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Physiology (Term 2) > Respiration 2 > Flashcards

Respiration 2 Flashcards

1
Q

Air flow =

A

Blood flow

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2
Q

What does blood flow through a vessel depends on?

A

–The pressure gradient

–Vascular resistance (r4)

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3
Q

In the case of smooth flow (laminar flow), What is the volume flow rate is given by?

A

the pressure difference divided by the viscous resistance (Poiseuille’s Law)

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4
Q

What does viscous resistance dependent on?

What is the fourth power dependent on?

A

This resistance depends linearly upon the viscosity and the length, but the fourth power dependence upon the radius is dramatically different.

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5
Q

Flow may be turbulent or laminar: Wherever a tube divides (airways, blood vessels) what happens to velocity and turbulent flow?

A

velocity increases and turbulent flow is more likely

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6
Q

What physical characterisitics is flow affected by?

A

Flow is affected by various physical characteristics:

    1. Flow requires a pressure gradient
    1. Flow depends on tube diameter

F ∝ r4

•3. Flow depends on tube length

F ∝ 1/l

•4. Flow depends on fluid/gas viscosity

F ∝ 1/η

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7
Q

F =

A

ΔP/R

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8
Q

What is resistance like in normal healthy airways?

What is airflow determined by?

A
  • In normal healthy airways, resistance is low
  • Airflow is determined by ΔP
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9
Q

What does Bronchoconstriction lead to?

A

Increased airway resistance e.g. in asthma

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10
Q

What is Bronchodilation?

A

Decrease airway resistance

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11
Q

What does Bronchodilation ensure?

How do inhalers work?

A

Pressure gradient established achieves maximum airflow with minimum resistance

e.g. ventolin and salbutmol inhalers that act on β-Adrenergic receptors across the smooth muscles that lines the bronciole tubules, causes blood vessels to dilate and open so breathing becomes easier

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12
Q

Describe Bronchoconstriction in disease (asthma)

A
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13
Q

Can respiratory conditions alter resistance?

A

Respiratory conditions can alter resistance

e.g. Asthma and Chronic obstructive pulmonary disease (COPD)

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14
Q

What happens if resistance increases?

A

If resistance increases then DPD must increase to maintain airflow Obstructive lung diseases with increased resistance = harder work to breathe

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15
Q

Can medication alter resistance?

A

understanding where particles may deposit along the respiratory tract e.g inhaled insulin

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16
Q

Is resistance altered by administering anaethetics?

A

Yes

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17
Q

What measures measures resistance via FEV1 and PEFR?

A

Spirometry

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18
Q

What makes resistance change in disease?

A

If the airways become narrowed because of disease (mucus blockage, inflammation, fibrosis), then resistance increases

Diseased lungs have altered tissue properties, not as flexible therefore more difficult to inflate

fibrotic livers are also problematic

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19
Q

When do lungs have to extend?

A

(inspiration) and return to their pre-inspiration volume/shape

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20
Q

What is pulmonary elasticity is governed by?

A
  • Elastance; elastic recoil dictates how readily lungs rebound after having been stretched = ease of deflation
  • Compliance; how much effort is required to stretch or distend the lungs = ease of inflation
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21
Q

How are Elastance and compliance related?

A

Elastance and compliance are inversely related

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22
Q

Explain some properties of stiff lungs

A
  • Stiff lungs are more difficult to inflate but deflate more easily
  • Stiff lungs have a high elastance, low compliance
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23
Q

What is the Elastic recoil of the lungs is partly due to?

A

properties of the parenchyma

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24
Q

Is elastin more/less compliant?

A

Elastin is more compliant

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25
Q

Is collagen more/less compliant?

A

collagen is less compliant

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26
Q

As well as elastin and collagen, Elastic recoil of the lungs is partly due to

A

Surface tension at the air-liquid interface in alveoli

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27
Q

What is surface tension?

A
  • Surface tension is the force that makes water form droplets
  • In liquids at air-liquid interfaces
  • Results from the greater attraction of liquid molecules to each other (due to cohesion) than to the molecules in the air (due to adhesion)
  • This creates surface tension
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28
Q

How does alveolar surface tension contribute to the lung’s elastic recoil?

A
  • Air-liquid interface is important in the airways
  • Pressure-volume curves of saline filled lungs demonstrate a lower elastance than air-filled lungs
  • Elastic recoil of the lungs is a function of alveolar surface tension
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29
Q

How is compliance calculated?

A
  • change in volume divided by change in pressure
  • C = ΔV / ΔP
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30
Q

What does a compliance curve measure?

A

•measure changes in pressure and volume

C = ΔV / ΔP

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31
Q

Volume changes are measured by

A

spirometry

32
Q

What are pressure changes measured by?

A

oesophageal balloon

33
Q

Compliance is reduced in various conditions:

How does this affect breathing?

A

–Collapsed alveoli (poor gas exchange)

–Pneumothorax (transmeural pressure gradient between lungs and external environment equilibriates)

–Obesity (More fat around thoracic cavity, more difficult for lungs to expand and relax)

–Musculoskeletal problems (e.g. sarcopenia- progressive and generalized loss of skeletal muscle mass and strength and intercoastal muscles deteriorate)

  • More work is needed to breathe in
  • Higher rate of breathing; lower tidal volume
34
Q

Is Compliance increased in emphysema?

A

YES

–Alveolar destruction (tissue damage)

Poor gas exchange

(A lung condition that causes shortness of breath. In people with emphysema, the air sacs in the lungs (alveoli) are damaged. Over time, the inner walls of the air sacs weaken and rupture — creating larger air spaces instead of many small ones)

35
Q

Give a clinical evaluation of compliance in relation to diseases that increase or decrease it

A
  • Obstructive lung disease (emphysema)
  • Curve shifted to the left

Increased compliance – tissue (alveoli) damage, poor gas exchange

  • Restrictive lung disease
  • Curve shifted to right

(fibrosis- lung tissue scarred and no longer mallaeble or able to expand to total capacity)

Reduced compliance, increased elastic recoil

36
Q

Other factors that contribute to healthy lung’s stability

A
  • Alveoli are not all the same size
  • If there was a constant surface tension at the air-liquid interface, lungs would be inherently unstable
  • Small alveoli would tend to collapse
37
Q

Which two factors help stabilise alveoli?

A
  1. Structural interdependence
  2. Pulmonary surfactant
38
Q

Describe the structural interdependence of alveoli

A
  • Alveoli are held open by the chest wall pulling on the outer surface of the lung
  • A collapsing alveolus increases the stress on adjacent alveoli- these would tend to hold it open
39
Q

Without pulmonary surfactant:

A

P1 (Small alveolar pressure) > P2 (Large alveolar pressure)

Smaller alveolus collapses becauses gases travel from higher to lower pressure

40
Q

Pulmonary surfactant- the law of LaPlace

A
  • LaPlace’s law explains the relationship between the pressure inside an alveolus and the tension of the alveolus wall
  • Pressure (P) = 2 x alveolar tension (T)/ alveolus radius (r)
41
Q

With pulmonary surfactant:

A

P1 = P2

No collapse

42
Q

what is pulmonary surfactant?

A

85-90% lipids (mostly phospholipids), 10-15% proteins

4 surfactant proteins – SP-A, SP-B, SP-C and SP-D (function as Opsonization agents because they bind to bacteria and allow alveolar macrophages to eat bacteria)

SP-A and SP-D- defence

SP-B- necessary for surfactant function

Makes a coating on the outer surface of the alveoli and reduces the surface tension

43
Q

What produces produce pulmonary surfactant?

A

Type II pneumocytes produce pulmonary surfactant

They are in a close environment to macrophages

Constant turnover (absorption and secretion) of pulmonary surfactant

Recycled by type II or cleared by AM (alveolar macrophages)

44
Q

The clinical importance of pulmonary surfactant: Infant respiratory distress syndrome

A

•Surfactant isn’t fully functional until about 7 months gestation

–Premature babies- lack pulmonary surfactant, tendency for spontaneous alveolar collapse :
Infant respiratory distress syndrome

Pulmonary surfactant can be injected

45
Q

Clinical importance of pulmonary surfactant: Adult respiratory distress syndrome

A

•Hypoxia (insufficient oxygen) may reduce surfactant production/levels in adults

Adult respiratory distress syndrome

  • Positive-pressure ventilation
  • Administer exogenous surfactant
46
Q

How can we measure lung function?

A

Spirometry uses an inverted canister in a water-filled space

Breathe into the tubing

Breathing pattern is traced on the rotating drum (kymograph)

47
Q

Describe a Spirogram of normal lung function

A
48
Q

Define Tidal volume VT

A

•volume of air per breath at rest

–500 ml per breath 70kg adult eupnea (normal, good, unlabored breathing, sometimes known as quiet breathing or resting respiratory rate)

49
Q

What is Residual volume RV?

A

volume remaining after max forced expiration

small amount of air that always stays in the lungs

about 1000ml

50
Q

What is Expiratory reserve volume ERV?

A

•volume expelled during max forced expiration starting at the end of normal tidal expiration

–FRC – RV

–1.5 L normally

IRV-Erv=

51
Q

What is Inspiratory reserve volume IRV?

A

•volume inhaled during max forced inspiration starting at the end of normal tidal inspiration

–2.5 L normally

52
Q

What is Functional Residual Capacity FRC?

A

• volume remaining at the end of normal tidal expiration

–RV + ERV; around 3L

53
Q

What is Inspiratory capacity IC?

A

•volume inhaled during max inspiratory effort at the end of normal tidal expiration

–VT + IRV; around 3L

54
Q

What is Total lung capacity TLC?

A

•volume in the lungs after max inspiratory effort

–RV + VT + IRV + ERV; about 6L

55
Q

What is Vital capacity VC?

A

•volume expelled during max forced expiration after max forced inspiration

–TLC – RV; about 4.5L

IRV-ERV

56
Q

What are the limitations of spirometry?

A

•Spirometry can only measure the lung volumes exchanged by a conscious, co-operative subject.These are:

Tidal volume, Inspiratory and expiratory reserve volumes, inspiratory capacity and Vital capacity

difficult for small children

•Spirometry cannot measure:

Residual volume, functional residual capacity or total lung capacity

57
Q

What are the characteristics of restrictive disease?

A

•(alveolar fibrosis) – reduced compliance and increased elastic recoil

–Reduced FRC, TLC, VC, IRV and ERV

–Increased breathing rate (compensatory)

58
Q

What are the characteristics of obstructive disease?

A

•(emphysema, chronic bronchitis) – increased resistance, decreased elastic recoil

–Increased RV, FRC and TLC

–Decreased VC and ERV

–Decreased breathing rate

59
Q

Restrictive - reduced TLC; reduced VC

Obstructive- increased TLC; reduced VC

A

Greater residual volume (RV) in obstructive

60
Q

What is minute volume?

A

The volume of air entering and leaving the nose every minute-but this is not the same as the volume entering and leaving the alveoli (some air dissapates)

61
Q

Is alveolar ventilation greater or less than minute volume

A

Alveolar ventilation < minute volume

62
Q

The last part of each respiration remains in

A

the conducting airways- does not reach alveoli

63
Q

Conducting airways do not exchange gas and are known as

A

anatomical dead space

64
Q

What is Pulmonary ventilation also called?

A

minute ventilation (Volume of air breathed in and out in one minute)

65
Q

How is Pulmonary ventilation calculated?

A

Pulmonary ventilation = tidal volume x respiratory rate

Does not take into account anatomical dead space

66
Q

Does increasing pulmonary ventilation always increase gas exchange?

A

increasing pulmonary ventilation does not always increase gas exchange

67
Q

Does anatomical deadspace participate in gas exchange

A

NO

Anatomical deadspace does not participate in gas exchange

68
Q

What are the properties of conducting airways?

A

–Good for defence and passage of air

–Not good for gas exchange

–Around 150ml volume lost

69
Q

For every 500ml VT, how many ml get to the alveoli for gas exchange

A

•For every 500ml VT, only 350 ml gets to the alveoli for gas exchange

70
Q

How is alveolar ventilation calculated?

A

Alveolar ventilation = (tidal volume – dead space (-150ml) x respiratory rate)

71
Q

What is alveolar ventilation?

A
  • Volume of air exchanged between the atmosphere and the alveoli per minute.
  • More important than pulmonary ventilation.
  • Less than pulmonary ventilation due to anatomic dead space. (-150ml)
72
Q

How do breathing patterns influence alveolar ventilation?

A

During exercise, deeper breathing is more effective than quicker shallow breaths

73
Q

Why is it said that ‘Not all alveoli are equal’?

A
  • Alveoli have dead space too
  • Not all alveoli (around 3-500 million of them) are ventilated equally OR perfused equally
  • Alveoli that do not participate in gas exchange make up the alveolar dead space
74
Q

What can alveolar dead space used to monitor?

Which diseases cause an increase in alveolar dead space?

A
  • Alveolar dead space can be used to monitor lung function under anaesthetic
  • This is fairly small in the healthy lung but may increase in disease

–Emphysematous lungs

–Decreased cardiac output

–Pulmonary embolism

75
Q

Give a summary of this lecture

A

Pressure volume relationships can help us to calculate lung compliance and elastic recoil (inverse of compliance)

Compliance= how stretchy

Elastic recoil= ease of rebound

Elastic recoil is partly defined by the tissue and partly by alveolar surface tension- generated by alveolar interdependence and surfactants

Surfactant stabilises the lungs- used clinically for pre-term babies

Spirometry can be used to measure some lung volumes

Lung volumes can be diagnostic for restrictive (reduced RV, reduced VC) and obstructive (increased RV, reduced VC) diseases

Dead spaces in the airways affect gas exchange

76
Q

How do you measure mean arterial pressure (MAP) from blood pressure values?

If blood pressure is 117/78

A

If blood pressure is 111/87

[(Diasolic blood pressure x 2) + systolic blood presure] / 3

→ MAP= [(78x2)+117]/3

Physiology (Term 2) (24 decks)

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