Airway Resistance & Compliance

Question 1

Outline the relative contribution of forces contributing to airway resistance and explain why the smallest airways do not create the greatest resistance to airflow

Answer 1

total resistance to flow of air in airways (Raw) is very little (2 cm H20/L/s)
Resistive forces:
A. intertia of resp. system (negligible)
B. Friction
- lung and chest wall surfaces gliding past
- airways gliding past other
- frictional resistance of air flowing through airways (80% total)
- UAW-60%, tracheobronchial tree-40%

number of airways increases as you go down, so total area gets larger, thus resistance decreases

major contributors to Raw are upper airways and TBT. in airway disease caused by smoking, major contributor are smaller airways with reduced luminal size

Question 2

Describe how airway size is controlled by the autonomic nervous system and apply this information to drug treatment for asthma.

Answer 2

PSNS: bronchoconstriction via ACh released from vagus nerve onto M3R on airway. Dominant control at rest regulating smooth muscle
SNS: bronchodilation via E release from adrenal medulla onto beta R on airway. sparse innervation.

• use anticholinergic and sympathomimetic medication for bronchodilation in asthma

Question 3

Outline the causes of increased airway resistance and expiratory airflow limitation in the obstructive lung diseases.

Answer 3

airway patency depends on transmural pressure.
forced expiration results in airflow limiting segment distal to an equal pressure point limiting max airflow.
- in ppl increased Raw, airway compliance, or both, flow limiting segment is increased, may collapse due to gas trapping

Increased Raw from airway narrowing, from:

• excess mucus production (asthma, bronchitis, CF)
• inflammation (asthma, bronchitis, COPD, bronchiolitis)
• bronchoconstriction (COPD, asthma)
• reduced elastic recoil, increased compliance (emphysema)

Question 4

  Explain the impact of lung volume, tissue elastance, and pulmonary surfactant on lung compliance.

Answer 4

1. tissue lung elasticity- connective tissue around airway. interstitium of elastin (extensible, low strength)/collagen(inextensible, strong) confers elasticity/compliance in small airways
   - loss of connective tissue (aging) –> loss elastin –> wrinkled, lung compliance increases, less elastic (floppy lungs). inflate easy, deflate poorly
   emphysema –> destroy alveolar wall –> floppy lungs
   PF –> collagen deposition wall –> decreased compliance, stiff lungs
2. Lung volume- change in V/P = compliance
   high compliance at lower volumes (and lower pressures)
3. alveolar surface tension- water molecules at liquid-gas interface are attracted to water molecules in liquid. air entering lungs is humidified. water molecules cover alveolar surface. creates surface tension. this surface tension creates inward recoil and alveolar collapse “atelectasis”. surfactant reduces surface tension

Question 5

Describe the static compliance of the lungs. Outline the key differences between the PV curve of the lungs in health, emphysema and pulmonary fibrosis

Answer 5

static compliance = change in v/p
emphysema (high compliance): air destroyed, easily distensible, cannot empty to FRC. very steep slope
PF (low compliance): can’t breathe in much, FRC might be fine. very flat slope.

Question 6

Describe the role of pulmonary surfactant in 1) determining

alveolar surface tension, 2) the compliance of the lungs 3) NRDS.

Answer 6

surfactant: reduces alveolar surface tension, prevents collapse and stabilizes alveoli

i guess it increases compliance

NRDS: premature babies, inadequate surfactant. stiff lungs, hard to inflate. ventilator dependent