Respiratory Flashcards

1
Q

functions of respiratory system

A

homeostatic regulation of blood gases: provides O2 and eliminates CO2
filtering action: protects against microbial infection
regulates blood pH
contributes to phonation + olfaction
reservoir for blood

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2
Q

upper airways

A

nasal cavity - nostrils
oral cavity - mouth
pharynx
larynx (vocal cords)

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3
Q

lower system

A

trachea
left + right main bronchi
left + right lungs
diaphragm

thoracic wall
parietal pleura (membrane)
intrapleural fluid
visceral pleura (membrane)

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4
Q

composition of structures

A

trachea + primary bronchi = C shape cartilage + smooth muscle
bronchi = plates of cartilage + smooth muscle
bronchioles = smooth muscle

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5
Q

conducting zone

A

pathway for gas to the respiratory zone
anatomical dead space = no alveoli + no gas exchange
~150mL

trachea
bronchi
bronchioles
terminal bronchioles = smallest airway without alveoli

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6
Q

respiratory zone

A

where gas exchange occurs
contains alveoli

respiratory bronchioles (sparse alveoli)
alveolar ducts
alveolar sacs (many alveoli)

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7
Q

pulmonary structures + blood vessels

A

pulmonary artery carries low-O2 blood to alveoli (500 million)
280 billion capillaries → in contact with alveoli for gas exchange
pulmonary vein carries high O2 blood to heart

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8
Q

alveoli

A

type I alveolar cells = simple squamous epithelium
type II alveolar cell
macrophage

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9
Q

type I alveolar cells

A

involved in gas exchange
epithelial cells forming surface of alveolus
do not divide

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10
Q

type II alveolar cells

A

produce surfactant
act as progenitor cells to differentiate into type I cells

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11
Q

respiratory membrane

A

alveolus → capillary
- alveolar fluid
- alveolar epithelium (type I + II pneumocytes)
- basement membrane of alveolar epithelium
- interstitial space
- basement membrane of capillary endothelium
- capillary endothelium

very thin = easily damaged

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12
Q

respiration steps

A
  1. ventilation
  2. gas exchange in lungs
  3. gas transport
  4. gas exchange in tissues
  5. cellular respiration
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13
Q
  1. ventilation
A

breathing = exchange of air between atmosphere and alveoli by bulk flow

steps:
1. CNS sends rhythmic excitatory drive to respiratory muscles
2. respiratory muscles contract rhythmically and in organized pattern
3. changes in volume and pressures at the level of chest + lungs
4. air flows in and out

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14
Q

bulk flow

A

movement due to pressure gradient → high to low
higher pressure in atmosphere compared to lungs = inspiration
F = (P alv - P atm)/R

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15
Q
  1. gas exchange in lungs
A

exchange of O2 + CO2 between alveolar air + blood in lung capillaries by diffusion

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16
Q

diffusion

A

movement due to concentration gradient (partial pressures)

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17
Q
  1. gas transport
A

transport of O2 + CO2 through pulmonary + systemic circulation by bulk flow

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18
Q
  1. gas exchange in tissues
A

exchange of O2 + CO2 between blood in tissue capillaries and cells by diffusion

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19
Q
  1. cellular respiration
A

cellular utilization of O2 and production of CO2

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20
Q

respiratory muscles

A

pump muscles
airway muscles
accessory muscles

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21
Q

pump muscles

A

INS:
- diaphragm
- external intercostals
- parasternal intercostals

EXP:
- internal intercostals
- abdominals (4 = external + internal abdominal oblique, transverse + rectus abdominus)

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22
Q

airway muscles

A

INS:
- tongue protruders (genioglossus)
- pharyngeal + laryngeal dilators

EXP:
- pharyngeal + laryngeal constrictors

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23
Q

accessory muscles

A

INS
- sternocleidomastoid
- scalene

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24
Q

normal/quiet inspiration

A

diaphragm contracts → pushes abdomen down + expands thorax as air comes in
external intercostals + parasternal intercostals → pull ribs up and out

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25
Q

maximal/forced inspiration

A

stronger contraction of diaphragm
recruitment of accessory muscles → further expansion of thoracic cavity
- sternocleidomastoid + scalenes move sternum up and out
- pectoralis minor elevates ribs

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26
Q

normal/quiet expiration

A

no active contraction of resp muscles
relaxation of inspiratory muscles → recoil of lungs = air moves out

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27
Q

maximal/forced expiration

A

abdominal muscles contract → compress organs + force diaphragm higher = push air out
internal intercostal muscles contract → pull ribs down and inward

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28
Q

spirometry

A

pulmonary function test to determine amount + rate of inspired + expired air
test lung volume + capacity
use spirometer

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29
Q

tidal volume

A

Vt
volume of air moved in/out of lungs during normal breath
~500 mL

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30
Q

inspiratory reserve volume

A

IRV
amount of air forcefully inhaled after normal inspiration
additional capacity
~3000 mL

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31
Q

expiratory reserve volume

A

ERV
amount of air forcefully exhaled after normal exhalation
~1100 mL (smaller than IRV)

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32
Q

residual volume

A

RV
volume of air remaining in lungs after maximal forceful expiration
~1200 mL
prevents lungs from collapsing
cannot be measured with spirometry

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33
Q

total lung capacity

A

volume of air in lungs at end of maximal inspiration
Vt + IRV + ERV + RV
5000-6000 mL

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34
Q

inspiratory capacity

A

Vt + IRV
total capacity for inspiration

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35
Q

vital capacity

A

Vt + IRV + ERV
max vol of air that can be forcibly exhaled after maximal inspiration

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36
Q

functional residual capacity

A

ERV + RV
vol remaining in lungs at end of normal expiration

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37
Q

total/min ventilation

A

total amount of air moved into respiratory system per minute
= Vt x resp frequency
= 0.5L x 12 brpm
= ~6L/min

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38
Q

alveolar ventilation

A

amount of air moved into alveoli per minute
less than minute ventilation
depends on anatomical dead space = 0.15 L
=(Vt - dead space) x resp frequency
= (0.5 - 0.15 L) x 12 brpm
= ~4.2 L/min

dead space is constant regardless of breath size
increased depth of breathing is more effective in increasing alveolar ventilation than increasing breathing rate

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39
Q

FEV1

A

spirometry test:
forced expiratory volume in one second
in healthy person: should approximate vital capacity

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40
Q

FVC

A

spirometry test:
forced vital capacity
total amount of air that is blown out in one breath after max inspiration as fast as possible
~ vital capacity

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41
Q

FEV1/FVC ratio

A

proportion of the amount of air that is blown out in one second
normal = ~80%

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42
Q

normal resp pattern

A

ratio = 83%
high FEV1 + high FVC

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43
Q

obstructive resp pattern

A

FEV1 is significantly reduced, FVC is normal/reduced
= ratio <70% → reduced
difficulty exhaling all air from lungs → shortness of breath
slower exhalation of air due to damage to lungs or narrowing of airways
high air vol in lungs after full exhalation

ex. bronchial asthma, COPD, cystic fibrosis

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44
Q

restrictive resp pattern

A

reduced vital capacity
FEV1 + FVC are reduced
ratio = 90% (almost normal)
cannot fill lungs completely (restricted from full expansion)
due to stiffness in lungs

ex. pulmonary fibrosis, neuromuscular disease, scarring of lung tissue

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45
Q

flow

A

F = ΔP/R
proportional to pressure difference between two points
inversely proportional to resistance

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46
Q

Boyle’s Law

A

P1V1 = P2V2
for a fixed amount of an ideal gas at a fixed temp, P and V are inversely proportional

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47
Q

compression of alveoli

A

↓ V = ↑ P
expiration

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48
Q

decompression of alveoli

A

↑ V = ↓ P
inspiration

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49
Q

elastic recoil

A
  • lungs have tendency to collapse
  • chest wall pulls thoracic cage outward

at equilibrium: inward elastic recoil of lungs balances outward elastic recoil of chest wall

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50
Q

intrapleural fluid

A

reduces friction of lungs against thoracic wall during breathing

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51
Q

intrapleural pressure

A

pressure within pleural cavity
fluctuates with breathing
always sub-atmospheric (-) → opposing directions of elastic recoil of lungs + thoracic cage

if P(ip) = P(alv) → lungs would collapse

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52
Q

alveolar pressure

A

pressure of air inside alveoli
changes during ventilation + determines direction of air flow

dynamic - directly involved in producing air flow

when P alv = P atm, F=0

53
Q

P(alv) - P(atm)

A

governs gas exchange between lungs and atmosphere
= flow

54
Q

transpulmonary pressure

A

force responsible for keeping alveoli open
pressure gradient across alveolar wall: P(tp) = P(alv) - P(ip)

static - does not cause airflow
determines lung volume

P(tp) > 0 to maintain lungs expanded in thorax (P alv > P ip)

55
Q

inspiration

A
  1. diaphragm + inspiratory intercostals contract
  2. thorax expands
  3. P(ip) becomes more subatmospheric = ↑ P(tp)
  4. lungs expand
  5. P(alv) becomes subatmospheric
  6. air flows into alveoli
56
Q

expiration

A
  1. diaphragm + inspiratory intercostals relax
  2. chest wall recoils inward
  3. ↑ P(ip) = ↓ P(tp) - return to preinspiration value
  4. lungs recoil
  5. air in alveoli becomes compressed = P(alv) > P(atm)
  6. air flows out of lungs
57
Q

airway resistance

A

small
→ small ΔP is enough to cause airflow

58
Q

resistive forces

A
  1. inertia
  2. friction
59
Q

inertia of resp system

A

negligible

60
Q

friction

A
  1. lung tissue past itself during expansion (negligible)
  2. lung and chest wall tissue surfaces past each other
    (reduced by IPF) (negligible)
  3. frictional resistance to flow of air = 80% of total airway resistance
61
Q

laminar airflow

A

gas particles move in linear fashion
low resistance
found in small airways (distal to terminal bronchioles)

62
Q

transitional flow

A

extra energy required → produce vortices
↑ resistance
found in most of bronchial tree

63
Q

turbulent flow

A

highest resistance
large airways (trachea, larynx, pharynx)

64
Q

Poiseuille’s law

A

for laminar flow
resistance is proportional to viscosity of gas + length of tube
inversely proportional to airway radius (^4)

65
Q

R in small airways

A

each small airway has high individual resistance
terminal bronchioles aligned in parallel = lower aggregated resistance

combined → lowest R

66
Q

R in disease conditions

A

R is determined primarily by small airways → easily occluded by:
- smooth muscle contraction around airway
- edema in walls of alveoli + bronchioles
- mucous collecting in lumen of bronchioles

67
Q

lung compliance

A

measure of elastic properties of lungs
how easily lungs can expand

determined by
- elastic components of lungs + airway tissue (elastin + collagen)
- surface tension

68
Q

C(L)

A

= (ΔV)/(ΔP(tp))
change in lung volume produced by given change in P(tp)
slope of pressure-volume curve

↑ C(L) = easier to expand (at given change in P(tp))

69
Q

emphysema

A

↑ compliance
floppy lungs due to destruction of elastin in walls of alveoli = collapse of smaller airways
less elastic recoil
large changes in lung vol due to little changes in P(tp)

low O2 due to less SA for gas exchange

70
Q

pulmonary fibrosis

A

↓ compliance
collagen deposition in alveolar walls
stiff lungs
higher P(tp) changes are necessary to generate changes in lung volume

poor gas exchange causes ↓ O2

71
Q

surface tension

A

property of surface of liquid that allows it to resist external force → cohesion of molecules

gives lungs elastic recoil (makes lungs collapse)
decreases lung compliance

72
Q

alveolar surface tension

A

air entering lungs is humidified → saturated with water
water molecules cover alveolar surface
cohesion of water → create surface tension
= creates inward recoil → alveolar collapse

decreases gas volume inside alveolar = increases pressure to prevent collapse

73
Q

Laplace’s equation

A

P = (2T)/r
[T = surface tension]
at equilibrium, tendency of increased pressure to expand the alveolus balances the tendency of surface tension to collapse

the smaller the radius, the greater the pressure needed to keep alveolus inflated

74
Q

different alveolar sizes

A

smaller alveoli = greater pressure → gas movement from high to low pressure = (POTENTIALLY) small alveoli collapse into larger ones

do not collapse because of surfactant → lowers surface tension = similar pressure across alveoli

75
Q

surfactant

A

produced by type II alveolar cells
made of lipoproteins = hydrophobic + hydrophilic properties → decreases density of water molecules covering alveolar surface
reduces surface tension of alveolar fluid
= ↑ lung compliance
stabilize alveoli against collapse

76
Q

IRDS

A

infant respiratory distress syndrome
born premature = under developed lungs → immature type II alveolar cells
can’t produce enough surfactant = ↓ O2
have abnormally low lung compliance

77
Q

partial pressures of gases

A

P increases with increased motion → due to change in temperature, concentration of gas molecules

78
Q

Dalton’s Law

A

in a mixture of gases, each gas acts independently
total pressure = sum of individual pressures

79
Q

P atm

A

= P (N2) + P (O2) + P (H2O) + P (CO2)
= 760 mmHg

P (p) = % of air x P total

78% N2 → P (N2) = 593 mmHg
21% O2
1% H2O
0.04% CO2

80
Q

Fick’s Law

A

V(gas) ∝ [A/T] x D x (P1 - P2)

rate of transfer of a gas through membrane (Vgas)
- is proportional to:
A = area of diffusion
ΔP = difference in gas partial pressure between two sides
D = diffusion constant
- is inversely proportional to:
T = thickness of membrane

81
Q

D = diffusion constant

A

D ∝ (sol)/√ (MW)

sol = solubility
MW = molecular weight

82
Q

diffusion of CO2 vs O2

A

solubility: CO2 > O2
similar molecular weights

CO2 diffuses 20x more rapidly than O2

P (CO2) is higher in alveoli than atm
P (O2) is higher in atm than alveoli

83
Q

P (O2) atm > P (O2) alveoli

A
  1. loss of O2 to blood by diffusion = ↓ P (O2)
  2. mixing of inspired air with functional residual vol = ↓ P (O2)

(3.) warming + humidification of air in resp tract = ↓ P (O2)

84
Q

alveolar partial pressures

A

determined by
- P (O2) + P (CO2) in atm
- alveolar ventilation [V(A) = (V(T) - V(D)) x resp frequency]
- metabolic rate
- perfusion

85
Q

increasing alveolar ventilation

A

= ↑ O2 intake + ↑ CO2 production
= ↑ P (O2) + ↓ P (CO2)

86
Q

increasing metabolic rate

A

= ↑ O2 intake + ↑ CO2 production
= ↓ P (O2) + ↑ P (CO2)

87
Q

lung perfusion

A

amount of blood that passes through pulmonary capillary system in the lung

using O2 from alveoli + adding CO2

88
Q

systemic circulation

A

high pressure system
overcome high resistance to deliver blood to peripheral tissue

89
Q

pulmonary circulation

A

low pressure system
only deliver blood to lungs

90
Q

ventilation/perfusion ratio

A

V/Q ratio
balance between ventilation + perfusion
one of major factors affecting alveolar (+ arterial) levels of O2 + CO2

91
Q

V/Q matching

A

local perfusion decreases to match a local decrease in ventilation (+ vice versa)
↓ airflow / blood flow to region of lung
↓ P (O2) in p. blood / ↓ P (CO2) in alveoli
vasoconstriction of p. vessels / bronchoconstriction
↓ blood flow / airflow

diversion of blood flow and airflow away from local area of disease to healthy areas of the lung

92
Q

ex. bronchoconstriction causes vasoconstriction

A

blockage of airway leads to poor gas exchange in alveoli → blood flow is diverted to better ventilated alveoli to compensate

93
Q

perfused alveoli that are not ventilated

A

blocked airway → ↓P(O2) + ↑P(CO2)
decreases V/Q ratio

94
Q

ventilated alveoli that lack perfusion

A

blocked blood flow → ↑P(O2) + ↓P(CO2)
increases V/Q ratio

95
Q

O2 transport

A

arterial blood = highly oxygenated
similar partial pressures of O2 and CO2 as seen in alveoli

majority of O2 is bound to Hb → in RBC
small amount is dissolved in plasma

96
Q

CO2 transport

A

venous blood = poorly oxygenated
↓ P(O2) + ↑ P(CO2) compared to alveoli

majority of CO2 is transported as bicarbonate
some is bound to Hb = carbaminohemoglobin
small amount is dissolved in plasma

97
Q

O2 uptake in lungs

A
  • diffuses from alveoli (↑[]) to p. capillary (↓[])
  • dissolved in plasma
  • moves to RBC
  • binds with Hb
98
Q

O2 delivery to tissues

A
  • diffuses from RBC to plasma
  • diffuses into tissue = dissolved O2 in ISF
  • moves into cells
  • consumed in cell mitochondria
99
Q

oxygen-hemoglobin dissociation curve

A

x = P (O2)
- systemic venous: ↓ P(O2)
- systemic arterial: ↑ P(O2)

y = Hb saturation (%)
- ↓ as O2 dissociates from Hb

difference between Hb sat of arterial and venous = amount of O2 unloaded in tissue capillaries

100
Q

effect of DPG concentration on Hb saturation

A

DPG = metabolic waste product

no DPG = high sat (L)
added DPG = low sat (shift curve to R)

same effect seen with CO2

101
Q

effect of temperature on Hb saturation

A

high metabolism increases temperature

↑t = ↓ sat
shifts curve to R

102
Q

effect of acidity on Hb saturation

A

high metabolic activity = high acidity (low pH = high [H+])
shifts curve to R

103
Q

effect of fetal hemoglobin on Hb saturation

A

high saturation during fetal development
decreases with aging

adult Hb = shift curve to R

104
Q

CO2 uptake from tissues

A

CO2 exits cells and is dissolved in ISF → diffuses to blood
in blood = 4 pathways
1. remains in plasma as dissolved CO2
2. enters RBC and remains as dissolved CO2
3. enters RBC and binds to deoxyHb = HbCO2
4. enters RBC and reacts with H2O → carbonic acid (CA catalyst) → dissociates to HCO3- + H+

[HCO3- exits RBC; H+ increases in venous blood = ↓ pH]

105
Q

CO2 delivery to lungs

A

HbCO2 dissociates → dissolved CO2
HCO3- moves back into RBC → binds with H+ → hydrolyzed into H20 + dissolved CO2

↓[CO2] in plasma drives diffusion of dissolved CO2 from RBC into plasma
→ diffuses into alveoli

106
Q

H+ transport

A

Hb from HbO2 + H+ from H2CO3- bind together
H+ is not dissolved in RBC or plasma to maintain stable pH

Hb buffers production of H+ in peripheral tissues + capillaries

107
Q

respiratory acidosis

A

high [H+] as a result of ↑ P(CO2)

hypoventilation causes CO2 production > CO2 elimination
= ↑ P(CO2) + ↑ [H+]

108
Q

respiratory alkalosis

A

low [H+] as a result of ↓ P(CO2)

hyperventilation causes CO2 production < CO2 elimination
= ↓ P(CO2) + ↓ [H+]

109
Q

metabolic acidosis

A

high blood [H+] as a result of metabolism

change is independent of changes in P(CO2)

110
Q

metabolic alkalosis

A

low blood [H+] as a result of metabolism

change is independent of changes in P(CO2)

111
Q

neural control of breathing

A

automatic process
regulated by neuronal network in pons + medulla (brainstem)

112
Q

breathing initiation

A

in medulla
by specialized neurons (PreBotC)

113
Q

medullary respiratory centre

A

dorsal respiratory group
ventral respiratory group
Pre-Botzinger Complex: sets basal resp rate

114
Q

DRG

A

fires during inspiration
stimulates inspiratory muscles = diaphragm + external intercostals

phrenic nerve → diaphragm
intercostal nerves → external intercostals

115
Q

VRG

A

expiration
contains Pre-Botzinger Complex in upper portion = respiratory rhythm generator

intercostal nerves → internal intercostals

116
Q

pons respiratory centres

A
  • pneumotaxic centre
  • apneustic centre
    = pontine respiratory group
117
Q

PRG

A

centres help modulate activity of medullary inspiratory neurons
- termination of inspiration at appropriate time
- smooth transition between inspiration + expiration

118
Q

pneumotaxic centre

A

descending inhibition to apneustic centre + DRG

119
Q

respiratory rhythmicity centre

A

DRG + VRG
send signals to one another
= local regulation of each other

120
Q

modification of breathing

A

by:
higher structures of CNS
inputs from central + peripheral chemoreceptors
inputs from mechanoreceptors in lung + chest wall
inputs from other peripheral receptors

121
Q

inhibitory modification

A

voluntary control of breathing
Hering-Breuer reflex (stretch receptors in lungs)

122
Q

stimulatory modification

A

voluntary control of breathing
medullary chemoreceptors
carotid + aortic body chemoreceptors
proprioceptors in muscles + joints
receptors for touch, temp, + pain stimuli

123
Q

peripheral chemoreceptors

A

carotid bodies + aortic bodies
respond to changes in arterial blood:
- hypoxia = ↓ P(O2)
- metabolic acidosis = ↑ [H+]
- respiratory acidosis = ↑ P(CO2)

124
Q

central chemoreceptors

A

located in medulla
respond to changes in brain extracellular fluid:
- ↑ P(CO2) via associated changes in [H+]

125
Q

hypoxia

A

stable ventilation between 60-120 mmHg arterial P(O2)

arterial P(O2) drops below 60 → stimulation of peripheral chemoreceptors

↓ inspired P(O2) = ↓ alveolar P(O2) = ↓ arterial P(O2)
↑ firing of peripheral chemoreceptors
→ reflex via medullary respiratory neurons (activation of DRG + VRG to control activity of resp muscles centrally = ↑ resp rate + tidal vol)
↑ contraction of resp muscles = ↑ ventilation
= return of P(O2) to normal

126
Q

hypercapnia

A

stable ventilation at 40 mmHg arterial P(CO2)

arterial P(CO2) increases above 40 → stimulation of central chemoreceptors (also peripheral)

↑ P(CO2) = ↑ alveolar P(CO2) = ↑ arterial P(CO2)
↑ brain extracellular fluid P(CO2) + ↑ brain extracellular fluid [H+] = respiratory acidosis
↑ firing of central chemoreceptors
→ reflex via medullary respiratory neurons (activation of DRG + VRG to control activity of resp muscles centrally = ↑ resp rate + tidal vol)
↑ contraction of resp muscles = ↑ ventilation
= return of P(CO2) to normal

127
Q

chemoreceptors + metabolic acidosis

A

H+ stimulates peripheral chemoreceptors
(does not cross blood brain barrier)

128
Q
A