Respiratory alkalosis is caused by
hyperventilation, resulting in a loss of
carbon dioxide. Compensatory mechanisms for this include release of hydrogen ion from tissue buffers and excretion of
bicarbonate in the kidneys, both of which lower blood
pH. Hyperventilation-induced alkalosis can be seen in several deadly
central nervous system diseases such as
strokes or
Rett syndrome. During exercise, due to the inability to utilize muscle glycogen as a substrate for ATP synthesis, plasma lactate does not significantly rise (and may fall below) compared to resting levels; consequently, McArdle disease individuals do not experience lactic acidosis. increased epinephrine, and/or increased oxygen demand for oxidative phosphorylation of blood borne substrates (free fatty acids and blood glucose). Metabolic alkalosis can be caused by repeated vomiting, resulting in a loss of
hydrochloric acid in the stomach contents. Severe
dehydration, and the consumption of
alkali, are other causes. It can also be caused by administration of diuretics and endocrine disorders such as
Cushing's syndrome. Compensatory mechanism for metabolic alkalosis involve slowed breathing by the lungs to increase
serum carbon dioxide, a condition leaning toward respiratory
acidosis. As respiratory acidosis often accompanies the compensation for metabolic alkalosis, and vice versa, a delicate balance is created between these two conditions. ==See also==