To summarize plasma pH problems, in metabolic acidosis there is eventual HCO–3 deficit, leading to decreased plasma pH and decreased CO2 content (or CO2 combining power). In respiratory acidosis there is primary H2CO3 excess, which causes decreased plasma pH, but the CO2 content is increased due to renal attempts at compensation. In metabolic alkalosis there is eventual bicarbonate excess leading to increased plasma pH and increased CO2 content. In respiratory alkalosis there is primary carbonic acid deficit, which causes increased plasma pH, but the CO2 content is decreased due to renal attempts at compensation. The urine pH usually reflects the status of the plasma pH except in hypokalemic alkalosis, where there is acid urine pH despite plasma alkalosis.

As noted, CO2 content or combining capacity essentially constitutes the numerator of the Henderson-Hasselbalch equation. PCO2 is essentially a measurement of the equation denominator and can be used in conjunction with pH to indicate acid-base changes. This is the system popularized by Astrup and Siggaard-Anderson. PCO2 follows the same direction as the CO2 content in classic acid-base syndromes. In metabolic acidosis, PCO2 is decreased, because acids other than H2CO3 accumulate, and CO2 is blown off by the lungs in attempts to decrease body fluid acidity. In metabolic alkalosis, PCO2 is increased if the lungs compensate by hypoventilation; in mild or acute cases, PCO2 may remain normal. In respiratory alkalosis, PCO2 is decreased because increased ventilation blows off more CO2. In respiratory acidosis, PCO2 is increased because of CO2 retention due to decreased ventilation.