Pie 944 :wow, amazing explanation..thx u..but i have other questions if u don't mind :
The explanation was not that amazing after I read it again.
Hopefully this isn't filled with errors like my prior posts. I apologize, it's a confusing enough subject without misinformation.
Background
Dead Space - Areas of ventilation without perfusion. At the extreme a V/Q of infinity.
Shunt - Areas of perfusion without ventilation. At the extreme a V/Q of zero.
The spectrum is everything in between.
So in units with a higher V/Q(excessive ventilation in relation to perfusion, or low perfusion in relation to ventilation) you are more towards the dead space spectrum, and have worse dead space/difficulties removing carbon dioxide compared to lung units with a normalized ratio.
Units with a lower V/Q(excessive perfusion in relation to ventilation, or low ventilation in relation to perfusion) you are more towards the shunt spectrum and have difficulties with oxygenation compared to a lung unit with a normalized ratio.
The cause of increased arterial carbon dioxide when giving COPD patients supplemental oxygen is not due to decreased respiratory drive. The respiratory drive has been shown not to change in multiple studies of COPD patients with supplemental oxygen.
The increase in arterial carbon dioxide is due to two effects, HPV and the Haldane effect in relation V/Q.
HPV:
The goal of HPV is to distribute blood flow to lung units with high V/Q, lowering this ratio and improving the match between ventilation and perfusion. It also diverts blood flow away from lung units with low V/Q and improve the ventilation and perfusion match between these units as well.
In the patient with COPD, lung units with poor ventilation have the blood(by HPV) forced to lung units with high ventilation. The lung units with high V/Q now by HPV have more blood being distributed to them and a lower V/Q ratio. Hence it transitions the lung unit away from the spectrum of dead space(improving ability to remove carbon dioxide). In addition, the poorly ventilated unit(low V/Q) now has blood flow diverted from it, increasing the V/Q, and reducing physiological shunt to improve oxygenation.
In addition, by driving blood to areas where oxygenation is more efficient it also utilizes the Haldane effect to help remove carbon dioxide.
Haldane Effect:
Deoxygenated hemoglobin binds H+ more efficiently than oxygenated blood, therefore blood will carry more carbon dioxide when deoxygenated. As the blood reaches an area of high oxygen concentration(lungs) the blood becomes oxygenated and binds H+ less efficiently leading to release carbon dioxide where it can be exchanged to the atmosphere.
Therefore, the greater oxygen gradient between the mixed venous and arterial blood(a-mV), the greater amount of CO2 will be displaced due to the Haldane effect and be able to be ventilated to the atmosphere. In situations where the oxygen difference between the mixed venous and arterial blood is smaller due to poor oxygenation, less CO2 will be displaced and unable to be removed by the lungs. This can be referred to as 'Haldane deadspace.'
In the COPD patient a poorly ventilated lung unit with normal perfusion is an example of this. Even though by V/Q ratio it appears low, hence would be on the shunt spectrum, because of the minimum change in the oxygen a-mV gradient, this also causes Haldane deadspace.
However, this effect is minimized by HPV which maximizes the displacement of CO2 by the Haldane effect by driving blood to lung units with adequate oxygen(large gradient, increased CO2 displacement).
Supplemental Oxygen:
When you give a patient with COPD supplemental oxygen it inhibits the above processes leading to an increase in arterial carbon dioxide, but not due to decreased ventilatory drive.
By giving supplemental oxygenation you are inhibiting the HPV as described above.
Now the blood that was diverted towards units with elevated V/Q helping to normalize them and improve dead space is now lost. Therefore, these lung units once again have excess ventilation in relation to perfusion and experience a relative worsening of dead space(the V/Q is increasing again)
In addition, by having this supplemental oxygen the blood is now once again flowing to poorly ventilated lung units due to the inhibition of HPV. This leads to a decreased oxygen gradient(a-mV) and less carbon dioxide being displaced by the Haldane effect and worsening of the Haldane deadspace.
Finally at higher levels of supplemental oxygenation your mixed venous saturation which is on the steeper portion of the oxyhemoglobin dissociation curve increases more than the arterial saturation on the flat portion of the curve. This also narrows your oxygen gradient(Arterial-mV) and further worsens Haldane deadspace.
I'm sorry for the prior posts and any confusion they caused. I've read this over a few times and am confident mistakes still exist in it.
