The acid-base changes that result from elevation of the partial pressure of carbon dioxide (PCO₂) are conventionally analyzed in terms of 'adaptive' increases in plasma bicarbonate concentration ([HCO₃^-]) and the effectiveness of the adaptation is judged by the resulting arterial hydrogen ion concentration ([H⁺]=24 PCO₂/[HCO₃^-]) (Henderson's equation). From studies dating back 40 years in animals and man (1,2), we learned that acute increases in PCO₂ are accompanied by smaller increases in [HCO₃^-] (approximately 0.1 mmol/L for each mmHg increase in PCO₂) than when increases in PCO₂ are sustained for weeks or longer, as in patients with chronic respiratory failure (approximately 0.35 mmol/L for each mmHg increase in PCO₂). This means that the expected increase in [H⁺] (fall in pH) resulting from a rapid increase in PCO₂ to, say, 60 mmHg is 55 nmol/L (a pH of 7.25) - greater than in the chronic state, when [H⁺] will usually be found around 46 nmol/L (pH 7.34). Thus, even in the chronic state, [H⁺] is still expected to be elevated, leading us to conclude that the 'adaptation' is never perfect. When normal arterial [H⁺] is encountered in chronic respiratory failure, the finding is usually explained by a complicating metabolic alkalosis secondary to diuretic or steroid therapy, or perhaps to transient hyperventilation at the time of arterial blood sampling.