Respiratory alkalosis results from increased alveolar respiration (hyperventilation) leading to decreased plasma carbon dioxide concentration. This leads to decreased hydrogen ion and bicarbonate concentrations.
There are two types of respiratory alkalosis: chronic and acute.
In acute respiratory alkalosis, increased levels of carbon dioxide are "blown off" by the lungs, which are hyperventilating. During acute respiratory alkalosis, the person may lose consciousness where the rate of ventilation will resume to normal.
In chronic respiratory alkalosis, for every 10 mM drop in pCO2 in blood, there is a corresponding 5 mM of bicarbonate ion drop. The drop of 5 mM of bicarbonate ion is a compensation effect which reduces the alkalosis effect of the drop in pCO2 in blood. This is termed metabolic compensation.
Causes of the alveolar hyperventilation seen in respiratory alkalosis include:
anxiety, hysteria and stress
moving into high altitude areas, when the low atmospheric pressure of oxygen stimulates increased ventilation
pyrexia in fever, which stimulates the respiratory centre in the brainstem
drugs, including doxapram and large doses of aspirin, which also stimulate the respiratory centre
CNS causes, including stroke, subarachnoid haemorrhage, meningitis
a hypoxic drive in lung disease, such as pneumonia
caffeine overdose and coffee abuse
In addition, a respiratory alkalosis is often produced accidentally by doctors (iatrogenically) during mechanical ventilation of patients.
Symptoms of respiratory alkalosis are related to the decreased blood carbon dioxide levels, and include peripheral paraesthesiae. In addition, the alkalosis may disrupt calcium ion balance, and cause the symptoms of hypocalcaemia (such as tetany) with no fall in total serum calcium levels.