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Health.2 > Respiratory system TT > Flashcards

Respiratory system TT Flashcards

1
Q

Topic 1: Intro to resp system

What are 8 common disorders that affect the respiratory system?

A
  • infections
  • allergic rhinitis
  • coughs
  • colds
  • congestion
  • asthma
  • COPD
  • COVID-19 (SARS-CoV-2)
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2
Q

What are 8 drug categories that affect the respiratory system?

A
  • antihistamines
  • decongestants
  • antitussives
  • mucolytics
  • expectorants
  • bronchodilators
  • leukotriene modifiers
  • mast cell stabilisers
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3
Q

What are the 2 types of respiration?

A
  • external: breathing

- internal: cellular

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4
Q

What does breathing do to O2 and CO2?

A

breathing brings in O2 from the atmosphere and transfers CO2 in the opposite direction

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5
Q

What are the 2 types of internal respiration?

where do they occur

A
  • aerobic
  • anaerobic

both energy-producing processes going on in cells

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6
Q

What is the respiration equation?

A

C6H12O6 + 6O2 —–> 6CO2 + 6H2O

ATP

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7
Q

energy required for life comes form what?

and what must happen to it to release energy stored inside it

A

comes form food.

must be OXIDISED, release energy

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8
Q

similarities between the cardiovascular and respiratory system?
(what type of flow do they use? what process allows the movement of gases?

A
  • highly efficient convective bulk flow systems (ventilatory + circulatory) for long-distance transport of gases or liquid
  • diffusion for short-distance movements: O2 & CO2
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9
Q

What is the metabolic rate also the rate of?

A

O2 consumption

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10
Q

What is V̇O2? What is the average value at rest?

A

O2 consumed per unit time

~250ml/min

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11
Q

What is V̇CO2? What is the average value at rest?

A

CO2 produced

200ml/min

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12
Q

What is RQ? What is the formula for it?

A

Respiratory quotient:

V̇O2/V̇CO2 = 200/250 = 0.8

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13
Q

When is the value of RQ 0.8?

A

when the person has a mixed diet of fats, carbohydrates and proteins

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14
Q

What is the RQ value for

  • fats
  • carbs
  • proteins
A
  • 0.7
  • 1
  • 0.8
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15
Q

How do V̇O2 and V̇CO2 change when exercising and why? How much is it?

A

BOTH: increase:
tissues consume more O2 so need more
tissues produce vast amounts of CO2

3000ml/min

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16
Q

Why is the respiratory system important with metabolic changes? (think V̇O2 and V̇CO2)

A
  • if blood O2 falls due to increased O2 consumption and respiratory system doesn’t restore, tissues become hypoxic
  • if blood CO2 rises and isn’t removed, pH would be disturbed
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17
Q

What is the consequence of blood O2 falling?

A

tissues become hypoxic

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18
Q

What is the consequence of blood CO2 rising?

A

pH disturbances

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19
Q

If the lungs regulate CO2 levels in the blood, what does that make it a regulator of?

A

an acid-base regulator

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20
Q

How does respiration change if V̇O2 doubles?

A

respiration also doubles - in direct proportion to the metabolic demand

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21
Q

What is the consequence of ventilation changing in direct proportion to metabolic demand?

A

the blood gases and pH are kept relatively constant

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22
Q

In a diseased state, can respiration meet metabolic demands? What are the consequences?

A

no, blood gases and pH are abnormal

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23
Q

In a less severe diseased state, when can respiration not meet the metabolic demand?

A

when the metabolic demand changes e.g. during exercise

blood gases and pH= abnormal

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24
Q

In a more severe diseased state, when can respiration not meet the metabolic demand?

A

at rest

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25
Q

What are 6 non-respiratory functions of the respiratory system?

A
  • traps/dissolves clots
  • defends against microbes (cilia, mucus)
  • ventilation through airways -> heat + water loss
  • blood reservoir (thin walls can inc volume)
  • phonation - sound production
  • metabolic functions (endothelial cells have role in uptake metabolism)
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26
Q

Topic 2: Partial pressures

What are the 3 different units for (P) pressure? What unit is used clinically?

A
  • kPa, mmHg, cmH2O

- kPa

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27
Q

What is PIO2 and PICO2?

A

Partial pressure of oxygen in Inspired air

Partial pressure of carbon dioxide in Inspired air

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28
Q

What is PAO2 and PACO2?

A

partial pressure of oxygen in Alveolus (BIG A)

partial pressure of carbon dioxide in Alveolus (big A)

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29
Q

What is PaO2 and PaCO2?

A

partial pressure of oxygen in arterial blood

partial pressure of carbon dioxide in arterial blood

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30
Q

What is PvO2 and PvCO2?

A

partial pressure of oxygen in venous blood

partial pressure of carbon dioxide in venous blood

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31
Q

How many mmHg is 1 kPa worth?

A

1 kPa = 7.5mmHg

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32
Q

How many mmHg is 1cmH2O worth?

A

1.3mmHg

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33
Q

What is a partial pressure?

A

the pressure of any gas whether alone/ in a mixture

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34
Q

What does the partial pressure of a gas depend on?

A

the number of molecules of the gas in given vol and temp

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35
Q

What is Dalton’s law of partial pressures?

A

Total pressure is the sum of the partial pressures of all constituent gases
TP = P1 + P2 = P3….
each gas exerting tis own PP

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36
Q

What is the equation for the total pressure in the atmospheric air, given the gases are nitrogen, oxygen, carbon dioxide and water vapour?

A

Total P = PN2 + PO2 + PCO2 + PH2O + other trace gases

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37
Q

What is the formula for the partial pressure of a gas? e.g. O2 in air

A

partial pressure = fractional conc of gas x total (atmospheric) pressure

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38
Q

What is the value of PIO2 at sea level if its fractional concentration is 21% and the barometric pressure is 95kPa?

A

partial pressure = fractional conc of gas x total pressure

therefore 0.21 x 95 = 20kPa

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39
Q

Reference ranges of arterial blood gases and alveolar gases

look at table!! p132 of sem2

A
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40
Q

Why are partial pressures important for diffusion?

A

because diffusion occurs down partial pressure gradients

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41
Q

How does the partial pressure of O2 change from the atmosphere to the mitochondria?

A
  • drops from air to alveolus
  • blood in alveolus removes O2 from air in alveolus, so then alveolar pp of O2 drops
  • pp drops very very low in tissues

air > alveolus > blood > tissue PaO2

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42
Q

What allows rapid diffusion between tissues and the capillaries? (hint: partial pressure)

A

there’s a massive PO2 gradient of >55mmHg

diffusion occurs down partial pressure gradients

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43
Q

effects of low alveolar PAO2 thus PaO2 in patient w resp disease?

A

dont have as much of gradient for diffusion= not as efficient.

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44
Q

Topic 2b: structure and function in airways

Schematic image of human airways: 4 parts in conducting zone and 3 in transitional + resp zones?

A

conducting zone: trachea, bronchi, bronchioles, terminal bronchioles

transitional + resp zones: resp bronchioles, alveolar ducts, alveolar sacs

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45
Q

What generations make up the conducting zone of the airways?

A

the first 16 generations

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46
Q

What is the function of the conducting zone? (2)

A
  • movement of inspired air to gas exchanging regions of lungs
  • warms and humidifies air so the alveoli aren’t damaged by cold dry air
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47
Q

What generations make up the transitional and respiratory zones?
and whats the function?

A

17-23

gas exchange

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48
Q

What type of flow moves gas through the conducting zone?

A

bulk flow

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49
Q

How and why does the cross sectional surface area increase from the conducting zone to the respiratory zone?

A
  • enormous increase

- due to continuous branching

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50
Q

What is the formula for total air flow?

A

total flow = speed x area

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51
Q

As area increases, what does the speed of flow do?

A

speed decreases

forward velocity of gas: good for diffusion

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52
Q

Why is the change in cross-sectional area from the conducting zone to the respiratory zone advantageous for gas exchange?

A
  • increases from conducting to respiratory
  • speed of air flow decreases
  • this decrease in velocity is advantageous for the diffusion of gas, the dominant mechanism of ventilation
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53
Q

What specialised cells are found within the conducting zone?

A
  • epithelia lined w cilia which beat constantly

- goblet cells which secrete mucus

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54
Q

How does nicotine affect cilia?

A

it paralyses the cilia, which allows bacteria to invade

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55
Q

How does inflammation/asthma affect mucus?

A

it increases the viscosity

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56
Q

What do the trachea and primary bronchi have that prevents their collapse?

A

U-shaped cartilage (blue on diagram)

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57
Q

Why are the bronchioles susceptible to collapse?

A

they don’t have cartilage

… COPD, asthma

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58
Q

The efficient flow of both what and what is necessary for efficient gas exchange?

A

air flow into the alveoli and blood flow through pulmonary capillaries

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59
Q

What is dead space (VD)?

A

the volume of gas within the respiratory system where no gas exchange takes place

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60
Q

Dead space occurs where? (2)

A
  • where there’s no effective airflow (aka no alveoli of unventilated alveoli)
  • where there’s no perfusion
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61
Q

Which is anatomical dead space: the conducting zone or the respiratory zone?

A

the conducting zone, where there’s no alveoli

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62
Q

What is the dead space within the conducting zone known as and how much is it in ml?

A

anatomic(al) dead space - 150ml

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63
Q

What affects the anatomic dead space? (4)

A
  • body size: 2ml/kg
  • age: increases
  • drugs: bronchodilators/constrictors
  • posture: decreased when lying
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64
Q

What is the dead space within the respiratory zone known as?

A

the alveolar dead space - inadequate perfusion for gas exchange (<5ml)

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65
Q

How does the alveolar dead space change in disease?

A

increases during disease e.g. pulmonary embolus

inspired gas reaches alveolus but alveolus if ineffective in oxygenating venous blood

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66
Q

What is the sum of anatomic dead space and alveolar dead space?

A

physiological dead space = anatomic dead space + alveolar dead space

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67
Q

What is the definition of tidal volume (VT)? What is the value for a 70kg healthy young adult?

A

volume of air breathed in & out in 1 breath - 500ml

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68
Q

What is the respiratory frequency (f)? What is the typical value?

A

number of breaths per min - 12 breaths/min

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69
Q

What is the equation for minute ventilation/volume (V̇E)?

A

V̇E (ml/min) = tidal volume x respiratory frequency

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70
Q

What is the definition of minute ventilation?

A

total air moving in and out of the respiratory system in 1 minute

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71
Q

total air moving in and out of the respiratory system in 1 minute

A

minute ventilation = tidal volume (VT) x respiratory frequency (f)
500 x 12 = 6000ml/min

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72
Q

how much air enters system every minute?

A

6L

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73
Q

what happens to total volume of air entering system a minute?

A

6L…

some: remains in anatomical dead space (not involved in gas exchange)
not all gets to resp zone: lower down

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74
Q

hows alveloar ventilation (VA) calulated?

A

VE = VT x f
= 500ml x 12
= 6000ml/min

VD = VD vol dead space x f
= 150ml x 12
= 1800ml/min
                                  so
VA = VE - VD
= 6000 - 1800
= 4200ml/min
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75
Q

alveolar ventilation use?

A

= best indication of whats actually going on

VD (dead space vent) not involved in gas exchange
VA: useful ventilation therefore. ☺

VE min total - VD (not used) = VA!!

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76
Q

what causes drug induced hypoventilation?

A

drug effects on alveolar vent

  • alcohol
  • tranquilisers
  • opiates
  • sedatives
  • hypnotics: benzodiazepines, barbiturates
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77
Q

Topic 3: mechanics of breathing

how are lung + chest wall organised and related at rest
3 parts of the lung?

A

parietal pleura- contact w chest wall
visceral pleaura (inner, covers lung)
pleural cavity: pleural fluid between

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78
Q

hows fragile lung tissue inflated?

A

visceral and parietal pleura- in intimate contact and pleural space has fluid that cant expand.

when thorax moves, lungs move too as linked with fluid

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79
Q

what must respiratory muscles do in order to breathe? (2)

A
  1. stretch elastic parts of resp system (lungs and chest wall)
  2. overcome resistance to flow (airways and lung tissues)

= takes 10% pf total body O2 consumption (VO2)

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80
Q

what 2 opposing forces act on lung and chest wall at rest?

A
  1. elastic recorl of chest wall tries to pull chest wall OUTWARD
  2. elastic recoil of lung creates INWARD pull
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81
Q

what kind of pressure is therefore in pleural space?

A

negative- less than PB

intrapleural space CANNOT EXPAND

2 surfaces held together by cohesion of pleural liquid space

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82
Q

what is FRC? func residual capacity

and value?

A

volume in lungs at end of expiration

approx 2.5L air

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83
Q

all pressures e.g. Palv in lung, relative to what?

A

pressure outside.
atmosphere can change!

stretching causes ⬇ in pressure
relative to atmos. not actually -

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84
Q

what is lung distending pressure at FRC calc?

and what does it show

A 
P in - P out
= Palv - PpI
= 0 - -0.5
=+0.5kPa
(preventing lung collapsing)
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85
Q

what is chest distending pressure at FRC calc?

and what does it show

A 
P in - P out
= PpI - PB
= -0.5 - 0
= -0.5kPa
(preventing chest springing outward)
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86
Q

at FRC, how are distending pressures across lung and chest wall described?

A

equal and opposite

+ dist press prevents lung collapsing
- dist press prevents chest wall springing out

eqm @ FRC. 2.3L in lung at rest= not empty

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87
Q

air flows from XX pressure -> YY pressure

A

high -> low

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88
Q

why does air move in and out of lungs? what allows this

A

because Palv is made alternately < and > than PB.

inspiration: Palv < PB
expiration: Palv < PB

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89
Q

chenges in Palv occur ass result of what?

A

changes in lung volume when thorax expands

i.e. BOYLES LAW

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90
Q

what is BOYLES LAW?

A

= pressure exerted by a constant number of gas molecules in container = inversely proportional to vol of container

P ∝ 1/V

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91
Q

main inspiratory muscle and role? when used

A

diaphragm- ONLY muscle used in quiet breathing. lengthens thorax

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92
Q

other inspiratory muscles- what are they used in? 3

A

exercise, coughing, vomiting

= need inc volume changes

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93
Q

name 3 other inspiratory muscles and use?

A

sternocleidomastoid
scalenes
external intercostal

1 and 3: forced breathing and inc metabolic demands

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94
Q

describe quiet breathing (insp + exp) using diaphragm. quiet breathing

A
  1. diaphragm relaxed at rest
  2. insp: D contracts, thoracic volume increases
  3. exp: D relaxes, thoracic volume decreases
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95
Q

what muscles also cause volume of thorax to increase during inspiration? NOT USED AT REST

A

external intercostal
bucket handle movement

rib moves up and sternum out

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96
Q

how does diaphragm behave in expiration? wb other muscles?

A

passive relaxation

… other muscles during forced breathing more

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97
Q

3 expiratory muscles?

A

internal intercostal

external and internal obliques

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98
Q

at start of breath, how do pressures INSIDE and OUTSIDE thoracic cavity (Palv and PB) relate?
what does this mean?

A

identical

PB= 0
Palv = 0

no air flows in or out

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99
Q

describe inspiration (4)

A
  1. thoracic cavity enlarges, diaphragm flattens
  2. due to pleural membranes, lungs move out w thorax
  3. lungs expand, vol ⬆
  4. alveolar P now < P outside
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100
Q

describe expiration (4)

A
  1. chest wall moves inward
  2. vol of thorax ⬇,
  3. lungs recoil- squeeze air
  4. alveolar P now > P outside
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101
Q

describe inspiration and expiration in terms of boyles law and give Palv values

A

as volume ⬆, pressure ⬇

INS: Palv= -0.1kPa, air IN
EXP: Palv= +0.1kPa, air OUT

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102
Q

Topic 4: Elasticity and compliance

What is elasticity? (2)

A
  • resistance of an object to deformation by external force (or stiffness)
  • ability to reform original shape after deformation e.g. balloons, lungs
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103
Q

What is compliance?

A

the ability to stretch

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104
Q

How do elasticity and compliance relate?

A

compliance is the inverse of elasticity or 1/E

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105
Q

HIGH elasticity means what for compliance, stretch, and recoil?

A

HIGH elasticity
LOW compliance
HARD to stretch
EASY to recoil!

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106
Q

LOW elasticity means what for compliance, stretch, and recoil?

A

LOW elasticity
HIGH compliance
EASY to stretch
HARD to recoil!

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107
Q

A balloon takes long to blow up but is quick to deflate. Is it low or high compliance/low or higher elasticity?

A
  • low compliance, high elasticity

- harder to stretch (blow up) but quick to recoil (deflate)

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108
Q

A balloon is quick to blow up but slow to deflate. Is it low or high compliance/low or higher elasticity?

A
  • high compliance, low elasticity

- easier to stretch (blow up) but slow to recoil (deflate)

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109
Q

The chest wall as high outward/inward elastic recoil

A

the chest wall has high outward elastic recoil (so wants to spring outwards like squeezing a tennis ball)

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110
Q

The lungs have high outward/inward elastic recoil

A

the lungs have high inward elastic recoil (so wants to collapse inwards like a balloon)

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111
Q

When are the lungs at rest?

A

at functional residual capacity (FRC)

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112
Q

At FRC, what is the lung distending pressure? (hint: alveolar pressure, interpleural pressure)

A
  • the distending pressure =difference between alveolar pressure and pleural pressure
  • therefore value is always +
  • prevents lungs from collapsing due to high inward elastic recoil
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113
Q

How does the lung distending pressure change during inspiration?

A

becomes more positive

because the alveolar pressure increases

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114
Q

degree of lung expansion= proportional to what?

and what does this generate?

A

distensing pressure

Pdist = Palv - PpI

= generates outward, distending Press -> greater change in lung volume.

represented by pressure-volume (compliance) curve

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115
Q

what does slope on pressure-volume curve show?

A

lung compliance.

magnitude of change in lung vol (δV) produced by a change in distending pressure (δ Pdist)

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116
Q

compliance=?

A

δV / δ Pdist

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117
Q

lung distending pressure is always what?

A

+

press inside lung

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118
Q

what is compliance like at

  • low vol
  • normal volumes
  • high volumes?
    (i. e. bottom of curve, flat steep slope up, and closer to top of curve on col/distending P compliance graph)
A

Low at v low lung vols

High at normal vols going up curve

Low at high volumes

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119
Q

what does diff in compliance mean in terms of breathing?

A

small change in distending pressure -> large change in volume (less work)

graph on p183.

larger than normal change in pressure needed to inflate lung (more work)

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120
Q

lung vol/ distending pressure compliance graph meaning in lung disease, emphysema?

A

easy to deflate lungs BUT ⬇ elastic recoil,
(⬆ compliance) = harder to get air out

e.g. intraresp distress syndrome/ restrictive interstitial fibrosis
need more pressure + work to inflate lungs the same

elastic, stiffer lungs

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121
Q

Topic 4b: determinants of lung compliance

what 2 things determine compliance of lung?

A

elastic properties of tissues (connective forces - stretchability)

!!! suface tension at air-water interfaces in alveoli (> half lung elastic recoil) !!!

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122
Q

type 1 alveolar cell: what does it do and what lines walls of alveoli?

A

role: aids diffusion of gases

thin layer of alveolar fluids

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123
Q

what type of force is surface tension and whys it present in alveoli?

A

collapsing force. (always wants to shrink+ resist stretch)

due to release of SURFACTANT from type 2 cells= overcome surface tension ☺
alveolar lining fluid!

high ST normally = collapse alveoli

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124
Q

how do surfactants reduce surface tensions in alveoli?

A

have strong attraction for each other…
low attraction for other mols.

accumulate at surface, ⬇ ST.
= easier to inflate ☺

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125
Q

how would compliance change if NO surfactant?

A

⬇.
need inc distending pressure to inflate lung = inc work for change.

no s= LESS lung volume at higher lung distending p (graph p 189)

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126
Q

what px at risk of low compliance as no surfactant?

A

newborns as born without it. released after wk 28 of gestation

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127
Q

area dependant effect of surfactant: how effective at smaller radius alveoli?

A

= lower SA.
> density of surfactant

more effective at ⬇ ST in smaller alveoli and during deflation (when alveoli size ⬇) of lung (expiration)

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128
Q

Topic 4c: chest wall & whole system compliance

how compliant is the chest wall?

A

chest distending P = always -
(tries to push chest in)

at FRC: Pdist =Pin -Pout
= PpI -PB
= -0.5 - 0 outside
= -0.5kPa 
pulling in

high elastic outward recoil

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129
Q

when can chest wall compliance change?

A

impairments:

obesity, pectus excavatum
inflammation of joints, fusion of bones in spine

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130
Q

lung distending pressure is always?

A

+

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131
Q

compliance of chest wall and “ of lung are…

A

equal!

  • and +
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132
Q

when chest wall and lung distending p hit 0 dist pressure i.e. change… where does this occur?

A

pneumothorax

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133
Q

how does compliance of total system compare with component parts

A

total is < comp parts

when lungs IN chest wall, less compliant

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134
Q

Topic 5: Airflow and Resistance

what 4 factors determine (Rate of) airflow into and out of resp system?

A

a. Density & viscosity of gas (constant)
b. driving pressure
c. types of airflow
d. airway resistance

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135
Q

a. Density & viscosity of gas (constant)

what has been used to inc rate of airflow and why?

A

Helium
as it has lower density

21% + 79%He used
e.g. Heliox for croup in children

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136
Q

what is b. driving pressure?

A

difference between pressure at 2 points

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137
Q

equation for flow of air? b. driving pressure

A

flow of air = press diff inside&outside (Palv - PB) / resistance

FOA= dir prop to driving pressure
FOA= inv prop to resistance
138
Q

what does b. driving pressure depend on?

A

c. types of airflow

certain types rew greater driving pressures to move air in and out of lung

139
Q

c.3 types of airflow and where?

A

laminar flow: v small airways, low velocity

turbulent flow: trachea, high vel flow, large radius

transitional flow: most of bronchial tree. mix of laminar + turbulent

140
Q

what does turbulent flow require? and when is it seen

A

exercise.

rew greater driving pressure (Palv-PB) to move air from mouth -> alveolus

141
Q

most of bronchial tree= transitional flow. what does it require?

A

inc turbulent flow = req more driving P to move air

as airflow inc from small airways, develops at bronchi

142
Q

what 2 things is resistance to airflow due to?

A
  1. friction between air + lung tissue (small contr)

2. friction between air + airways (BIG contr)

143
Q

when may friction between air + lung tissue increase?

A

e.g. in interstitial fibrosis- scarring of tissue and laying down of collagen

144
Q

why must resistance to airflow be small?

A

since a pressure diff between PB and Palv of 0.1kPa moves 500mL of air/breath

flow prop to pressure/ resistance

small resistance = greater flow

145
Q

where does airway resistance arise from?

A

40-50% upper resp tract
50-60% lower resp tract (larger airways)

(Gen 7- most resistance)
after 15th gen (term bronchioles, res = 0)

146
Q

how is airway resistance in upper resp tract sig reduced?

A

switch from nose to mouth breathing… more air to alveoli

147
Q

whats resistance directly prop to?

what has biggest effect on resistance?

A

L n / r^4
(Length, n: viscosity, radius)

r^4: airway calibre has LARGEST EFFECT on resistance as small airway radius change = big change to res and thus flow!

148
Q

resistance inc with 1/r^4, so where does most resistance lie?
is this actually true?

A

in narrow airways, with small r
… true if airways in series

BUT airways are in parallel, not series so TOTAL res of small airways = w small
(branched)

R total = 1/ R1 + R2 + R3

149
Q

whats radial traction and what does it affect?

A

force exerted by the lung parenchyma to keep the airways open

inflate= outward force on airways.

inc elastic recoil, alv want to collapse.

affects airways resistance

150
Q

affect of changing elastic recoil of alveolli e.g. in interstitial fibrosis/ emphysema on radial traction

A

walls of alveoli stiffen, lose elastic recoil

151
Q

Topic 5: Importance and control of airway resistance

how does contraction of smooth muscles lining in bronchioles –> decrease airflow?

A
  • > dec airway radius (a bit)
  • -> inc resistance to airflow (a lot)
  • –> dec airflow
152
Q

3 ways that airway resistance can be controlled by?

A

autonomic control
local chemical mediators
bronchoconstriction by ⬇ in CO2 in over-ventilated areas

153
Q

how is airway resistance controlled autonomically?

example??

A

vagal parasymp fibres evoke bronchoconstriction
bind to and activates M3 receptor
inc mucus secreted by submucosal gland= inc resistance to airflow too

anticholinergics (antimuscarinics) treat COPD

154
Q

autonomic control of airway resistance: hm symp fibres innervate airways?

and affect of evoking B2 rec? by what?
example drug

A

not many

circ Ad/ other adrenergic agonists/ sympathomimetics acting on B2 receptors evokes bronchodilation

treat asthma e.g. salbutamol
mimic Ad

155
Q

drugs used for local chem mediators used to control airway resistance?

used in what conditions?

A

mast cell stabilisers
leukotriene antagonist
antihistamines

asthma
allergic conjuctivitis
rhinitis
sinusitis

156
Q

how do irritant and allergens affect bronchi?

example substance?

A

activate mast cell: inflamm substances released
bronchi release mucus and constrict= hard to breathe
inc resistance to airflow

e.g. histamine: causes airway muscle contraction

157
Q

if resistance is so small, whys it important in: upper airway?

A

intraluminal airway obstruction: stuck in normal passages +up airways

aspiration of foreign objects

abdominal thrusts: inc in Palv= expel object when choking

bronchospasms, mucus, oedema

obstruction by tongue/tonsils (sleep/ unconsciousness)
= inc resistance in upper airways

158
Q

if resistance is so small, whys it important in: lower airway?
in what disease?**

A

COPD

e.g. bronchitis, asthma, emphysema

159
Q

how to treat high resistance in lower airways: COPD
e.g. bronchitis, asthma, emphysema

(3)

A

long and short acting BRONCHODILATORS

  • b rec agonists (relievers)
  • anticholinergics
  • theophylline

STEROIDS

ANTI-INFLAMM DRUGS

160
Q

Topic 6: alveolar gases

what is referred to by PIO2, PAO2, PaO2, PvO2?

A

Inspired
Alveolar
arterial
venous

161
Q

PO2 in inspired air (PIO2) = 20kPa
PO2 in alveoli (PAO2) = 13kPa

why is lower PO2 in lung than air?

A

bc O2 constantly removed from alveolus into blood = satisfy metabolism (VO2)

O2 in blood= 250ml/min at rest

162
Q

PCO2 in inspired air (PICO2) = 0kPa
PCO2 in alveoli (PACO2) = 5kPa

why is more PCO2 in lung than air?

A

bc CO2 produced by metabolism - constantly added from blood -> alveolar air

CO2 in blood: 200ml/min, removed into alv ☺

163
Q

what are alveolar gases similar to?

values?

A

arterial gases
PaO2 = 12
PaCO2 = 5

…
alveolar:
PAO2 = 13
PACO2 = 5

164
Q

normally alveolar levels of PO2 and PCO2 determine systemic artial levels too, but what determines alveolar gas:

  • PAO2? (3)
A
  1. PO2 in atmosphere (inpspired) air.. altitude
  2. rate of replenishment of O2 by alv ventilation (VA)
  3. rate of removal of O2 by pulmonary cap blood (level of metab rate, VO2)
165
Q

rate of replenishment of O2 by alv ventilation (VA)

determines PAO2. if VO2 unchanged,how is VA linked w PAO2?

A

VA inc = PAO2 inc
…
dir prop

166
Q

rate of removal of O2 by pulmonary cap blood (level of metab rate, VO2). if VA unchanged,how is VO2 linked w PAO2?

A

inc VO2 = dec PAO2
…
dec VO2 = inc PAO2

indirectly/ reverse prop

167
Q

normally alveolar levels of PO2 and PCO2 determine systemic arterial levels too, but what determines alveolar gas:

-PACO2 (2)
5kPa

A
  1. rate of metabolism (VCO2) if breathing unchanged: PACO2 ∝ VCO2

so… if CO2: 5% of alveolar air… CO2: 200ml/min= transfer
if increases,both increase!

  1. alveolar ventilation (VA)
168
Q

PACO2 is also affected by: alveolar ventilation (VA) - if VCO2 unchanged, how does VA link with PACO2

A

inc VA = dec PACO2
dec VA = inc PAO2

inversely proportional (alveolar ventilation!)

169
Q

how is ventilation linked to metabolic demand?

A

directly proportional ☺

if metab x2, VA x2
if metab halves, VA halves

alveolar gases, blood gases, pH kept rel constant :)

170
Q

effect of disease on alveolar gases, blood gases, pH and why?

A

abnormal

resp cant meet metabolic demand at rest (severe) or changes in demand (less severe)

171
Q

what happens in

  • hypoventilation
  • hyperventilation
A
  • underbreathing: PACO2 ⬆ and PAO2 ⬇.
    alveolar ventilation doesnt keep pace with CO2 production
  • overbreathing: PACO2 ⬇ and PAO2 ⬆
    no change in metabolic rate
    alveolar ventilation to great for CO2 production
172
Q

what 2 things are
increased in hypoventilation
decreased in hyperventilation?

A

PACO2 and PaCO2

173
Q

whats hyperventilation no same as and why?

A 
increased ventilation (during exercise)
as ven STILL matched to metabolism
174
Q

whats hyperpnoea?

A

breathing: deeper and more rapid than normal

but ⬆ in CO2 produced is exactly ∝ to ⬆ ventilation

175
Q

3 signs/ indicators of hyperventilation

A
  1. PaCO2 lower than normal (<4.5kPA, but need blood gases)
  2. dizzy: low PaCO2 = vasoconstriction of cerebral vessels
  3. tetany: spasm, numbness
176
Q

why may hyperventilation cause tetany?

A

fall in PaCO2-> hyperexcitability of membranes
= inc perm
= AP initiation

177
Q

how to treat hyperventilation?

A

slow deep breaths

not breathing in a bag = inc in CO2!

178
Q

Topic 6b: diffusion of gases across alveolar membranes

whats diffusion through tissues described by?
and whats it dependant on?

A

Ficks law of diffusion

  • SA
  • barrier thickness
  • PP difference between 2 sides (P1-P2)
  • diffusion constant for that gas through that barrier
179
Q

what does diffusion constant for gas through barrier depend on?

A

MW and solubility of gas

180
Q

diffusion ability of CO2 and O2 compared.. which one diffuses more easily?

A

CO2 diff 20x more easily than O2

more soluble, need less gradient ☺

181
Q

in what conditions may SA of alveoli in contact with capillaries be decreased and what will this affect for diffusion?

A

lung infections/ pulmonary oedema….

thus increase distance O2 has to diffuse

182
Q

normally and in thickened diffusion barrier:

how does inc in % pulmonary cap length affect PO2 in pulmonary cap?

A

normally: proportional. inc together

in TDB: up to 25% length, VERY STEEP inc in PO2, then plateu. same alveolar PO2 regardless of length

PP gradient dec, rate of diffusion and blood flow= SLOW= eqm before end of cap!

OR OTHER WAY around? checkkk

183
Q

affect on exercise and PO2 pulmonary capillary?

A

HR inc,
time for complete cardiac cycle dec
= less time spent in cap
= time for eqm decreases

184
Q

p361 learn PPs!

A
185
Q

define:
dyspnoea
tachypnoae
apnoea

A
  • sensation of shortness of breath
  • rapid breathing
  • cessation of breathing
186
Q

Topic 7: Ventilation and perfusion

control of gases: how does blood enter the capillary and what happens to gases?

A

CO2 rich, O2 poor

CO2 given up to alveolar air, O2 taken up

after exchange: alveolar air AND blood = 12kPa O2 and 5kPa CO2

187
Q

alveolar air and blood contain same levels of O2 and CO2. whats responsible for setting blood gases?

A

alveolar gases

188
Q

whys there a small difference in PAO2 (alveoli 13kPa) and PaO2 (arterial 12kPa)?

A

ventilation- perfusion (V/Q) matching

189
Q

if given lung unit = equally well V and Q (ventilated and perfused) with blood, what is optimised?

A
  • gas exchange
  • uptake of O2 form alveolar gas -> blood
  • elim of CO2 from blood -> alveolar gas
190
Q

V/Q matching in the whole lung = calculate the value

wb ideal value?

A

VA (V) = 4L/min

blood flow to lung= CO (Q) = 5L/min

V/Q = 4/5 = 0.8

**ideally equal so ratio = 1

191
Q

whys V/Q not exactly matched and = 1 irl?

2 scenarios

A

alveolus may be:
underventilated/ overperfused VQ ratio infinite
or opposite with VQ of zero

192
Q

A: blood returning to heart from an undervent/overperfused alveolus is….

A

hypoxic and hypercapnic….
exactly same as when entered

PvO2: 5kPa –> PaO2: 5kPa
PvCO2: 6kPa –> PaCO2: 6kPa

no ventilation received (fresh air)

193
Q

A: blood returning to heart from an undervent/overperfused alveolus.
this is seen in what condition?

A

COPD
V/Q<1

alveolar and arterial blood gases equilibriate w venous gases (shunt)

194
Q

b: alveolus may be overventilated/ underperfused V>Q ratio infinite

when may this occur?

A

pulmonary embolism

alveolar dead space
..
well ventilated but no blood flow

195
Q

what happens to alveolar gases in an overventilated/ underperfused alveolus?

A

equilibriate with inspired gases..
as no O2 extracted/ CO2 added to alveolus

so dont contribute to gas exchange.
can inc in disease state!

196
Q

how does lung adjust to match V and Q in… undervent alveolus?

A

hypoxic blood = localised hypoxic vasoconstriction

blood directed away = Q inc

197
Q

how does lung adjust to match V and Q in… overvent alveolus?

A

low PCO2 in airways = localised bronchoconstriction

198
Q

look at lung/ flow unit vol lung graph p373

A
199
Q

Topic 8: Oxygen transport

normal values of arterial: PaO2, PaCO2
venous: PvO2, PvCO2?

A

PaO2: 12.6-13.3
PaCO2: 5

PvO2: 5
PvCO2: 6

kPa

200
Q

what 2 forms is oxygen carried in throughout body?

A
  • dissolved in plasma

- combined with Hb (majority!)

201
Q

whats the total O2 content (in 1L of arterial blood)?

and what does each factor depend on?

A

200ml total O2..

3ml dissolved O2
- dep on PaO2

197ml O2 bound to Hb
- dep on [Hb] and % Hb sat (which depends on PaO2)

202
Q

Hb is not a plasma protein… what 3 problems would be caused i it were in plasma?

A

viscosity of blood would be high: high resistance to flow

Hb would be lost by kidney: size, filtered in glom.. has to be constantly made

Hb could be attacked by free enz in plasma

203
Q

whats haemoglobin made of?

A

4x globin: polypeptide chains (2 alpha and 2 beta) each containing 1 haem

4x heam: has centtral Fe atom - can combine reversibly w 1 molecule of O2

204
Q

1 molecule of Hb combines with what…
whats formed?

equation?

A

4 molecules of O2 to form 4 molecules of O2..-> oxyhaemoglobin

Hb + O2 HbO2

205
Q

what does amount of oxygen that blood will carry therefore depend on?

A

[Hb]

i.e. O2 binding capacity = proportional to Hb of blood.

206
Q 
normal Hb values (g/dL) in 
men
women
birth
child
A

men: 13-18
women: 12-15
birth: 12-24
child: 10-14

207
Q

whats theoretical O2 binding capacity not dependant on?

A

PO2

theoretical= if ALL Hb binding sites are saturated w O2

208
Q

whats the theoretical value O2 binding capacity in normal person.. and anaemic?

1g Hb can combine w 1.34ml O2
each 100ml blood has [Hb]= 15g

A

normal:
[Hb] x 1.34
15 x 1.34
20.1ml O2/dL

anaemic:
10 x 1.34
13.4ml O2/dL

       as drop in [Hb]
209
Q

whats saturation of Hb and how is it calculated?

A

% of Hb binding sites in bloodstream occupied by O2..

% sat = O2 bound to Hb/ O2 capacity x 100

210
Q

whats %saturation of Hb dependant on?

A

PO2

in arterial (PO2: 13kPa) = 99%
mixed venous (PO2: 5kPa) = 75%
211
Q

how will mixed venous % Hb sat (SpO2) change if metabolism increases?

A

inc metab… more O2 removed to meet metabolic demand… would DECREASE

212
Q

O2 dissociation curve. what does the O2 bound to Hb depend on?

A

partial pressure of O2 in blood

SIGMOIDAL SHAPE
… doesnt account dissolved O2!!

213
Q

why is the % Hb saturation/ PO2 curve sigmoidal?

A

haem-haem interaction

= how O2 binds + dissoc from Haem groups on Hb molecule

as Hb sat inc… affinity for O2 inc
snowball effect of attaching: + or - of O2 to Hb

214
Q

physiological significance of sigmoidal shape of Hb curve?

A

steepest: at levels of PO2 in tissues

= O2 can be given up readily w/out need to fall in PO2… high diffusion gradient maintained ☺

215
Q

PO2 in lungs (top of Hb curve)… how does % sat link to alveolar PO2?

A

large fall in alveolar PO2, small fall in % sat

216
Q

what does the steep part of Hb curve mean/ whys it useful?

A

PO2 in tissues (not lungs…)

if inc demand for O2, more O2 removed for small change in PO2. easily dissociated

217
Q

dissolved o2 at bottom of curve… whys this a safety net for altitude/ disease?

A

still have high %.

alveolar thus arterial PO2 can fall w/out change in Hb☺

218
Q

describe the Bohr effect

what happens and why?

A

right shift of Hb curve…
O2 affinity ⬇, P50 ⬆

Hb sensitive to needs of tissue. can change affinity to O2 to promote unloading when tissue demand increases

219
Q

what is right shift (decreased affinity) of Hb curve caused by? 4

A

⬆ PCO2
⬆ H+ conc
⬆ temp
⬆ 2,3-DPG (made in RBC by metabolism. fairly constant conc, changed in hypoxia + disease)

220
Q

what 2 points of Hb curve do not change?

A

top and bottom

221
Q

what is left shift (increased affinity) of Hb curve caused by? 4

A

⬇ PCO2
⬇ H+ conc
⬇ temp
⬇ 2,3-DPG (made in RBC by metabolism. fairly constant conc, changed in hypoxia + disease)

222
Q

physiological significance of Bohr effect?

on lungs

A

LUNG: LEFT shift
⬇ CO2, H+
⬆ Hb affinity

more O2 uptake in lung.
CO2 release.. ⬇ acidity

223
Q

physiological significance of Bohr effect?

on Tissues

A

TISSUES: RIGHT shift
⬆ CO2 to blood, H+
⬇⬇ Hb affinity

more O2 uptake in tissues.
O2 dissoc AWAY from Hb

224
Q

how will anaemia affect Hb dissociation curve?

A

low [Hb]
reduce carrying capacity,
LEFT shift

225
Q

how will CO poisoning affect Hb dissociation curve?

A

HbCO = drop by half (the top point)
inc O2 affinity lower

curve now: O2 content/ PO2 !!!
PaO2 normal not affected but P50 ⬇ LEFT SHIFT = ⬆ affinity

226
Q

when will symptoms occur for CO poisoning (O2 content curve) and why?

A

CO has 200x greater affinity for Hb, symptoms when COHb >10%

difficult to remove form Hb, .. dizzy, nausea, hypoxic

227
Q

2 types of Hb? which is in

  • adults
  • newborns?
A 
Hb A (2 a, 2 b chains)
Hb F (2 a, 2 y chains)
228
Q

newborns have Hb F (2 a, 2 y chains) instead of Hb A. how does this affect Hb saturation curve? benefits?

A

LEFT: inc affinity (compared to maternal curve)
as doesnt interact with 23DPG.
aids uptake O2 from placenta: inc saturation = dec PO2
diffusion distance inc

compared to lungs = helps O2 uptake

229
Q

affect of sickly cell (Hb A) mutation of B chains …

A

abnormal Hb molecule, poorly soluble deformed RBC can be destroyed.
genetic
carry less O2

230
Q

myoglobin: how the % sat/ PO2 curve different?

A

independant of pH/ PCO2… LEFT shift a lot.

P50: 0.5kPa
90% saturated at PO2 of 2.6kPa

made of 1 Haem, 1 globin, can only bind 1 O2 at a time

231
Q

roles of myoglobin?

A

stores O2 for use during v heavy exercise

enhances o2 diffusion through cells by carrying o2 through cytosol

232
Q

Topic 8b: CO2 transport

in what 3 forms is CO2 carried in the blood?

A
  • dissolved in physical solution (same as O2)
  • bound to proteins inc Hb, as carbamino compounds (20% more soluble than O2)
  • as bicarbonate (carbonic acid) MAJORITY
233
Q

how are carbamino compounds formed?

A

reversible

CO2 + terminal amino group of proteins esp Hb

CO2 + Hb-NH2 Hb-NHCOO + H+

H+ is removed. if not buffered = change in pH

234
Q

60% of CO2 produced is carried as bicarbonate. whats the eqn?

what accelerates the slow step?

A

CO2 + H2O -> H2CO3 -> HCO3- + H+
SLOW in plasma
- accel by carbonic acid (CA) in RBC.
helps maintain strong pp gradient between tissues + blood during CO2 diffusion ☺

p403 for diagram!!

235
Q

how does the CO2 dissociation curve differ from O2?

A

more than twice O2 content of blood
steeper slope= greater change in content for given change in CO2
no plateau or maximum (p404)

236
Q

effect of inc PO2 on CO2 content/ PCO2 curve?

name for this?

A

shifts CO2 curve down and left i.e. less CO2 carried = less CO2 in blood

HALDANE EFFECT

237
Q

why does haldane effect happen? (inc PO2 shifts CO2 curve down and left i.e. less CO2 carried)
(2)

A
  1. deoxyHb = better buffer to mop up H+.. favours formation of bicarbonate
    H2CO3 eqn.. H+ goes to..
    H+ + HbO2 H+-Hb +O2
    oxyHb deoxyHb
  2. deoxyHb = better ability to bind CO2 and form carbamino compounds
238
Q

importance of haldane effect

on. .. capacity for co2 carriage
and. .. CO2 given up ?

A

as blood gives up O2 in tissue, CO2 carriage capacity INC = transported back to lungs

as oxygenation of Hb occurs in lung blood gives up CO2 into alveoli.
excreted in lung

239
Q

how do Bohr effect and Haldane effect compare in terms of mol and affinities?

A

BOHR: CO2/H+ affecting affinity of Hb for O2
HALDANE: O2 affecting affinity of Hb for CO2/H+

240
Q

Topic 9: Role of respiratory system in acid-base balance

what does H2CO3 affect if not monitored and regulated?

A

weak but <20mls made a day.

will affect normal tissue func!

241
Q

what may cause plasma and RBC acidity to increase?

A

H+ made from carbonic acid disso and carbamino compounds, if not buffered

242
Q

3 methods that buffer H+ atoms…

role of carbonic acid system as an important buffer system

A
  1. plasma proteins: bind H+ + R-NH2 –> R-NH3+
  2. globin chain of Hb
    HbO2 dissoc into O2 and Hb.
    Hb + H+ -> HbH
  3. carbonic acid-bicarbonate system
    moved to left.. CO2 excreted at lung
243
Q

whats the ideal arterial pH (pHa) for enzymatic activity and (how calculated)?

A

7.40

pH = -log [H+]

244
Q

what 3 solns in body contain weak acids and buffer changes in H+ by adding acid/alkali?

A

blood
intracellular fluid
extracellular fluid

245
Q

henderson-hasselback eqn relates to pH solution to… (2)

A

A)!! pKa of buffer system
b) ionised [A-] and unionised [HA] forms

pKa = pH
when
[A-] = [HA]

246
Q

whats the unionised and in=onised forms in CO2-bicarbonate system and thus…

A 
H2CO3 = unionised (BUT quicly dissociates)
[HCO3-]= ionised

since [H2CO3] ∝ PaCO2
= use PaCO2 as unioninsed measure

247
Q

what systems control: [HCO3-] and [PaCO2]?

A
  1. kidney

2. resp systems

248
Q

whats meant by:
metabolic acidosis
metabolic alkalosis

carbonic acid eqn

A
  1. [H+] rises, mass reaction pushed left
  2. loss of body acids -> dec in breathing + retention of CO2

i.e. lungs take care

249
Q

whats meant by:
Resp acidosis
Resp alkalosis

carbonic acid eqn

A
  1. if [CO2] inc, mass reaction pushed RIGHT… but also inc CO2 and bicarb
  2. opposite if CO2 decreases

i.e. kidneys take care
HCO3- reabsorbed by kidney
H+ secreted by kidney

250
Q

metabolic acidosis process of returning pH back to normal?

A 
acidemia
sensed by chemoreceptors
inc ventilation
inc CO2 excretion
pH normal now ☺
251
Q

examples of

  • metabolic acidosis
  • metabolic alkalosis
A
  • diarrhoea
    diabetic ketoacidosis
    lactic acidosis
  • vomiting
    diuretics
252
Q

examples of

  • Resp acidosis
  • Resp alkalosis
A
  • hypoventilation (COPD)

- hyperventilation (response to hypoxia, anxiety)

253
Q

Topic 10: chemical control of breathing

location and properties of receptors: monitor art BGs and ECF
changes in vent evoked by breathing diff gas mixtures

3 basic elements of a control system?

A

central controller –> output: effectors –> sensors (then input back to CC)

254
Q

22 examples of sensors that then input to central controller?

A

chemical: chemoreceptors
mechanical

gather info form environment

255
Q

where are chemorec sensors and where do they send info to?

A

in upper airways, chets wall, lungs, joints/muscles…
info back to brain stem (CC)
to act on effectors: ventilatory muscles

256
Q

function of respiratory system: has exchange and pH maintenance… hm O2 consumes and CO2 produced in young adult at rest?

A

VO2: 250ml/min
VCO2: 200ml/min

257
Q

what would happen to blood O2 and blood CO2 if metabolism changed and no change in respiration? and consequence?

A

blood O2: fall (tissues -> hypoxic)

blood CO2: rise (pH disturbances)

258
Q

whats alveolar ventilation (VA) increased by? (3 instances)

i.e. what should be staying constant?… and what detects the change

A

low arterial PO2
high arterial PCO2
low arterial pH

.. chemoreceptors detect

259
Q

how do chemoreceptors maintain homeostasis of PaO2, PaCO2, and pH?

A

assist in ensuring VA is appropriate to level of metabolism…

260
Q

whats name of difference in O2 content between arterial and mixed venous blood?

A

arteriovenous difference

261
Q

what do fairly constant levels of PaO2 and PaCO2 gases after exercise/ anaerobic threshold ensure?

A

constant by inc ventilation to meet metab demand… = constant delivery of gases ☺

262
Q

2 types of chemoreceptors and what do they each respond to?

A

Peripheral:
low PaO2 (arterial)
high PaCO2
high [H+] (low pH)

central:
only- high PaCO2
- majority of CO2 response

263
Q

where are peripheral chemoreceptors located?

A

2 sets, same as arterial baroreceptors…

*carotid bodies (in c sinus)
distinct nodules, most important for refled
*aortic bodies

264
Q

where does carotid sinus nerve join into?

peripheral chemorec

A

carotid body (chemos) next to sinus.

.. glossopharyngeal (IX) nerve

265
Q

what type of blood flow is supplied by branch of external carotid artery?
wb AV O2 difference?

A

high blood flow… and little O2 consumption= O2 leave similar to in.

= small AV O2 difference

266
Q

how do carotid bodies work to signal CNS?

4

A

fall in PO2-> K+ channel closes, Vm depolarises
Ca2+ channels open
Ca2+ influx triggers NT release
sensory afferents signal to CNA

267
Q

4 properties of carotid bodies i.e. what do they repond to?

A

low activity at normal PaO2

respond to

  • PaO2 (not O2 content)… therefore no response to anaemia/CO
  • H+ (change in pH) derived from acids other than CO2 e.e. lactic acid, ketone bodies
268
Q

why dont carotid bodies respond to anaemia/ CO?

A

as they respond to PaO2 not O2 content…

CO poisoning affects O2 content and delivery to tissues BUT NOT PO2.
-> affects breathing thus no change seen as not affected
= VERY DANGEROUS

269
Q

what does removal of carotid bodies (peripheral chemoreceptors) –>?

A

decreases in ventilatinon during hypoxia (direct effect of hypoxia on brainstem)

270
Q

how are aortic bodies different to carotid? peripheral chemoreceptors

A

less important in resp control

less vascular, lower blood flow (sluggish)

dont respnd to changes in pH (without change in PCO2)

271
Q

what do aortic bodies respond to?

A

increase in PaCO2
fall in PaO2
O2 content… thus can detect anaemia/CO

272
Q

what are aortic bodies innervated by? and what role do they play?

A

vagus (x) nerve

role in cardiovasc reflexes - haemmhorage

273
Q

whats the resp response to hypoxia? low O2

A

only peripheral chemoreceptors…
VE starts to ⬆ when PaO2<8kPa
carotid bodies start to respond when Hb sat drops

ventilation/PaO2 curve: L shape moves up
simultaneous hypoxia and hypercapnia have multiplicative effect

274
Q

affect of moderate hypoxemia on VE?

A

(PaO2 5-8kPa) only doubles VE (⬆ ventilation)

275
Q

where are central chemoreceptors located?

A

ventrolateral medulla of brainstem (midbrain, pons, medulla oblongata)

276
Q

central chemoreceptors are stimulated when?

and account for minority/ majority of response to hypercapnia (⬆ CO2)?

A

when arterial PCO2 increases
only slightly stim by ⬆ in arterial acidity (H+ ions) bc separated from blood by BBB

account for 60-80%… majority

277
Q

what are central chemorec insensitive to?

A

hypoxia (change in arterial O2)

278
Q

process of stimulation of central chemoreceptors?

A
  1. BBB prevents H+, HCO3- from affecting brain ECF/CSF
  2. CO2 crosses… goes in CSF .. carbonic acid eqn
  3. H+ made -> ECF,stim response in chemorec
279
Q

stimulation of central chemoreceptors summarised: what stimulates the cc neurons?

A

acidification of CSF and ECF

280
Q

CSF is a poor buffer so small changes in PaCO2 ->?

A

significant CSF acidosis

281
Q

resp response to hypercapnia (high CO2): what would graoh look like (AV/PaCO2)

A

resp system: VERY sensitive to CO2 levels

peripheral and cetral chemor detect
steeper slope than hypoxia response
⬆ of <1kPa can double VA

282
Q

how would (AV/PaCO2) graoh change in CO2 resp responses to

  • awake normal
  • sleep
  • morphine, barbs, COPS
  • anaesthetics
A
  • VERY steep and high
  • steep and high
  • flatter and lower
  • VERY flat and low
283
Q

Topic 10: Central control of breathing intro 1/4

effectors: in vent muscles. whats output of system? CC, sensors, effectors

A

change in thoracic volume and airflow

284
Q

what 3 thingsmust any model of rhythm generation account for?

A
  • maintenance of invol breathing (automatic)
  • adj of vent for gas exch (metabolic demand)
  • adj of breathing pattern for speech, swallowing… (voluntary)
285
Q

minute ventilation (VE) =?

A 
VE = VT x Rf
VE = tidal volume x respiratory frequency
         (infinite combos)
286
Q

minute ventilation (VE) how is it determined/ whats pattern aimed at?

and whats meant by resonance?

A

aimed at minimising work done by resp muscles to reach required VE

res: right timing = req less effort
(pushing someone on a swing- timing)

287
Q

neural control must affect what 2 nerves before affect on resp muscles?

A

phrenic (inspiratory)
+
internal intercostal (exp)

288
Q

what does alternating activity in muscles: inspand exp lead to?

A

phrenic and intercostal….

change in thoracic vol thus change in pressure and airflow

289
Q

what do accessory insp muscles do?

A

sternocleidomastoid, scalene, external intercostal:

raise ribs and expand chest cavity

290
Q

what would airway flow and airway pressure EMG recording look like?

A

airway flow:
insp = curve up
exp: curve down
then flat= exp pause

airway pressure:
reverse (upside down)
with same flat, exp pause in between

291
Q

exp muscles at rest: what takes part in passive relaxation?

A

diaphragm

292
Q

role of other muscles during exp? internal intercostal, externala nd internal oblique?

A

suppress: shrink cavity push air out of lungs

forced expiration!

293
Q

central respiratory rhythm –> what ?

in insp and exp muscles

A

-> reciprocal motor activity

294
Q

on EMG, what muscle active in

  • inspiration
  • expiration?
A
  • diaphragm (thick small lines vertical)

- internal intercostal (thin long lines vertical)

295
Q

exp and insp nerves: intercostal and diaphragm … where do they get intrinsic activity input form?

A

have none themselves… from CNS

= central controller in brain must be driving

296
Q

Topic 10b: CC of breathing 2- neural control centres

what part of brainstem is important in rhythm generation? how we know?

A

medulla
bc when cut off, complete cessation of rhythmic breathing pattern
has all neural mechs to gen rhythm.

PRG interacts w medullary centres to smooth resp rhyhtm timing!

297
Q

2 main areas of CNS involved in breathing?

A

pons
- pontine resp group PRG

medulla
-medullary respiratory centre

either side of midline can generate rhythm independantly (even tho normally funcn as 1 unit)

298
Q

p545 dorsal view of brainstem image: identify

  • Botzinger complex (expiratory),
  • prebotzinger (Pacemaker?),
  • ventral resp group (VRG insp +exp),
  • dorsal resp group (DRG insp)
A
299
Q

what do neurones in DRG do?

A

discharge AP prior to inspiration -> control lateral phrenic nerve- control diaphragm

300
Q

where is DRG in?

A

dorsal resp group… in NTS (Nucleus Tractus Solitarius)

301
Q

what info does NTS (Nucleus Tractus Solitarius) receive and what does it do with it?

A

resp and CV afferent inputs, integrates info from chemo and mechanorec afferents related to breathing

302
Q

Topic 10c: cc of breathing 3: resp rhythm generation in medulla

what drives inspiration during quiet breathing?

A

Prebotzinger complex…

  • DRG neurones ACTIVE –> C spinal cord–> diaphragm contracts-> inspiration
  • VRG neurones INactive
303
Q

what causes diaphragm to contract?

A

motor neurones inc activity of phrenic nerve… d innervated by AP generation

304
Q

what causes expiration during quiet breathing?

A

passive!

  • DRG neurones INactive
  • VRG neurones INactive –> diaphragm relaxes and passive recoil-> expiration to FRC

(inhibition of motor neurones in SC that control diaphragm)

305
Q

VRG neurones action in insp and expiration in quiet breathing

A

inactive in both insp and expiration in quiet breathing

has insp and exp neurones but no breathing movements in quiet breathing

306
Q

what about the DRG is responsible for basic rhythm of breathing?

A

cyclical electrical activity of DRG

307
Q

what nerve responsible for contraction and relaxation of diaphragm using DRG in quiet breathing?

A

phrenic motor nerve

308
Q

What happens when demand for ventilation increases? i.e. no longer just quiet breathing
inspiration?

A 
sensory info (chemo, mechanor) to NTS
stimulates
  • DRG = MORE active… C SC…. diaphragm contracts harder
  • VRG = ACTIVE….Thoracic T SC… accessory insp muscles contract

== more forceful indpiration (and freq may change)

309
Q

What happens when demand for ventilation increases? i.e. no longer just quiet breathing
expiration?

A 
sensory info (chemo, mechanor) to NTS
stimulates (BOTZ (E) as well)
  • DRG = INactive…diaphragm relaxes
  • VRG = I inactive… other insp muscles relax
  • VRG = E neurones ACTIVE… accessory exp muscles contract == more forceful expiration !

p549

310
Q

Topic 10d: cc of breathing: outside the medulla

role of pontine group (PRG)?

A

influences switching between inspiration and expiration

sectioning through diff levels of pons= change breathing pattern esp TIMING

311
Q

how does PRG shut off inspiration?

A

inhibits DRG insp neurones

vagal afferent role

312
Q

higher brain centres affect DRG: +/-

outside medulla and pons, when are hypothalamus, limbic system, motor cortex involved in breathing changes?

A

H: temp, fight/flight (hypervent)
L: emotion/pain
M: limb receptors, exercise. activates DRG rec in propn to exercise demands

313
Q

how is voluntary control (large breaths, hypervent, speaking, breath hold) done?

A

cerebral cortex direct to SC…
bypasses medullary centres.
directly affect motor neurones in Sc -> control respiratory muscles

314
Q

Topic 11: Neural reflex control of breathing 1

most of sensory influence comes from where?

A

vagal afferents.

main role: protect resp centre + feedback on situation

315
Q

where is vagus nerve located and what info does it carry and what is it important in?

A

parallel to trachea.

info to and from parts of body + important in resp control

316
Q

what do irritant receptord in bronchi
sense?
effect?

A

chemicals, dust, cold air

cough, bronchoconstriction

317
Q

what do J receptors in bronchioles/alveoli
sense?
effect?

A

chemicals, stretch, pulmonary oedema

shallow breathing, cronchoconstr, mucus secrtn

318
Q

what do stretch receptors in lung
sense?
effect?

A

lung inflation

inflation terminates

319
Q

4 types of mechanoreceptors? location

A

lung + airways
nose + upper airways
joints and muscles
arterial baroreceptors

320
Q

mechanoreceptors respond to what?

A

pressure/ distortion

321
Q

where are PSR? pulmonary stretch rec

A

vagal nerve endings in SM of trachea + local airways

322
Q

what are PSR pulmonary stretch rec stimulated by?

A

lung inflation (greater lung inf = more airways tension)

slowly adapting stretch receptors

breathe in= stretch rec ∝ to lung inflation stimuli

vagus nerve carries the afferent activity

323
Q

what are the 2 diff patterns from PSRs?

A
  1. rec which continues to be active during expiration IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII
  2. rec with phasic activity and high threshold- only active at inspiration IIII———-IIIIIIIIII———–IIIIIIIIII———IIIIIIIIII———–IIIIIIIII-
324
Q

when is hering-breuer reflex present? and whos it more powerful in?
whos it important in?

A

during sleep

babies as inhib influences from cortex not deveolped,
animals (need inflation >1L)

important in px w low lung compliance

325
Q

describe Hering-Breaur reflex when dec lung comlpiance

give example disease

A

stiffer lungs
more pull on stretch receptors
insp switched off earlier
= breathing shallow and rapid… restrictive diseases (interstitial fibrosis)

326
Q

central mechanism PSR? link to hering -breuer

A

inhibit inspiration and promote expiration (HB reflex)

vagal input from stretch rec VT> 1L –> NTS direct - inhib DRG (insp)
+ excite PRG

prolonged insp (cut vagi) = inc tidal volume

327
Q

lung irritant receptors- where are the vagal nerve endings and what are they stim by? speed of action?

A

between epithelia of trachea and lower airways

stim by noxious gases, smoke, dust, cold air,
rapidly acting receptors!

role in asthma induced bronchitis

328
Q

if stimulus maintained, how would this affect lung irritant rec action?

A

afferent impulse num dec over time

329
Q

how do lung irritant rec prevent noxious substance getting down to lungs and affecting lung tissue?

A

cig smoke, oxidants, inhald irritants stim irritant rec
info down vagal afferent
through vagal efferent
–> smooth muscle = bronchoconstriction ☺

330
Q

what else other than bronchoconstriction, may irritant rec initiate?

A

augmented breaths

natural sigh

  • occur naturally every few mins in man, more than animals
  • reverse slow collapse of lung during quiet breathing

lung vol increases, basic same phrenic nerve activity

331
Q

pulmonary C/ J receptors are located where?

A 
bronchial walls (unmyelinated C- fibres)
alveolar walls (J receptors juxtacapillary)- close to caps
332
Q

pulmonary C/ J receptors are usually what? and what stimulates them?

A

silent.

stim by: mechanical distortion and inc in interstitial fluid (oedema)

333
Q

what type of breathing do pulmonary C/ J receptors evoke?

A

rapid shallow or apnoea

responsible for rapid shallow breathing and dyspnoea in interstitial lung disease + LVHF?

334
Q

Topic 11b: Neural reflex control of breathing 2: nose and upper airways receptors

what initiates:

  • sneeze + diving reflex
  • cough
A 
nasal mucosa (trigeminal nerve endings)
- superimposed insp, rapid strong exp + exp pause

larynx + trachea (vagal nerve endings)
- inc exp air flow velocity and expel irritants

335
Q

what do proprioreceptors respond to?

examples of some

A

position/length
to position and movement, sense, stretch, tension, proprioception
in NTS (DRG)

golgi tendon organs
muscle spindles in diaphragm
intercostal muscles –> elongate, reflex control strength + resp of muscle contraction

336
Q

what do proprioreceptors allow for if movement is impeded?

A

inc force of insp and expiration

337
Q

what receptors are responsible for sensation of dyspnoea (breathlessness) if large effort required? e.g. obstruction

A

proprioreceptors

muscle spindles in intercostal muscles (calf) = certain tidal volume achieve if airway resistance increases

338
Q

joint and muscle rec in moving limbs.. have afferent activity into where and what does this lead to?

A

DRG

= inc ventilation upon at onset during exercise? esp early stages

339
Q

what do baroreceptors control and how?

A

BP

⬆ BP–> reflex hypoventilation/ apnoea e.g. Ad apnoea
⬇ BP–> reflex hyperventilation (e.g. due to haemorrhage)

340
Q

when may baroreceptors action be important?

A

in complex stimuli (haemorrhage) - many reflexes occur at once!

pathways unknown

Health.2 (19 decks)

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