respiratory: gaseous diffusion and transport Flashcards
Henry’s law
C=kP
C is concentration of dissolved gas
K is Henry’s constant (different for different gases)
P is partial pressure of gas
What is alveolar water vapour pressure? Why is it constant
6.3kPa
Water vapour pressure depends on temperature and saturation
Temperature is constant at 37C
Saturation is 100% after passing over moist surfaces
Equation for PIO2
(Pb-6.3)x0.209
How to measure pAO2? Why cant we measure this directly
Co2 diffuses into alveolus to replace o2 diffusing into capillary
Usually more o2 is used than co2, co2 production:o2 consumption = 4:5 (R=0.8)
PAo2= pIo2-pAco2/R
PO2, PCO2, PH2O of atm, mixed expired air, trachea and alveolar gas
Atm: po2=21kpa; pco2=0kpa; ph2o=variable
Expired air: po2=16kpa; pco2=3.5kpa; ph2o=variable
Trachea (during inspiration): po2=20kpa; pco2=0kpa; ph2o=6.3kpa
Alveolar gas: po2=13.5kpa; pco2=5.3kpa; ph2o=6.3kpa
What is po2 at venous end of capillary? When does capillarypo2=alveolarpo2
5.3kpa;
About 1/3 along capillary
Solubility co-efficient of co2 and o2;
Which gas will diffuse faster? How many times faster
O2=0.03ml/L/mmhg
Co2=0.7ml/L/mmhg
Co2 diffuses faster. It is 85% of the molecular weight of o2; it is 0.7/0.03=23x more soluble
Diffuses 23x0.85=20x faster
What factors are diffusion across a membrane affected by? How is the rate of transfer of gas calculated in the lungs?
Proportional to area; proportional to pressure gradient; inversely proportional to thickness
DLG is the transfer factor (area and thickness considered)
Rate of transfer=DLG (P2-P1)
How is oxygen diffusing capacity calculated (DLO2)
DLO2= oxygen uptake from lungs/(pAo2-pco2)
How is carbon monoxide diffusing capacity measured (DLCO) measured?
Inhale Low amount of CO + tracer gas -> composition of exhaled gas examined
DLCO=CO uptake from lungs/(pAco-pcCO)
PcCO assumed to be zero as haemoglobin has great affinity for CO-> most CO binds to haemoglobin once in blood
What is DLCO reduced and increased by
Reduced by: anaemia/ increased thickness (eg fibrosis/oedema)/ reduced area (eg emphysema/emboli)
Increased by: polycythaemia (too many blood cells)/increased pulmonary blood volume (increases area)
Haemoglobin content in blood Haemoglobin carrying capacity Oxygen capacity in blood Oxygen saturation of pulmonary venous blood Oxygen saturation in Vena cava
Haemoglobin content=150g/L Haemoglobin carrying capacity=1.34ml/g Oxygen capacity=150 x 1.34= 200ml/L Oxygen saturation in pulmonary venous=100% Oxygen saturation in VC=75%
How does haemoglobin dissociation curve change from arterial-> venous blood? Why is there a change like that?
Moves right wards;
Bohr shift: ph decreases/pco2 increases/temperature increases/2,3DPG increases
How much o2 do tissues extract
How much co2 do tissues produce
5ml of o2/dL
4ml of co2/dL
How does anaemia affect oxygen dissociation curve? Why are anaemics fatigued?
Causes a downward shift
Hb capacity is halved, venous capacity Low at 3.6kpa
Anaemia limits o2 extraction during exercise-> fatigue
Negative effects of CO binding to Hb
How does CO shift oxygen dissociation curve
Problems caused
Reduces o2 bound to Hb Increases o2 affinity of remaining binding sites on Hb -> decreases unloading of o2 Downward shift, now a plateauing shape Venous po2=2kpa Headache coma death
Cyanosis types; what is it?
Central and peripheral
O2 supply to tissues is deficient-> content of de-oxy hb in tissue capillaries is high-> blueish tinge
Peripheral cyanosis
Causes
Reduced blood flow to a region-> hypoxic tissue
Causes of reduced blood flow: cardiovascular shock/Low temp/reduced CO/poor arterial supply
Central cyanosis
Causes
Arterial hypoxaemia (reduction in o2 content)
Blood contains 1.5-2 g/dL of deoxyhb; o2 saturation is 85%
COPD/right to left heart shunts
Forms and percentages in which co2 is carried
60% HCO3
30% HbCO2
10% dissolved
What happens to H and HCO3 formed by CA in RBC
H is buffered by deoxyhaemoglobin
HCO3 enters plasma via HCO3/CL antiporter
Formation of carbamino compounds
Co2 reacts with nh2 on plasma proteins + deoxy-hb
Oxygenation of hb-> co2 unloaded
Haldane effect and causes
At any pco2, venous blood carries more co2 than arterial blood
This is bc hb forms carbamino compounds more readily when deoxygenated
And hb buffers H+ more readily when deoxygenated-> formation of HCO3 favoured
Whats respiratory quotient
Co2 produced: o2 utilised
Consequences of hyperventilation
Low paco2-> cerebral vasoconstriction-> cerebral hypoxia-> dizziness
Alkalosis-> decreased free ca (proteins bind more strongly to ca at higher pH)-> increased excitability of VGCC
Hypoventilation consequences
Hypercapnia
Acidosis
Vasodilation/flushed skin/full pulse
Very high pco2-> CNS depressed-> confusion/drowsiness/coma
Values for PAO2 PaO2 Arterial o2 content Mixed venous po2 Mixed venous o2 content Mixed venous hb saturation
PAO2=13.5 kpa PaO2=12.5 kpa Arterial o2 content= 200ml/L Mixed venous po2= 5.3kpa Mixed venous o2 content=150ml/L Mixed venous hb saturation= 75%
PACO2 PaCO2 Arterial co2 content Mixed venous paco2 Mixed venous co2 content Arterial HCO3
PACO2= 5.3kpa PaCO2=5.3kpa Arterial co2 content= 480 ml/L Mixed venous pco2= 6.1kpa Mixed venous co2 content= 520ml/L Arterial HCO3= 21-27mmol/L