: V/Q ~0.6, with lower PAO2 and higher PACO2. This is the site of best absolute ventilation and perfusion. - With exercise, perfusion of the apex increases (recruitment/distention of capillaries), so V/Q becomes more uniform across the lung.

**Extremes** - **V/Q = 0 (airway obstruction / shunt):** Perfusion without ventilation. Alveolar gas equilibrates with mixed venous blood (PO2 ~40, PCO2 ~45). Examples are pneumonia, atelectasis, mucus plug, ARDS, and foreign body aspiration. Anatomic shunts (intracardiac right-to-left, as in Eisenmenger or tetralogy of Fallot) behave similarly. - Hypoxemia is **not corrected (or only minimally corrected) by 100% O2**, because the shunted blood never contacts ventilated alveoli. This is the classic way to separate shunt from other causes of hypoxemia. - **V/Q = ∞ (blood flow obstruction / dead space):** Ventilation without perfusion. Alveolar gas equals inspired gas (PO2 ~150, PCO2 0). Examples are pulmonary embolism, and also emphysema (loss of capillary bed) and severe hypotension/shock. - Physiologic dead space increases. Hypoxemia **is corrected by 100% O2** in the unaffected areas, although this is more nuanced in PE, where redistribution of flow to other regions causes V/Q mismatch. - **V/Q < 0.8 (low):** Seen in COPD (chronic bronchitis), asthma, and interstitial/pulmonary edema. - **V/Q > 0.8 (high):** Seen in PE, emphysema, and decreased cardiac output.

**Hypoxic pulmonary vasoconstriction** - Low alveolar PO2 constricts pulmonary arterioles and diverts blood to better-ventilated areas, which optimizes V/Q matching. This is the opposite of the systemic response, in which hypoxia causes vasodilation. - It is impaired by vasodilators (e.g., nitroprusside) and inflammation, and it contributes to pulmonary hypertension at altitude and in chronic hypoxia (cor pulmonale).

**Clinical/exam correlations** - **A-a gradient** = PAO2 − PaO2. Normal ≈ 10–15 mmHg (increases with age). It is **elevated** in V/Q mismatch, shunt, and diffusion limitation. It is **normal** in hypoventilation and at high altitude. - Causes of hypoxemia: (1) high altitude (↓ FiO2), (2) hypoventilation, (3) diffusion limitation, (4) V/Q mismatch, (5) shunt. Of these, V/Q mismatch is the most common cause of hypoxemia, and the only one in which hypoxemia is classically O2-responsive and the A-a gradient is elevated is V/Q mismatch (shunt has an elevated A-a gradient but is O2-unresponsive). - Diffusion-limited gases (O2 in fibrosis, exercise) vs. perfusion-limited gases (O2 in a healthy lung, CO2, N2O): perfusion-limited gases equilibrate early along the capillary. - Dead space: V_D = V_T × (PaCO2 − PECO2)/PaCO2 (Bohr equation). - PE: sudden-onset dyspnea, pleuritic chest pain, tachycardia, ↓ PaO2 and ↓ PaCO2 (hyperventilation) with a ↑ A-a gradient. CT pulmonary angiography is the diagnostic test; V/Q scan is used when contrast is contraindicated (renal failure, allergy) or in pregnancy. - V/Q scan interpretation: PE shows a **ventilation-perfusion mismatch** (normal ventilation, absent perfusion). Pneumonia/COPD shows a matched defect (both reduced). - Management: V/Q mismatch improves with supplemental O2 and treating the underlying cause. Shunt requires PEEP/recruitment, because O2 alone is not enough.

**Mnemonic** - Airway obstruction → V/Q → 0 (shunt). Blood flow obstruction → V/Q → ∞ (dead space).