Dalton’s Law
A rise in PCO2 leads to a fall in PO2 for a fixed inspired O2 (FiO2) as the preservation of pressures is dictated by Dalton’s law.
Dalton’s Law
Each gas in a mixed gas environment produces its own partial pressure with the result that the sum of the pressures of the different gases provides the total pressure created by the mixture. This is defined in Dalton’s law of partial pressure. The pressure of a mixture of gases is equal to the sum of the pressures of all of the constituent gases alone.
Mathematically P Total = P1 + P2 … Pn
The higher the baseline PaCO2, the more it will rise for a given fall in VA, e.g. a 1 L/min decrease in VA will raise PaCO2 a larger amount when the baseline PaCO2 is 6.7 kPa than when it is 5.3 kPa. A direct consequence of raised CO2 is the rise in [H+] as previously outlined, leading to respiratory acidosis. This acidification has varying consequences:
Pulmonary vasoconstriction which, in a hypoxic environment, contributes even further to reducing the availability of O2 with potential life threatening consequences. Therefore, in the situation of a normal or raised PCO2 with acidosis, non invasive ventilation (NIV) is indicated so as to assist the excretion of CO2 thus preventing further increases in pulmonary vascular resistance which would reduce oxygenation yet further.
There is augmented release of adrenaline and noradrenaline in acute respiratory acidosis and in the milieu of proton excess and hypoxia the myocardium becomes irritable and is prone to arrhythmias.
Learning Bite
For acute respiratory disturbances a PaCO2 variation from normal by 1.33 kPa is accompanied by pH shift of about 0.08 units and 1.5 mmol change in HCO3–. Whereas for chronic cases PaCO2 variation by 1.33 kPa is followed by a smaller pH shift of 0.03 units and 3 mmol/L change in HCO3–
The effects of an acute rise in PCO2 >8 kPa are headache and confusion, while levels >9.3 kPa lead to CO2 narcosis manifesting as drowsiness, depressed consciousness or coma. Unlike the lungs, the cerebral vascular resistance decreases with raised PCO2 with consequent increased cerebral blood flow (CBF). The extracellular acidosis of the CSF is mitigated within 36 hours in the face of a persistent hypercarbic state.
In acute hypercarbia, CO2 rapidly diffuses across the blood-brain barrier, with resultant rise in CSF [H+]. The fall in pH is readily registered at the brainstem leading to increased minute ventilation to expel more CO2. This effect is responsible for about 85% of respiratory drive.
It used to be believed that in patients with chronic hypercapnia, giving oxygen removed their hypoxic drive causing PaCO2 levels to rise. We now know that the rise in CO2 levels is caused by the Haldane effect, with oxygenated haemoglobin off-loading CO2 into the plasma, and the reversal of hypoxic pulmonary vasoconstriction leading to blood being diverted to unventilated parts of the lung increasing the V/Q mismatch. Please see the RCEM learning podcast “Hypoxic drive: Fact or fiction?” for further details.
The caveat must be that oxygen is still required in the hypoxic COPD patient.