Respiratory acidosis

Respiratory acidosis may be acute or chronic. Acute conditions occur within minutes or hours. They are uncompensated. Renal compensation has no time to develop as the mechanisms that adjust bicarbonate reabsorption take 48–72 hours to become fully effective. The primary problem in acute respiratory acidosis is alveolar hypoventilation. If airflow is completely or partially reduced, the PCO₂ in the blood will rise immediately and the [H⁺] will rise quickly (Fig 22.2). A resulting low PO₂ and high PCO₂ causes coma. If this is not relieved rapidly, death results.

Examples of acute, and hence uncompensated, respiratory acidosis are:

Chronic respiratory acidosis usually results from chronic obstructive airways disease (COAD) and is usually a long-standing condition, accompanied by maximal renal compensation. In a chronic respiratory acidosis the primary problem again is usually impaired alveolar ventilation, but renal compensation contributes markedly to the acid–base picture. Compensation may be partial or complete. The kidney increases hydrogen ion excretion and ECF bicarbonate levels rise. Blood [H⁺] tends back towards normal (Fig 22.3).

It takes some time for the kidneys to respond to a high PCO₂ and a high [H⁺], and therefore compensation will only be maximal some days after the onset of the clinical problem. In many patients with chronic respiratory conditions, extensive renal compensation will keep the blood [H⁺] near normal, despite grossly impaired ventilation. In stable chronic bronchitis the [H⁺] may be within the reference interval despite a very high PCO₂. This is achieved only by maintaining a plasma bicarbonate concentration twice that of normal. The PO₂ is usually depressed, and becomes more so as lung damage increases with time (pp. 46–47). Examples of chronic respiratory disorders are:

The causes of respiratory acidosis are summarized in Figure 22.4.

Respiratory alkalosis

Respiratory alkalosis is much less common than acidosis but can occur when respiration is stimulated or is no longer subject to feedback control (Fig 22.4). Usually these are acute conditions, and there is no renal compensation. The treatment is to inhibit or remove the cause of the hyperventilation, and the acid–base balance should return to normal. Examples are:

Mixed acid–base disorders

It is not uncommon for patients to have more than one acid–base disorder. A patient may have both a metabolic and respiratory acidosis, such as the chronic bronchitic patient who develops renal impairment. In such a patient with a raised [H⁺], the PCO₂ will be increased and the bicarbonate concentration will be low, both expected findings in primary respiratory and primary metabolic acidosis.

Where the two acid–base conditions are antagonistic in the way they affect the [H⁺], one of the disorders may mimic the compensatory response. A patient may present with a metabolic acidosis and a coexistent respiratory alkalosis. The respiratory disorder may appear, at first sight, to be simply the compensatory response.

Other examples of mixed acid–base disorders commonly encountered are:

Care must be taken in the interpretation of the blood gas results in these patients. Knowledge of the clinical picture is essential. Theoretically, the limits of the compensatory responses in simple primary acid–base disorders are known (Fig 22.5). When compensation apparently falls outside of these expected limits, it is likely that a second acid–base disorder is present.

There is further discussion on the interpretation of blood gas results on pages 48–49.