Makindo Medical Notes

Related Subjects: |Pulmonary Physiology |Pancreas Physiology |Renal Physiology |Pulmonary Physiology |Cardiac Anatomy and Physiology |Coronary Anatomy and Physiology |Cardiac Electrophysiology |Cardiac Embryology |Cardiac Physiology |Cardiac Physiology |Gastrointestinal tract Physiology |Autonomic Nervous System

🫁 Pulmonary physiology examines how the respiratory system sustains life through the mechanics of breathing, the exchange of gases, and the neural–chemical control of ventilation. The lungs provide the interface between the external environment and the bloodstream — delivering oxygen to fuel cellular metabolism and removing carbon dioxide, the major acid–base by-product. Effective respiration depends on ventilation (airflow), perfusion (blood flow), and diffusion (gas movement across alveolar membranes), all precisely regulated to maintain arterial blood gases within narrow limits.

🏗️ Anatomy and Organisation

• Upper Respiratory Tract: Nose, nasal cavity, pharynx, and larynx — warm, filter, and humidify inspired air.
• Lower Respiratory Tract: Trachea, bronchi, bronchioles, and alveoli — the functional units of gas exchange.
• Alveoli: ~300 million microscopic sacs providing ~70 m² surface area; surrounded by dense pulmonary capillaries lined by type I pneumocytes (gas exchange) and type II pneumocytes (surfactant secretion).
• Surfactant: Reduces alveolar surface tension (Laplace’s law), preventing collapse at low volumes — deficiency leads to neonatal respiratory distress syndrome.

⚙️ Mechanics of Breathing

• Inspiration: Active process driven by diaphragm contraction (75%) and external intercostals; thoracic volume ↑, intrapulmonary pressure ↓ (~–1 to –2 mmHg), air flows in.
• Expiration: Passive during quiet breathing; active during exertion via internal intercostals and abdominal muscles.
• Compliance: Measure of lung distensibility (ΔV/ΔP); decreased in fibrosis, increased in emphysema.
• Elastic recoil: Due to lung tissue and surface tension; opposes expansion, aids passive expiration.
• Airway Resistance (Raw): ~80% from large bronchi; small airways become important in disease (asthma, COPD). Flow is governed by Poiseuille’s law: radius⁴ relationship means small decreases cause large resistance changes.
• Dead Space: ~150 mL of inspired air that does not participate in gas exchange (anatomical + alveolar).

💨 Lung Volumes and Capacities

• Tidal Volume (TV): ~500 mL per breath.
• Inspiratory Reserve Volume (IRV): ~3 L; extra air inhaled beyond TV.
• Expiratory Reserve Volume (ERV): ~1.2 L; extra air exhaled beyond TV.
• Residual Volume (RV): ~1.2 L; air remaining after maximal exhalation.
• Vital Capacity (VC) = IRV + TV + ERV
• Total Lung Capacity (TLC) = VC + RV
• Functional Residual Capacity (FRC): Volume at end-tidal expiration; balance between inward recoil of lungs and outward recoil of chest wall.

🌬️ Gas Exchange and Transport

• Alveolar Gas Equation: PAO₂ = (FiO₂ × [P_atm – P_H₂O]) – (PaCO₂ / R) ≈ 100 mmHg on room air at sea level (FiO₂ = 0.21, R = 0.8).
• Diffusion: Fick’s law — gas transfer ∝ surface area × ΔP / thickness. Thickened membranes (fibrosis, oedema) impair diffusion → ↓ PaO₂.
• Ventilation–Perfusion (V/Q) Matching:
  • Apex: High V/Q (ventilation > perfusion) → relative dead space → higher PO₂, lower PCO₂.
  • Base: Low V/Q → relative shunt → lower PO₂, higher PCO₂.
  • Normal overall V/Q ≈ 0.8 for optimal gas exchange.
• Oxygen Transport:
  • 98% bound to haemoglobin (Hb); 1 g Hb binds 1.34 mL O₂.
  • Oxyhaemoglobin dissociation curve is sigmoid; right shift (↓ affinity) with ↑ CO₂, ↑ temperature, ↓ pH — the Bohr effect.
  • Clinical Example: During exercise or fever, right shift facilitates O₂ unloading to active tissues.
• Carbon Dioxide Transport:
  • ~10% dissolved in plasma, ~20% bound to Hb (carbamino-Hb), ~70% as bicarbonate (HCO₃⁻).
  • Formation catalysed by carbonic anhydrase: CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻.
  • Haldane effect: Deoxygenated Hb binds more CO₂, enhancing transport from tissues to lungs.

🧬 Regulation of Respiration

• Central Control:
  • Medulla oblongata: Dorsal respiratory group (inspiration) and ventral group (active expiration).
  • Pons: Pneumotaxic and apneustic centres fine-tune rhythm and transition.
• Chemoreceptors:
  • Central: Located in medulla; respond primarily to ↑ CO₂ (via ↓ CSF pH).
  • Peripheral: Carotid and aortic bodies; respond to ↓ PaO₂ (<60 mmHg), ↑ CO₂, or ↓ pH.
  • Clinical Case: In chronic hypercapnia (e.g. COPD), central chemoreceptors desensitised → ventilation driven by hypoxia — giving high O₂ can suppress breathing.
• Mechanoreceptors: Stretch receptors in lungs prevent over-inflation (Hering–Breuer reflex).
• Higher Centres: Cortex allows voluntary control (speaking, breath-holding); hypothalamus integrates emotion-driven changes (fear, pain → tachypnoea).

🩺 Clinical Correlations

• Asthma: Airway hyper-responsiveness and reversible bronchoconstriction → ↑ resistance, ↓ peak flow. Example: Night-time wheeze triggered by allergen exposure; treated with β₂-agonists and inhaled corticosteroids.
• Chronic Obstructive Pulmonary Disease (COPD): Fixed airflow limitation due to chronic bronchitis and emphysema. ↓ elastic recoil → air trapping, ↑ FRC, ↑ work of breathing. Hypoxic vasoconstriction → pulmonary hypertension → cor pulmonale.
• Pulmonary Fibrosis: Thickened alveolar membranes → ↓ diffusion capacity, ↓ compliance, rapid shallow breathing. Case: Patient with dry cough, bibasal crackles, clubbing; HRCT shows honeycombing.
• Acute Respiratory Distress Syndrome (ARDS): Diffuse alveolar damage and protein-rich exudate → impaired gas exchange and stiff lungs. Managed with low tidal volume ventilation and PEEP to prevent alveolar collapse.
• High-Altitude Physiology: ↓ atmospheric PO₂ → hypoxaemia → hyperventilation and respiratory alkalosis; adaptation via ↑ 2,3-BPG and erythropoietin.
• Anaesthesia and Mechanical Ventilation: Loss of diaphragmatic tone and positive-pressure ventilation alter normal pressure gradients; excessive PEEP may reduce venous return → ↓ cardiac output.

📊 Summary and Integration

Pulmonary physiology integrates mechanics (ventilation), diffusion (gas exchange), and control (neural–chemical regulation) to maintain arterial blood gases and acid–base balance. Disruption at any level — whether mechanical (obstruction), structural (fibrosis), or control (CNS depression) — impairs oxygen delivery and CO₂ clearance. Understanding these interdependent systems underpins the management of respiratory failure, anaesthesia, and critical care.

💡 Teaching Tip: Think of the lungs as a “two-stage engine”: the pump (chest wall and diaphragm) moves air in and out, while the filter (alveoli and capillaries) exchanges gases. When either component fails — the pump in neuromuscular disease or the filter in ARDS — oxygen delivery collapses, and your job is to restore pressure, perfusion, and partnership between the two.