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
What are 6 non-respiratory functions of the respiratory system?
- 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)
26
Topic 2: Partial pressures What are the 3 different units for (P) pressure? What unit is used clinically?
- kPa, mmHg, cmH2O | - kPa
27
What is PIO2 and PICO2?
Partial pressure of oxygen in Inspired air | Partial pressure of carbon dioxide in Inspired air
28
What is PAO2 and PACO2?
partial pressure of oxygen in Alveolus (BIG A) | partial pressure of carbon dioxide in Alveolus (big A)
29
What is PaO2 and PaCO2?
partial pressure of oxygen in arterial blood | partial pressure of carbon dioxide in arterial blood
30
What is PvO2 and PvCO2?
partial pressure of oxygen in venous blood | partial pressure of carbon dioxide in venous blood
31
How many mmHg is 1 kPa worth?
1 kPa = 7.5mmHg
32
How many mmHg is 1cmH2O worth?
1.3mmHg
33
What is a partial pressure?
the pressure of any gas whether alone/ in a mixture
34
What does the partial pressure of a gas depend on?
the number of molecules of the gas in given vol and temp
35
What is Dalton's law of partial pressures?
Total pressure is the sum of the partial pressures of all constituent gases TP = P1 + P2 = P3.... each gas exerting tis own PP
36
What is the equation for the total pressure in the atmospheric air, given the gases are nitrogen, oxygen, carbon dioxide and water vapour?
Total P = PN2 + PO2 + PCO2 + PH2O + other trace gases
37
What is the formula for the partial pressure of a gas? e.g. O2 in air
partial pressure = fractional conc of gas x total (atmospheric) pressure
38
What is the value of PIO2 at sea level if its fractional concentration is 21% and the barometric pressure is 95kPa?
partial pressure = fractional conc of gas x total pressure therefore 0.21 x 95 = 20kPa
39
Reference ranges of arterial blood gases and alveolar gases | look at table!! p132 of sem2
40
Why are partial pressures important for diffusion?
because diffusion occurs down partial pressure gradients
41
How does the partial pressure of O2 change from the atmosphere to the mitochondria?
- 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
42
What allows rapid diffusion between tissues and the capillaries? (hint: partial pressure)
there's a massive PO2 gradient of >55mmHg diffusion occurs down partial pressure gradients
43
effects of low alveolar PAO2 thus PaO2 in patient w resp disease?
dont have as much of gradient for diffusion= not as efficient.
44
Topic 2b: structure and function in airways Schematic image of human airways: 4 parts in conducting zone and 3 in transitional + resp zones?
conducting zone: trachea, bronchi, bronchioles, terminal bronchioles transitional + resp zones: resp bronchioles, alveolar ducts, alveolar sacs
45
What generations make up the conducting zone of the airways?
the first 16 generations
46
What is the function of the conducting zone? (2)
- movement of inspired air to gas exchanging regions of lungs - warms and humidifies air so the alveoli aren't damaged by cold dry air
47
What generations make up the transitional and respiratory zones? and whats the function?
17-23 | gas exchange
48
What type of flow moves gas through the conducting zone?
bulk flow
49
How and why does the cross sectional surface area increase from the conducting zone to the respiratory zone?
- enormous increase | - due to continuous branching
50
What is the formula for total air flow?
total flow = speed x area
51
As area increases, what does the speed of flow do?
speed decreases forward velocity of gas: good for diffusion
52
Why is the change in cross-sectional area from the conducting zone to the respiratory zone advantageous for gas exchange?
- 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
53
What specialised cells are found within the conducting zone?
- epithelia lined w cilia which beat constantly | - goblet cells which secrete mucus
54
How does nicotine affect cilia?
it paralyses the cilia, which allows bacteria to invade
55
How does inflammation/asthma affect mucus?
it increases the viscosity
56
What do the trachea and primary bronchi have that prevents their collapse?
U-shaped cartilage (blue on diagram)
57
Why are the bronchioles susceptible to collapse?
they don't have cartilage | ... COPD, asthma
58
The efficient flow of both what and what is necessary for efficient gas exchange?
air flow into the alveoli and blood flow through pulmonary capillaries
59
What is dead space (VD)?
the volume of gas within the respiratory system where no gas exchange takes place
60
Dead space occurs where? (2)
- where there's no effective airflow (aka no alveoli of unventilated alveoli) - where there's no perfusion
61
Which is anatomical dead space: the conducting zone or the respiratory zone?
the conducting zone, where there's no alveoli
62
What is the dead space within the conducting zone known as and how much is it in ml?
anatomic(al) dead space - 150ml
63
What affects the anatomic dead space? (4)
- body size: 2ml/kg - age: increases - drugs: bronchodilators/constrictors - posture: decreased when lying
64
What is the dead space within the respiratory zone known as?
the alveolar dead space - inadequate perfusion for gas exchange (<5ml)
65
How does the alveolar dead space change in disease?
increases during disease e.g. pulmonary embolus inspired gas reaches alveolus but alveolus if ineffective in oxygenating venous blood
66
What is the sum of anatomic dead space and alveolar dead space?
physiological dead space = anatomic dead space + alveolar dead space
67
What is the definition of tidal volume (VT)? What is the value for a 70kg healthy young adult?
volume of air breathed in & out in 1 breath - 500ml
68
What is the respiratory frequency (f)? What is the typical value?
number of breaths per min - 12 breaths/min
69
What is the equation for minute ventilation/volume (V̇E)?
V̇E (ml/min) = tidal volume x respiratory frequency
70
What is the definition of minute ventilation?
total air moving in and out of the respiratory system in 1 minute
71
total air moving in and out of the respiratory system in 1 minute
minute ventilation = tidal volume (VT) x respiratory frequency (f) 500 x 12 = 6000ml/min
72
how much air enters system every minute?
6L
73
what happens to total volume of air entering system a minute?
6L... some: remains in anatomical dead space (not involved in gas exchange) not all gets to resp zone: lower down
74
hows alveloar ventilation (VA) calulated?
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 ```
75
alveolar ventilation use?
= 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!!
76
what causes drug induced hypoventilation?
drug effects on alveolar vent - alcohol - tranquilisers - opiates - sedatives - hypnotics: benzodiazepines, barbiturates
77
Topic 3: mechanics of breathing how are lung + chest wall organised and related at rest 3 parts of the lung?
parietal pleura- contact w chest wall visceral pleaura (inner, covers lung) pleural cavity: pleural fluid between
78
hows fragile lung tissue inflated?
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
79
what must respiratory muscles do in order to breathe? (2)
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)
80
what 2 opposing forces act on lung and chest wall at rest?
1. elastic recorl of chest wall tries to pull chest wall OUTWARD 2. elastic recoil of lung creates INWARD pull
81
what kind of pressure is therefore in pleural space?
negative- less than PB intrapleural space CANNOT EXPAND 2 surfaces held together by cohesion of pleural liquid space
82
what is FRC? func residual capacity | and value?
volume in lungs at end of expiration approx 2.5L air
83
all pressures e.g. Palv in lung, relative to what?
pressure outside. atmosphere can change! stretching causes ⬇ in pressure relative to atmos. not actually -
84
what is lung distending pressure at FRC calc? | and what does it show
``` P in - P out = Palv - PpI = 0 - -0.5 =+0.5kPa (preventing lung collapsing) ```
85
what is chest distending pressure at FRC calc? | and what does it show
``` P in - P out = PpI - PB = -0.5 - 0 = -0.5kPa (preventing chest springing outward) ```
86
at FRC, how are distending pressures across lung and chest wall described?
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
87
air flows from XX pressure -> YY pressure
high -> low
88
why does air move in and out of lungs? what allows this
because Palv is made alternately < and > than PB. inspiration: Palv < PB expiration: Palv < PB
89
chenges in Palv occur ass result of what?
changes in lung volume when thorax expands i.e. BOYLES LAW
90
what is BOYLES LAW?
= pressure exerted by a constant number of gas molecules in container = inversely proportional to vol of container P ∝ 1/V
91
main inspiratory muscle and role? when used
diaphragm- ONLY muscle used in quiet breathing. lengthens thorax
92
other inspiratory muscles- what are they used in? 3
exercise, coughing, vomiting | = need inc volume changes
93
name 3 other inspiratory muscles and use?
sternocleidomastoid scalenes external intercostal 1 and 3: forced breathing and inc metabolic demands
94
describe quiet breathing (insp + exp) using diaphragm. quiet breathing
1. diaphragm relaxed at rest 2. insp: D contracts, thoracic volume increases 3. exp: D relaxes, thoracic volume decreases
95
what muscles also cause volume of thorax to increase during inspiration? NOT USED AT REST
external intercostal bucket handle movement rib moves up and sternum out
96
how does diaphragm behave in expiration? wb other muscles?
passive relaxation | ... other muscles during forced breathing more
97
3 expiratory muscles?
internal intercostal | external and internal obliques
98
at start of breath, how do pressures INSIDE and OUTSIDE thoracic cavity (Palv and PB) relate? what does this mean?
identical ``` PB= 0 Palv = 0 ``` no air flows in or out
99
describe inspiration (4)
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
100
describe expiration (4)
1. chest wall moves inward 2. vol of thorax ⬇, 3. lungs recoil- squeeze air 4. alveolar P now > P outside
101
describe inspiration and expiration in terms of boyles law and give Palv values
as volume ⬆, pressure ⬇ INS: Palv= -0.1kPa, air IN EXP: Palv= +0.1kPa, air OUT
102
Topic 4: Elasticity and compliance What is elasticity? (2)
- resistance of an object to deformation by external force (or stiffness) - ability to reform original shape after deformation e.g. balloons, lungs
103
What is compliance?
the ability to stretch
104
How do elasticity and compliance relate?
compliance is the inverse of elasticity or 1/E
105
HIGH elasticity means what for compliance, stretch, and recoil?
HIGH elasticity LOW compliance HARD to stretch EASY to recoil!
106
LOW elasticity means what for compliance, stretch, and recoil?
LOW elasticity HIGH compliance EASY to stretch HARD to recoil!
107
A balloon takes long to blow up but is quick to deflate. Is it low or high compliance/low or higher elasticity?
- low compliance, high elasticity | - harder to stretch (blow up) but quick to recoil (deflate)
108
A balloon is quick to blow up but slow to deflate. Is it low or high compliance/low or higher elasticity?
- high compliance, low elasticity | - easier to stretch (blow up) but slow to recoil (deflate)
109
The chest wall as high outward/inward elastic recoil
the chest wall has high outward elastic recoil (so wants to spring outwards like squeezing a tennis ball)
110
The lungs have high outward/inward elastic recoil
the lungs have high inward elastic recoil (so wants to collapse inwards like a balloon)
111
When are the lungs at rest?
at functional residual capacity (FRC)
112
At FRC, what is the lung distending pressure? (hint: alveolar pressure, interpleural pressure)
- the distending pressure =difference between alveolar pressure and pleural pressure - therefore value is always + - prevents lungs from collapsing due to high inward elastic recoil
113
How does the lung distending pressure change during inspiration?
becomes more positive | because the alveolar pressure increases
114
degree of lung expansion= proportional to what? | and what does this generate?
distensing pressure Pdist = Palv - PpI = generates outward, distending Press -> greater change in lung volume. represented by pressure-volume (compliance) curve
115
what does slope on pressure-volume curve show?
lung compliance. magnitude of change in lung vol (δV) produced by a change in distending pressure (δ Pdist)
116
compliance=?
δV / δ Pdist
117
lung distending pressure is always what?
+ | press inside lung
118
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)
Low at v low lung vols High at normal vols going up curve Low at high volumes
119
what does diff in compliance mean in terms of breathing?
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)
120
lung vol/ distending pressure compliance graph meaning in lung disease, emphysema?
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
121
Topic 4b: determinants of lung compliance what 2 things determine compliance of lung?
elastic properties of tissues (connective forces - stretchability) !!! suface tension at air-water interfaces in alveoli (> half lung elastic recoil) !!!
122
type 1 alveolar cell: what does it do and what lines walls of alveoli?
role: aids diffusion of gases thin layer of alveolar fluids
123
what type of force is surface tension and whys it present in alveoli?
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
124
how do surfactants reduce surface tensions in alveoli?
have strong attraction for each other... low attraction for other mols. accumulate at surface, ⬇ ST. = easier to inflate ☺
125
how would compliance change if NO surfactant?
⬇. need inc distending pressure to inflate lung = inc work for change. no s= LESS lung volume at higher lung distending p (graph p 189)
126
what px at risk of low compliance as no surfactant?
newborns as born without it. released after wk 28 of gestation
127
area dependant effect of surfactant: how effective at smaller radius alveoli?
= lower SA. > density of surfactant more effective at ⬇ ST in smaller alveoli and during deflation (when alveoli size ⬇) of lung (expiration)
128
Topic 4c: chest wall & whole system compliance how compliant is the chest wall?
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
129
when can chest wall compliance change?
impairments: obesity, pectus excavatum inflammation of joints, fusion of bones in spine
130
lung distending pressure is always?
+
131
compliance of chest wall and " of lung are...
equal! - and +
132
when chest wall and lung distending p hit 0 dist pressure i.e. change... where does this occur?
pneumothorax
133
how does compliance of total system compare with component parts
total is < comp parts when lungs IN chest wall, less compliant
134
Topic 5: Airflow and Resistance what 4 factors determine (Rate of) airflow into and out of resp system?
a. Density & viscosity of gas (constant) b. driving pressure c. types of airflow d. airway resistance
135
a. Density & viscosity of gas (constant) | what has been used to inc rate of airflow and why?
Helium as it has lower density 21% + 79%He used e.g. Heliox for croup in children
136
what is b. driving pressure?
difference between pressure at 2 points
137
equation for flow of air? b. driving pressure
flow of air = press diff inside&outside (Palv - PB) / resistance ``` FOA= dir prop to driving pressure FOA= inv prop to resistance ```
138
what does b. driving pressure depend on?
c. types of airflow certain types rew greater driving pressures to move air in and out of lung
139
c.3 types of airflow and where?
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
what does turbulent flow require? and when is it seen
exercise. rew greater driving pressure (Palv-PB) to move air from mouth -> alveolus
141
most of bronchial tree= transitional flow. what does it require?
inc turbulent flow = req more driving P to move air as airflow inc from small airways, develops at bronchi
142
what 2 things is resistance to airflow due to?
1. friction between air + lung tissue (small contr) | 2. friction between air + airways (BIG contr)
143
when may friction between air + lung tissue increase?
e.g. in interstitial fibrosis- scarring of tissue and laying down of collagen
144
why must resistance to airflow be small?
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
where does airway resistance arise from?
40-50% upper resp tract 50-60% lower resp tract (larger airways) (Gen 7- most resistance) after 15th gen (term bronchioles, res = 0)
146
how is airway resistance in upper resp tract sig reduced?
switch from nose to mouth breathing... more air to alveoli
147
whats resistance directly prop to? | what has biggest effect on resistance?
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
resistance inc with 1/r^4, so where does most resistance lie? is this actually true?
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
whats radial traction and what does it affect?
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
affect of changing elastic recoil of alveolli e.g. in interstitial fibrosis/ emphysema on radial traction
walls of alveoli stiffen, lose elastic recoil
151
Topic 5: Importance and control of airway resistance how does contraction of smooth muscles lining in bronchioles --> decrease airflow?
- > dec airway radius (a bit) - -> inc resistance to airflow (a lot) - --> dec airflow
152
3 ways that airway resistance can be controlled by?
autonomic control local chemical mediators bronchoconstriction by ⬇ in CO2 in over-ventilated areas
153
how is airway resistance controlled autonomically? | example??
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
autonomic control of airway resistance: hm symp fibres innervate airways? and affect of evoking B2 rec? by what? example drug
not many circ Ad/ other adrenergic agonists/ sympathomimetics acting on B2 receptors evokes bronchodilation treat asthma e.g. salbutamol mimic Ad
155
drugs used for local chem mediators used to control airway resistance? used in what conditions?
mast cell stabilisers leukotriene antagonist antihistamines asthma allergic conjuctivitis rhinitis sinusitis
156
how do irritant and allergens affect bronchi? | example substance?
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
if resistance is so small, whys it important in: upper airway?
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
if resistance is so small, whys it important in: lower airway? in what disease?**
COPD | e.g. bronchitis, asthma, emphysema
159
how to treat high resistance in lower airways: COPD e.g. bronchitis, asthma, emphysema (3)
long and short acting BRONCHODILATORS - b rec agonists (relievers) - anticholinergics - theophylline STEROIDS ANTI-INFLAMM DRUGS
160
Topic 6: alveolar gases what is referred to by PIO2, PAO2, PaO2, PvO2?
Inspired Alveolar arterial venous
161
PO2 in inspired air (PIO2) = 20kPa PO2 in alveoli (PAO2) = 13kPa why is lower PO2 in lung than air?
bc O2 constantly removed from alveolus into blood = satisfy metabolism (VO2) O2 in blood= 250ml/min at rest
162
PCO2 in inspired air (PICO2) = 0kPa PCO2 in alveoli (PACO2) = 5kPa why is more PCO2 in lung than air?
bc CO2 produced by metabolism - constantly added from blood -> alveolar air CO2 in blood: 200ml/min, removed into alv ☺
163
what are alveolar gases similar to? | values?
arterial gases PaO2 = 12 PaCO2 = 5 ... alveolar: PAO2 = 13 PACO2 = 5
164
normally alveolar levels of PO2 and PCO2 determine systemic artial levels too, but what determines alveolar gas: - PAO2? (3)
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
rate of replenishment of O2 by alv ventilation (VA) | determines PAO2. if VO2 unchanged,how is VA linked w PAO2?
VA inc = PAO2 inc ... dir prop
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rate of removal of O2 by pulmonary cap blood (level of metab rate, VO2). if VA unchanged,how is VO2 linked w PAO2?
inc VO2 = dec PAO2 ... dec VO2 = inc PAO2 indirectly/ reverse prop
167
normally alveolar levels of PO2 and PCO2 determine systemic arterial levels too, but what determines alveolar gas: -PACO2 (2) 5kPa
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! 2. alveolar ventilation (VA)
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PACO2 is also affected by: alveolar ventilation (VA) - if VCO2 unchanged, how does VA link with PACO2
inc VA = dec PACO2 dec VA = inc PAO2 inversely proportional (alveolar ventilation!)
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how is ventilation linked to metabolic demand?
directly proportional ☺ if metab x2, VA x2 if metab halves, VA halves alveolar gases, blood gases, pH kept rel constant :)
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effect of disease on alveolar gases, blood gases, pH and why?
abnormal | resp cant meet metabolic demand at rest (severe) or changes in demand (less severe)
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what happens in - hypoventilation - hyperventilation
- 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
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what 2 things are increased in hypoventilation decreased in hyperventilation?
PACO2 and PaCO2
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whats hyperventilation no same as and why?
``` increased ventilation (during exercise) as ven STILL matched to metabolism ```
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whats hyperpnoea?
breathing: deeper and more rapid than normal | but ⬆ in CO2 produced is exactly ∝ to ⬆ ventilation
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3 signs/ indicators of hyperventilation
1. PaCO2 lower than normal (<4.5kPA, but need blood gases) 2. dizzy: low PaCO2 = vasoconstriction of cerebral vessels 3. tetany: spasm, numbness
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why may hyperventilation cause tetany?
fall in PaCO2-> hyperexcitability of membranes = inc perm = AP initiation
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how to treat hyperventilation?
slow deep breaths | not breathing in a bag = inc in CO2!
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Topic 6b: diffusion of gases across alveolar membranes whats diffusion through tissues described by? and whats it dependant on?
Ficks law of diffusion - SA - barrier thickness - PP difference between 2 sides (P1-P2) - diffusion constant for that gas through that barrier
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what does diffusion constant for gas through barrier depend on?
MW and solubility of gas
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diffusion ability of CO2 and O2 compared.. which one diffuses more easily?
CO2 diff 20x more easily than O2 | more soluble, need less gradient ☺
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in what conditions may SA of alveoli in contact with capillaries be decreased and what will this affect for diffusion?
lung infections/ pulmonary oedema.... | thus increase distance O2 has to diffuse
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normally and in thickened diffusion barrier: | how does inc in % pulmonary cap length affect PO2 in pulmonary cap?
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
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affect on exercise and PO2 pulmonary capillary?
HR inc, time for complete cardiac cycle dec = less time spent in cap = time for eqm decreases
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p361 learn PPs!
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define: dyspnoea tachypnoae apnoea
- sensation of shortness of breath - rapid breathing - cessation of breathing
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Topic 7: Ventilation and perfusion control of gases: how does blood enter the capillary and what happens to gases?
CO2 rich, O2 poor CO2 given up to alveolar air, O2 taken up after exchange: alveolar air AND blood = 12kPa O2 and 5kPa CO2
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alveolar air and blood contain same levels of O2 and CO2. whats responsible for setting blood gases?
alveolar gases
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whys there a small difference in PAO2 (alveoli 13kPa) and PaO2 (arterial 12kPa)?
ventilation- perfusion (V/Q) matching
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if given lung unit = equally well V and Q (ventilated and perfused) with blood, what is optimised?
- gas exchange - uptake of O2 form alveolar gas -> blood - elim of CO2 from blood -> alveolar gas
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V/Q matching in the whole lung = calculate the value | wb ideal value?
VA (V) = 4L/min blood flow to lung= CO (Q) = 5L/min V/Q = 4/5 = 0.8 **ideally equal so ratio = 1
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whys V/Q not exactly matched and = 1 irl? | 2 scenarios
alveolus may be: underventilated/ overperfused VQ ratio infinite or opposite with VQ of zero
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A: blood returning to heart from an undervent/overperfused alveolus is....
hypoxic and hypercapnic.... exactly same as when entered PvO2: 5kPa --> PaO2: 5kPa PvCO2: 6kPa --> PaCO2: 6kPa no ventilation received (fresh air)
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A: blood returning to heart from an undervent/overperfused alveolus. this is seen in what condition?
COPD V/Q<1 alveolar and arterial blood gases equilibriate w venous gases (shunt)
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b: alveolus may be overventilated/ underperfused V>Q ratio infinite when may this occur?
pulmonary embolism alveolar dead space .. well ventilated but no blood flow
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what happens to alveolar gases in an overventilated/ underperfused alveolus?
equilibriate with inspired gases.. as no O2 extracted/ CO2 added to alveolus so dont contribute to gas exchange. can inc in disease state!
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how does lung adjust to match V and Q in... undervent alveolus?
hypoxic blood = localised hypoxic vasoconstriction blood directed away = Q inc
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how does lung adjust to match V and Q in... overvent alveolus?
low PCO2 in airways = localised bronchoconstriction
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look at lung/ flow unit vol lung graph p373
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Topic 8: Oxygen transport normal values of arterial: PaO2, PaCO2 venous: PvO2, PvCO2?
PaO2: 12.6-13.3 PaCO2: 5 PvO2: 5 PvCO2: 6 kPa
200
what 2 forms is oxygen carried in throughout body?
- dissolved in plasma | - combined with Hb (majority!)
201
whats the total O2 content (in 1L of arterial blood)? | and what does each factor depend on?
200ml total O2.. 3ml dissolved O2 - dep on PaO2 197ml O2 bound to Hb - dep on [Hb] and % Hb sat (which depends on PaO2)
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Hb is not a plasma protein... what 3 problems would be caused i it were in plasma?
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
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whats haemoglobin made of?
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
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1 molecule of Hb combines with what... whats formed? equation?
4 molecules of O2 to form 4 molecules of O2..-> oxyhaemoglobin Hb + O2 HbO2
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what does amount of oxygen that blood will carry therefore depend on?
[Hb] | i.e. O2 binding capacity = proportional to Hb of blood.
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``` normal Hb values (g/dL) in men women birth child ```
men: 13-18 women: 12-15 birth: 12-24 child: 10-14
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whats theoretical O2 binding capacity not dependant on?
PO2 theoretical= if ALL Hb binding sites are saturated w O2
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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
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]
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whats saturation of Hb and how is it calculated?
% of Hb binding sites in bloodstream occupied by O2.. % sat = O2 bound to Hb/ O2 capacity x 100
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whats %saturation of Hb dependant on?
PO2 ``` in arterial (PO2: 13kPa) = 99% mixed venous (PO2: 5kPa) = 75% ```
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how will mixed venous % Hb sat (SpO2) change if metabolism increases?
inc metab... more O2 removed to meet metabolic demand... would DECREASE
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O2 dissociation curve. what does the O2 bound to Hb depend on?
partial pressure of O2 in blood SIGMOIDAL SHAPE ... doesnt account dissolved O2!!
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why is the % Hb saturation/ PO2 curve sigmoidal?
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
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physiological significance of sigmoidal shape of Hb curve?
steepest: at levels of PO2 in tissues | = O2 can be given up readily w/out need to fall in PO2... high diffusion gradient maintained ☺
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PO2 in lungs (top of Hb curve)... how does % sat link to alveolar PO2?
large fall in alveolar PO2, small fall in % sat
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what does the steep part of Hb curve mean/ whys it useful?
PO2 in tissues (not lungs...) if inc demand for O2, more O2 removed for small change in PO2. easily dissociated
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dissolved o2 at bottom of curve... whys this a safety net for altitude/ disease?
still have high %. | alveolar thus arterial PO2 can fall w/out change in Hb☺
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describe the Bohr effect | what happens and why?
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
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what is right shift (decreased affinity) of Hb curve caused by? 4
⬆ PCO2 ⬆ H+ conc ⬆ temp ⬆ 2,3-DPG (made in RBC by metabolism. fairly constant conc, changed in hypoxia + disease)
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what 2 points of Hb curve do not change?
top and bottom
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what is left shift (increased affinity) of Hb curve caused by? 4
⬇ PCO2 ⬇ H+ conc ⬇ temp ⬇ 2,3-DPG (made in RBC by metabolism. fairly constant conc, changed in hypoxia + disease)
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physiological significance of Bohr effect? | on lungs
LUNG: LEFT shift ⬇ CO2, H+ ⬆ Hb affinity more O2 uptake in lung. CO2 release.. ⬇ acidity
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physiological significance of Bohr effect? | on Tissues
TISSUES: RIGHT shift ⬆ CO2 to blood, H+ ⬇⬇ Hb affinity more O2 uptake in tissues. O2 dissoc AWAY from Hb
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how will anaemia affect Hb dissociation curve?
low [Hb] reduce carrying capacity, LEFT shift
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how will CO poisoning affect Hb dissociation curve?
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
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when will symptoms occur for CO poisoning (O2 content curve) and why?
CO has 200x greater affinity for Hb, symptoms when COHb >10% difficult to remove form Hb, .. dizzy, nausea, hypoxic
227
2 types of Hb? which is in - adults - newborns?
``` Hb A (2 a, 2 b chains) Hb F (2 a, 2 y chains) ```
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newborns have Hb F (2 a, 2 y chains) instead of Hb A. how does this affect Hb saturation curve? benefits?
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
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affect of sickly cell (Hb A) mutation of B chains ...
abnormal Hb molecule, poorly soluble deformed RBC can be destroyed. genetic carry less O2
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myoglobin: how the % sat/ PO2 curve different?
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
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roles of myoglobin?
stores O2 for use during v heavy exercise enhances o2 diffusion through cells by carrying o2 through cytosol
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Topic 8b: CO2 transport in what 3 forms is CO2 carried in the blood?
- 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
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how are carbamino compounds formed?
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
60% of CO2 produced is carried as bicarbonate. whats the eqn? what accelerates the slow step?
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
how does the CO2 dissociation curve differ from O2?
more than twice O2 content of blood steeper slope= greater change in content for given change in CO2 no plateau or maximum (p404)
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effect of inc PO2 on CO2 content/ PCO2 curve? | name for this?
shifts CO2 curve down and left i.e. less CO2 carried = less CO2 in blood HALDANE EFFECT
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why does haldane effect happen? (inc PO2 shifts CO2 curve down and left i.e. less CO2 carried) (2)
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
importance of haldane effect on. .. capacity for co2 carriage and. .. CO2 given up ?
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
how do Bohr effect and Haldane effect compare in terms of mol and affinities?
BOHR: CO2/H+ affecting affinity of Hb for O2 HALDANE: O2 affecting affinity of Hb for CO2/H+
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Topic 9: Role of respiratory system in acid-base balance what does H2CO3 affect if not monitored and regulated?
weak but <20mls made a day. | will affect normal tissue func!
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what may cause plasma and RBC acidity to increase?
H+ made from carbonic acid disso and carbamino compounds, if not buffered
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3 methods that buffer H+ atoms... | role of carbonic acid system as an important buffer system
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
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whats the ideal arterial pH (pHa) for enzymatic activity and (how calculated)?
7.40 pH = -log [H+]
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what 3 solns in body contain weak acids and buffer changes in H+ by adding acid/alkali?
blood intracellular fluid extracellular fluid
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henderson-hasselback eqn relates to pH solution to... (2)
A)!! pKa of buffer system b) ionised [A-] and unionised [HA] forms pKa = pH when [A-] = [HA]
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whats the unionised and in=onised forms in CO2-bicarbonate system and thus...
``` H2CO3 = unionised (BUT quicly dissociates) [HCO3-]= ionised ``` since [H2CO3] ∝ PaCO2 = use PaCO2 as unioninsed measure
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what systems control: [HCO3-] and [PaCO2]?
1. kidney | 2. resp systems
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whats meant by: metabolic acidosis metabolic alkalosis carbonic acid eqn
1. [H+] rises, mass reaction pushed left 2. loss of body acids -> dec in breathing + retention of CO2 i.e. lungs take care
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whats meant by: Resp acidosis Resp alkalosis carbonic acid eqn
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
metabolic acidosis process of returning pH back to normal?
``` acidemia sensed by chemoreceptors inc ventilation inc CO2 excretion pH normal now ☺ ```
251
examples of - metabolic acidosis - metabolic alkalosis
- diarrhoea diabetic ketoacidosis lactic acidosis - vomiting diuretics
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examples of - Resp acidosis - Resp alkalosis
- hypoventilation (COPD) | - hyperventilation (response to hypoxia, anxiety)
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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?
central controller --> output: effectors --> sensors (then input back to CC)
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22 examples of sensors that then input to central controller?
chemical: chemoreceptors mechanical gather info form environment
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where are chemorec sensors and where do they send info to?
in upper airways, chets wall, lungs, joints/muscles... info back to brain stem (CC) to act on effectors: ventilatory muscles
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function of respiratory system: has exchange and pH maintenance... hm O2 consumes and CO2 produced in young adult at rest?
VO2: 250ml/min VCO2: 200ml/min
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what would happen to blood O2 and blood CO2 if metabolism changed and no change in respiration? and consequence?
blood O2: fall (tissues -> hypoxic) | blood CO2: rise (pH disturbances)
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whats alveolar ventilation (VA) increased by? (3 instances) i.e. what should be staying constant?... and what detects the change
low arterial PO2 high arterial PCO2 low arterial pH .. chemoreceptors detect
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how do chemoreceptors maintain homeostasis of PaO2, PaCO2, and pH?
assist in ensuring VA is appropriate to level of metabolism...
260
whats name of difference in O2 content between arterial and mixed venous blood?
arteriovenous difference
261
what do fairly constant levels of PaO2 and PaCO2 gases after exercise/ anaerobic threshold ensure?
constant by inc ventilation to meet metab demand... = constant delivery of gases ☺
262
2 types of chemoreceptors and what do they each respond to?
Peripheral: low PaO2 (arterial) high PaCO2 high [H+] (low pH) central: only- high PaCO2 - majority of CO2 response
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where are peripheral chemoreceptors located?
2 sets, same as arterial baroreceptors... *carotid bodies (in c sinus) distinct nodules, most important for refled *aortic bodies
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where does carotid sinus nerve join into? | peripheral chemorec
carotid body (chemos) next to sinus. .. glossopharyngeal (IX) nerve
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what type of blood flow is supplied by branch of external carotid artery? wb AV O2 difference?
high blood flow... and little O2 consumption= O2 leave similar to in. = small AV O2 difference
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how do carotid bodies work to signal CNS? | 4
fall in PO2-> K+ channel closes, Vm depolarises Ca2+ channels open Ca2+ influx triggers NT release sensory afferents signal to CNA
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4 properties of carotid bodies i.e. what do they repond to?
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
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why dont carotid bodies respond to anaemia/ CO?
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
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what does removal of carotid bodies (peripheral chemoreceptors) -->?
decreases in ventilatinon during hypoxia (direct effect of hypoxia on brainstem)
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how are aortic bodies different to carotid? peripheral chemoreceptors
less important in resp control less vascular, lower blood flow (sluggish) dont respnd to changes in pH (without change in PCO2)
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what do aortic bodies respond to?
increase in PaCO2 fall in PaO2 O2 content... thus can detect anaemia/CO
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what are aortic bodies innervated by? and what role do they play?
vagus (x) nerve | role in cardiovasc reflexes - haemmhorage
273
whats the resp response to hypoxia? low O2
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
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affect of moderate hypoxemia on VE?
(PaO2 5-8kPa) only doubles VE (⬆ ventilation)
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where are central chemoreceptors located?
ventrolateral medulla of brainstem (midbrain, pons, medulla oblongata)
276
central chemoreceptors are stimulated when? | and account for minority/ majority of response to hypercapnia (⬆ CO2)?
when arterial PCO2 increases only slightly stim by ⬆ in arterial acidity (H+ ions) bc separated from blood by BBB account for 60-80%... majority
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what are central chemorec insensitive to?
hypoxia (change in arterial O2)
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process of stimulation of central chemoreceptors?
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
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stimulation of central chemoreceptors summarised: what stimulates the cc neurons?
acidification of CSF and ECF
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CSF is a poor buffer so small changes in PaCO2 ->?
significant CSF acidosis
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resp response to hypercapnia (high CO2): what would graoh look like (AV/PaCO2)
resp system: VERY sensitive to CO2 levels peripheral and cetral chemor detect steeper slope than hypoxia response ⬆ of <1kPa can double VA
282
how would (AV/PaCO2) graoh change in CO2 resp responses to - awake normal - sleep - morphine, barbs, COPS - anaesthetics
- VERY steep and high - steep and high - flatter and lower - VERY flat and low
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Topic 10: Central control of breathing intro 1/4 effectors: in vent muscles. whats output of system? CC, sensors, effectors
change in thoracic volume and airflow
284
what 3 thingsmust any model of rhythm generation account for?
- maintenance of invol breathing (automatic) - adj of vent for gas exch (metabolic demand) - adj of breathing pattern for speech, swallowing... (voluntary)
285
minute ventilation (VE) =?
``` VE = VT x Rf VE = tidal volume x respiratory frequency ``` (infinite combos)
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minute ventilation (VE) how is it determined/ whats pattern aimed at? and whats meant by resonance?
aimed at minimising work done by resp muscles to reach required VE res: right timing = req less effort (pushing someone on a swing- timing)
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neural control must affect what 2 nerves before affect on resp muscles?
phrenic (inspiratory) + internal intercostal (exp)
288
what does alternating activity in muscles: inspand exp lead to?
phrenic and intercostal.... change in thoracic vol thus change in pressure and airflow
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what do accessory insp muscles do?
sternocleidomastoid, scalene, external intercostal: | raise ribs and expand chest cavity
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what would airway flow and airway pressure EMG recording look like?
airway flow: insp = curve up exp: curve down then flat= exp pause airway pressure: reverse (upside down) with same flat, exp pause in between
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exp muscles at rest: what takes part in passive relaxation?
diaphragm
292
role of other muscles during exp? internal intercostal, externala nd internal oblique?
suppress: shrink cavity push air out of lungs | forced expiration!
293
central respiratory rhythm --> what ? | in insp and exp muscles
-> reciprocal motor activity
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on EMG, what muscle active in - inspiration - expiration?
- diaphragm (thick small lines vertical) | - internal intercostal (thin long lines vertical)
295
exp and insp nerves: intercostal and diaphragm ... where do they get intrinsic activity input form?
have none themselves... from CNS | = central controller in brain must be driving
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Topic 10b: CC of breathing 2- neural control centres what part of brainstem is important in rhythm generation? how we know?
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!
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2 main areas of CNS involved in breathing?
pons - pontine resp group PRG medulla -medullary respiratory centre either side of midline can generate rhythm independantly (even tho normally funcn as 1 unit)
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p545 dorsal view of brainstem image: identify - Botzinger complex (expiratory), - prebotzinger (Pacemaker?), - ventral resp group (VRG insp +exp), - dorsal resp group (DRG insp)
299
what do neurones in DRG do?
discharge AP prior to inspiration -> control lateral phrenic nerve- control diaphragm
300
where is DRG in?
dorsal resp group... in NTS (Nucleus Tractus Solitarius)
301
what info does NTS (Nucleus Tractus Solitarius) receive and what does it do with it?
resp and CV afferent inputs, integrates info from chemo and mechanorec afferents related to breathing
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Topic 10c: cc of breathing 3: resp rhythm generation in medulla what drives inspiration during quiet breathing?
Prebotzinger complex... - DRG neurones ACTIVE --> C spinal cord--> diaphragm contracts-> inspiration - VRG neurones INactive
303
what causes diaphragm to contract?
motor neurones inc activity of phrenic nerve... d innervated by AP generation
304
what causes expiration during quiet breathing?
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
VRG neurones action in insp and expiration in quiet breathing
inactive in both insp and expiration in quiet breathing has insp and exp neurones but no breathing movements in quiet breathing
306
what about the DRG is responsible for basic rhythm of breathing?
cyclical electrical activity of DRG
307
what nerve responsible for contraction and relaxation of diaphragm using DRG in quiet breathing?
phrenic motor nerve
308
What happens when demand for ventilation increases? i.e. no longer just quiet breathing inspiration?
``` 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
What happens when demand for ventilation increases? i.e. no longer just quiet breathing expiration?
``` 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
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Topic 10d: cc of breathing: outside the medulla role of pontine group (PRG)?
influences switching between inspiration and expiration sectioning through diff levels of pons= change breathing pattern esp TIMING
311
how does PRG shut off inspiration?
inhibits DRG insp neurones | vagal afferent role
312
higher brain centres affect DRG: +/- | outside medulla and pons, when are hypothalamus, limbic system, motor cortex involved in breathing changes?
H: temp, fight/flight (hypervent) L: emotion/pain M: limb receptors, exercise. activates DRG rec in propn to exercise demands
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how is voluntary control (large breaths, hypervent, speaking, breath hold) done?
cerebral cortex direct to SC... bypasses medullary centres. directly affect motor neurones in Sc -> control respiratory muscles
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Topic 11: Neural reflex control of breathing 1 most of sensory influence comes from where?
vagal afferents. | main role: protect resp centre + feedback on situation
315
where is vagus nerve located and what info does it carry and what is it important in?
parallel to trachea. | info to and from parts of body + important in resp control
316
what do irritant receptord in bronchi sense? effect?
chemicals, dust, cold air cough, bronchoconstriction
317
what do J receptors in bronchioles/alveoli sense? effect?
chemicals, stretch, pulmonary oedema shallow breathing, cronchoconstr, mucus secrtn
318
what do stretch receptors in lung sense? effect?
lung inflation inflation terminates
319
4 types of mechanoreceptors? location
lung + airways nose + upper airways joints and muscles arterial baroreceptors
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mechanoreceptors respond to what?
pressure/ distortion
321
where are PSR? pulmonary stretch rec
vagal nerve endings in SM of trachea + local airways
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what are PSR pulmonary stretch rec stimulated by?
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
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what are the 2 diff patterns from PSRs?
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-
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when is hering-breuer reflex present? and whos it more powerful in? whos it important in?
during sleep babies as inhib influences from cortex not deveolped, animals (need inflation >1L) important in px w low lung compliance
325
describe Hering-Breaur reflex when dec lung comlpiance | give example disease
stiffer lungs more pull on stretch receptors insp switched off earlier = breathing shallow and rapid... restrictive diseases (interstitial fibrosis)
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central mechanism PSR? link to hering -breuer
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
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lung irritant receptors- where are the vagal nerve endings and what are they stim by? speed of action?
between epithelia of trachea and lower airways stim by noxious gases, smoke, dust, cold air, rapidly acting receptors! role in asthma induced bronchitis
328
if stimulus maintained, how would this affect lung irritant rec action?
afferent impulse num dec over time
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how do lung irritant rec prevent noxious substance getting down to lungs and affecting lung tissue?
cig smoke, oxidants, inhald irritants stim irritant rec info down vagal afferent through vagal efferent --> smooth muscle = bronchoconstriction ☺
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what else other than bronchoconstriction, may irritant rec initiate?
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
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pulmonary C/ J receptors are located where?
``` bronchial walls (unmyelinated C- fibres) alveolar walls (J receptors juxtacapillary)- close to caps ```
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pulmonary C/ J receptors are usually what? and what stimulates them?
silent. | stim by: mechanical distortion and inc in interstitial fluid (oedema)
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what type of breathing do pulmonary C/ J receptors evoke?
rapid shallow or apnoea responsible for rapid shallow breathing and dyspnoea in interstitial lung disease + LVHF?
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Topic 11b: Neural reflex control of breathing 2: nose and upper airways receptors what initiates: - sneeze + diving reflex - cough
``` 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
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what do proprioreceptors respond to? | examples of some
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
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what do proprioreceptors allow for if movement is impeded?
inc force of insp and expiration
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what receptors are responsible for sensation of dyspnoea (breathlessness) if large effort required? e.g. obstruction
proprioreceptors | muscle spindles in intercostal muscles (calf) = certain tidal volume achieve if airway resistance increases
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joint and muscle rec in moving limbs.. have afferent activity into where and what does this lead to?
DRG | = inc ventilation upon at onset during exercise? esp early stages
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what do baroreceptors control and how?
BP ⬆ BP--> reflex hypoventilation/ apnoea e.g. Ad apnoea ⬇ BP--> reflex hyperventilation (e.g. due to haemorrhage)
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when may baroreceptors action be important?
in complex stimuli (haemorrhage) - many reflexes occur at once! pathways unknown