- Metabolic Alkalosis is a pathophysiological category of alkalosis that refers to any cause of increased ECF pH not due to a ventilatory defect (i.e. Respiratory Alkalosis). Although the primary metabolic disturbance can cause a significant increase in blood pH, respiratory compensatory mechanisms can largely correct the pH over several hours.
- The fundamental primary disturbance in a metabolic alkalosis is an increase in the levels of ECF bicarbonate concentration ([HCO3-]) relative to the partial pressure of arterial carbon dioxide (PaCO2). Increased bicarbonate relative to PaCO2 results in an misalignment of the Henderson-Hasselbalch Equation for the bicarbonate buffer which largely determines the pH of the extracellular fluid. Mathematically, the increased ECF pH results from an decrease in the ratio between PaCO2 relative to the ECF concentration of bicarbonate ([HCO3-]).
- Metabolic Alkaloses can be compensated by the actions of the lungs which serve to realign the bicarbonate buffer Henderson-Hasselbalch Equation over a period of hours. As described in Respiratory Acid-Base Control, the lungs respond to alkalosis by decreasing alveolar ventilation, essentially a physiological hypoventilation, which in turn increases the partial pressure of arterial carbon dioxide (PaCO2). The increased PaCO2 realigns the Henderson-Hasselbalch Equation for the bicarbonate buffer and thus largely corrects the ECF pH. Consequently, a respiratory-compensated metabolic alkalosis is characterized by increased levels of ECF bicarbonate (caused by the primary metabolic disturbance) as well as increased levels of PaCO2 (caused by the respiratory compensation). More colloquially, the lungs compensate for the metabolic alkalosis by slowing "Breathing Off" of acid in the form of CO2, thus helping reduce ECF pH. However, it is important to point out that respiratory compensation cannot completely correct the ECF pH and thus the ECF will still remain slightly acidotic even after compensation.
- Metabolic Alkaloses are relatively uncommon and occur either due to exogenous ingestion of bicarbonate or loss of acid. Excessive ingestion of bicarbonate may occur in patients attempting to treat their peptic ulcer disease with Sodium Bicarbonate. Major bouts of vomiting can lead to direct loss of stomach acid. Alternatively, in those with primary hyperaldosteronism a mild metabolic alkalosis occurs due to the capacity of aldosterone to promote renal acid excretion.
- An uncompensated metabolic alkalosis is characterized by a blood pH far above 7.45, increased blood bicarbonate, and a largely normal PaCO2. A respiratory-compensated metabolic alkalosis is characterized by a blood pH only slightly above 7.45, increased blood bicarbonate, and increased PaCO2.