What acid base and electrolyte changes are associated with hypovolemia?
• Gastric secretions contain high concentrations of H + and Cl − . Therefore vomiting and nasogastric suction often cause metabolic alkalosis. The increased filtered load of bicarbonate leads to increased delivery of sodium and bicarbonate to the collecting tubule. Because of volume depletion, aldosterone secretion is enhanced. This hyperaldosteronism enhances sodium reabsorption and potassium secretion in the collecting tubule. Therefore vomiting and nasogastric suction may also be accompanied by hypokalemia.
• Secretions from the gallbladder, pancreas, and intestines have high concentrations of bicarbonate. Losses of these fluids, as from diarrhea or external drainage, may cause normal anion gap metabolic acidosis. Because these secretions contain potassium, hypokalemia may also be present.
• Overuse of diuretics is typically accompanied by hypokalemia and metabolic alkalosis. Diuretics lead to contraction of the ECF volume around a constant amount of bicarbonate, leading to contraction alkalosis. Loop and thiazide diuretics increase sodium delivery to the collecting tubule. Hyperaldosteronism secondary to volume contraction promotes sodium reabsorption and potassium secretion in the collecting tubule, leading to hypokalemia.
• Osmotic diuresis from uncontrolled diabetes mellitus can cause perturbations in plasma sodium and potassium concentrations. Hyperglycemia causes movement of water from the intracellular space to the extracellular space, depressing the plasma sodium concentration. However, the plasma sodium concentration is often higher than expected because of free water loss caused by the osmotic diuresis. Osmotic diuresis from uncontrolled diabetes mellitus generally causes a large total body potassium deficit because of urinary losses from the osmotic diuresis. Despite this potassium deficit, the plasma potassium concentration is usually normal or elevated. There are two reasons for this phenomenon. Because insulin promotes uptake of potassium by cells, insulin deficiency promotes hyperkalemia. In addition, the hyperosmolality caused by hyperglycemia causes water to move out of the cells into the ECF. Potassium will be “dragged” out of the cells in a process called solvent drag. Even if the initial plasma potassium concentration is normal, then, one must monitor it closely. Insulin administration will reverse the processes described above and can lead to severe hypokalemia. Uncontrolled Type I diabetes mellitus may be accompanied by diabetic ketoacidosis.
• Diabetes insipidus leads to water losses and can cause severe hypernatremia in patients who do not have access to water.
• Any case of hypovolemia, if severe enough, can cause shock and lactic acidosis.
