PY6.1-13 | Respiratory Physiology — Gate Quiz

Correct! Tidal volume (TV) is the volume of air moved in a single normal resting breath — approximately 500 mL (0.5 L) in an adult. During exercise, TV increases and breathing frequency increases, raising minute ventilation.

Key concept: Lung volumes — TV (~500 mL), IRV (~3000 mL), ERV (~1200 mL), RV (~1200 mL, cannot be measured by spirometry). Capacities: IC = TV+IRV (~3500 mL); VC = TV+IRV+ERV (~4600 mL); FRC = ERV+RV (~2400 mL); TLC = VC+RV (~5800 mL). RV and FRC cannot be measured by simple spirometry (need gas dilution or body plethysmography).

Incorrect. Tidal volume is the volume of air in each normal resting breath (~500 mL). Vital capacity is the maximum exhalation after maximum inhalation (~4.6 L).

Correct! Anatomical dead space (~150 mL) is the volume of the conducting airways (nose, pharynx, larynx, trachea, bronchi to terminal bronchioles) where no gas exchange occurs. Physiological dead space = anatomical + alveolar dead space. In healthy lungs, physiological ≈ anatomical dead space.

Key concept: Dead space — Anatomical (~150 mL): conducting airways; Alveolar: ventilated but not perfused; Physiological = anatomical + alveolar. Bohr's formula: Vd/Vt = (PaCO₂ - PECO₂)/PaCO₂. Alveolar ventilation = (TV - Vd) × RR = (500-150) × 12 = 4200 mL/min (more relevant than minute ventilation for gas exchange).

Incorrect. Anatomical dead space (~150 mL) is the conducting airway volume where no gas exchange occurs. Alveolar dead space = ventilated but non-perfused alveoli. Total = physiological dead space.

Correct! ~98.5% of O₂ is transported bound to haemoglobin as oxyhaemoglobin (HbO₂). Only ~1.5% is dissolved in plasma (responsible for PaO₂ measurement). Each gram of Hb can carry 1.34 mL O₂; at 15 g/dL, Hb carries ~20 mL O₂ per 100 mL blood (O₂ content).

Key concept: O₂ transport — Dissolved (~1.5%, proportional to PaO₂): 0.003 mL/mmHg/dL; Bound to Hb (~98.5%). O₂ content = (Hb × 1.34 × SaO₂) + (PaO₂ × 0.003). Normal CaO₂ ≈ 20 mL/dL. CO₂ transport: 70% as bicarbonate, 23% bound to Hb (carbaminohaemoglobin), 7% dissolved.

Incorrect. ~98.5% of O₂ is carried by haemoglobin as oxyhaemoglobin; only ~1.5% is dissolved in plasma.

Correct! CO poisoning causes anaemic hypoxia — CO binds to Hb with 240× greater affinity than O₂, forming carboxyhaemoglobin (HbCO), reducing O₂-carrying capacity. Additionally, HbCO shifts the ODC leftward, reducing O₂ release to tissues. PaO₂ is paradoxically NORMAL (dissolved O₂ in plasma).

Key concept: Types of hypoxia — Hypoxic: ↓PaO₂ (altitude, hypoventilation, V/Q mismatch, shunt); Anaemic: ↓O₂ content with normal PaO₂ (IDA, CO poisoning, metHb); Stagnant/ischaemic: ↓blood flow (shock, heart failure); Histotoxic: ↓O₂ utilisation with normal PaO₂ and O₂ content (cyanide poisoning — blocks cytochrome c oxidase). CO: SpO₂ falsely normal.

Incorrect. CO poisoning = anaemic hypoxia (reduced O₂ carrying capacity). The PaO₂ is normal because CO does not affect plasma O₂ — it blocks Hb binding. This is why pulse oximetry is UNRELIABLE in CO poisoning.

Correct! Normal alveolar ventilation ≈ 4 L/min; pulmonary blood flow ≈ 5 L/min; V/Q = 4/5 = 0.8. Regional variation: V/Q is highest at the lung apex (~3.3, dead space-like) and lowest at the base (~0.6, shunt-like) in upright posture due to gravity effects on perfusion.

Key concept: V/Q ratio — Normal overall: 0.8. Regional (upright): apex ~3.3 (ventilation > perfusion, dead space-like), base ~0.6 (perfusion > ventilation, shunt-like). V/Q mismatch is the most common cause of hypoxaemia in lung disease. V/Q = 0 = shunt (perfused but not ventilated); V/Q = ∞ = dead space (ventilated but not perfused). Corrected by O₂ in V/Q mismatch but not in true shunt.

Incorrect. Normal V/Q ratio = alveolar ventilation (4 L/min) / pulmonary blood flow (5 L/min) = 0.8.

Correct! Low pH (acidosis) + elevated PaCO₂ (primary ↑CO₂ → ↑H₂CO₃) + normal HCO₃⁻ = respiratory acidosis with no metabolic compensation (acute). This occurs in acute hypoventilation: COPD exacerbation, respiratory muscle failure, opioid overdose.

Key concept: ABG interpretation — Step 1: pH (acidosis <7.35, alkalosis >7.45). Step 2: primary disorder (↑PaCO₂ = resp acidosis; ↓PaCO₂ = resp alkalosis; ↓HCO₃⁻ = met acidosis; ↑HCO₃⁻ = met alkalosis). Step 3: compensation (renal for resp; respiratory for met). Acute respiratory acidosis: HCO₃⁻ normal; chronic: HCO₃⁻ rises 3.5 per 10 mmHg ↑PaCO₂.

Incorrect. pH is low (acidosis) + PaCO₂ is HIGH (the primary problem = CO₂ retention/hypoventilation) + HCO₃⁻ is normal (no compensation yet) = acute respiratory acidosis.

Correct! CO₂ (hypercapnia) is the most potent respiratory stimulant. CO₂ crosses the blood-brain barrier and lowers CSF pH → stimulates central chemoreceptors in the medulla. Even a 1 mmHg rise in PaCO₂ causes measurable increase in ventilation. O₂ (peripheral chemoreceptors) is a weaker stimulus, active only when PaO₂ falls below ~60 mmHg.

Key concept: Chemoreceptors — Central (medulla): respond to ↑CO₂/↑H⁺ in CSF (most powerful); Peripheral (carotid/aortic bodies): respond to ↓PaO₂ (<60 mmHg), ↑PaCO₂, ↑H⁺. In COPD with chronic CO₂ retention, central chemoreceptors are blunted — patients depend on hypoxic drive (peripheral chemoreceptors). High-flow O₂ in such patients removes hypoxic drive → ↓ventilation.

Incorrect. Increased PaCO₂ (hypercapnia) is the strongest respiratory stimulus. PaO₂ only becomes a significant stimulus when it falls below ~60 mmHg (the steep part of the O₂-Hb dissociation curve).

Correct! Surfactant is produced by Type II pneumocytes (granular/great alveolar cells). It is composed primarily of DPPC (dipalmitoylphosphatidylcholine). It reduces alveolar surface tension (especially in smaller alveoli), preventing alveolar collapse (atelectasis) and reducing the work of breathing.

Key concept: Surfactant — produced by Type II pneumocytes (appear at 24–26 weeks gestation, mature at 34–36 weeks); composition: DPPC (~80%), other phospholipids, surfactant proteins (SP-A, B, C, D). Reduces surface tension (especially variable with area — flattens Laplace pressure difference). Deficiency: neonatal respiratory distress syndrome (hyaline membrane disease). Treatment: antenatal steroids (↑synthesis), postnatal exogenous surfactant.

Incorrect. Surfactant is produced by Type II pneumocytes. Its primary function is to reduce alveolar surface tension, preventing small alveoli from collapsing (by Laplace's law: P = 2T/r — without surfactant, small alveoli would have high inward pressure).

Correct! ~70% of CO₂ is transported as bicarbonate ions (HCO₃⁻) in plasma. The reaction: CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ is catalysed by carbonic anhydrase inside RBCs. HCO₃⁻ exits RBCs (in exchange for Cl⁻, the chloride shift) and travels to the lungs where the reaction reverses.

Key concept: CO₂ transport — Bicarbonate (70%): CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ (carbonic anhydrase in RBCs); HCO₃⁻ exits via Cl⁻/HCO₃⁻ exchanger (chloride shift/Hamburger shift); Carbaminohaemoglobin (23%): binds to globin amino groups (not haem); Dissolved CO₂ (7%). Haldane effect: oxygenation of Hb at lungs reduces CO₂ binding, facilitating CO₂ release.

Incorrect. ~70% of CO₂ is transported as bicarbonate (HCO₃⁻) in plasma; ~23% as carbaminohaemoglobin (bound to Hb); ~7% dissolved.

Correct! Obstructive lung disease (asthma, COPD) shows reduced FEV₁ (obstructed expiratory flow) with a disproportionately less-reduced FVC, giving a reduced FEV₁/FVC ratio (<0.7 or <0.70 per GOLD criteria for COPD). The hallmark is airflow limitation on expiration.

Key concept: Spirometry patterns — Obstructive (asthma, COPD, bronchiectasis): ↓FEV₁, ↓FEV₁/FVC (<70%), FVC may be ↓; Restrictive (pulmonary fibrosis, obesity, kyphoscoliosis, neuromuscular): ↓FVC, ↓FEV₁, normal/↑FEV₁/FVC, ↓TLC. Reversibility: FEV₁ improves >12% with bronchodilator = reversible obstruction (asthma vs COPD).

Incorrect. Obstructive pattern: ↓FEV₁, ↓FEV₁/FVC (<0.7), FVC may be reduced but less so. Restrictive pattern: ↓FVC, ↓FEV₁, NORMAL or increased FEV₁/FVC ratio (>0.80), ↓TLC.