Respiratory alkalosis is an elevation in pH secondary to reduced arterial partial pressure of carbon dioxide (pCO₂) in the setting of hyperventilation. It can be either acute or chronic and is the most common acid-base disturbance in critically ill patients. Hyperventilation often leads to hypocapnia, which in turn leads to a slight reduction in bicarbonate, hypokalemia, and hypophosphatemia due to an intracellular shift of potassium and phosphate, and hypocalcemia due to increased calcium binding to albumin in the setting of increased pH.

The symptoms of acute respiratory alkalosis are often secondary to hypocalcemia and include paresthesias, circumoral numbness, and tetany. Dizziness and confusion are secondary sequelae from cerebral vasoconstriction in the setting of hypocapnia.

Causes of respiratory alkalosis are broad and include hyperventilation syndrome, pain, central nervous system tumors, pneumonia, pulmonary emboli, interstitial lung disease, congestive heart failure, high altitude, alcohol withdrawal, and medications including salicylates and progesterone. It is rare for patients to have a pure respiratory alkalosis unless they are on mechanical ventilation.

Respiratory alkalosis can be divided into acute and chronic phases:

• Acute – Occurs within minutes and causes an acute decrease in the serum bicarbonate concentration. In acute respiratory alkalosis, the serum bicarbonate should fall by 2 mEq/L for every 10 mm Hg decline in the pCO₂.
• Chronic – Occurs secondary to renal adaptations and takes 3-5 days as the kidneys reduce acid excretion and increase bicarbonate excretion, both of which increase the serum bicarbonate concentration. In chronic respiratory alkalosis, the serum HCO₃ concentration should fall by about 4-5 mEq/L for every 10 mm Hg reduction in the pCO₂.

Alkalosis can decrease tissue oxygen delivery through 2 mechanisms:

1. Increased pH decreases hemoglobin's ability to offload oxygen via the Bohr effect.
2. Increased pH causes vasoconstriction of vasculature to the brain.