Compensatory Responses: Respiratory Acidosis
Respiratory Acidosis is an acid base disturbance characterized by an elevation in the partial pressure of dissolved CO2 leading to an elevation in the PCO2/[HCO3-] ratio which subsequently increases the hydrogen ion concentration according to the following equation:
[H+] = 24 × PCO2 / [HCO3-]
In Respiratory Acidosis, the elevation in PCO2 result from a reduction in alveolar ventilation. Elevation in PCO2 is never due to an increase in CO2 production.
In response to the increase in [H+] and reduction of the pH, the body responds by trying to increase the plasma [HCO3-] to match the increase in PCO2 and thus maintain the PCO2/HCO3- ratio. This is accomplished via two mechanisms; a) rapid cell buffering and b) an increase in net acid excretion.
Because these mechanisms occur at different moments in time, acute respiratory acidosis can be distinguished from chronic respiratory acidosis.
Acute Respiratory Acidosis
Cell buffering occur within minutes after the onset of respiratory acidosis.
The elevation in CO2 levels lead to an increase in carbonic or volatile acid in the plasma. Unlike nonvolatile acids, carbonic acid (H2CO3 ) cannot be buffered by HCO3- in the extracellular fluid. Therefore, in contrast to metabolic acidosis, bicarbonate levels do not fall in respiratory acidosis..
In this setting, carbonic acid (H2CO3 ) can only be buffered by the limited intracellular buffers (primarily hemoglobin and proteins).
H2CO3 + Hb- → HHb + HCO3-
As shown above, each buffering reaction produces HCO3-, which leads to an increase in plasma [HCO3-].
Due to this process, acutely, there is an increase in the plasma [HCO3-], averaging 1 meq/L for every 10 mmHg rise in the PCO2.
Chronic Respiratory Acidosis
In chronic respiratory acidosis, the persistent elevation in PCO2 stimulates increased excretion of titratable acid and ammonium, resulting in the addition of new HCO3- to the extracellular fluid.
This process is complete after 3-5 days resulting in a new steady state in which there is approximately a 3.5 meq/L increase in the plasma HCO3- concentration for every 10 mmHg increase in the PCO2.
To put into perspective the impact of cell buffering vs renal adaptation on protecting the pH in respiratory acidosis, consider the following examples:
If the PCO2 is acutely increased to 80 mmHg, there will be approximately a 4meq/L elevation in the plasma [HCO3-] to 28 meq/L and a potentially serious reduction in extracellular pH to 7.17.
Change in PCO2 = 80- 40 = 40.
Therefore elevation in [HCO3-] = 40/10 ×1 = 4
According to the Henderson-Hasselbach equation, pH = 6.1 + log[HCO3-]/0.03 PCO2
Hence pH = 6.1 + log (28/ 0.03×80) = 7.17.
In another example: If the PCO2 were chronically increased to 80 mmHg, the plasma [HCO3-] should rise by 14 ([(80-40)/10] × 3.5) to a new concentration of 38 meq/L (24+14)
The pH in this situation would be:
pH = 6.1 + log (38/ 0.03×80) = 7.30
Thus renal compensation offers more significant pH protection in the setting of chronic respiratory acidosis in contrast to intracellular buffering in the acute situation.
Chronic respiratory acidosis is commonly caused by COPD. These patients can tolerate a PCO2 of up to 90-110 mmHg and not have a severe reduction in pH due to renal compensation.
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