Respiratory acidosis is a clinical disorder characterized by a low arterial pH (< 7.36), an elevation in the pCO2 (hypercapnia) and a compensatory increase in the plasma [HCO3-].
Hypercapnia also occurs in metabolic alkalosis, but this is rather a response to the high arterial pH, which distinguishes the two.
As mentioned previously, breakdown of carbohydrates and fats result in the endogenous production of up to 20 mol of CO2. This CO2, if not excreted via ventilation will combine with H2O to form carbonic acid in the following reaction:
CO2 + H2O ↔ H2CO3 (CA) ↔ H+ + HCO3-
Any increase in PCO2 due to increased CO2 production is rapidly handled by increased alveolar ventilation. Because of the lung’s excellent capacity to excrete excess CO2, increases in PCO2 are always due to hypoventilation and never to increased CO2 production.
Hypoventilation can occur with any interference in the respiratory process. See table. Common etiologies are neuromuscular disorders, CNS depression, disorders of the chest wall, chronic obstructive lung disease and acute airway obstruction.
For a discussion on the compensatory mechanisms of respiratory acidosis, click here.
Causes of respiratory acidosis
A) CNS depression
4) Disorders affecting gas exchange
Symptoms are caused by acute respiratory acidosis and not by chronic respiratory acidosis and usually include neurologic abnormalities. Initial symptoms include headache, blurry vision, restlessness, and anxiety, which can progress to tremors, asterixis, delirium, and somnolence or coma (CO2 narcosis). Severe hypercapnia increases cerebral blood flow and cerebrospinal fluid pressure. Signs of increased intracranial pressure such as papilledema may be seen.
The tendency to develop neurologic abnormalities in acute respiratory acidosis is due to the rapid reduction in CSF pH. CO2 is lipid soluble and rapidly crosses the blood brain border, leading to a decline in CSF pH. In contrast, HCO3- is a polar compound that does not readily cross the blood border and thus is not available to counteract the actions of CO2. Thus acute respiratory acidosis promotes a greater fall in CSF pH than acute metabolic acidosis, which may explain why neurologic abnormalities are seen less often in the latter. In chronic respiratory acidosis, the CO2 accumulates at a much slower rate, allowing renal compensation to return the arterial pH and ultimately CSF pH toward normal. Therefore neurologic abnormalities are also seldom seen in chronic respiratory acidosis.
- Treat underlying disorder
- Supply oxygen
- Corticosteroids and bronchodilators to reduce airway inflammation and resistance.
- Mechanical ventilator if ventilation fails.