Serum chloride levels sometimes increase to abnormal levels as an undesirable side effect of medical treatment with sodium chloride or ammonium chloride. The toxicity of chloride results not from the chloride itself, but from the fact that the chloride occurs as the acid, hydrogen chloride (more commonly known as hydrochloric acid, or HCl). An overdose of chloride may cause the accumulation of hydrochloric acid in the bloodstream, with consequent acidosis. Renal tubular acidosis, one of many kidney diseases, involves the failure to release acid into the urine. The acidosis produces weakness, headache, nausea, and cardiac arrest. Low plasma chloride leads to the opposite situation: a decline in the acid content of the bloodstream. This is known as alkalization of the bloodstream, or alkalosis. Hydrochloric acid, originally from extracellular fluids, can be lost by vomiting. At its most severe, alkalosis results in paralysis (tetany).
Hyperphosphatemia occurs at serum phosphate levels above 5 mg/dL. It can result from the failure of the kidneys to excrete phosphate into the urine, causing phosphate to accumulate in the bloodstream. Hyperphosphatemia can also be caused by the impaired action of parathyroid hormone and by phosphate poisoning. Severe hyperphosphatemia can cause paralysis, convulsions, and cardiac arrest. These symptoms result because the phosphate, occurring in elevated levels, complexes with free serum calcium, resulting in hypocalcemia. Tests for heart function (an electrocardiogram) and parathyroid hormone levels are used in the diagnosis of hyperphosphatemia. Hypophosphatemia occurs if serum phosphorus falls to2.0 mg/dL or lower. It often results from a shift of inorganic phosphate from the bloodstream to various organs and tissues. This shift can be caused by a rise in pH (alkalization) of the bloodstream, which can occur during hyperventilation, a reaction in various disease states. A shift in phosphate to intracellular tissues may draw calcium away from the bloodstream via the formation of insoluble calcium phosphate crystals within cells, with consequent hypocalcemia. Thus, tests for abnormalities in phosphate metabolism also involve tests for serum calcium.
Bicarbonate metabolism involves several compounds. When dietary starches, sugars, and fats are broken down for energy production, carbon dioxide is created. Much of this carbon dioxide (CO2) spontaneously converts to carbonic acid (H2CO3), and some of the carbonic acid spontaneously converts to bicarbonate (HCO3) plus a hydrogen ion (H+). Eventually, almost every molecule of carbon dioxide produced in the body, whether in the form of carbon dioxide, carbonic acid, or bicarbonate, must convert back to carbon dioxide in order to leave via the lungs during normal breathing.
If one holds one's breath, carbon dioxide cannot escape from the lungs, but continues to be generated within the body. This results in an increase in production of carbonic acid. A portion of the carbonic acid breaks apart (dissociates), causing an increase in hydrogen ions in the plasma, with a resulting acidosis. Tests for serum bicarbonate levels are accompanied by tests for acidosis (pH test). Conversely, when one breathes too rapidly (hyperventilation), the carbon dioxide is drawn off from the bloodstream and expelled in the breath at an increased rate. This results in an increase in the rate of combination of bicarbonate with hydrogen ions, resulting in alkalosis. Acidosis and alkalosis can be produced by means other than by altering the rate of breathing. The carbonic acid and bicarbonate in the bloodstream minimize (or buffer) any trend to acidosis or alkalosis. Tests for bicarbonate are generally accompanied by tests for blood pH and possibly tests for kidney malfunction, abnormal hormone function, or gastrointestinal disorders.
Tom Brody PhD, The Gale Group Inc., Gale, Detroit,