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Gas transport and pulmonary blood flow (Oxygen carriage (Haemoglobin (Hb),…
Gas transport and pulmonary blood flow
Oxygen carriage
O2 poorly soluble in plasma. So need Hb
Haemoglobin (Hb)
4 x haem units each with associated with globin chain
Each haem can bind one O2 (so each Hb can bind 4 O2)
Haem = pigment molecule containing Fe2+
1g Hb can carry 1.36ml O2
Mammalian blood average [Hb] = 150g/l
Maximum capacity = about 200ml per 1L blood
Cooperative binding - binding of O2 increases the affinity of the other sites for O2 (until fully bound)
Produces the sigmoid shape graph
-allows you to deal with moderate drop in environmental pO2
-if v.hypoxic environment large drop in % sat v.quickly
Sigmoidal shape graph
-fast binding at lung
-fast dissociation at tissue
Oxygen dissociation curve altered by
Increase Temperature - Curve to right (reduced affinity)
Increase pH (
more basic
) - Curve to left (Increased affinity)
Increase CO2 - Curve to right (Reduced affinity)
Increase in 2.3-DPG - Curve to right (Reduced affinity)
Carbon dioxide carriage
Dissolved in plasma (5%)
Carbamino compounds (30%)
Bicarbonate ions (65%)
Carbamino compounds
CO2 combined with protein
Mostly with Hb = Carbaminohaemoglobin
CO2 binds more readily to deoxyHb
Bicarbonate ions
CO2 + H2O <--> H2CO3 <--> HCO3- + H+ happens within erythrocyte. (Step 1 uses Carbonic anhydrase)
HCO3- diffuses out into plasma
Cl- moves into cell to maintain electrochemical neutrality = chloride shift
Opposite way round at lungs
Oxygen and CO2 interaction to Hb
Oxygen binding to Hb is facilitated by relatively low CO2 and pH
CO2 binds more readily to deoxyHb as does H+
Bronchovascular bundle (and vascular resistance)
Protective sheet surrounding attached to visceral pleura. So when lung expands (inspiration) dilates blood vessels lowering resistance
Diameter of blood vessels affected by transmural pressure
At super high lung volume alveolar capillary squished so vascular resistance increases
As lung volume increases initially extra-alveolar vessels dilated so reduced vascular resistance
Pulmonary vascular resistance
PVR = (P of pulm.artery - P of left atrium) / Cardiac output
Capillaries contribute more to resistance than arteries in pulmonary
Capillary flow in lungs is pulsatile
Control
Smooth muscle in walls which can contract (in arteries and arterioles)
Relaxation = dilation of arteries = decrease in PVR
Contraction = constriction of arteries = Increase in PCR
Nervous control
Sympathetic net effect is vasoconstriction (undesired)
Parasympathetic net effect is vasodilation
Autonomic nervous system has small impact
Humoral control
Nitric oxide
Causes vasodilation
Released from endothelial cells in response to:
-Parasympathetic stim.
-Bradykinin
-Increased speed of blood flow in vessel
Alveolar hypoxia
Causes vasoconstriction - opposite to normal hypoxia effect
Aims to maintain VA:Q. Reduced blood flow so reduced perfusion so matches reduced ventilation so balance
Problematic if general