Respiratory Physiology: The Mechanics of Breathing

The Core Principle: Pressure Gradients

Breathing, or pulmonary ventilation, is a mechanical process entirely governed by physics. The fundamental principle is that air flows from an area of high pressure to an area of low pressure. To inhale, the pressure inside the alveoli (intrapulmonary pressure) must become lower than the atmospheric pressure. To exhale, the intrapulmonary pressure must rise above atmospheric pressure. The respiratory system achieves these pressure changes by rhythmically altering the volume of the thoracic cavity, the closed compartment housing the lungs. This is Boyle’s Law in action: for a given amount of gas at a constant temperature, pressure and volume are inversely related. Increase the volume, pressure decreases. Decrease the volume, pressure increases.

The Architectural Framework: Bones and Muscles

The thoracic cavity is a conical enclosure bounded by the sternum anteriorly, the vertebral column posteriorly, and the rib cage laterally. The floor is formed by a critical muscle: the diaphragm. The lungs are not directly attached to these walls; instead, they are surrounded by the pleural membranes. The visceral pleura clings to the lung surface, while the parietal pleura lines the inside of the thoracic wall and the superior surface of the diaphragm. The potential space between these membranes, the pleural cavity, contains a thin layer of pleural fluid. This fluid creates a hydrostatic seal, coupling the lungs to the chest wall. As the chest wall expands or contracts, the lungs are compelled to follow due to this pleural linkage.

The Muscles of Ventilation

The Primary Inspiratory Muscle: The Diaphragm
The diaphragm is a large, dome-shaped skeletal muscle that separates the thoracic and abdominal cavities. When it contracts, its dome flattens and descends, like a piston moving downward. This action increases the vertical diameter of the thoracic cavity, which is the primary driver of quiet inhalation, accounting for about 75% of the air entering the lungs.

The Accessory Inspiratory Muscles
During exercise or forced inhalation, additional muscles assist. The external intercostal muscles, located between the ribs, contract to lift the rib cage upward and outward, increasing the anteroposterior and lateral dimensions of the thorax—the “bucket handle” effect. Other accessory muscles include the scalenes and sternocleidomastoids, which lift the sternum and upper ribs.

The Muscles of Exhalation
Exhalation during quiet breathing is primarily a passive process. It results from the elastic recoil of the lungs and chest wall once the inspiratory muscles relax. The diaphragm ascends passively, and the rib cage descends. For active or forced exhalation, such as during exercise or coughing, internal intercostal muscles contract to pull the ribs down and in. The most powerful expiratory muscles are those of the abdominal wall (e.g., rectus abdominis, external and internal obliques). Their contraction increases intra-abdominal pressure, forcing the diaphragm upward and pushing air out of the lungs.

The Process of Inhalation (Inspiration)

Neural Stimulus: The inspiratory neurons in the medulla oblongata send action potentials via the phrenic and intercostal nerves.
Muscle Contraction: The diaphragm and external intercostal muscles contract.
Volume Increase: The thoracic cavity expands in three dimensions: vertically (diaphragm descent), laterally, and anteroposteriorly (rib movement).
Pleural Pressure Drop: The expansion of the thoracic wall pulls the parietal pleura outward. Due to the pleural fluid’s cohesion, the visceral pleura and the lungs themselves are also pulled outward. This stretching increases the volume of the pleural cavity, causing a drop in intrapleural pressure (the pressure within the pleural space). It becomes more subatmospheric (e.g., from -4 mm Hg to -6 mm Hg).
Lung Expansion: The negative intrapleural pressure transmurally pulls the alveolar walls outward, increasing lung volume.
Pressure Gradient Creation: According to Boyle’s Law, the increase in lung volume causes a decrease in intrapulmonary pressure inside the alveoli (e.g., from 760 mm Hg to 758 mm Hg).
Airflow: A pressure gradient is now established, with atmospheric pressure higher than alveolar pressure. Air rushes down this pressure gradient through the airways and into the alveoli until the pressures equalize.

The Process of Exhalation (Expiration)

Cessation of Stimulus: The inspiratory neurons stop firing, and the phrenic and intercostal nerves become silent.
Muscle Relaxation: The diaphragm and external intercostal muscles relax.
Elastic Recoil: The lungs contain elastic tissue that was stretched during inspiration. The chest wall also possesses elasticity. With the inspiratory muscles relaxed, these structures passively recoil to their resting positions.
Volume Decrease: The thoracic cavity volume decreases as the diaphragm rises and the rib cage descends.
Pleural Pressure Rise: The decrease in thoracic volume reduces the stretch on the pleural membranes, and the intrapleural pressure returns to its resting, less-negative value (e.g., from -6 mm Hg back to -4 mm Hg).
Lung Recoil: The loss of the expanding force from the pleural space allows the elastic lungs to recoil inward, decreasing lung volume.
Pressure Gradient Reversal: The decrease in lung volume increases the intrapulmonary pressure above atmospheric pressure (e.g., from 760 mm Hg to 762 mm Hg).
Airflow Out: The pressure gradient is now reversed. Alveolar pressure is higher than atmospheric pressure, so air flows out of the lungs until the pressures equalize.

Key Pressure Concepts

Atmospheric Pressure (P_atm): The pressure exerted by the air surrounding the body (760 mm Hg at sea level). This is the reference point.

Intrapulmonary Pressure (Alveolar Pressure): The pressure within the alveoli. It fluctuates above and below atmospheric pressure during the breathing cycle. During quiet breathing, these changes are small (±1 mm Hg), but they become larger during forced breathing.

Intrapleural Pressure (P_ip): The pressure within the pleural cavity. It is always negative (subatmospheric) under normal conditions, typically around -4 mm Hg at rest. This negativity is critical and is maintained by two opposing forces: the inward elastic recoil of the lungs, which tends to pull the visceral pleura away from the parietal pleura, and the outward spring of the chest wall. The pleural fluid resists this separation. This negative pressure keeps the lungs partially inflated even after exhalation and prevents lung collapse (atelectasis).

Transpulmonary Pressure: The difference between the intrapulmonary pressure and the intrapleural pressure (P_pul – P_ip). It is the pressure gradient that effectively keeps the air spaces of the lungs open and is the best index of the forces acting to inflate the lungs. A greater transpulmonary pressure means a more inflated lung.

Lung Compliance and Airway Resistance

The ease with which the lungs can be expanded is determined by two main factors: compliance and resistance.

Lung Compliance (C_L) is a measure of the distensibility of the lungs—how much effort is required to stretch them. It is defined as the change in lung volume (ΔV) for a given change in transpulmonary pressure (ΔP). High compliance means the lungs expand easily (e.g., low elastic recoil). Low compliance means they are “stiff” and require more work to inflate, as seen in conditions like pulmonary fibrosis. Compliance is influenced by two primary factors:

Elasticity of the Lung Tissue: The elastic fibers in the lung parenchyma.
Surface Tension at the Air-Water Interface: The alveoli are lined with a thin film of water, creating a surface tension that acts to collapse the alveoli. This is counteracted by pulmonary surfactant, a detergent-like complex of lipids and proteins secreted by Type II alveolar cells. Surfactant reduces surface tension, decreasing the work of breathing and increasing compliance. It also prevents smaller alveoli from collapsing into larger ones, contributing to alveolar stability.

Airway Resistance is the resistance to airflow within the respiratory passages. According to Poiseuille’s Law, resistance is inversely proportional to the fourth power of the radius of the airway. Therefore, small changes in airway diameter have a massive impact on resistance. Bronchoconstriction, as in asthma, dramatically increases resistance and the work of breathing. Bronchodilation, often mediated by the sympathetic nervous system, decreases resistance. Resistance is normally very low in the healthy lung due to the extensive branching and large total cross-sectional area of the airways.

The Work of Breathing

The energy required for ventilation is used for three main purposes:

Compliance Work (Elastic Work): The work required to stretch the elastic tissues of the lungs and chest wall. This is the major component during normal quiet breathing.
Tissue Resistance Work: The work required to overcome the viscosity of the lung and chest wall structures.
Airway Resistance Work: The work required to overcome the resistance to airflow through the bronchial tree.

In obstructive lung diseases (e.g., COPD, asthma), the airway resistance work increases significantly. In restrictive lung diseases (e.g., fibrosis), the compliance work increases due to lung stiffness.

Pulmonary Volumes and Capacities

Spirometry is used to measure the volumes of air moved during breathing.

Tidal Volume (V_T): The amount of air inhaled or exhaled during normal, quiet breathing (approx. 500 ml).
Inspiratory Reserve Volume (IRV): The maximum amount of air that can be forcibly inhaled beyond a normal tidal inhalation.
Expiratory Reserve Volume (ERV): The maximum amount of air that can be forcibly exhaled beyond a normal tidal exhalation.
Residual Volume (RV): The amount of air remaining in the lungs after a maximal exhalation. This prevents lung collapse.

Capacities are combinations of two or more volumes:

Inspiratory Capacity (IC): V_T + IRV (the total air that can be inspired after a normal expiration).
Functional Residual Capacity (FRC): ERV + RV (the amount of air remaining in the lungs after a normal tidal expiration). This is a crucial volume representing the equilibrium point where the inward elastic recoil of the lungs is balanced by the outward recoil of the chest wall.
Vital Capacity (VC): IRV + V_T + ERV (the total amount of exchangeable air).
Total Lung Capacity (TLC): The sum of all lung volumes (IRV + V_T + ERV + RV).

Neural Control of the Respiratory Muscles

Breathing is an automatic rhythm generated by networks of neurons in the brainstem. The dorsal respiratory group (DRG) in the medulla is primarily responsible for initiating inspiration. The ventral respiratory group (VRG) contains neurons that fire during forced inspiration and expiration. The pontine respiratory group (PRG) in the pons smooths the transition between inhalation and exhalation. This central pattern generator sends rhythmic signals to the spinal cord motor neurons that control the diaphragm and intercostal muscles. This automaticity is finely modulated by chemoreceptors (sensitive to CO2, O2, and pH) and mechanoreceptors in the lungs and joints to match ventilation to metabolic demands.