Ventilation question Watch

Revenged
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#1
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1) What would overventilation in an alveolus cause local airway smooth muscle to do?

2) What would underventilation in an alveolus cause local pulmoary arteriolear smooth muscle to do?

3) What role does parasympathetic inneravation have on blood vessels?

Edit: I worked out some of it... i think it's to do with V/Q matching... So... 1) Contract (reduces ventilation) 2) Vasoconstriction (reduces perfusion)


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j00ni
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I don't have my textbooks to hand to check this but...

1. Overventilation will cause CO2 to transfer into the alveolus from the bloodstream. This will cause an increase in concentration of CO2 in the airways. IIRC airway smooth muscle responds to hypercapnia by relaxing, thus dilating the airways.

2. Underventilation will cause carboxaemia in the bloodstream. Pulmonary vascular smooth muscle responds to hypercapnia by constricting, so as to shunt blood flow to better ventilated vessels, thus preventing hypoxia/hypercapnia in the systemic circulation by shunting deoxygenated blood to areas of the lung which are ventilating.

3. The parasympathetic nervous system innervation of the cardiovascular system is mostly just the innervation of the heart by the vagus nerve. There is little or no innervation of the blood vessels, although ACh released by the parasympathetic nervous system can bind to receptors in the endothelium causing the release of EDRF, which relaxes vascular smooth muscle
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Revenged
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(Original post by j00ni)
I don't have my textbooks to hand to check this but...

1. Overventilation will cause CO2 to transfer into the alveolus from the bloodstream. This will cause an increase in concentration of CO2 in the airways. IIRC airway smooth muscle responds to hypercapnia by relaxing, thus dilating the airways.

2. Underventilation will cause carboxaemia in the bloodstream. Pulmonary vascular smooth muscle responds to hypercapnia by constricting, so as to shunt blood flow to better ventilated vessels, thus preventing hypoxia/hypercapnia in the systemic circulation by shunting deoxygenated blood to areas of the lung which are ventilating.

3. The parasympathetic nervous system innervation of the cardiovascular system is mostly just the innervation of the heart by the vagus nerve. There is little or no innervation of the blood vessels, although ACh released by the parasympathetic nervous system can bind to receptors in the endothelium causing the release of EDRF, which relaxes vascular smooth muscle
1) So overventilation means hyperventilation...

More CO2 leaves the blood, high alveolar CO2, relaxation of muscles

So would this reduce the airway resistance and cause more air to leave the airway?

2) Underventilation (reduced rate or depth of breathing)

Underventilation in alveoli, high CO2 in arteriolar blood, local constriction to alveoli, blood passes into other alveoli that are well ventilated, prevents high CO2 in the system...

What are these shunt vessels?


Ok that makes sense...

3) This must be a bit of a trick question then


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j00ni
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1. yeah i think so

2. Shunting is basically just when blood is redirected to different vessels. So it's not like new vessels are formed, just that blood that would normally go to say the lower lobe is shunted to the upper lobe, so the vessels to the upper lobe have a higher flow volume than normal

3. Not really, there are parasympathetic effects on vascular smooth muscle as i said, just not direct effects that you would see in other areas
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arvin_infinity
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(Original post by j00ni)

2. Shunting is basically just when blood is redirected to different vessels. So it's not like new vessels are formed, just that blood that would normally go to say the lower lobe is shunted to the upper lobe, so the vessels to the upper lobe have a higher flow volume than normal

s
I know this is really old..

Just would be epic if you could tell me what else I need to know about shunt vessels!?
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DeeWave
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The shunting effect isn't due to designated shunt vessels as would be found bypassing cutaneous capillaries, for example. In under-ventilated areas, vasoconstriction occurs to reduce the blood flow through that portion of lung. Since cardiac output is maintained, the same amount of blood flow occurs through the pulmonary vascular bed, so the blood is divided across the rest of the lung. This is ventilation-perfusion matching - it has the effect of increasing PO2 in the left atrium as high as possible, since less blood is wasted through lung where it isn't properly oxygenated. The rest of the lung can respond by capillary recruitment and distension so it can accommodate the extra blood flow.

This can cause problems at altitude - low alveolar PO2 due to lower atmospheric pressure makes all parts of the lung appear under-ventilated, so a generalised vasoconstriction occurs. This raises pulmonary vascular pressure causing oedema. Oedema increases the path length for diffusion in gaseous exchange and thus impairs it, compounding the problem.

HTH
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