Respiratory system TT Flashcards
Topic 1: Intro to resp system
What are 8 common disorders that affect the respiratory system?
- infections
- allergic rhinitis
- coughs
- colds
- congestion
- asthma
- COPD
- COVID-19 (SARS-CoV-2)
What are 8 drug categories that affect the respiratory system?
- antihistamines
- decongestants
- antitussives
- mucolytics
- expectorants
- bronchodilators
- leukotriene modifiers
- mast cell stabilisers
What are the 2 types of respiration?
- external: breathing
- internal: cellular
What does breathing do to O2 and CO2?
breathing brings in O2 from the atmosphere and transfers CO2 in the opposite direction
What are the 2 types of internal respiration?
where do they occur
- aerobic
- anaerobic
both energy-producing processes going on in cells
What is the respiration equation?
C6H12O6 + 6O2 —–> 6CO2 + 6H2O
ATP
energy required for life comes form what?
and what must happen to it to release energy stored inside it
comes form food.
must be OXIDISED, release energy
similarities between the cardiovascular and respiratory system?
(what type of flow do they use? what process allows the movement of gases?
- highly efficient convective bulk flow systems (ventilatory + circulatory) for long-distance transport of gases or liquid
- diffusion for short-distance movements: O2 & CO2
What is the metabolic rate also the rate of?
O2 consumption
What is V̇O2? What is the average value at rest?
O2 consumed per unit time
~250ml/min
What is V̇CO2? What is the average value at rest?
CO2 produced
200ml/min
What is RQ? What is the formula for it?
Respiratory quotient:
V̇O2/V̇CO2 = 200/250 = 0.8
When is the value of RQ 0.8?
when the person has a mixed diet of fats, carbohydrates and proteins
What is the RQ value for
- fats
- carbs
- proteins
- 0.7
- 1
- 0.8
How do V̇O2 and V̇CO2 change when exercising and why? How much is it?
BOTH: increase:
tissues consume more O2 so need more
tissues produce vast amounts of CO2
3000ml/min
Why is the respiratory system important with metabolic changes? (think V̇O2 and V̇CO2)
- 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
What is the consequence of blood O2 falling?
tissues become hypoxic
What is the consequence of blood CO2 rising?
pH disturbances
If the lungs regulate CO2 levels in the blood, what does that make it a regulator of?
an acid-base regulator
How does respiration change if V̇O2 doubles?
respiration also doubles - in direct proportion to the metabolic demand
What is the consequence of ventilation changing in direct proportion to metabolic demand?
the blood gases and pH are kept relatively constant
In a diseased state, can respiration meet metabolic demands? What are the consequences?
no, blood gases and pH are abnormal
In a less severe diseased state, when can respiration not meet the metabolic demand?
when the metabolic demand changes e.g. during exercise
blood gases and pH= abnormal
In a more severe diseased state, when can respiration not meet the metabolic demand?
at rest
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)
Topic 2: Partial pressures
What are the 3 different units for (P) pressure? What unit is used clinically?
- kPa, mmHg, cmH2O
- kPa
What is PIO2 and PICO2?
Partial pressure of oxygen in Inspired air
Partial pressure of carbon dioxide in Inspired air
What is PAO2 and PACO2?
partial pressure of oxygen in Alveolus (BIG A)
partial pressure of carbon dioxide in Alveolus (big A)
What is PaO2 and PaCO2?
partial pressure of oxygen in arterial blood
partial pressure of carbon dioxide in arterial blood
What is PvO2 and PvCO2?
partial pressure of oxygen in venous blood
partial pressure of carbon dioxide in venous blood
How many mmHg is 1 kPa worth?
1 kPa = 7.5mmHg
How many mmHg is 1cmH2O worth?
1.3mmHg
What is a partial pressure?
the pressure of any gas whether alone/ in a mixture
What does the partial pressure of a gas depend on?
the number of molecules of the gas in given vol and temp
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
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
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
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
Reference ranges of arterial blood gases and alveolar gases
look at table!! p132 of sem2
Why are partial pressures important for diffusion?
because diffusion occurs down partial pressure gradients
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
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
effects of low alveolar PAO2 thus PaO2 in patient w resp disease?
dont have as much of gradient for diffusion= not as efficient.
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
What generations make up the conducting zone of the airways?
the first 16 generations
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
What generations make up the transitional and respiratory zones?
and whats the function?
17-23
gas exchange
What type of flow moves gas through the conducting zone?
bulk flow
How and why does the cross sectional surface area increase from the conducting zone to the respiratory zone?
- enormous increase
- due to continuous branching
What is the formula for total air flow?
total flow = speed x area
As area increases, what does the speed of flow do?
speed decreases
forward velocity of gas: good for diffusion
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
What specialised cells are found within the conducting zone?
- epithelia lined w cilia which beat constantly
- goblet cells which secrete mucus
How does nicotine affect cilia?
it paralyses the cilia, which allows bacteria to invade
How does inflammation/asthma affect mucus?
it increases the viscosity
What do the trachea and primary bronchi have that prevents their collapse?
U-shaped cartilage (blue on diagram)
Why are the bronchioles susceptible to collapse?
they don’t have cartilage
… COPD, asthma
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
What is dead space (VD)?
the volume of gas within the respiratory system where no gas exchange takes place
Dead space occurs where? (2)
- where there’s no effective airflow (aka no alveoli of unventilated alveoli)
- where there’s no perfusion
Which is anatomical dead space: the conducting zone or the respiratory zone?
the conducting zone, where there’s no alveoli
What is the dead space within the conducting zone known as and how much is it in ml?
anatomic(al) dead space - 150ml
What affects the anatomic dead space? (4)
- body size: 2ml/kg
- age: increases
- drugs: bronchodilators/constrictors
- posture: decreased when lying
What is the dead space within the respiratory zone known as?
the alveolar dead space - inadequate perfusion for gas exchange (<5ml)
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
What is the sum of anatomic dead space and alveolar dead space?
physiological dead space = anatomic dead space + alveolar dead space
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
What is the respiratory frequency (f)? What is the typical value?
number of breaths per min - 12 breaths/min
What is the equation for minute ventilation/volume (V̇E)?
V̇E (ml/min) = tidal volume x respiratory frequency
What is the definition of minute ventilation?
total air moving in and out of the respiratory system in 1 minute
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
how much air enters system every minute?
6L
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
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
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!!
what causes drug induced hypoventilation?
drug effects on alveolar vent
- alcohol
- tranquilisers
- opiates
- sedatives
- hypnotics: benzodiazepines, barbiturates
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
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
what must respiratory muscles do in order to breathe? (2)
- stretch elastic parts of resp system (lungs and chest wall)
- overcome resistance to flow (airways and lung tissues)
= takes 10% pf total body O2 consumption (VO2)
what 2 opposing forces act on lung and chest wall at rest?
- elastic recorl of chest wall tries to pull chest wall OUTWARD
- elastic recoil of lung creates INWARD pull
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
what is FRC? func residual capacity
and value?
volume in lungs at end of expiration
approx 2.5L air
all pressures e.g. Palv in lung, relative to what?
pressure outside.
atmosphere can change!
stretching causes ⬇ in pressure
relative to atmos. not actually -
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)
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)
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
air flows from XX pressure -> YY pressure
high -> low
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
chenges in Palv occur ass result of what?
changes in lung volume when thorax expands
i.e. BOYLES LAW
what is BOYLES LAW?
= pressure exerted by a constant number of gas molecules in container = inversely proportional to vol of container
P ∝ 1/V
main inspiratory muscle and role? when used
diaphragm- ONLY muscle used in quiet breathing. lengthens thorax
other inspiratory muscles- what are they used in? 3
exercise, coughing, vomiting
= need inc volume changes
name 3 other inspiratory muscles and use?
sternocleidomastoid
scalenes
external intercostal
1 and 3: forced breathing and inc metabolic demands
describe quiet breathing (insp + exp) using diaphragm. quiet breathing
- diaphragm relaxed at rest
- insp: D contracts, thoracic volume increases
- exp: D relaxes, thoracic volume decreases
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
how does diaphragm behave in expiration? wb other muscles?
passive relaxation
… other muscles during forced breathing more
3 expiratory muscles?
internal intercostal
external and internal obliques
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
describe inspiration (4)
- thoracic cavity enlarges, diaphragm flattens
- due to pleural membranes, lungs move out w thorax
- lungs expand, vol ⬆
- alveolar P now < P outside
describe expiration (4)
- chest wall moves inward
- vol of thorax ⬇,
- lungs recoil- squeeze air
- alveolar P now > P outside
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
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
What is compliance?
the ability to stretch
How do elasticity and compliance relate?
compliance is the inverse of elasticity or 1/E
HIGH elasticity means what for compliance, stretch, and recoil?
HIGH elasticity
LOW compliance
HARD to stretch
EASY to recoil!
LOW elasticity means what for compliance, stretch, and recoil?
LOW elasticity
HIGH compliance
EASY to stretch
HARD to recoil!
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)
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)
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)
The lungs have high outward/inward elastic recoil
the lungs have high inward elastic recoil (so wants to collapse inwards like a balloon)
When are the lungs at rest?
at functional residual capacity (FRC)
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
How does the lung distending pressure change during inspiration?
becomes more positive
because the alveolar pressure increases
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
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)
compliance=?
δV / δ Pdist
lung distending pressure is always what?
+
press inside lung
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
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)
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
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) !!!
type 1 alveolar cell: what does it do and what lines walls of alveoli?
role: aids diffusion of gases
thin layer of alveolar fluids
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
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 ☺
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)
what px at risk of low compliance as no surfactant?
newborns as born without it. released after wk 28 of gestation
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)
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
when can chest wall compliance change?
impairments:
obesity, pectus excavatum
inflammation of joints, fusion of bones in spine
lung distending pressure is always?
+
compliance of chest wall and “ of lung are…
equal!
- and +
when chest wall and lung distending p hit 0 dist pressure i.e. change… where does this occur?
pneumothorax
how does compliance of total system compare with component parts
total is < comp parts
when lungs IN chest wall, less compliant
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
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
what is b. driving pressure?
difference between pressure at 2 points
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
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
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
what does turbulent flow require? and when is it seen
exercise.
rew greater driving pressure (Palv-PB) to move air from mouth -> alveolus
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
what 2 things is resistance to airflow due to?
- friction between air + lung tissue (small contr)
2. friction between air + airways (BIG contr)
when may friction between air + lung tissue increase?
e.g. in interstitial fibrosis- scarring of tissue and laying down of collagen
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
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)
how is airway resistance in upper resp tract sig reduced?
switch from nose to mouth breathing… more air to alveoli
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!
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
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
affect of changing elastic recoil of alveolli e.g. in interstitial fibrosis/ emphysema on radial traction
walls of alveoli stiffen, lose elastic recoil
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
3 ways that airway resistance can be controlled by?
autonomic control
local chemical mediators
bronchoconstriction by ⬇ in CO2 in over-ventilated areas
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
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
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
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
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
if resistance is so small, whys it important in: lower airway?
in what disease?**
COPD
e.g. bronchitis, asthma, emphysema
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
Topic 6: alveolar gases
what is referred to by PIO2, PAO2, PaO2, PvO2?
Inspired
Alveolar
arterial
venous
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
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 ☺
what are alveolar gases similar to?
values?
arterial gases
PaO2 = 12
PaCO2 = 5
…
alveolar:
PAO2 = 13
PACO2 = 5
normally alveolar levels of PO2 and PCO2 determine systemic artial levels too, but what determines alveolar gas:
- PAO2? (3)
- PO2 in atmosphere (inpspired) air.. altitude
- rate of replenishment of O2 by alv ventilation (VA)
- rate of removal of O2 by pulmonary cap blood (level of metab rate, VO2)
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
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
normally alveolar levels of PO2 and PCO2 determine systemic arterial levels too, but what determines alveolar gas:
-PACO2 (2)
5kPa
- rate of metabolism (VCO2) if breathing unchanged: PACO2 ∝ VCO2
so… if CO2: 5% of alveolar air… CO2: 200ml/min= transfer
if increases,both increase!
- alveolar ventilation (VA)
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!)
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 :)
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)
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
what 2 things are
increased in hypoventilation
decreased in hyperventilation?
PACO2 and PaCO2
whats hyperventilation no same as and why?
increased ventilation (during exercise) as ven STILL matched to metabolism
whats hyperpnoea?
breathing: deeper and more rapid than normal
but ⬆ in CO2 produced is exactly ∝ to ⬆ ventilation
3 signs/ indicators of hyperventilation
- PaCO2 lower than normal (<4.5kPA, but need blood gases)
- dizzy: low PaCO2 = vasoconstriction of cerebral vessels
- tetany: spasm, numbness
why may hyperventilation cause tetany?
fall in PaCO2-> hyperexcitability of membranes
= inc perm
= AP initiation
how to treat hyperventilation?
slow deep breaths
not breathing in a bag = inc in CO2!
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
what does diffusion constant for gas through barrier depend on?
MW and solubility of gas
diffusion ability of CO2 and O2 compared.. which one diffuses more easily?
CO2 diff 20x more easily than O2
more soluble, need less gradient ☺
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
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
affect on exercise and PO2 pulmonary capillary?
HR inc,
time for complete cardiac cycle dec
= less time spent in cap
= time for eqm decreases
p361 learn PPs!
define:
dyspnoea
tachypnoae
apnoea
- sensation of shortness of breath
- rapid breathing
- cessation of breathing
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
alveolar air and blood contain same levels of O2 and CO2. whats responsible for setting blood gases?
alveolar gases
whys there a small difference in PAO2 (alveoli 13kPa) and PaO2 (arterial 12kPa)?
ventilation- perfusion (V/Q) matching
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
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
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
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)
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)
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
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!
how does lung adjust to match V and Q in… undervent alveolus?
hypoxic blood = localised hypoxic vasoconstriction
blood directed away = Q inc
how does lung adjust to match V and Q in… overvent alveolus?
low PCO2 in airways = localised bronchoconstriction
look at lung/ flow unit vol lung graph p373
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
what 2 forms is oxygen carried in throughout body?
- dissolved in plasma
- combined with Hb (majority!)
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)
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
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
1 molecule of Hb combines with what…
whats formed?
equation?
4 molecules of O2 to form 4 molecules of O2..-> oxyhaemoglobin
Hb + O2 HbO2
what does amount of oxygen that blood will carry therefore depend on?
[Hb]
i.e. O2 binding capacity = proportional to Hb of blood.
normal Hb values (g/dL) in men women birth child
men: 13-18
women: 12-15
birth: 12-24
child: 10-14
whats theoretical O2 binding capacity not dependant on?
PO2
theoretical= if ALL Hb binding sites are saturated w O2
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]
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
whats %saturation of Hb dependant on?
PO2
in arterial (PO2: 13kPa) = 99% mixed venous (PO2: 5kPa) = 75%
how will mixed venous % Hb sat (SpO2) change if metabolism increases?
inc metab… more O2 removed to meet metabolic demand… would DECREASE
O2 dissociation curve. what does the O2 bound to Hb depend on?
partial pressure of O2 in blood
SIGMOIDAL SHAPE
… doesnt account dissolved O2!!
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
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 ☺
PO2 in lungs (top of Hb curve)… how does % sat link to alveolar PO2?
large fall in alveolar PO2, small fall in % sat
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
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☺
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
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)
what 2 points of Hb curve do not change?
top and bottom
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)
physiological significance of Bohr effect?
on lungs
LUNG: LEFT shift
⬇ CO2, H+
⬆ Hb affinity
more O2 uptake in lung.
CO2 release.. ⬇ acidity
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
how will anaemia affect Hb dissociation curve?
low [Hb]
reduce carrying capacity,
LEFT shift
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
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
2 types of Hb? which is in
- adults
- newborns?
Hb A (2 a, 2 b chains) Hb F (2 a, 2 y chains)
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
affect of sickly cell (Hb A) mutation of B chains …
abnormal Hb molecule, poorly soluble deformed RBC can be destroyed.
genetic
carry less O2
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
roles of myoglobin?
stores O2 for use during v heavy exercise
enhances o2 diffusion through cells by carrying o2 through cytosol
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
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
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!!
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)
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
why does haldane effect happen? (inc PO2 shifts CO2 curve down and left i.e. less CO2 carried)
(2)
- deoxyHb = better buffer to mop up H+.. favours formation of bicarbonate
H2CO3 eqn.. H+ goes to..
H+ + HbO2 H+-Hb +O2
oxyHb deoxyHb - deoxyHb = better ability to bind CO2 and form carbamino compounds
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
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+
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!
what may cause plasma and RBC acidity to increase?
H+ made from carbonic acid disso and carbamino compounds, if not buffered
3 methods that buffer H+ atoms…
role of carbonic acid system as an important buffer system
- plasma proteins: bind H+ + R-NH2 –> R-NH3+
- globin chain of Hb
HbO2 dissoc into O2 and Hb.
Hb + H+ -> HbH - carbonic acid-bicarbonate system
moved to left.. CO2 excreted at lung
whats the ideal arterial pH (pHa) for enzymatic activity and (how calculated)?
7.40
pH = -log [H+]
what 3 solns in body contain weak acids and buffer changes in H+ by adding acid/alkali?
blood
intracellular fluid
extracellular fluid
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]
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
what systems control: [HCO3-] and [PaCO2]?
- kidney
2. resp systems
whats meant by:
metabolic acidosis
metabolic alkalosis
carbonic acid eqn
- [H+] rises, mass reaction pushed left
- loss of body acids -> dec in breathing + retention of CO2
i.e. lungs take care
whats meant by:
Resp acidosis
Resp alkalosis
carbonic acid eqn
- if [CO2] inc, mass reaction pushed RIGHT… but also inc CO2 and bicarb
- opposite if CO2 decreases
i.e. kidneys take care
HCO3- reabsorbed by kidney
H+ secreted by kidney
metabolic acidosis process of returning pH back to normal?
acidemia sensed by chemoreceptors inc ventilation inc CO2 excretion pH normal now ☺
examples of
- metabolic acidosis
- metabolic alkalosis
- diarrhoea
diabetic ketoacidosis
lactic acidosis - vomiting
diuretics
examples of
- Resp acidosis
- Resp alkalosis
- hypoventilation (COPD)
- hyperventilation (response to hypoxia, anxiety)
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)
22 examples of sensors that then input to central controller?
chemical: chemoreceptors
mechanical
gather info form environment
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
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
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)
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
how do chemoreceptors maintain homeostasis of PaO2, PaCO2, and pH?
assist in ensuring VA is appropriate to level of metabolism…
whats name of difference in O2 content between arterial and mixed venous blood?
arteriovenous difference
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 ☺
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
where are peripheral chemoreceptors located?
2 sets, same as arterial baroreceptors…
*carotid bodies (in c sinus)
distinct nodules, most important for refled
*aortic bodies
where does carotid sinus nerve join into?
peripheral chemorec
carotid body (chemos) next to sinus.
.. glossopharyngeal (IX) nerve
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
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
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
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
what does removal of carotid bodies (peripheral chemoreceptors) –>?
decreases in ventilatinon during hypoxia (direct effect of hypoxia on brainstem)
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)
what do aortic bodies respond to?
increase in PaCO2
fall in PaO2
O2 content… thus can detect anaemia/CO
what are aortic bodies innervated by? and what role do they play?
vagus (x) nerve
role in cardiovasc reflexes - haemmhorage
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
affect of moderate hypoxemia on VE?
(PaO2 5-8kPa) only doubles VE (⬆ ventilation)
where are central chemoreceptors located?
ventrolateral medulla of brainstem (midbrain, pons, medulla oblongata)
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
what are central chemorec insensitive to?
hypoxia (change in arterial O2)
process of stimulation of central chemoreceptors?
- BBB prevents H+, HCO3- from affecting brain ECF/CSF
- CO2 crosses… goes in CSF .. carbonic acid eqn
- H+ made -> ECF,stim response in chemorec
stimulation of central chemoreceptors summarised: what stimulates the cc neurons?
acidification of CSF and ECF
CSF is a poor buffer so small changes in PaCO2 ->?
significant CSF acidosis
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
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
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
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)
minute ventilation (VE) =?
VE = VT x Rf VE = tidal volume x respiratory frequency
(infinite combos)
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)
neural control must affect what 2 nerves before affect on resp muscles?
phrenic (inspiratory)
+
internal intercostal (exp)
what does alternating activity in muscles: inspand exp lead to?
phrenic and intercostal….
change in thoracic vol thus change in pressure and airflow
what do accessory insp muscles do?
sternocleidomastoid, scalene, external intercostal:
raise ribs and expand chest cavity
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
exp muscles at rest: what takes part in passive relaxation?
diaphragm
role of other muscles during exp? internal intercostal, externala nd internal oblique?
suppress: shrink cavity push air out of lungs
forced expiration!
central respiratory rhythm –> what ?
in insp and exp muscles
-> reciprocal motor activity
on EMG, what muscle active in
- inspiration
- expiration?
- diaphragm (thick small lines vertical)
- internal intercostal (thin long lines vertical)
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
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!
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)
p545 dorsal view of brainstem image: identify
- Botzinger complex (expiratory),
- prebotzinger (Pacemaker?),
- ventral resp group (VRG insp +exp),
- dorsal resp group (DRG insp)
what do neurones in DRG do?
discharge AP prior to inspiration -> control lateral phrenic nerve- control diaphragm
where is DRG in?
dorsal resp group… in NTS (Nucleus Tractus Solitarius)
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
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
what causes diaphragm to contract?
motor neurones inc activity of phrenic nerve… d innervated by AP generation
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)
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
what about the DRG is responsible for basic rhythm of breathing?
cyclical electrical activity of DRG
what nerve responsible for contraction and relaxation of diaphragm using DRG in quiet breathing?
phrenic motor nerve
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)
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
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
how does PRG shut off inspiration?
inhibits DRG insp neurones
vagal afferent role
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
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
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
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
what do irritant receptord in bronchi
sense?
effect?
chemicals, dust, cold air
cough, bronchoconstriction
what do J receptors in bronchioles/alveoli
sense?
effect?
chemicals, stretch, pulmonary oedema
shallow breathing, cronchoconstr, mucus secrtn
what do stretch receptors in lung
sense?
effect?
lung inflation
inflation terminates
4 types of mechanoreceptors? location
lung + airways
nose + upper airways
joints and muscles
arterial baroreceptors
mechanoreceptors respond to what?
pressure/ distortion
where are PSR? pulmonary stretch rec
vagal nerve endings in SM of trachea + local airways
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
what are the 2 diff patterns from PSRs?
- rec which continues to be active during expiration IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII
- rec with phasic activity and high threshold- only active at inspiration IIII———-IIIIIIIIII———–IIIIIIIIII———IIIIIIIIII———–IIIIIIIII-
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
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)
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
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
if stimulus maintained, how would this affect lung irritant rec action?
afferent impulse num dec over time
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 ☺
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
pulmonary C/ J receptors are located where?
bronchial walls (unmyelinated C- fibres) alveolar walls (J receptors juxtacapillary)- close to caps
pulmonary C/ J receptors are usually what? and what stimulates them?
silent.
stim by: mechanical distortion and inc in interstitial fluid (oedema)
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?
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
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
what do proprioreceptors allow for if movement is impeded?
inc force of insp and expiration
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
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
what do baroreceptors control and how?
BP
⬆ BP–> reflex hypoventilation/ apnoea e.g. Ad apnoea
⬇ BP–> reflex hyperventilation (e.g. due to haemorrhage)
when may baroreceptors action be important?
in complex stimuli (haemorrhage) - many reflexes occur at once!
pathways unknown
