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

Humoral control

Sympathetic net effect is vasoconstriction (undesired)

Parasympathetic net effect is vasodilation

Autonomic nervous system has small impact

Nitric oxide

Alveolar hypoxia

Causes vasodilation

Released from endothelial cells in response to:
-Parasympathetic stim.
-Bradykinin
-Increased speed of blood flow in vessel

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