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+ CAPS 301: Respiratory, Renal, GI, Endocrinology, Reproduction > Airway Resistance and Compliance > Flashcards

Airway Resistance and Compliance Flashcards

1
Q

Describe the characteristics of smoker’s lungs. Compare them to healthy lungs.

A
  • high resistance and compliance
  • inflamed, narrowed, and destroyed airways
  • lots of holes (alveoli in healthy lung are much more compact)
  • bigger (compared to healthy lung)
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2
Q

How much resistance to air flow (Raw) is there in airways of lungs? Why?

A
  • total resistance is very little
  • bifurcations and branching make resistance very small
  • good for gas exchange
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3
Q

What are the two resistive forces of airways?

A
  • inertia (negligible)

- friction

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4
Q

Where does friction cause resistance in airways?

A

lung and chest wall surfaces (connected to each other) gliding past each other

airways gliding past each other

frictional resistance of air molecules flowing through airways (and resistance they have against each other, and walls of that airway) represents 80% of total airways resistance

  • upper airways (nose to trachea) – 60%
  • tracheobronchial tree – 40%
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5
Q

Describe changes in diameter of airways through branching of the lung.

A

diameter of individual airway decreases after each generation, from central airways to peripheral airways as you go deeper into lungs to alveolar sacs

diameter of all airways lying parallel to one another in any given generation initially gets smaller, then gets much larger – due to presence of more alveolar sacs as you get deeper into lung

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6
Q

What are the advantages of the parallel design of the airways?

A

reduces frictional resistance to airflow by increasing total cross-sectional area

  • individual airway is getting narrower, BUT division/branching of airways results in more and more airways arranged in parallel, and therefore total cross-sectional area is much larger with every generation
  • air can go through two or more airways with greater cross-sectional area
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7
Q

What are the major contributors to airway resistance in health individuals?

A

larger airways (upper airways and TBT generations 1-6)

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8
Q

What are the major contributors to airway resistance in individuals with airway disease?

A

smaller respiratory airways with reduced luminal size

  • BUT these airways represent ‘silent zone’
  • to quantify their impact on resistance, airflow is measured instead of airway resistance
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9
Q

Where in the airways is resistance the highest? Where is it lowest?

A

starts off high in beginning of conducting zone, and peaks at medium-sized bronchi

exponentially decreases throughout conducting zone

small resistance in respiratory zone, where gas exchange occurs

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10
Q

If respiratory zone airways are contributing very little to resistance, what are they said to be acting as?

A

silent zone

  • problems in small airways results in very small change in resistance, therefore will not significantly change overall value of resistance
  • measure airflow instead of resistance – much better indicator of what’s happening
  • can’t measure resistance of some parts of TBT
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11
Q

Will you see a change by measuring resistance if there’s an obstruction to airflow?

A

NO – need to know relationship between resistance and flow

ie. mucus produced in airways and they’re getting plugged, airways getting inflamed and airway size is reduced

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12
Q

What is the Poiseuille relationship?

A

relationship between flow, driving pressure, and resistance

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13
Q

What is the equation for flow?

A

flow (V) = ΔP / R

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14
Q

What is the equation for resistance?

A

resistance (R) = ΔP / V

where V = volume moving per unit time
where resistance ∝ 1/radius4

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15
Q

What is the equation for resistance of airways?

A

for a normal quiet breath when breathing out:

Raw = (PA - PB) / V
= (1 cm H2O) / (0.5 L/sec)
= 2 cm H2O/L/sec at peak flow

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16
Q

If radius of an airway is halved, how much does pressure need to increase to keep the same flow rate?

A

must increase pressure 16x

  • expand chest cavity more to increase pressure difference
  • respiratory muscles must work exponentially harder
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17
Q

How does the parasympathetic nervous system control smooth muscles of the airway?

A

contraction of smooth muscle (bronchoconstriction)

  • via acetylcholine release from vagus nerve on to cholinergic (muscarinic, M3) receptors on airway smooth muscle
  • dominant control at rest regulating airway smooth muscle tone
18
Q

How does the sympathetic nervous system control smooth muscles of the airway?

A

relaxation of smooth muscle (bronchodilation)

  • via adrenaline release from adrenal medulla into circulation, stimulating β2 adrenergic receptors (parasympathetic type) on airway smooth muscle
19
Q

Why is sympathetic innervation of airway smooth muscle in humans sparse?

A

muscle itself has adrenergic receptors, therefore if adrenal medulla releases adrenaline/epinephrine into system, muscles will relax

20
Q

How is asthma treated?

A

both mechanisms of parasympathetic and sympathetic nervous systems are exploited in treatment of asthma with use of anticholinergic and sympathomimetic bronchodilator medication

21
Q

What does airway patency (being open) depend on?

A

airway transmural pressure

22
Q

What does maximal forced expiration result in (that doesn’t occur in normal quiet breathing or routine exercise)?

A

results in flow limiting segment distal to an equal
pressure point, limiting maximum airflow

in patients with increases in airway resistance, airway compliance, or both, flow limited segment is increased and may collapse and lead to gas trapping

23
Q

Describe the flow limiting segment.

A

large intrathoracic pressure generated with expiratory muscles also creates very large positive pressure

  • as air leaves airways, there can be a place where pressure inside airway relative to outside (pleura) becomes the same
  • distal to mouth there could be a place where pressure on outside > inside (narrowing of airway, can collapse if there isn’t adequate cartilage)
  • as air moves out, flow will be limited in getting out of airway
  • further narrowing (muscle contracts, mucus produced, inflammation) results in greater airway limitation – can see this in airflow a person generates when breathing out
24
Q

During routine exercise, why is Ppl higher compared to normal breathing?

A

because use of chest wall, internal intercostals, and abdominal muscles generates huge pressure

  • contraction of chest wall
  • pushing abdominals against diaphragm
25
Q

What are mechanisms of expiratory airflow limitation?

A

increased airway resistance from airway narrowing leads to reduced maximal expiratory flow

  • excess mucus production: asthma / chronic bronchitis / cystic fibrosis
  • inflammation: asthma / chronic bronchitis / COPD / bronchiolitis
  • bronchoconstriction: asthma / COPD
  • reduced elastic recoil / increased compliance: emphysema
26
Q

What is lung compliance?

A

how easily lung can be stretched

thicker = decrease in compliance

27
Q

What is elastance?

A

tendency of object to oppose stretch, and its ability to return to its original form after distorting force is removed

inverse of compliance (1/elastance)

thicker = increase in elastance

28
Q

What contributes to determination of lung tissue elasticity?

A

connective tissues that surrounds all airways

  • collagen: high tensile strength, inextensible
  • elastin: low tensile strength, extensible
29
Q

How does aging affect elastance?

A

results in loss of elastin fibers

  • lung compliance increases → less elastic (floppy lungs), inflate easily, deflate poorly
  • wrinkled skin
30
Q

What is emphysema? What is it caused by? How does it affect the lungs?

A

“disappearing lung disease”

caused by:

  • cigarette smoking
  • genetic/inherited alpha 1 antitrypsin deficiency

results in:

  • destruction of alveolar wall
  • lung compliance increases → floppy lungs
  • reduces elastance
  • lungs are really stretched due to air inside – can fill lungs, but can’t empty
31
Q

What is pulmonary fibrosis? How does it affect the lungs?

A

collagen deposition in alveolar walls in response to lung injury (ie. asbestosis)

  • lung compliance decreases → stiff lungs
  • hard to inflate/fill lungs
32
Q

What are physical properties that determine lung compliance? (3)

A
  • lung tissue elasticity
  • lung volume
  • alveolar surface tension
33
Q

What is static compliance of the lung? What can change it?

A

change in volume for a given difference in pressure (slope)

  • changes at end of normal breath (normally breathing tidally – FRC)
  • changes if compliance is being measured at top (normally don’t breathe at top of lungs)
34
Q

When is lung compliance much greater?

A

much greater at normal volumes closest to FRC (end of expiration during normal breathing), compared to breathing at top of lung

35
Q

What is static compliance of the lungs determined by?

A

pressure/volume slope at FRC

  • relationship of PV differ across
36
Q

In a lung volume vs. Ptp graph, describe how high compliance (emphysema) shifts the graph for static compliance compared to normal.

A
  • shifted left
  • higher FRC
  • higher TLC
  • need much lower pressures to get into a given volume
  • at very low pressure, you have reached highest lung volume that this individual can reach
37
Q

What is surface tension?

A

cohesive force in which water molecules at liquid-gas interface are attracted strongly to water molecules within liquid mass

38
Q

How is alveolar surface tension created ?

A

created by cohesive forces of surface water molecules

  • air entering lungs is humidified and saturated with water vapour at body temperature
  • water molecules cover alveolar surface
  • surface water molecules create substantial surface tension by the time air reaches alveoli
39
Q

What is atelectasis? How can it be avoided?

A

complete or partial collapse of lung, caused by inward recoil created by alveolar surface tension

to avoid collapse and stabilize alveoli, pulmonary surfactant secreted from type II alveolar cells reduces alveolar surface tension

40
Q

What is neonatal respiratory distress syndrome (NRDS)?

A

high alveolar surface tension

  • increases elastance
  • reduces compliance

premature babies with inadequate pulmonary surfactant production by type II pneumocytes have stiff lungs that are hard to inflate at birth

  • surfactant is produced between 24-28 weeks gestations – adequacy greatest the closer to term
  • life threatening – 25% babies born at 30 weeks require ventilation
  • treated with semi-synthetic surfactant delivered intra-tracheally
  • mother is treated with corticosteroids during pregnancy

+ CAPS 301: Respiratory, Renal, GI, Endocrinology, Reproduction (32 decks)

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