Respiratory Physiology

Ventilation is the mechanical process of moving air in and out of the lungs, driven by pressure gradients created by the diaphragm and intercostal muscles. Boyle's Law explains how changes in thoracic volume alter intrapulmonary pressure. Lung compliance (ease of expansion) and airway resistance are key determinants of the work of breathing. Gas exchange occurs across the thin alveolar-capillary membrane via passive diffusion, governed by Fick's Law (surface area, thickness, partial pressure gradient). The Ventilation/Perfusion (V/Q) ratio is crucial: an ideal ratio of 0.8 ensures efficient gas exchange, but regional variations exist (higher at apices, lower at bases). Oxygen is primarily transported bound to haemoglobin, while carbon dioxide is mainly transported as bicarbonate. Understanding the factors affecting haemoglobin's affinity for oxygen (e.g., Bohr effect) is vital. Breathing is centrally controlled by the medulla, primarily responding to PaCO2 and pH.

The sigmoid shape of the oxyhaemoglobin dissociation curve reflects cooperative binding: binding of one O2 molecule to haemoglobin increases the affinity for subsequent O2 molecules. Surfactant, a lipoprotein, acts to reduce the surface tension in alveoli, preventing smaller alveoli from collapsing into larger ones (as predicted by Laplace's Law: P = 2T/r). Lung compliance (ΔVolume/ΔPressure) is reduced in stiff lungs (e.g., fibrosis) and increased in emphysema. The work of breathing involves overcoming elastic recoil and airway resistance. Respiratory rhythm is generated by medullary centres (DRG/VRG). Central chemoreceptors in the medulla are highly sensitive to H+ concentration in the CSF, which is primarily influenced by CO2 levels (CO2 crosses BBB, then converts to H+). Peripheral chemoreceptors (carotid and aortic bodies) respond mainly to severe hypoxaemia (PaO2 <8 kPa), and also to H+ and PaCO2. The Haldane effect describes how deoxygenated haemoglobin has a higher affinity for CO2, facilitating CO2 transport from tissues to lungs.

V/Q mismatch is the most common cause of hypoxaemia (e.g., pulmonary embolism, pneumonia, COPD, asthma). Obstructive lung diseases (e.g., COPD, asthma) are characterised by reduced FEV1/FVC ratio, while restrictive lung diseases (e.g., pulmonary fibrosis) show reduced total lung volumes with a preserved or increased FEV1/FVC ratio. Respiratory failure is classified as Type 1 (hypoxaemic, PaO2 <8 kPa with normal/low PaCO2) or Type 2 (hypercapnic, PaCO2 >6 kPa with or without hypoxaemia). Patients with chronic CO2 retention (e.g., severe COPD) may rely on a 'hypoxic drive' for breathing, where peripheral chemoreceptors become the primary stimulus due to desensitisation of central chemoreceptors to chronic hypercapnia.

Spirometry is essential for assessing lung function, measuring FEV1, FVC, and their ratio to differentiate obstructive from restrictive patterns. Peak Expiratory Flow Rate (PEFR) is used for monitoring asthma control. Arterial Blood Gases (ABGs) are crucial for assessing gas exchange (PaO2, PaCO2) and acid-base status (pH, HCO3-). Pulse oximetry provides a non-invasive estimate of oxygen saturation (SpO2) but can be inaccurate in conditions like carbon monoxide poisoning or poor peripheral perfusion.

Acute management of respiratory distress involves controlled oxygen therapy, aiming for target saturations (e.g., 94-98% for most, 88-92% for those at risk of CO2 retention). Bronchodilators (short-acting beta-agonists, anticholinergics) are used to relieve bronchoconstriction. Non-invasive ventilation (NIV) such as CPAP (for Type 1 respiratory failure, e.g., acute pulmonary oedema) or BiPAP (for Type 2 respiratory failure, e.g., COPD exacerbation) provides ventilatory support and improves gas exchange.