Medical School · Year 1 · Respiratory · includes a quiz and discussion video

Lecture 2: Pulmonary Ventilation

Unit 1.8: Respiratory System

Learning Objectives

By the end of this lecture, students will be able to:

1. Define lung volumes and capacities and their measurement
2. Explain the mechanics of breathing including pressure changes
3. Describe the elastic properties of the lung and chest wall
4. Explain the roles of compliance and resistance in ventilation
5. Describe the work of breathing and its components
6. Apply ventilation concepts to clinical scenarios

Lecture Content

I. Lung Volumes and Capacities

The respiratory system handles approximately 12,000 liters of air daily, moving gases through airways and exchanging oxygen and carbon dioxide at the alveolar surface. Understanding lung volumes and capacities provides essential information about respiratory function and helps identify patterns of pulmonary disease.

Lung volumes represent non-overlapping compartments of air within the respiratory system. Tidal volume refers to the air moved during a normal, quiet breath, typically around 500 milliliters in adults. When a person makes an extra inspiratory effort beyond a normal breath, the additional volume inhaled represents the inspiratory reserve volume, which averages 3000 milliliters. Similarly, after a normal expiration, one can force additional air out by contracting the expiratory muscles; this expiratory reserve volume amounts to approximately 1100 milliliters. Even after the most forceful expiration possible, air remains trapped within the lungs due to the structural support of airways and alveoli. This residual volume, normally about 1200 milliliters, cannot be expelled no matter how hard one tries.

Lung capacities combine two or more volumes and provide clinically useful information. The inspiratory capacity equals the tidal volume plus inspiratory reserve volume, totaling approximately 3500 milliliters and representing the maximum air that can be inspired from the end of a normal expiration. Functional residual capacity represents the volume remaining in the lungs after a passive expiration, calculated as the sum of expiratory reserve volume and residual volume, yielding roughly 2300 milliliters. This capacity marks the resting equilibrium point of the respiratory system. Vital capacity encompasses all exchangeable air, combining tidal volume, inspiratory reserve, and expiratory reserve volumes to yield about 4600 milliliters. Total lung capacity represents the sum of all four primary volumes, approximately 5800 milliliters in a healthy adult male.

Different measurement techniques access different volumes. Spirometry, the most common pulmonary function test, directly measures tidal volume, inspiratory reserve, expiratory reserve, and vital capacity through breathing maneuvers into a closed system. However, spirometry cannot measure residual volume because the air never leaves the lungs. Determining residual volume and functional residual capacity requires specialized techniques. Helium dilution involves breathing a known concentration of helium and measuring its dilution to calculate the volume of gas it dispersed into. This method measures only communicating gas volumes and may underestimate lung volume if trapped gas exists. Body plethysmography, conducted in a sealed box, uses pressure-volume relationships based on Boyle's law to measure total thoracic gas volume, including trapped air. Nitrogen washout measures functional residual capacity by having subjects breathe pure oxygen while measuring exhaled nitrogen concentration.

Minute ventilation represents the total volume of air moved in one minute, calculated by multiplying tidal volume by respiratory rate. With typical values of 500 milliliters and 12 breaths per minute, minute ventilation equals 6000 milliliters per minute. However, not all inspired air participates in gas exchange. The conducting airways, comprising about 150 milliliters of anatomical dead space, receive fresh air with each breath but lack alveoli for gas exchange. Alveolar ventilation, the volume actually reaching gas-exchanging surfaces, equals tidal volume minus dead space volume, multiplied by respiratory rate. With the values above, alveolar ventilation calculates to approximately 4200 milliliters per minute, representing the clinically important ventilation for maintaining blood gases.

<image>Panel A: Volume-versus-time spirometry tracing showing quiet breathing oscillating around functional residual capacity level. Panel B: Maximal inspiration to total lung capacity and maximal expiration to residual volume with tidal volume amplitude marked. Panel C: Four primary volumes (TV, IRV, ERV, RV) with typical milliliter values shown as horizontal brackets. Panel D: Four capacities (IC, FRC, VC, TLC) as combinations of volumes with shaded residual volume indicating unmeasurable by spirometry.</image>

II. Dead Space

Dead space represents ventilated regions that do not participate in effective gas exchange. Understanding dead space explains why alveolar ventilation differs from minute ventilation and why certain disease states cause respiratory failure despite apparently adequate breathing.

Anatomical dead space comprises the conducting airways from the nose and mouth down to the terminal bronchioles. These passages, totaling approximately 150 milliliters in an adult, warm, humidify, and filter inspired air but contain no alveoli for gas exchange. The air filling these passages at end-inspiration represents "wasted" ventilation that never reaches gas-exchanging surfaces.

Alveolar dead space consists of alveoli that receive ventilation but lack adequate perfusion. In healthy individuals at rest, alveolar dead space approaches zero because nearly all ventilated alveoli also receive blood flow. However, conditions reducing pulmonary perfusion create significant alveolar dead space.

Physiological dead space, the sum of anatomical and alveolar components, represents the total volume of wasted ventilation. In health, physiological dead space approximately equals anatomical dead space. In disease, physiological dead space may increase substantially due to added alveolar dead space.

The Bohr equation quantifies physiological dead space by comparing arterial carbon dioxide tension to mixed expired carbon dioxide. The ratio of dead space to tidal volume normally approximates 0.3, meaning roughly 30 percent of each breath does not participate in gas exchange. This calculation uses the principle that arterial PCO2 reflects alveolar PCO2 in gas-exchanging regions, while expired air represents a mixture from both dead space and alveolar compartments.

Multiple factors affect dead space. Pulmonary embolism dramatically increases alveolar dead space by blocking blood flow to ventilated regions. Emphysema destroys alveolar septa, enlarging air spaces while reducing perfusion, thereby increasing dead space. Deep breathing reduces the dead space to tidal volume ratio because anatomical dead space remains constant while tidal volume increases. Conversely, rapid shallow breathing increases this ratio, potentially impairing gas exchange despite normal or elevated minute ventilation.

<image>Panel A: Conducting airways from nose to terminal bronchioles highlighted in blue representing anatomical dead space of approximately 150 mL. Panel B: Normal alveolus with matched ventilation and perfusion showing oxygen and carbon dioxide exchange across intact capillary. Panel C: Unperfused alveolus representing alveolar dead space with fresh air entering but no blood flow for gas exchange. Panel D: Bar diagram comparing normal versus pathological physiological dead space states with Bohr equation and normal values.</image>

III. Mechanics of Breathing

Breathing results from pressure differences between the atmosphere and the alveoli, created by the mechanical action of respiratory muscles. Understanding these pressure relationships explains how air flows into and out of the lungs and why certain conditions impair ventilation.

Several pressure terms require definition. Atmospheric pressure represents the pressure outside the body, conventionally set as zero for reference at sea level (760 mmHg absolute). Intrapleural pressure, the pressure within the pleural space between the visceral and parietal pleura, remains subatmospheric throughout the breathing cycle, typically around minus 5 centimeters of water at rest. Alveolar pressure equals atmospheric pressure at rest when no air flows. Transpulmonary pressure, the difference between alveolar and intrapleural pressure, maintains lung inflation against elastic recoil.

Inspiration begins when the diaphragm and external intercostal muscles contract. The diaphragm descends and the rib cage expands, increasing thoracic volume. As the chest wall expands, the pleural space enlarges, making intrapleural pressure more negative, dropping to approximately minus 8 centimeters of water. This increasingly negative intrapleural pressure pulls the lung outward through the intact pleural seal. As lung volume increases, alveolar pressure briefly drops below atmospheric pressure, to approximately minus 1 centimeter of water. This pressure difference drives air flow from the atmosphere into the alveoli. As air fills the expanding lungs, alveolar pressure returns to zero and airflow ceases, marking the end of inspiration.

Quiet expiration occurs passively, without muscle contraction. When the diaphragm relaxes, the elastic recoil of the lungs and chest wall compresses the alveoli. Intrapleural pressure becomes less negative, returning toward minus 5 centimeters of water. Alveolar pressure rises slightly above atmospheric, to approximately plus 1 centimeter of water. Air flows down this pressure gradient from alveoli to atmosphere until alveolar pressure again equals atmospheric pressure.

Forced expiration requires active muscle contraction. The internal intercostals and abdominal muscles contract, actively compressing the thoracic cavity and generating positive intrapleural and alveolar pressures. This forces air out more rapidly than passive recoil alone but can also cause dynamic airway compression, discussed later in the context of airway resistance.

<image>Panel A: Time-based graph showing lung volume, alveolar pressure, and intrapleural pressure traces through one complete breathing cycle. Panel B: Four chest diagrams at different respiratory phases showing diaphragm position and airflow direction with pressure values. Panel C: Pressure gradients driving airflow with arrows indicating flow from high to low pressure during each phase. Panel D: Color-coded phases distinguishing inspiration in blue and expiration in red with vertical phase demarcations.</image>

IV. Elastic Properties of the Respiratory System

Both the lungs and chest wall possess elastic properties that determine the resting lung volume and influence the work required for breathing. These elastic forces create a balance point at functional residual capacity and contribute significantly to lung mechanics.

Lung elastic recoil arises from two sources. Approximately one-third comes from elastic and collagen fibers woven throughout lung parenchyma, which stretch during inspiration and recoil during expiration. The remaining two-thirds derives from surface tension at the air-liquid interface lining alveoli. Together, these forces create an inward-directed recoil that constantly tends to collapse the lungs.

The chest wall also exhibits elastic properties, but with different characteristics. Below functional residual capacity, the chest wall tends to spring outward, opposing further lung collapse. At functional residual capacity, chest wall recoil outward exactly balances lung recoil inward. Above functional residual capacity, both the lungs and the chest wall recoil inward, favoring expiration.

Functional residual capacity represents the equilibrium point where these opposing forces balance. At this volume, intrapleural pressure remains subatmospheric because the lung's inward recoil creates tension on the visceral pleura while the chest wall's outward recoil creates tension on the parietal pleura. The pleural space, normally containing only a thin layer of fluid, transmits these forces while maintaining the functional seal between lung and chest wall.

Transpulmonary pressure, the difference between alveolar and intrapleural pressure, keeps the lungs inflated. This positive pressure (approximately plus 5 centimeters of water at rest) counteracts the elastic recoil that would otherwise collapse the lungs.

Pneumothorax demonstrates the importance of transpulmonary pressure. When air enters the pleural space through a chest wall wound or ruptured bleb, intrapleural pressure equilibrates with atmospheric pressure. Transpulmonary pressure drops to zero, and the lung collapses inward following its elastic recoil. Simultaneously, the chest wall, freed from the counterbalancing lung tension, springs outward. Treatment requires evacuating air from the pleural space and re-establishing the subatmospheric intrapleural pressure that maintains lung inflation.

<image>Panel A: Cross-section of thorax with arrows indicating inward lung recoil and outward chest wall recoil forces. Panel B: Graph plotting recoil tendency versus lung volume showing force vectors crossing at FRC equilibrium point. Panel C: Normal anatomy with intact pleural seal showing negative intrapleural pressure and pressure values. Panel D: Pneumothorax illustration showing air in pleural space, collapsed lung, and expanded chest wall with tissue movement arrows.</image>

V. Compliance

Compliance quantifies the distensibility of the respiratory system, relating volume change to the pressure required to produce that change. High compliance indicates an easily distensible system, while low compliance describes a stiff system requiring more pressure for equivalent volume changes.

Mathematical compliance equals the change in volume divided by the change in pressure, expressed in milliliters per centimeter of water. Normal lung compliance measures approximately 200 milliliters per centimeter of water, meaning a pressure change of 1 centimeter of water produces a 200 milliliter volume change. Chest wall compliance also approximates 200 milliliters per centimeter of water when measured independently. However, because these two elastic components act in series, total respiratory system compliance follows the reciprocal sum rule. The calculated total system compliance equals approximately 100 milliliters per centimeter of water.

The compliance curve demonstrates a sigmoid relationship between pressure and volume. At functional residual capacity, where normal breathing occurs, the curve reaches its steepest portion, indicating optimal compliance and efficient breathing. At very low lung volumes approaching residual volume, small airways collapse and alveoli resist inflation, flattening the curve. At very high lung volumes approaching total lung capacity, elastic fibers reach their extensibility limits and the curve again flattens.

Multiple conditions alter lung compliance. Emphysema destroys alveolar septa and elastic tissue, dramatically increasing compliance. The lungs become overly distensible and lose their elastic recoil, trapping air and making expiration difficult. Pulmonary fibrosis deposits excessive collagen in lung parenchyma, reducing compliance. The stiff lungs require excessive pressure to inflate, increasing the work of breathing. Acute respiratory distress syndrome floods alveoli with protein-rich edema and inflammatory cells, markedly decreasing compliance. Pulmonary edema similarly fills air spaces with fluid, reducing the volume available for gas exchange and stiffening the lungs. Surfactant deficiency, as in neonatal respiratory distress syndrome, increases surface tension and decreases compliance. Normal aging gradually increases lung compliance as elastic fibers degenerate, while chest wall compliance often decreases due to rib cage stiffening.

Chest wall compliance also varies with disease. Obesity decreases chest wall compliance by adding weight to the thoracic cage and restricting diaphragmatic descent. Kyphoscoliosis distorts thoracic geometry, limiting chest wall excursion. Ankylosing spondylitis fuses spinal and costovertebral joints, severely restricting chest wall movement.

<image>Panel A: Normal sigmoid pressure-volume curve showing lung volume versus transpulmonary pressure with slope at FRC representing compliance. Panel B: Left-shifted curve in blue representing increased compliance in emphysema with listed conditions. Panel C: Right-shifted curve in red representing decreased compliance in fibrosis with listed conditions. Panel D: Series relationship diagram between lung and chest wall compliance with formula for total compliance calculation.</image>

VI. Surface Tension and Surfactant

Surface tension at the air-liquid interface lining alveoli significantly influences lung mechanics. Without mechanisms to reduce surface tension, alveoli would be unstable and breathing extremely difficult. Pulmonary surfactant, produced by specialized alveolar cells, provides the essential solution to this physical challenge.

Surface tension arises when water molecules at an air interface attract each other more strongly than they attract air molecules. This creates an inward-directed force that tends to minimize surface area. In spherical alveoli, surface tension creates a collapsing pressure directed toward the alveolar center.

LaPlace's law quantifies this collapsing pressure: pressure equals twice the surface tension divided by the radius. This relationship predicts a serious problem for the lung. Smaller alveoli, having smaller radii, would experience higher collapsing pressures than larger alveoli. Without correction, small alveoli would empty into large alveoli, creating progressively fewer, larger air spaces rather than the millions of tiny alveoli needed for efficient gas exchange.

Surfactant solves this problem elegantly. Produced by type II pneumocytes, surfactant consists primarily of dipalmitoyl phosphatidylcholine along with surfactant proteins that regulate its function. Surfactant molecules accumulate at the air-liquid interface with their hydrophobic fatty acid tails pointing toward the air and hydrophilic heads in the aqueous layer.

The key to surfactant function lies in its behavior during breathing. As alveoli shrink during expiration, surfactant molecules become more concentrated at the reduced surface area, dramatically lowering surface tension. According to LaPlace's law, the decreased surface tension in small alveoli reduces their collapsing pressure, preventing emptying into larger alveoli. As alveoli expand during inspiration, surfactant molecules spread apart, allowing surface tension to rise and assisting elastic recoil that will drive the next expiration.

Surfactant provides several benefits beyond alveolar stability. By reducing surface tension, surfactant increases lung compliance, reducing the pressure needed to inflate the lungs and decreasing the work of breathing. Surfactant also reduces the hydrostatic pressure that would otherwise draw fluid from capillaries into alveoli, helping to keep alveoli dry.

Clinical conditions involving surfactant deficiency cause severe respiratory failure. Neonatal respiratory distress syndrome affects premature infants whose type II pneumocytes have not yet matured sufficiently to produce adequate surfactant. These infants develop atelectasis, hypoxemia, and require mechanical ventilation. Exogenous surfactant administration has transformed outcomes in this population. Acute respiratory distress syndrome in adults involves surfactant dysfunction from inflammatory damage, contributing to the decreased compliance and oxygenation difficulties characteristic of this condition.

<image>Panel A: LaPlace's law diagram showing large and small spheres experiencing different collapsing pressures at constant surface tension. Panel B: Surfactant molecules at alveolar air-liquid interface with phospholipid hydrophobic tails and hydrophilic heads. Panel C: Paired alveoli without surfactant showing small alveolus collapsing into large one due to higher pressure. Panel D: Paired alveoli with surfactant showing concentrated surfactant equalizing pressure and maintaining stability with color-coded components.</image>

VII. Airway Resistance

Airway resistance represents the opposition to airflow through the tracheobronchial tree. While the lungs' elastic properties determine how much pressure is needed to hold the lungs at a given volume, airway resistance determines how much pressure is needed to generate airflow.

Resistance mathematically equals the pressure difference divided by flow rate, expressed in centimeters of water per liter per second. Normal airway resistance measures 1 to 2 centimeters of water per liter per second during quiet breathing.

Poiseuille's law describes factors affecting resistance in tubes. Resistance relates inversely to the fourth power of radius, making airway caliber the dominant determinant of resistance. A reduction of airway radius by half increases resistance sixteen-fold. Resistance also increases proportionally with tube length and fluid viscosity. While these factors have less impact than radius, they become relevant in certain clinical conditions.

The distribution of airway resistance may seem counterintuitive. Despite their small individual diameters, the small airways contribute less than 10 percent of total airway resistance in healthy lungs. This occurs because the progressive branching creates an enormous aggregate cross-sectional area at the peripheral airways, dramatically reducing the contribution of each individual airway to total resistance. The upper airways, including the nose, pharynx, and larynx, contribute 40 to 50 percent of total resistance. Medium-sized bronchi contribute another 40 to 50 percent. This distribution has clinical implications: small airway disease may progress substantially before manifesting in standard pulmonary function tests, a phenomenon called the "silent zone" of the lung.

Multiple mechanisms increase airway resistance pathologically. Bronchoconstriction from smooth muscle contraction narrows airways in asthma and chronic obstructive pulmonary disease exacerbations. Mucus hypersecretion in chronic bronchitis reduces effective airway caliber. Airway wall edema from inflammation further narrows the lumen. External compression by tumors or lymph nodes may obstruct airways.

Dynamic airway compression represents a unique phenomenon during forced expiration. When expiratory muscles contract forcefully, they generate positive pleural pressure that compresses intrathoracic airways. At some point along the airways, called the equal pressure point, airway pressure exactly equals pleural pressure. Downstream from this point toward the mouth, pleural pressure exceeds airway pressure, causing airway compression. Flow becomes limited regardless of additional expiratory effort, creating the effort-independent portion of expiration visible on flow-volume loops.

<image>Panel A: Bronchial tree with color-coded resistance contributions showing upper airways, medium bronchi, and small airways with percentage bar graph. Panel B: Poiseuille's law illustration with tubes of different radii demonstrating the fourth-power relationship. Panel C: Cross-section through thorax during forced expiration showing positive pleural pressure and equal pressure point. Panel D: Dynamic airway compression with arrows indicating pressure values and flow direction where pleural exceeds airway pressure.</image>

VIII. Flow-Volume Loops

Flow-volume loops provide a visual representation of airflow during forced breathing maneuvers, offering valuable diagnostic information about obstructive and restrictive lung diseases. Understanding normal loop morphology and pathological patterns enables interpretation of pulmonary function testing.

To generate a flow-volume loop, the subject inhales maximally to total lung capacity, then exhales as forcefully and completely as possible to residual volume, followed by rapid inhalation back to total lung capacity. The test plots flow rate on the vertical axis against volume on the horizontal axis, with expiration above the baseline and inspiration below.

The normal expiratory limb rises sharply to peak expiratory flow early in expiration, then descends relatively linearly as lung volume decreases. The early peak occurs when lung elastic recoil is greatest and airways are widest. As expiration continues, decreasing lung volume reduces the driving pressure while dynamic compression limits flow, creating the characteristic declining pattern. The inspiratory limb forms a smooth curve, remaining effort-dependent throughout because negative pleural pressure during inspiration tends to open rather than compress intrathoracic airways.

Key measurements from flow-volume testing include forced vital capacity, the total volume exhaled during the maneuver. Forced expiratory volume in one second represents the volume exhaled in the first second and normally exceeds 80 percent of predicted values. The ratio of forced expiratory volume in one second to forced vital capacity normally exceeds 0.70 in adults, though this threshold decreases with age. Forced expiratory flow at 25 to 75 percent of vital capacity measures average flow during the middle portion of expiration, providing sensitivity to small airway dysfunction.

Obstructive diseases produce characteristic flow-volume loop changes. The expiratory limb shows a scooped or concave appearance as flow decreases disproportionately relative to volume. Peak expiratory flow diminishes. The ratio of forced expiratory volume in one second to forced vital capacity falls below 0.70. Total lung capacity often increases from hyperinflation, while residual volume rises substantially from air trapping.

Restrictive diseases produce a different pattern. The loop maintains a relatively normal shape but appears miniaturized, as if the normal loop were proportionally reduced in all dimensions. Both forced vital capacity and forced expiratory volume in one second decrease, but their ratio remains normal or even increases. Total lung capacity and residual volume both decrease.

Upper airway obstruction creates distinct patterns depending on location and whether the obstruction is fixed or variable. Fixed obstruction, as from tracheal stenosis, flattens both inspiratory and expiratory limbs equally. Variable extrathoracic obstruction, such as vocal cord paralysis, primarily affects inspiration because negative pressure during inspiration draws the floppy obstruction into the airway. Variable intrathoracic obstruction primarily affects expiration because positive pressure during forced expiration compresses the already compromised airway.

<image>Panel A: Normal flow-volume loop with labeled peak expiratory flow, volume axis from RV to TLC, and flow axis showing expiration above zero line. Panel B: Obstructive disease pattern with scooped expiratory limb and preserved TLC alongside restrictive disease miniature loop. Panel C: Fixed upper airway obstruction showing flattened inspiratory and expiratory limbs with clinical example. Panel D: Variable obstruction patterns showing extrathoracic with flattened inspiratory limb and intrathoracic with flattened expiratory limb.</image>

IX. Work of Breathing

Breathing requires metabolic work to overcome the elastic and resistive properties of the respiratory system. In health, this work represents a small fraction of total energy expenditure, but disease states may dramatically increase respiratory work, leading to dyspnea and potentially respiratory failure.

Total respiratory work divides into elastic and resistive components. Elastic work overcomes the recoil of the lungs and chest wall, stretching these structures during inspiration. This work is stored as potential energy and released during expiration, which normally occurs passively. Resistive work overcomes airway resistance and tissue viscous resistance, dissipating energy as heat. Unlike elastic work, resistive work cannot be recovered and must be performed during both inspiration and expiration.

Normal respiratory work consumes approximately 5 percent of total body oxygen consumption at rest. During exercise, both ventilation and respiratory work increase, but the proportion of total energy devoted to breathing remains manageable in healthy individuals.

Disease states alter the distribution and magnitude of respiratory work. Obstructive diseases such as asthma and chronic obstructive pulmonary disease increase resistive work. Narrowed airways require greater pressure gradients to generate adequate airflow. Additionally, expiration may require active muscle contraction rather than passive recoil, adding inspiratory and expiratory muscle work. Restrictive diseases such as pulmonary fibrosis increase elastic work. Stiff lungs require greater pressure to achieve adequate tidal volumes. Conditions affecting both properties may push total respiratory work beyond sustainable levels, leading to respiratory muscle fatigue and failure.

The respiratory system adapts breathing patterns to minimize work. Patients with obstructive disease tend toward slow, deep breathing, which reduces the flow rate and therefore the resistive work per breath. Patients with restrictive disease tend toward rapid, shallow breathing, which reduces the volume change per breath and therefore the elastic work. These adaptive patterns develop unconsciously but may be recognized clinically as characteristic breathing patterns in different disease states.

<image>Panel A: Pressure-volume loop during breathing cycle with area inside representing total work of breathing. Panel B: Elastic work as triangular area and resistive work as additional area between dynamic loop and static compliance curve. Panel C: Work distribution comparison in normal lungs, obstructive disease with blue-shaded resistive work, and restrictive disease with red-shaded elastic work. Panel D: Compensatory breathing patterns showing deep slow breaths in obstructive and rapid shallow breaths in restrictive disease.</image>

X. Clinical Applications

Pulmonary function testing translates the physiological concepts of ventilation into clinical practice, enabling diagnosis and monitoring of respiratory diseases. Understanding how to interpret these tests requires integrating knowledge of volumes, compliance, resistance, and flow-volume relationships.

The fundamental distinction in pulmonary function test interpretation separates obstructive from restrictive patterns. Obstructive disease, characterized by difficulty expelling air, produces a reduced forced expiratory volume in one second to forced vital capacity ratio, with the threshold typically set at 0.70. Forced expiratory volume in one second decreases disproportionately to forced vital capacity because airflow limitation primarily affects the active expiratory phase. Restrictive disease, characterized by difficulty taking a deep breath, shows reduced total lung capacity as the defining feature. Both forced expiratory volume in one second and forced vital capacity decrease, but their ratio remains normal or may even increase because the proportionally smaller lungs empty normally.

Bronchodilator response helps distinguish asthma from chronic obstructive pulmonary disease. In asthma, administration of an inhaled bronchodilator produces significant improvement in forced expiratory volume in one second, typically defined as an increase of at least 12 percent and 200 milliliters. Chronic obstructive pulmonary disease shows less reversibility, though some patients demonstrate partial responses.

Specific diseases produce recognizable patterns. Asthma exacerbation shows decreased forced expiratory volume in one second with air trapping evidenced by increased residual volume, substantially reversible with bronchodilators. Chronic obstructive pulmonary disease produces persistent airflow obstruction, increased total lung capacity from hyperinflation, and incomplete reversibility. Pulmonary fibrosis demonstrates decreased total lung capacity, decreased vital capacity, and a normal or increased ratio, with reduced diffusing capacity reflecting impaired gas transfer. Neuromuscular weakness reduces vital capacity and maximal inspiratory and expiratory pressures, with relatively preserved lung compliance.

Understanding these patterns enables appropriate diagnosis, guides therapy selection, and permits monitoring of disease progression or treatment response. Pulmonary function testing remains a cornerstone of respiratory medicine practice.

<image>Panel A: Flowchart beginning with spirometry branching based on FEV1/FVC ratio less than or greater than 0.70. Panel B: Obstructive pathway leading to bronchodilator testing distinguishing asthma from COPD based on reversibility. Panel C: Restrictive pathway with TLC measurement, diffusing capacity, and maximal pressures distinguishing parenchymal from neuromuscular causes. Panel D: Summary table comparing FVC, FEV1, ratio, TLC, and RV values across obstructive and restrictive patterns with common diagnoses.</image>

Summary

Lung volumes and capacities describe the compartmentalization of air within the respiratory system. Tidal volume, inspiratory reserve, expiratory reserve, and residual volume combine in various ways to form the clinically important capacities. Functional residual capacity, the resting lung volume after passive expiration, represents the equilibrium between inward lung recoil and outward chest wall recoil.

Breathing mechanics depend on pressure differences created by respiratory muscles. Diaphragm contraction increases thoracic volume, making intrapleural pressure more negative. This expanding negative pressure lowers alveolar pressure below atmospheric, driving air into the lungs. Expiration reverses these changes, with passive elastic recoil raising alveolar pressure above atmospheric and driving air out.

Compliance describes the distensibility of the respiratory system, with high compliance in emphysema where elastic tissue is destroyed, and low compliance in fibrosis where collagen deposition stiffens the lungs. Surfactant, produced by type II pneumocytes, reduces alveolar surface tension, increases compliance, and stabilizes alveoli of different sizes against collapse.

Airway resistance follows Poiseuille's law, with radius as the dominant determinant due to the fourth-power relationship. Major resistance occurs in medium-sized bronchi, while the small airways contribute relatively little due to their enormous aggregate cross-sectional area. Dynamic airway compression during forced expiration limits flow regardless of effort, creating the characteristic shape of flow-volume loops.

Work of breathing combines elastic work to overcome recoil with resistive work to generate airflow. Obstructive diseases increase resistive work, while restrictive diseases increase elastic work. Breathing pattern adaptations minimize total work under different conditions.

Pulmonary function testing distinguishes obstructive from restrictive patterns. An FEV1/FVC ratio below 0.70 indicates obstruction, while reduced total lung capacity confirms restriction. Bronchodilator responsiveness, diffusing capacity, and other measurements further refine the diagnosis.

Key Terms

This content is subject to the MIT License. © 2024–2026 Hibbert School of Medicine.

Read this lecture as Markdown