Lung elasticity is one of the most important mechanical properties of the respiratory system. Every breath depends on the lungs’ ability to expand during inspiration and recoil during expiration. This balance between stretch and recoil allows ventilation to occur efficiently with minimal energy expenditure.
When elasticity is altered, breathing mechanics change significantly and can lead to respiratory distress or chronic disease.
For respiratory therapists, understanding lung elasticity is essential for interpreting compliance, managing mechanical ventilation, and recognizing disorders such as emphysema and pulmonary fibrosis.
What Is Lung Elasticity?
Lung elasticity refers to the natural tendency of the lungs to return to their original resting size after being stretched or inflated. This property is primarily determined by elastic fibers, including elastin and collagen, located within the lung parenchyma. When these fibers are stretched during inspiration, they generate tension. When the inspiratory muscles relax, the stored elastic energy causes the lungs to recoil, allowing air to flow out passively.
This concept can be compared to a spring. The more a spring is stretched, the greater the force pulling it back toward its original length. However, there is a limit. As the lungs approach total lung capacity, progressively greater pressure is required to achieve further expansion. At very high volumes, the pressure-volume curve flattens, indicating increasing resistance to additional stretch. If excessive force is applied, structural damage can occur, just as a spring can break when overstretched.
Elastic recoil is essential for normal breathing. During quiet respiration, expiration does not require active muscular effort. Instead, it is driven almost entirely by the elastic recoil of the lungs and chest wall. Without sufficient recoil, air becomes trapped and exhalation becomes inefficient.
The Role of Surface Tension and Hysteresis
Lung elasticity is not determined solely by tissue fibers. Surface tension within the alveoli also contributes significantly to the lung’s recoil properties. The alveoli are lined with a thin liquid layer. The surface tension at the air-liquid interface creates inward forces that promote alveolar collapse. During inflation, additional pressure is needed to overcome these forces. During deflation, surface tension decreases, which alters the pressure-volume relationship.
This difference between inflation and deflation is known as hysteresis. On a pressure-volume curve, the path of inflation does not exactly match the path of deflation. At a given pressure, lung volume during deflation is slightly greater than during inflation. One reason for this is the behavior of collapsed alveoli. During inspiration, extra pressure may be required to open previously collapsed alveoli. Once opened, they tend to remain open during expiration until very low lung volumes are reached.
Hysteresis has important clinical implications, particularly in conditions where alveolar collapse is common. It explains why certain ventilator strategies, such as applying positive end-expiratory pressure (PEEP), help maintain alveolar stability and reduce the work of reopening lung units with each breath.
Lung Compliance vs. Elasticity
Although closely related, compliance and elasticity describe opposite mechanical characteristics. Compliance refers to the ease with which the lungs expand, while elasticity refers to the tendency of the lungs to recoil. A highly compliant lung stretches easily but has reduced recoil. A stiff lung has low compliance but strong recoil.
Compliance is calculated as the change in volume divided by the change in pressure. For respiratory therapists, compliance measurements provide insight into lung mechanics and disease states. Static compliance, measured when airflow is momentarily zero, reflects elastic properties without the influence of airway resistance. Changes in compliance can indicate worsening pathology, improvement after treatment, or complications such as pneumothorax or pulmonary edema.
Understanding the balance between compliance and elasticity allows clinicians to interpret ventilator data accurately and adjust settings appropriately.
Lung Elasticity in Obstructive Diseases
One of the most clinically relevant examples of altered lung elasticity occurs in emphysema, a form of chronic obstructive pulmonary disease (COPD). In emphysema, destruction of elastin fibers within the alveolar walls reduces elastic recoil. As a result, the lungs become more compliant but less capable of returning to their resting size.
Although inflation may seem easier, expiration becomes impaired. Small airways, which rely on surrounding elastic tissue to remain open, are more prone to collapse during exhalation. This leads to air trapping, hyperinflation, and increased residual volume. Patients often experience prolonged expiration and dyspnea.
For respiratory therapists, recognizing increased compliance on ventilator measurements or pulmonary function testing can signal loss of elastic recoil. Management strategies must account for the risk of dynamic hyperinflation and intrinsic PEEP in these patients.
Lung Elasticity in Restrictive Diseases
The opposite pattern is seen in restrictive lung diseases such as pulmonary fibrosis. In these conditions, lung tissue becomes stiff due to increased collagen deposition and scarring. Compliance decreases, and higher pressures are required to achieve adequate lung expansion.
Patients with restrictive disorders often exhibit rapid, shallow breathing because large tidal volumes require significant effort. On mechanical ventilation, elevated plateau pressures may reflect reduced compliance. Careful ventilator management is necessary to prevent barotrauma while ensuring sufficient ventilation.
Note: Understanding elasticity helps respiratory therapists distinguish between obstructive and restrictive patterns and tailor interventions accordingly.
Relevance to Mechanical Ventilation and Respiratory Care
Lung elasticity is central to mechanical ventilation management. Ventilators deliver pressure or volume to inflate the lungs, but the response depends on the lung’s elastic properties. In stiff lungs, higher pressures may be required. In highly compliant lungs, overdistention can occur if volumes are not carefully controlled.
Monitoring plateau pressure provides insight into alveolar pressure and static compliance. Trends in compliance can reveal improvement or deterioration in lung condition. Adjusting tidal volume, inspiratory pressure, and PEEP requires a thorough understanding of how elastic forces influence lung mechanics.
Elasticity also affects oxygenation strategies. Recruitment maneuvers and PEEP help stabilize alveoli in conditions characterized by collapse. By maintaining open lung units, clinicians reduce the pressure required to inflate the lungs on subsequent breaths and improve gas exchange efficiency.
Note: Beyond mechanical ventilation, lung elasticity plays a role in pulmonary function testing, assessment of dyspnea, and long-term disease monitoring. It connects foundational physiology with everyday clinical decision-making in respiratory care.
Lung Elasticity Practice Questions
1. What is lung elasticity?
The tendency of the lungs to return to their resting volume after being stretched during inspiration.
2. What are the two primary components that determine lung elasticity?
Elastic fibers (elastin and collagen) in the lung parenchyma and surface tension within the alveoli.
3. How does lung recoil contribute to normal breathing?
Elastic recoil drives passive expiration during quiet breathing.
4. What happens to elastic fibers during inspiration?
They stretch and store potential energy.
5. What occurs when inspiratory effort ends?
Stored elastic energy causes the lungs to recoil passively.
6. Which law describes the proportional relationship between stretch and tension in elastic structures?
Hooke’s law
7. What is meant by transpulmonary pressure?
The difference between alveolar pressure and pleural pressure.
8. How is lung elasticity studied experimentally?
By placing an excised lung in an airtight chamber and altering transpulmonary pressure.
9. Why is airflow stopped during pressure-volume measurements?
To eliminate resistive forces and measure only elastic properties.
10. What does the pressure-volume (P-V) curve represent?
The relationship between transpulmonary pressure and lung volume.
11. What happens to the P-V curve as the lungs approach total lung capacity (TLC)?
The curve flattens, indicating decreased compliance and increased resistance to stretch.
12. Why is more pressure required to inflate the lungs at high volumes?
Elastic fibers are maximally stretched and oppose further expansion.
13. What is hysteresis in lung mechanics?
The difference between inflation and deflation pressure-volume curves.
14. During deflation, how does lung volume compare to inflation at the same pressure?
Volume is slightly greater during deflation.
15. What is the main cause of hysteresis in the lungs?
Surface tension effects and recruitment of collapsed alveoli.
16. Why is more pressure required to inflate collapsed alveoli?
Additional pressure is needed to overcome surface tension and open them.
17. How does surfactant influence lung elasticity?
It reduces alveolar surface tension and decreases the work required for inflation.
18. What contributes to lung recoil?
Elastic tissue fibers and alveolar surface tension.
19. What happens to lung compliance in emphysema?
Compliance increases due to destruction of elastic fibers.
20. Why do patients with emphysema have difficulty exhaling?
Reduced elastic recoil leads to air trapping.
21. How does fibrosis affect lung elasticity?
It increases stiffness and reduces compliance.
22. What is compliance?
The change in lung volume per unit change in transpulmonary pressure.
23. How is compliance related to elasticity?
High elasticity corresponds to low compliance, and vice versa.
24. What happens to pleural pressure during inspiration?
It becomes more negative.
25. Why does negative pleural pressure inflate the lungs?
It increases transpulmonary pressure, expanding alveoli.
26. What is total lung capacity (TLC)?
The maximum volume of air the lungs can hold.
27. Why does the lung not collapse completely in the intact chest?
Opposing forces between lung recoil and chest wall expansion maintain functional residual capacity (FRC).
28. What role does the chest wall play in lung elasticity?
It has its own elastic properties that interact with lung recoil.
29. How does lung volume history affect elasticity?
Prior inflation or deflation alters surfactant distribution and hysteresis.
30. What is the clinical significance of reduced elastic recoil?
It impairs passive expiration and may lead to hyperinflation.
31. Why is elastic recoil important for effective coughing?
It generates expiratory flow necessary to clear secretions.
32. What happens to elastic recoil in aging?
It gradually decreases due to structural changes in lung tissue.
33. How does ARDS affect lung elasticity?
It decreases compliance due to alveolar collapse and inflammation.
34. What is the relationship between elasticity and work of breathing?
Increased stiffness increases the work required for inspiration.
35. Why does the P-V curve shift in diseased lungs?
Changes in compliance alter the pressure required for inflation.
36. What occurs if excessive tension is applied to lung tissue?
Overdistention may cause lung injury or barotrauma.
37. How does elastic recoil influence expiratory airflow?
Greater recoil increases driving pressure for exhalation.
38. Why is surface tension a major component of lung recoil?
Because alveoli are lined with fluid that naturally resists expansion.
39. What is the effect of decreased surfactant on elasticity?
Surface tension increases, making inflation more difficult.
40. Why must pressure increase disproportionately near maximal lung inflation?
Because elastic fibers approach their limit of stretch and strongly resist expansion.
41. What are the primary pathophysiologic mechanisms that contribute to airflow obstruction in COPD?
Inflammation and narrowing of small airways (<2 mm in diameter), loss of elastic recoil (as in emphysema), and bronchospasm.
42. How does destruction of elastin in emphysema contribute to airflow limitation?
Loss of elastic recoil reduces radial traction on small airways, promoting airway collapse during exhalation.
43. Why are small airways particularly vulnerable to collapse in emphysema?
They lack cartilaginous support and rely on surrounding elastic tissue to remain open.
44. Using a balloon analogy, how does high compliance relate to elasticity?
A balloon that inflates easily is highly compliant but has reduced elasticity (poor recoil).
45. How does a golf ball compared to a tennis ball illustrate elasticity?
A golf ball resists deformation and returns to shape (high elasticity), whereas a tennis ball is more compliant and compresses easily.
46. How do diseases of the lung or chest wall affect total respiratory system compliance?
They alter the pressure required to inflate the lungs by changing lung or thoracic compliance.
47. How does acute respiratory distress syndrome (ARDS) affect lung compliance?
ARDS reduces lung compliance, requiring higher pressures to achieve adequate ventilation.
48. How does kyphoscoliosis impact respiratory mechanics?
It decreases chest wall compliance, increasing the work required for lung expansion.
49. How does emphysema affect pulmonary compliance?
Pulmonary compliance increases due to loss of elastic fibers.
50. Why does emphysema require less pressure to inflate the lungs?
Because the lungs are more compliant due to reduced elastic recoil.
51. What does the pressure-volume (P-V) curve illustrate?
The relationship between transpulmonary pressure and lung volume.
52. How is lung elasticity studied using a laboratory model?
An excised lung is placed in an airtight chamber, and changes in transpulmonary pressure are measured against volume changes.
53. Why is increasingly negative pleural pressure required at higher lung volumes?
Because elastic forces opposing inflation increase as lung volume rises.
54. What happens to compliance as lung volume approaches total lung capacity (TLC)?
Compliance decreases as the P-V curve flattens.
55. What is hysteresis in lung mechanics?
The difference between the inflation and deflation limbs of the pressure-volume curve.
56. During deflation, how does lung volume compare to inflation at the same pressure?
Lung volume is slightly greater during deflation than inflation at the same pressure.
57. What does hysteresis indicate about lung mechanics?
That surface tension and alveolar recruitment influence lung elasticity beyond tissue fiber forces.
58. How does alveolar surface tension contribute to elastic recoil?
Surface tension creates inward forces that promote alveolar collapse.
59. Why is additional pressure required during lung inflation?
To overcome both elastic tissue resistance and alveolar surface tension.
60. How does surfactant improve lung compliance?
It reduces alveolar surface tension, lowering the pressure required for inflation.
61. What happens to lung compliance in neonatal respiratory distress syndrome?
Compliance decreases due to insufficient surfactant.
62. How are compliance and elasticity mathematically defined?
Compliance = Change in Volume / Change in Pressure; elasticity is the tendency to recoil.
63. What is the relationship between compliance and elasticity?
They are inversely related; high compliance corresponds to low elasticity.
64. How does a stiff lung differ from a highly compliant lung?
A stiff lung has low compliance and strong recoil; a compliant lung expands easily but recoils poorly.
65. Why is monitoring compliance important in mechanically ventilated patients?
Changes may indicate disease progression, improvement, or ventilator-induced lung injury.
66. In healthy lungs, how does elastic recoil assist breathing?
It promotes passive expiration and maintains airway patency.
67. How does elastic recoil help maintain functional residual capacity (FRC)?
It balances outward chest wall forces to establish a stable resting lung volume.
68. What role does radial traction play in airway patency?
Elastic tissue exerts outward pull on small airways, preventing collapse during exhalation.
69. Why are small airways (<2 mm) dependent on elastic support?
They lack cartilage and rely on surrounding parenchymal tethering.
70. How does loss of elasticity affect expiratory airflow?
Reduced recoil decreases driving pressure, leading to airflow limitation and air trapping.
71. What structural changes occur in emphysema that alter lung elasticity?
Destruction of elastin fibers and alveolar walls leads to increased compliance and decreased elastic recoil.
72. How does increased compliance in emphysema affect lung inflation?
The lungs inflate more easily but lack the ability to recoil effectively during exhalation.
73. Why does loss of elastic recoil in emphysema lead to air trapping?
Reduced radial traction allows small airways to collapse during exhalation, preventing complete emptying of the lungs.
74. How does emphysema affect residual volume (RV) and total lung capacity (TLC)?
Both RV and TLC are typically increased due to hyperinflation and air trapping.
75. What clinical signs are associated with decreased elastic recoil in emphysema?
Prolonged expiration, wheezing, dyspnea, and hyperinflated lungs.
76. On a ventilator, what finding may suggest increased lung compliance in a patient with emphysema?
Lower airway pressures for a given tidal volume, indicating reduced elastic resistance.
77. How does pulmonary fibrosis alter lung elasticity compared with emphysema?
Fibrosis decreases compliance and increases elastic recoil, making the lungs stiff.
78. Why do patients with pulmonary fibrosis often exhibit rapid, shallow breathing?
Large tidal volumes require excessive pressure due to low compliance, increasing the work of breathing.
79. What ventilator pressure pattern is commonly observed in fibrotic lungs?
Elevated peak and plateau pressures due to reduced compliance.
80. Why is barotrauma a concern in patients with pulmonary fibrosis?
Higher pressures are required to ventilate stiff lungs, increasing the risk of alveolar injury.
81. What is the clinical significance of hysteresis in lung mechanics?
It explains why higher pressures are needed to open collapsed alveoli than to keep them open.
82. Why are recruitment maneuvers used in conditions such as ARDS?
To apply sufficient pressure to open collapsed alveoli and improve oxygenation.
83. How does positive end-expiratory pressure (PEEP) improve oxygenation?
PEEP prevents alveolar collapse at end expiration, stabilizing lung units and reducing shunt.
84. In what clinical conditions is hysteresis particularly relevant?
ARDS, atelectasis, and postoperative lung collapse.
85. What does plateau pressure primarily reflect during mechanical ventilation?
Alveolar pressure and static compliance of the respiratory system.
86. What does an elevated plateau pressure suggest about lung mechanics?
Decreased compliance due to stiffness, edema, fibrosis, or other pathology.
87. Why must tidal volume be carefully adjusted in patients with stiff lungs?
To prevent ventilator-induced lung injury from excessive pressures.
88. What could a sudden decrease in measured compliance indicate in a ventilated patient?
Worsening ARDS, pneumothorax, pulmonary edema, or mucus plugging.
89. Why should overdistention be avoided in patients with highly compliant lungs?
Overinflation can worsen hyperinflation and increase the risk of barotrauma.
90. How does understanding lung elasticity help individualize ventilator settings?
It allows clinicians to tailor pressures, volumes, and PEEP based on lung mechanics.
91. In obstructive lung disease such as emphysema, how are expiratory flow rates affected?
Expiratory flow rates are reduced due to airway collapse and decreased recoil.
92. What pulmonary function test (PFT) pattern is typical of emphysema?
Increased compliance, increased RV and TLC, and decreased expiratory flow rates.
93. What PFT findings are typical of restrictive lung disease such as fibrosis?
Decreased compliance and reduced lung volumes with preserved or increased recoil.
94. How does elastic recoil influence expiratory airflow?
Greater recoil increases the driving pressure for exhalation.
95. How does decreased elastic recoil affect functional residual capacity (FRC)?
FRC increases due to incomplete lung emptying and hyperinflation.
96. Why is elastic recoil essential for maintaining airway patency during exhalation?
It provides radial traction that keeps small airways open.
97. How does increased collagen deposition in fibrosis affect lung mechanics?
It stiffens lung tissue, decreasing compliance and increasing recoil.
98. Why is monitoring compliance trends important in critical care?
Changes may reflect improvement or deterioration in lung condition.
99. How does elasticity influence the distribution of ventilation?
Altered elastic properties can cause uneven filling and emptying of lung units.
100. Why is knowledge of lung elasticity essential for lung-protective ventilation strategies?
Because setting appropriate pressures and volumes depends on understanding compliance and recoil.
Final Thoughts
Lung elasticity is a fundamental property that allows the lungs to expand and recoil with each breath. It results from the combined effects of elastic tissue fibers and surface tension within the alveoli. When elasticity is balanced, breathing is efficient and largely passive during expiration. When it is altered, as in emphysema or fibrosis, respiratory mechanics change dramatically.
For respiratory therapists, understanding lung elasticity is essential for interpreting compliance, managing ventilators, applying PEEP appropriately, and recognizing disease progression. Mastery of this concept strengthens clinical judgment and enhances the quality of patient care across all areas of respiratory practice.
Written by:
John Landry is a registered respiratory therapist from Memphis, TN, and has a bachelor's degree in kinesiology. He enjoys using evidence-based research to help others breathe easier and live a healthier life.
References
- Bhana RH, Magan AB. Lung Mechanics: A Review of Solid Mechanical Elasticity in Lung Parenchyma. J Elast. 2023.