Respiratory Physiology RS

Air flows when respiratory muscles create pressure gradients. Lung and chest-wall elastic properties, airway resistance and surfactant determine the work required to ventilate alveoli.

Follow muscle action → thoracic volume → pressure change → airflow.

Asthma, fibrosis, emphysema and pneumothorax alter different mechanical components.

Air is not actively pulled by the lung; it moves down a pressure gradient created by changes in thoracic volume.

Minute ventilation includes air reaching gas-exchanging alveoli and air occupying dead space. Alveolar ventilation therefore depends on tidal volume minus dead-space volume, multiplied by respiratory rate.

Do not judge effective ventilation from respiratory rate alone; consider depth and dead space.

Rapid shallow breathing may produce poor alveolar ventilation despite a high minute respiratory rate.

Minute ventilation and alveolar ventilation are not interchangeable.

Gas transfer depends on partial-pressure gradients, surface area, diffusion distance and gas properties. Efficient exchange also requires matching ventilation to perfusion.

Separate diffusion limitation from ventilation-perfusion mismatch and shunt-like physiology.

Many causes of hypoxaemia can be classified by ventilation, diffusion, perfusion and inspired-oxygen mechanisms.

A well-ventilated alveolus cannot exchange much gas without perfusion, and a well-perfused alveolus cannot oxygenate blood without ventilation.

Oxygen is transported mainly bound to haemoglobin; carbon dioxide travels dissolved, as bicarbonate and in carbamino compounds. Brainstem networks and chemoreceptors adjust ventilation in response to chemical signals.

Connect metabolism → CO2/H+ signal → chemoreception → ventilatory response.

Respiratory failure can involve inadequate ventilation, impaired gas exchange or both.

Oxygen saturation, PaO2 and oxygen content describe different aspects of oxygen transport.

Ventilation is driven by pressure gradients created by respiratory-muscle activity. During quiet inspiration, contraction of the diaphragm enlarges the thoracic cavity, lowering alveolar pressure below atmospheric pressure so air flows inward. Expiration at rest is largely passive as elastic structures recoil.

Compliance describes the change in volume produced by a change in distending pressure. Surface tension at the air-liquid interface tends to favour alveolar collapse; pulmonary surfactant lowers surface tension, improves compliance and stabilizes alveoli of different sizes. Airway resistance is strongly influenced by airway radius.

Clinical reasoning: obstructive disease primarily raises resistance to airflow, whereas restrictive processes reduce compliance or available lung volume. These categories describe mechanics and can coexist.

Teach it back: explain how surfactant simultaneously reduces work of breathing and helps stabilize small alveoli.

Minute ventilation equals tidal volume multiplied by respiratory rate, but not all inspired air reaches gas-exchanging alveoli. Anatomical dead space occupies conducting airways. Alveolar ventilation is therefore approximately (tidal volume − dead-space volume) × respiratory rate.

This distinction explains why rapid shallow breathing may produce a seemingly large minute ventilation while delivering little fresh gas to alveoli. Effective carbon dioxide elimination depends strongly on alveolar ventilation.

Clinical reasoning: when ventilation changes, PaCO2 provides useful information about effective alveolar ventilation if metabolic CO2 production is considered.

Teach it back: compare two breathing patterns with the same minute ventilation but different tidal volumes and predict which gives greater alveolar ventilation.

Oxygen and carbon dioxide cross the respiratory membrane down partial-pressure gradients. Transfer is influenced by surface area, membrane thickness, diffusion properties and the time blood spends in pulmonary capillaries. But diffusion alone is not enough: ventilation must be appropriately matched to perfusion.

A region with ventilation but little perfusion behaves like dead space; a region with perfusion but no effective ventilation behaves like a shunt-like unit. Between these extremes lies a spectrum of V/Q mismatch, an important mechanism of hypoxaemia.

Clinical reasoning: disease can impair oxygenation by hypoventilation, V/Q mismatch, diffusion limitation, shunt or low inspired oxygen. Identifying the mechanism is more informative than merely observing low saturation.

Teach it back: explain why giving more ventilation to an unperfused alveolus cannot substantially improve gas exchange from that unit.

Most oxygen is carried bound to haemoglobin, while only a small fraction is dissolved. Carbon dioxide is transported in several forms, importantly as bicarbonate after reversible reactions in red cells and tissues. Ventilation is controlled by brainstem networks receiving chemical information from central and peripheral chemoreceptors plus neural and behavioural inputs.

Carbon dioxide and hydrogen-ion physiology are closely linked. Changes in alveolar ventilation alter PaCO2, which can rapidly affect acid-base status. Peripheral chemoreceptors also respond importantly to low arterial oxygen, particularly when hypoxaemia becomes substantial.

Teach it back: explain why a patient can have 100% haemoglobin saturation yet still have inadequate oxygen content if haemoglobin concentration is very low.