Respiratory Physiology 1: Introduction

Respiration encompasses two linked processes. External respiration describes the exchange of oxygen and carbon dioxide between the atmosphere and the blood at the lung surface. Internal respiration describes the exchange of those same gases between the blood and the metabolising tissues throughout the body. Understanding both processes requires a firm grasp of gas laws and the physical principles governing diffusion.

Dalton's law of partial pressures states that the total pressure of a gas mixture equals the sum of the pressures each gas would exert alone. At sea level the atmospheric pressure is 101.3 kPa. Oxygen makes up approximately 21% of dry air, giving an inspired partial pressure of oxygen (PiO2) of roughly 21 kPa. Once air enters the airways it is humidified; water vapour exerts its own partial pressure (6.3 kPa at body temperature), which reduces the effective PiO2 that reaches the alveoli to approximately 20 kPa. This humidity correction is clinically important when calculating alveolar oxygen levels.

At the alveolar surface, oxygen moves down its partial pressure gradient from the alveolar gas into the pulmonary capillary blood. Carbon dioxide moves in the opposite direction. The driving force for each gas is the partial pressure difference across the alveolar-capillary membrane. Fick's law of diffusion formalises this: the rate of diffusion is proportional to the surface area of the membrane and the partial pressure difference, and inversely proportional to membrane thickness. The healthy lung has approximately 70 m² of surface area and a membrane thickness of less than 0.5 µm, making it ideally suited for rapid gas exchange.

Alveolar ventilation is the volume of fresh gas that reaches the alveoli per minute and is the clinically useful measure of ventilatory efficiency. Total minute ventilation is tidal volume multiplied by respiratory rate, but a portion of each breath occupies anatomical dead space (approximately 150 mL in adults) and does not participate in gas exchange. Alveolar ventilation therefore equals (tidal volume minus dead space) multiplied by respiratory rate. An increase in alveolar ventilation lowers alveolar PCO2 and raises alveolar PO2, whereas hypoventilation has the opposite effect.

Arterial hypoxaemia can arise through several distinct mechanisms. Hypoventilation reduces alveolar PO2 proportionally. Ventilation-perfusion mismatch, the most common clinical cause, occurs when areas of lung receive ventilation and perfusion in mismatched proportions. Diffusion impairment reduces the rate at which oxygen equilibrates across the membrane, particularly during exercise. An anatomical shunt allows deoxygenated blood to bypass alveoli entirely, meaning that supplemental oxygen has little corrective effect on the resulting hypoxaemia. Finally, a low inspired PO2 at high altitude reduces the driving gradient for oxygen uptake regardless of lung function.

These foundational principles underpin the interpretation of arterial blood gas results and the rational management of respiratory failure in clinical practice.