Compensatory Responses: Respiratory Alkalosis

Respiratory alkalosis is caused by an elevation in the frequency of alveolar ventilation and more importantly tidal volume that result in an increase in minute ventilation. The increase in ventilation leads to the excretion of CO2 at a rate greater than that of cellular CO2 production.

This leads to a net reduction in PCO2 and subsequently to a reduction in the PCO2 / [HCO3-] ratio which reduces the hydrogen ion concentration (and increases the pH) according to the following equation: [H+] = 24 × PCO2 / [HCO3-]

In response to the decrease in [H+] and elevation in pH, the body responds by trying to reduce the plasma [HCO3-] to match the reduction in PCO2 and thus maintain the ratio. There are two mechanisms responsible for this compensation to respiratory alkalosis; 1) rapid cell buffering and 2) a decrease in net renal acid excretion.

As in respiratory acidosis, these responses occur in different moments of time, distinguishing acute respiratory alkalosis from chronic respiratory alkalosis.
 

Acute Respiratory Alkalosis  

About 10 minutes after the onset of respiratory alkalosis, hydrogen ions move from the cells into the extracellular fluid, where they combine with [HCO3- to form carbonic acid in the following reaction:
                  H+   + HCO3-      →      H2CO3 (CA)   

The hydrogen ions are primarily derived from intracellular buffers such as hemoglobin, protein and phosphates. The reaction with bicarbonate ions in this reaction leads to a mild reduction in plasma [HCO3-].

In acute respiratory alkalosis, as a result of cell buffering, for every 10 mmHg decrease in the PCO2, there is a 2meq/L decrease in the plasma HCO3- concentration.

Please note that the cellular buffering does not offer adequate protection against respiratory alkalosis. For example:

If the PCO2, were reduced to 20 mmHg, the change in PCO2 would be 20 (40-20) and therefore the fall in plasma [HCO3-] would be 4 meq/L (20/10 × 2). The new plasma [HCO3-] would be 20 meq/L (24-4).
The pH in this circumstance would be:
           pH = 6.1 + log (20/ 0.03×20) = 7.63

 Had no cell buffering occurred, then the pH would be
           pH = 6.1 + log (24/ 0.03×20) = 7.70

 As you can see, really not much of a change.

 

Chronic Respiratory Alkalosis

      If respiratory alkalosis persist for longer than 2- 6 hours, the kidney will respond by lowering hydrogen secretion, excretion of titratable acids, ammonium production and ammonium excretion. There will also be an increase in the amount of HCO3- excreted due to decreased reabsorption of filtered HCO3- .

Completion of this process occurs after 2-3 days after which a new steady state is achieved.

Renal compensation result in a 4 meq/L reduction in plasma [HCO3-] for every 10 mmHg reduction in PCO2.


In comparison, to acute respiratory alkalosis, this compensation offers a much better protection of the arterial pH. To put this into perspective, consider the same 20 mmHg fall in PCO2 as before in the acute scenario. Now, due to renal compensation, the plasma [HCO3-] falls by 8 meq/L to 16 meq/L. The pH now in the chronic situation would be :
                pH = 6.1 + log (16/ 0.03×20) = 7.53.

 

 

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