respiratory physiology Flashcards
external respiration
exchange of oxygen and CO2 between organism and env
control of respiration:pacemaker for breathing
detection of partial pressure
how much lungs expand
found in brain
changes volume of thorax and lungs
in respiratory centres
stretch receptors in respiratory muscle feed into brain
part of spinal cord responsible for breathing
expiratory rhythm generated by?
pre-Bot. C controls inspiration
pFRG
3 neurones involved in sensing arteriole gases
RM
Rob
RPa
in medulla
3 central controls of breathing
reflex/automatic - brainstem
voluntary/behavioural - motor cortex
emotional - limbic system (overrides everything)
brainstem
pons and medulla
2 types of pulmonary stretch receptors
fire quickly and for some time, long term changes
same inflation but quick bursts and die off, acute changes
lung compliance
how much can stretch something for a given pressure
very compliant if can stretch something a lot with not a lot of pressure
magnitude of change in lung volume produced by given change in transpulmonary pressure (Ptp)
like blowing up balloon (hard at first then easy)
2 determinants - stretchability of tissues and surface tension within alveoli
alveoli
surface is moist
surface tension at air-water interface resists stretching
surface tension lowered (by water) and lung compliance is increased by pulmonary surfactant
want bubble - water with air inside not just water droplet
pulmonary surfactant
phospholipids and protein
makes lung easier to expand
secreted by type II alveolar cells
deep breath increases secretion
like lipid bilayer
hypercapnia
hypoxia
CO2 excess
lack O2
how much does partial pressure of O2 have to fall before breathing is stimulated?
half
accessory respiratory muscles
sternocleidomastoid and scalenes
pull lungs up
human inspiration and expiration control
active inspiration but passive expiration (relaxing and recoiling)
sometimes active expiration when extreme exercise
phrenic nerve
innervates diaphragm
70% of your tidal volume
internal intercostal muscles
external
active expiration
close ribs, move down and in
for inspiration
external and internal obliques
bottom of ribcage
force lower ribs inwards when contract
transverse abdominis
stitch when running
force abdomen in and liver up into thorax
pushes air out
genioglossus
tongue
inspiration and active expiration
contracts and strengthens airways so resist change of pressure, keep wide open
widens airway so more air movement
thorax
closed compartment
separated from abdomen by diaphragm
lungs and walls of thorax covered by thing membranes (pleurae)
fluid inside pleurae sticks lungs and muscle together
lung and muscle not physically connected but vacuum connects them
visceral pleura
parietal pleura
pleural cavity
intrapleural fluid
epithelium covering lung
inner surface of walls of thorax, muscle, diaphragm, heart, bones
partial vacuum helps lungs keep expanding
creates vacuum and freedom of pleurae to slide over one another
what stops lung collapsing?
ribs being pulled outwards by muscles
lung being pulled in due to recoil
but vacuum keeps connected so doesn’t pull anywhere
pneumothorax
collapsed lung
break vacuum
so air comes in
elastic recoil of lung takes over
decrease in pressure also pulls heart over centrally
transpulmonary pressure
lung stay inflated if?
alveoli pressure (in lungs) intrapleural (outside lungs in thorax)
alveoli higher than intrapleural
more flow if
higher difference in pressure
why is there a delay in pressure change of alveoli after volume change?
resistance by airway so no more gas molecules, so pressure decreases
then high pressure to low pressure so air moves in - till difference is 0
same happens with exhaling
creates wave graph of pressure but semicircle volume graph
inspiration
muscles and diaphragm contract
ribs pulled upwards and diaphragm flattens
thorax enlarges
intrapleural pressure decreases so transpulmonary pressure increases
expiration
muscles and diaphragm relax
volume of thorax decreases
intrapleural pressure increases so transpulmonary pressure decreases
FEV1
volume expired in first second
FVC
forced vital capacity
total volume expired
80% healthy
lung structure
3 lobes in right lung
2 lobes in left lung
bronchioles structure
divide to terminal bronchioles then split to respiratory bronchioles then alveoli
conducting zone
functions
from mouth and nose to end of terminal bronchioles
conducts air but doesn’t exchange gas
low-resistance pathway for airflow
warms and moistens air
defends against microbes
most resistance in conducting zone
in upper parts - larger but lots of bronchiles larger than 1 trachea
disorders of the conducting zone - asthma
chronic inflammation of airways
smooth muscle is hyper-responsive to lots of triggers
thickened airway wall and less open area
disorders of conducting zone - bronchitis
inflammation of bronchial walls, thickened walls
increase mucus secreting cells and loss ciliated cells
obstruction of airway
respiratory zone
function
respiratory bronchioles to alveolar sacs
provides O2 and removes CO2
regulate blood pH in coordination with kidneys
influence arterial conc. of chemical messengers like converts angiotensin 1 to vasoconstrictor angiotensin 2
dissolves blood clots
how many alveoli?
500 million
pulmonary circulation
blood from right ventricle to left atrium
low pressure
from heart to lungs to get oxygen
ventilation-perfusion mismatching
stop blood supplying areas with poor gas exchange
hypoxia (lack O2) shuts down blood supply to that region
bottom of lung has low flow
ventilation
amount of gas getting to lungs
perfusion
amount of blood getting to lungs
TUC
time of useful consciousness
decreases as altitude increases
3rd man factor
hallucinate someone else when extreme stress from little O2 at high altitude
sleep at high altitude
impaired, frequent awakenings, unpleasant dreams, no feeling of refreshment
periodic breathing is the cause
high altitude and lung capacity
increased erythrocytes and increased blood oxygen carrying capacity
develops over several weeks
high altitude diseases
acute mountain sickness
pulmonary edema
cerebral edema
acute mountain sickness
cure
higher than 3000m
headache, fatigue,insomnia,nausea
last 2-3 days
reverse symptoms if go to low altitude so not long term
acetazolamide - carbonic anhydrase inhibitor so increase excretion of HCO3 and reduce alkalosis, maintain normal pH
high altitude pulmonary edema
above 3000m
people who suffer once likely to suffer again
laboured breathing, reduced exercise tolerance, dry cough, rapid breathing and heartbeat, raised body temp
treat by moving to low altitude
high altitude cerebral edema
potentially fatal
above 4500m
confusion, rapid mood changes, hallucination, loss control of body, coma
only rapid descent will cure it
birds
highest rate of O2 consumption relative to body weight
air only goes in 1 direction so air coming in not same tube as going out (like humans)
2 cycles:
air sac expands and draws air in, contracts and blow through system, both sacs expand and suck air in sack, air out, only travels 1 way through system
also very thing blood gas barrier
powerful heart
less sensitive to lowered PCO2
Cx26
CO2-gated receptor that releases ATP
ATP signals to breathe more
mole rats
underground
rebreathe own air
elephants
don’t have pleural space
filled with dense connective tissue instead
