Airway Resistance: Overview and Practice Questions (2025)

Airway resistance plays a crucial role in the mechanics of breathing and overall lung function. It refers to the opposition to airflow within the respiratory tract, primarily caused by friction as air moves through the airways.

Understanding airway resistance is essential for students, clinicians, and anyone involved in respiratory care, as it influences how easily air can enter and exit the lungs. Factors such as airway diameter, flow rate, and lung volume all affect resistance, which can vary significantly between healthy individuals and those with respiratory conditions like asthma or COPD.

In this article, we’ll explore what airway resistance is, how it’s measured, and why it matters in both normal and diseased states.

What Is Airway Resistance?

Airway resistance (Raw) refers to the resistance to airflow as gas moves through the respiratory tract. This resistance results from friction between the gas molecules and the walls of the airways. It is a key component of the total respiratory resistance and has a direct effect on the work of breathing. In simple terms, the narrower the airway, the more resistance the air will encounter, making it harder to breathe.

Airway resistance is one of the main factors that determine how easily air can move in and out of the lungs during breathing. It is especially relevant in conditions such as asthma, chronic obstructive pulmonary disease (COPD), and bronchitis, where the airways become inflamed or narrowed, thereby increasing resistance and causing breathing difficulties.

Formula for Airway Resistance

In respiratory physiology, resistance is calculated using the ratio of pressure to flow:

Resistance = ΔP / V̇

Where:

• ΔP is the pressure difference required to produce airflow
• V̇ is the flow rate (in liters per second)

For airway resistance specifically, the pressure difference used is called transairway pressure (ΔPTA)—the difference between the pressure at the mouth and the pressure inside the alveoli.

Thus, the equation for airway resistance becomes:

Raw = ΔPTA / V̇

The units of measurement are typically cmH₂O/L/sec.

Normal Values and Clinical Relevance

In healthy adults, airway resistance typically ranges from 0.5 to 2.5 cmH₂O/L/sec. This means that to generate a flow of 1 liter per second, a pressure of only 0.5 to 2.5 cm H₂O is required. When airway resistance increases—due to bronchospasm, inflammation, or obstruction—greater pressure is needed to move the same volume of air, increasing the work of breathing.

Elevated airway resistance can be a sign of:

• Bronchoconstriction (as in asthma)
• Airway inflammation or edema
• Mucus plugging
• Foreign body obstruction

Note: Monitoring and managing airway resistance is critical in ventilated patients and those with chronic respiratory diseases.

How Is Airway Resistance Measured?

Airway resistance is typically measured in a pulmonary function laboratory, especially in patients who are breathing spontaneously. Two key tools are used:

• Pneumotachometer: Measures the flow rate of air entering and exiting the lungs.
• Body Plethysmograph: An airtight box that the patient sits in to measure changes in pressure and volume.

During the test:

• The airway is momentarily occluded.
• With no airflow, the mouth pressure equals alveolar pressure.
• The device calculates airway resistance by relating pressure changes in the plethysmograph to airflow measurements.

Note: This method allows for an accurate assessment of airway resistance under controlled conditions.

Factors That Influence Airway Resistance

Several factors can influence airway resistance, and understanding them helps in both diagnosis and treatment planning. These include:

• Airway Diameter: The most significant factor affecting airway resistance is the diameter of the airways. According to Poiseuille’s law, resistance is inversely proportional to the fourth power of the radius of the airway. This means even a small decrease in airway diameter can lead to a dramatic increase in resistance. Conditions like asthma, bronchitis, and anaphylaxis can cause airway narrowing and lead to increased resistance.
• Lung Volume: At higher lung volumes, the airways are stretched open, reducing resistance. Conversely, at lower lung volumes, airways become narrower, increasing resistance. This is why patients with obstructive lung disease often breathe at higher lung volumes to keep their airways more open.
• Airflow Pattern: Turbulent airflow, which occurs in larger airways and during rapid breathing, increases resistance compared to laminar flow, which is smooth and occurs at slower rates in smaller airways. Factors like airway obstruction or artificial airways (e.g., endotracheal tubes) can also cause turbulence.
• Gas Properties: The viscosity and density of the gas being inhaled can influence resistance. For example, breathing a dense gas like oxygen increases resistance more than a low-density gas like helium. This is why heliox therapy (a mixture of helium and oxygen) is sometimes used to reduce airway resistance in severe obstruction.

Airway Resistance in Disease States

In healthy individuals, airway resistance remains low, allowing for effortless breathing. However, in disease states, resistance often increases significantly:

• Asthma: Bronchospasm, inflammation, and mucus plugging lead to narrowed airways, dramatically increasing Raw.
• COPD: Chronic inflammation and structural changes in the lungs cause persistent elevation in airway resistance.
• Bronchiectasis: Damaged and dilated airways can trap secretions, increasing resistance and impairing ventilation.
• Croup or Epiglottitis: In children, even minimal swelling in small airways can result in dangerously high resistance.

Note: Understanding how resistance changes in these conditions helps guide the use of bronchodilators, corticosteroids, and other therapeutic interventions.

Airway Resistance in Mechanical Ventilation

Airway resistance is a crucial parameter when managing patients on mechanical ventilation. Elevated resistance can lead to increased peak inspiratory pressures (PIP), making it harder to deliver adequate tidal volumes. Causes in ventilated patients may include:

• Kinked or blocked endotracheal tubes
• Bronchospasm
• Airway secretions
• Patient-ventilator asynchrony

Note: Monitoring Raw in these patients helps identify airway problems early and guides appropriate interventions, such as suctioning or bronchodilator therapy.

Airway Resistance Practice Questions

1. What is airway resistance?
It refers to the resistance to airflow within the respiratory tract during breathing.

2. What is the primary cause of airway resistance?
Internal friction between gas molecules and friction between the gas and the airway walls.

3. Which airway segment contributes the most to total airway resistance?
The medium-sized bronchi (around the 7th generation of airway branching).

4. Why do smaller airways contribute less to resistance than medium-sized bronchi?
They are numerous and arranged in parallel, reducing total resistance like capillaries.

5. What factors can increase airway resistance?
Rapid breathing, airway narrowing, low lung volume, bronchospasm, increased gas density or viscosity.

6. Which has a greater effect on airway resistance: gas density or viscosity?
Gas density has a greater effect, especially during turbulent flow.

7. How is residual volume (RV) affected in obstructive lung diseases?
It is increased due to air trapping.

8. What physiological change does restrictive lung disease primarily cause?
It reduces lung expansion, not airway resistance.

9. What physiological change does obstructive lung disease primarily cause?
It increases airway resistance.

10. Where is the major site of airway resistance in the lung?
The segmental bronchi (approximately Z3–Z7).

11. Why don’t alveoli significantly contribute to airway resistance?
There are hundreds of millions of alveoli arranged in parallel with laminar flow.

12. What type of muscle surrounds the segmental bronchi?
Smooth muscle, controlled by both sympathetic and parasympathetic nervous systems.

13. What effect does sympathetic stimulation have on bronchial smooth muscle?
It causes relaxation and bronchodilation via epinephrine and norepinephrine.

14. What effect does parasympathetic stimulation have on bronchial smooth muscle?
It causes contraction and bronchoconstriction via acetylcholine.

15. Why do epinephrine and norepinephrine cause opposite effects in blood vessels vs. airways?
They act on different receptors: alpha receptors cause vasoconstriction, beta-2 receptors cause bronchodilation.

16. What happens to airway resistance during an asthma attack?
It significantly increases due to smooth muscle hyperconstriction and inflammation.

17. What determines the balance of airway tone at rest?
The relative influence of sympathetic and parasympathetic nervous system activity.

18. What is a typical treatment for mild, exercise-induced asthma?
A short-acting beta-2 agonist like albuterol.

19. What is the usual treatment for allergen-induced moderate asthma?
Albuterol and antihistamines such as diphenhydramine (Benadryl).

20. What must be treated in severe asthma to reduce airway resistance?
Airway inflammation using corticosteroids like prednisone.

21. Why can increased airway resistance be beneficial at low lung volumes?
It helps preserve residual volume (RV) and prevents complete alveolar collapse.

22. What happens to pleural pressure during maximum expiration?
It rises to approximately +30 cm H₂O, which compresses the airways.

23. Why don’t alveoli collapse under high pleural pressure during exhalation?
Because the pressure drop occurs in the bronchi, not the alveoli, allowing airways to stay open.

24. What is the role of segmental bronchi during forced expiration?
They act as a resistor, increasing pressure below and reducing airflow, protecting alveoli.

25. How does airway resistance help maintain the lungs’ residual volume?
It prevents complete exhalation by limiting airflow at very low lung volumes.

26. What is the benefit of high resistance at the end of exhalation?
It helps maintain alveolar patency and allows a prolonged exhalation time (~5 seconds).

27. Why does airflow stop even when airways remain open at RV?
Resistance becomes so high that the pressure gradient can no longer drive flow.

28. How does cartilage help airways resist collapse during forced exhalation?
It provides structural support above the resistor to keep airways partially open.

29. What are the two main benefits of airway resistance during forced exhalation?
It ensures residual volume and prevents damage to delicate alveolar structures.

30. What condition is characterized by dynamic airway compression and increased resistance during exhalation?
Obstructive lung disease, such as asthma or COPD.

31. What is the equal pressure point (EPP)?
It is the point during forced expiration where alveolar pressure equals intrapleural pressure.

32. Where does the EPP normally occur in healthy lungs?
In the segmental bronchi, where cartilage helps keep the airways open during exhalation.

33. What can cause the EPP to shift distally towards smaller airways?
Diseases such as emphysema weaken airway walls, moving the EPP closer to the alveoli.

34. What is the consequence of the EPP moving to the alveolar region (e.g., Z16–Z17)?
Increased airway collapse and significant air trapping, which raises residual volume.

35. Why does the EPP move distally as expiration progresses?
Because alveolar pressure decreases along the airway path while intrapleural pressure remains high.

36. What happens if the EPP occurs in smaller, cartilage-free airways?
The airways may collapse, leading to airflow limitation and air trapping.

37. Can increasing expiratory effort overcome EPP?
No, because both alveolar and intrapleural pressures increase equally, so the EPP does not change favorably.

38. What is dynamic airway compression?
Airway narrowing that occurs during forced expiration when intrapleural pressure exceeds airway pressure.

39. What is the Starling resistor effect?
When greater pleural pressure compresses the airway at or beyond the EPP, limiting airflow despite increased effort.

40. What happens during forced expiration in a patient with airway disease?
Weakened airways collapse prematurely, causing air-trapping and obstructed airflow.

41. What characterizes restrictive lung diseases?
Decreased total lung capacity (TLC) and vital capacity (VC) due to impaired lung inflation.

42. What characterizes obstructive lung diseases?
Increased residual volume (RV) and decreased VC due to airflow obstruction.

43. Why is it easier for asthmatics to inhale than to exhale?
Because airway resistance decreases during inhalation and increases during exhalation.

44. What does the FEV1/FVC ratio measure?
The proportion of air exhaled in the first second relative to the total forced vital capacity.

45. What is the normal FEV1/FVC ratio?
Approximately 0.80 or 80%, meaning 80% of the air is exhaled in the first second.

46. What are normal FEV1 and FVC values?
FVC is about 5 liters, and FEV1 is about 4 liters.

47. How does the FEV1/FVC ratio appear in restrictive disease?
It remains normal or high (>0.80), despite both FEV1 and FVC being reduced.

48. How does the FEV1/FVC ratio appear in obstructive disease?
It is significantly reduced (<0.80), due to decreased airflow in the first second.

49. What four factors influence the FVC or how fast we can exhale?
Muscle strength, airway resistance, lung size, and lung elasticity.

50. Why is vital capacity reduced in both restrictive and obstructive disease?
In restrictive disease due to decreased TLC; in obstructive disease due to increased RV.

51. What is laminar airflow?
Smooth flow that requires the least energy, typically in the alveolar region (Reynolds number <2000).

52. What is transitional airflow?
Mixed flow pattern requiring more pressure to maintain, common in bronchi (Reynolds number 2000–4000).

53. What is turbulent airflow?
Disorganized flow that requires greater pressure change, common in the trachea (Reynolds number >4000).

54. How does airflow change in chronic bronchitis?
Turbulence extends deeper into the airways, increasing resistance and effort needed to breathe.

55. What causes crackles heard on auscultation?
Air reopening previously collapsed airways; also associated with turbulent airflow.

56. Who is most likely to have audible crackles?
Infants, elderly patients, or those with airway disease and premature airway closure.

57. What role does dynamic airway compression play in expiration?
It limits airflow and helps establish the residual volume by preventing full lung deflation.

58. How does airway resistance change with lung volume?
It increases at lower lung volumes, especially during forced expiration.

59. What is the formula for airway resistance (Raw)?
Raw = ∆P / V, where ∆P is pressure change and V is airflow.

60. What does ∆P represent in the airway resistance formula?
The pressure difference between two points in the airway.

61. What is represented by “V” in the airway resistance formula?
Flow rate of gas through the airways.

62. How is pressure change (∆P) typically measured?
By subtracting plateau pressure from peak inspiratory pressure during mechanical ventilation.

63. What two pressures are used to calculate airway resistance?
Peak Inspiratory Pressure (PIP) and Plateau Pressure.

64. What does Peak Inspiratory Pressure (PIP) represent?
The maximum pressure achieved when air is being delivered into the lungs.

65. When is Plateau Pressure measured?
It is measured during an inspiratory hold when airflow is momentarily stopped.

66. What is the normal range of airway resistance in a healthy, non-intubated patient?
0.6 – 2.4 cm H₂O/L/sec.

67. What is the normal airway resistance in an intubated patient?
Approximately 5 cm H₂O/L/sec.

68. What is the standard flow rate used to measure normal airway resistance?
30 L/min, or 0.5 L/sec.

69. Does an endotracheal tube increase airway resistance?
Yes, due to its smaller diameter and added length.

70. How do you convert a flow rate from L/min to L/sec?
Divide the L/min value by 60.

71. What does PIP stand for in mechanical ventilation?
Peak Inspiratory Pressure.

72. What is the formula for calculating airway resistance (Raw)?
Raw = (PIP – Plateau Pressure) / Flow rate in L/sec.

73. A patient has PIP of 35 cm H₂O, Plateau Pressure of 20 cm H₂O, and flow rate of 60 L/min. What is the airway resistance?
15 cm H₂O/L/sec.

74. What is the relationship between airway resistance (Raw) and pressure difference (∆P)?
They are directly proportional.

75. What does an increase in ∆P suggest in terms of WOB?
Increased work of breathing.

76. If Raw increases, what happens to work of breathing (WOB)?
WOB increases.

77. If Raw decreases, what happens to work of breathing (WOB)?
WOB decreases.

78. What does WOB stand for?
Work of Breathing.

79. When is WOB a critical factor in clinical decision-making?
When determining if mechanical ventilation is needed.

80. What is the relationship between airway resistance (Raw) and flow (V)?
They are inversely proportional.

81. If Raw increases, what happens to flow (V)?
Flow decreases.

82. If Raw decreases, what happens to flow (V)?
Flow increases.

83. What causes airway resistance?
Obstruction or narrowing of the airways.

84. Airway resistance is directly proportional to what factor?
Airway length.

85. Airway resistance is inversely proportional to what factor?
Airway diameter.

86. If airway diameter decreases, what happens to resistance?
Resistance increases.

87. What clinical conditions increase airway resistance?
COPD, mechanical obstructions, and infections.

88. Which diseases under COPD contribute to increased Raw?
Emphysema, chronic bronchitis, asthma, and bronchiectasis.

89. What mechanical conditions can increase Raw?
ET tube obstruction, foreign body, post-intubation narrowing, and ventilator tubing condensation.

90. What infections can increase airway resistance?
Croup, epiglottitis, and bronchiolitis.

91. What is the relationship between ∆P and flow (V)?
They are directly proportional.

92. If ∆P increases, what happens to flow?
Flow increases.

93. If ∆P decreases, what happens to flow?
Flow decreases.

94. What does severe, uncorrected airflow obstruction lead to?
Increased work of breathing (WOB).

95. What can happen if the patient cannot sustain elevated WOB?
Ventilatory and oxygenation failure.

96. What does increased bowing on the flow-volume loop suggest?
Increased airway resistance (Raw).

97. What causes bowing of the inspiratory limb on the flow-volume loop?
Inspiratory flow exceeding the patient’s needs.

98. What does bowing of the expiratory limb indicate?
Increased expiratory airway resistance, often from bronchospasm.

99. When is the greatest pressure observed on the pressure-volume loop?
During inspiration.

100. What happens to pressure and tidal volume during exhalation?
Both pressure and volume decrease.

101. What happens to pressure and tidal volume during inhalation?
Both pressure and volume increase.

102. When is mechanical ventilation necessary?
When the patient cannot sustain adequate ventilation to maintain gas exchange.

103. What are some indications for mechanical ventilation?
Physiologic changes, disease states, procedures, or other causes.

104. What is a physiologic indication for mechanical ventilation?
Deterioration of the lung parenchyma.

105. What disease state commonly leads to the need for ventilation?
Respiratory Distress Syndrome (RDS).

106. What is the most frequent use of mechanical ventilation in clinical settings?
Postoperative patients recovering from anesthesia and sedative medications.

107. Along with lung elasticity, what other major force must be overcome during breathing?
Airway resistance.

108. Which formula represents the key contributors to airway resistance?
Resistance ∝ (viscosity × length) / radius⁴.

109. Where in the lungs is airway resistance the highest and lowest?
Highest: Segmental bronchi (Z3–Z7); Lowest: Alveoli and terminal bronchioles.

110. Why isn’t resistance highest in the alveoli, despite their small radius?
The massive number of alveoli and laminar airflow result in overall low resistance.

111. Why do the segmental bronchi have the highest airway resistance?
They contain a thick smooth muscle layer responsive to autonomic input.

112. What is the effect of sympathetic tone on pulmonary airways?
It causes bronchodilation, decreasing airway resistance and increasing airflow.

113. What is the effect of parasympathetic tone on pulmonary airways?
It causes bronchoconstriction, increasing airway resistance and decreasing airflow.

114. Why do epinephrine and norepinephrine relax pulmonary airways but constrict blood vessels?
They bind to different receptors—β-receptors in the lungs vs. α-receptors in the vasculature.

115. How does asthma increase airway resistance?
Hyperconstriction of airway smooth muscle reduces radius, drastically increasing resistance.

116. What determines the level of airway constriction in asthma?
The balance of sympathetic (relaxing) and parasympathetic (constricting) tone.

117. Describe mild asthma and its treatment.
Exercise- or cold-induced; treat with a beta-agonist like albuterol via nebulizer.

118. Describe moderate asthma and its treatment.
Allergen-induced inflammation; treat with albuterol and antihistamines like diphenhydramine.

119. Describe severe asthma and its treatment.
Extensive inflammatory response; treat with corticosteroids like prednisone, not just bronchodilators.

120. Why does airway resistance increase at lower lung volumes?
Airway radius decreases, causing resistance to rise exponentially.

121. Why does airway conductance decrease as lung volume decreases?
Smaller airway radius reduces conductance linearly.

122. How high can pleural pressure rise during maximum forced expiration?
Up to +30 cm H₂O.

123. What happens when airway resistance becomes infinite during maximal expiration?
No airflow occurs—conductance is zero, leaving behind residual lung volume (~1.2 L).

124. Why don’t alveoli collapse during max expiration despite high pleural pressures?
Backpressure from narrowed segmental bronchi prevents alveolar collapse.

125. What is the equal pressure point (EPP)?
The point where intrapleural pressure equals airway pressure, typically in segmental bronchi.

126. How does the EPP contribute to residual volume?
It marks the site beyond which airway collapse occurs, trapping air and preserving residual volume.

127. If airway pressure is doubled, what happens to airflow through the airway?
Airflow will also double (assuming linear flow conditions).

128. What happens to airway resistance if the length of the airway is cut in half?
Resistance decreases by 50%.

129. Where is the major site of airway resistance in the lungs?
Segmental bronchi.

130. What are the primary sympathetic hormones?
Epinephrine and norepinephrine.

131. What effect does decreased parasympathetic tone have on airway diameter?
It increases the diameter (radii) of the segmental bronchi.

132. True or false: Decreased sympathetic tone can worsen asthma.
True.

133. True or false: The alveoli are the main site of increased airway resistance during an asthma attack.
False. The segmental bronchi are.

134. True or false: Airway resistance is highest at total lung capacity.
False. It’s lowest due to maximal airway diameter.

135. True or false: Above the equal pressure point, airway pressure exceeds pleural pressure.
False. It’s less, favoring airway collapse.

136. True or false: The equal pressure point normally occurs in the trachea.
False. It occurs in the segmental bronchi.

137. Airway resistance is lowest when:
Airway radius is large and tube length is short.

138. As lung volume increases from residual volume to total lung capacity, what happens to airway resistance?
Airway resistance decreases exponentially.

139. What effect does having many small airways in parallel have on airway resistance?
Although each small airway has high resistance, their parallel arrangement significantly reduces overall airway resistance.

140. Which airway generations contribute the most to total airway resistance?
Generations 3 to 5 contribute the most to airway resistance.

141. What percentage of total airway resistance is contributed by small airways less than 2 mm in diameter?
Approximately 20% of total resistance.

142. Where is airway resistance primarily located in the respiratory system?
A) Nose, pharynx, and larynx; B) Within the lungs: medium-sized bronchi.

143. What is the “silent zone” of the lungs and why is it called that?
The small airways are the silent zone because damage occurs gradually and symptoms often appear late.

144. What are the two main factors that affect airway resistance?
1) Airway conditions (e.g., inflammation, secretions) and 2) Pressure across the airway wall.

145. Which nervous system innervates bronchoconstriction?
The parasympathetic nervous system.

146. Which receptor does acetylcholine act on to cause bronchoconstriction?
M3 muscarinic receptors.

147. Which neurotransmitter causes bronchoconstriction of bronchial smooth muscle?
Acetylcholine (ACh).

148. What happens to airway resistance during bronchoconstriction?
Airway resistance increases.

149. Which neurotransmitter causes bronchodilation of bronchial smooth muscle?
Epinephrine.

150. Which receptors mediate bronchodilation in the lungs?
Beta-2 adrenergic receptors.

Final Thoughts

Airway resistance is a vital concept in respiratory physiology that affects every breath we take. It plays a central role in both normal breathing and in the pathophysiology of respiratory disorders.

Whether assessing a patient with asthma, managing someone on mechanical ventilation, or interpreting pulmonary function tests, understanding how airway resistance works—and how to measure and manage it—is essential.

By recognizing the factors that influence Raw and its implications in health and disease, healthcare providers can better diagnose issues and optimize respiratory care.