Respiratory compensation is a vital physiological process that stabilizes blood plasma pH by regulating the partial pressure of carbon dioxide (P_CO2), a key determinant of pH levels. Most carbon dioxide in the blood dissolves and converts into carbonic acid (H₂CO₃). It dissociates into hydrogen ions (H⁺) and bicarbonate ions (HCO₃⁻). There is also an inverse relationship between PCO₂​​ and pH.

When carbon dioxide levels increase in the blood, more H⁺and HCO₃⁻ are produced, leading to a decrease in blood pH (acidosis). Conversely, when carbon dioxide diffuses from the bloodstream into the alveoli during exhalation, H⁺levels decrease, causing a rise in blood pH (alkalosis). Bicarbonate levels remain relatively stable due to renal compensation mechanisms, which act over a longer timescale.

A negative feedback loop governs the interaction between blood pH and respiratory activity. Central chemoreceptors in the medulla oblongata and peripheral chemoreceptors in the aortic and carotid bodies detect increased blood acidity (lower pH). These chemoreceptors stimulate respiratory centers in the medulla oblongata, triggering an increased rate and depth of breathing. This enhanced respiratory effort expels more CO₂, reducing carbonic acid formation, decreasing H⁺concentration, and raising blood pH toward normal levels.

In contrast to acidosis, during alkalosis, blood pH rises, and the respiratory center activity decreases, leading to slower and shallower breathing. This reduction in breathing rate allows CO₂to accumulate in the blood, increasing H⁺concentration and lowering pH to restore balance. Respiratory compensation is a rapid and dynamic mechanism to stabilize blood pH, complementing slower but longer-lasting renal compensation processes.