gas exchange and breathing Flashcards
Dalton’s law
law of partial pressure
pressure of gas mixture = sum of pressures of gases in the mixture
fick’s law
law of diffusion
molecules defuse down conc gradient, proportional to the conc gradient, SA, and diffusion capacity (numerator)
inversely proportional to thickness of exchange surface (denominator)
Vgas = [AD(P1-P2)]/T
henry’s law
law of solubility
conc of gas that dissolves in fluid is proportional to pp gas and solubity of gas
Boyle’s law
law of pressure
vol of gas inversely proportional to the pressure at constant temp
Charles’ law
volume gas proportional to temperature of the gas
why do you need to know composition of air people have been breathing
might explain clinical symptoms
different compositions of air
oxygen therapy >21% O2
smoking - make O2 and CO2
high altitude - same proportion of O2 but a lower volume, because of low biometric pressure
what happens to air as it goes down the respiratory tube
it is warmed
humidified
slowed and mixed
air in the conducting pathways
100% saturation with H2O - know because you breathe out saturated air
less oxygen because of air mixing
air in the respiratory airways
supersaturated - fascilitates GE
greater mixing of air so more dilution - gas particles move by diffusion, alveoli don’t change size
high CO2 conc so moves down gradient until it reaches airflow
problem with oxygen solubility
CdO2 = 16ml/min but the vol of O2 consumption = 250ml/min
so cant rely on oxygen solubility alone
describe haemoglobin
different genes = different globin monomers - all have 2a and then either 2 B, d, gamma
has Fe2+ at centre of tetrapyrrole porpyrin connected to globin covalently joined at histamine residue
90% = HbA
2% = HbA2
HbF - foetal
proportions change through development
describe O2 transport
Hb low affinity to O2
coincidently bump into each other and bind
conformational change
higher affinity to other oxygen - exponential increase up to 300x, however there are fewer binding sites left
this is cooperative binding
also generate binding site for 2,3-DGB - push Hb into a more tense state - forcing oxygen out - allosteric action
relationship between affinity and ‘tense’
lower affinity = more tense state
describe methaemoglobin
.5-1% of Hb
Fe3+ - doesn’t bind to O2
involved in redox reaction in terms of ETC and managing electron donors and receivers, in equilibrium - constant flux from Hb
use methyl blue to increase Hb if methaemoglobin is too high
why can methaemoglobin change our colour
Hb is a pigment
why would linear oxygen dissociation curve be bad
too big range in lung and too small in tissue
in pul circulation - pp varies so have large range of binding
in systemic circulation - only small range that you could get O2
describe oxygen dissociation curve
curve looks different at different parts of the body
steepness gives greater scope for removing oxygen from the blood
even if low PP in lungs - still get high percentage of saturation
what causes a rightward shift in the oxygen dissociation curves
increase in temp from exothermic metabolic reactions
acidosis - from accumulation of protons and high CO2
hypercapnia - increased CO2
increased 2,3-DPG
what causes a leftward shift in the oxygen dissociation curve
low temp
alkalosis
hypocapnia
low 2,3- DPG
effect of shifts on O dissociation curves
L - more O2 bound at given pO2
R less O2 bound at pO2
what causes an upward shift in O dissociation curve
polycythaemia - increased O carrying capability
tumour that increases erythropoiesis
greater conc of Hb in blood
what causes a downward shift in O dissociation curve
anaemia - impaired O carrying capacity - lost 1/4 blood
saturation 100% but not enough vol
what causes a downward and L shift
CO2 binding (carboxyhaemoglobin) - takes binding sites
reduces capacity
however increases affinity - less willing to get rid of O2
foetal Hb
greater affinity than adult Hb
to extract blood from mother in placenta
myoglobin
steeper than even foetal
provide O2 for early stage of exercise
high energy for a short time
higher affinity to get O2 for early stage exercise
describe O transport
diffuse into plasma until pp = alveolar pp
o enter RBC and bind to Hb
blood returning to lungs - large drop in pO but only small drop in Hb conc
why does blood arriving at the tissues have less O than in the lungs
lung tissue has brinchial circulation and a little bid drains into pulmonary circulation = haemodilution
how do you calculate flux
net change in arterial oxygen/CO2 content
multiple by 50 - because CO 5L per minute
describe co2 transport
co2 move into RBC react h2o in RBC with carbonic anhydrase enzyme - H2CO3 dissociate - bicarbonate moves out and cl- enters
or binds to amine end of Hb chain
protons mopped up by binding to -ve aa in Hb eg histidine
or co2 in blood react with h2o = bicarbonate and H+
change in dissolved vol of co2 is significant - no sigmoidal shape
the co2 dissociation curve
means the Hbco2 is more in deox blood
Haldane effect
when Hb saturated with o2 - Hb not bind to co2
what is transit time
time it takes for o2 to do GE - ie equilibrate in plasma and alveoli
CO2 more soluble so even faster than o2 (.75s)
during exercise blood goes faster so transit time = .25s
describe ventilation perfusion matching
lung tissue and circulation are under the effect of gravity - gravity squashes the pleural space at the bottom and expands it at the top
at top - higher transmural pressure because pulled down - so less scope for them to be stretched more - take more pressure to inflate more
at bottom alveoli compliant and so airway ventilate more
also at top lower jintravascular pressure - less recruitment, more resistance so lower flow rate - more perfusion at the bottom
greater impact of perfusion in the zones than ventilation - because blood flow is denser
divide one by other = ventilation perfusion ratio
at top - wasted ventilation - because v little perfusion
at bottom wasted perfusion
