Anatomy and Physiology - Respiratory System

Overview

Respiratory physiology links airway anatomy and mechanics to gas exchange and control of ventilation. Questions commonly test spirometry interpretation, V/Q concepts, and O₂/CO₂ transport.

Anatomy and zones

• Conducting zone: nose → pharynx → larynx → trachea → bronchi → bronchioles (terminal). Functions: air conduction, humidification, filtration (mucociliary escalator).
• Respiratory zone: respiratory bronchioles → alveolar ducts → alveoli; type I pneumocytes (gas exchange), type II (surfactant, regeneration), alveolar macrophages (defense).

Mechanics of breathing

• Compliance (ΔV/ΔP): lung and chest wall; surfactant reduces surface tension to prevent alveolar collapse (Laplace law concept: P ∝ 2T/r).
• Resistance: R ∝ 1/r⁴ (Poiseuille). Medium bronchi contribute most resistance; small airways dominate in disease.
• Work of breathing: elastic (overcoming recoil) + resistive (airway resistance). At high rates, resistive work dominates.

Lung volumes and capacities (qualitative)

• TV, IRV, ERV, RV; VC = IRV+TV+ERV; TLC = VC+RV. RV cannot be measured by simple spirometry.
• Dead space: anatomic (conducting airways) vs physiologic (anatomic + alveolar that does not exchange). In healthy states, physiologic ≈ anatomic.

Gas exchange and transport

• Diffusion: proportional to area × ΔP / thickness; emphysema (↓area), fibrosis (↑thickness) reduce DLCO.
• O₂ transport: carried mostly bound to Hb; O₂–Hb dissociation curve sigmoidal (cooperativity). Right shift (↓affinity) with ↑CO₂, ↓pH, ↑temperature, ↑2,3‑BPG (Bohr effect) → improved tissue unloading. Left shift opposite.
• CO₂ transport: dissolved, carbaminohemoglobin, as bicarbonate (major). Haldane effect: oxygenation of blood in lungs displaces CO₂, aiding CO₂ unloading.

V/Q relationships (qualitative)

• Ideal ≈ 1. Apex: low perfusion relative to ventilation (V/Q > 1), high PAO₂, low PACO₂; Base: high perfusion (V/Q < 1), lower PAO₂, higher PACO₂.
• Shunt (V/Q → 0): perfusion without ventilation (e.g., mucus plug) → low PAO₂ unresponsive to O₂. Dead space (V/Q → ∞): ventilation without perfusion (e.g., PE) → wasted ventilation.

Control of ventilation

• Central chemoreceptors: respond to CSF pH (PaCO₂ proxy). Peripheral (carotid/aortic bodies): respond to PaO₂ (especially <60 mmHg), PaCO₂, pH.
• Ventilatory drive integrates in medullary/pons centers with mechanoreceptor feedback; higher centers modulate behaviorally.

Worked micro‑examples

1. Spirometry pattern recognition

• Obstructive: ↓FEV₁, ↓FVC (less), ↓FEV₁/FVC; scooped flow–volume loop. Restrictive: ↓FEV₁, ↓FVC, normal/↑FEV₁/FVC; smaller loop with preserved shape.

2. V/Q mismatch reasoning

• Lobar pneumonia: shunt physiology in affected region (V/Q ~ 0) → hypoxemia refractory to O₂; PE: increased dead space (V/Q → ∞) → hyperventilation and hypocapnia possible.

3. O₂ curve shift

• Fever and acidosis in exercising muscle shift right → improved unloading; at lungs (cooler, higher pH), curve left → loading.

Pitfalls

• Confusing dead space with shunt; misreading apex–base gradients.
• Equating low PaO₂ causes: hypoventilation vs diffusion limitation vs V/Q mismatch vs shunt—respond differently to O₂.
• Forgetting that CO₂ retention is more sensitive to ventilation than O₂ at moderate ranges.

Practice prompts

• Classify obstructive vs restrictive from provided spirometry and draw expected flow–volume loop.
• Explain PaO₂ and PaCO₂ changes in high altitude adaptation (hyperventilation, 2,3‑BPG).
• Predict DLCO changes in emphysema vs fibrosis.

References

• SciOly Wiki – Anatomy & Physiology (Respiratory)
• OpenStax Anatomy & Physiology (Respiratory system)