There are several possible explanations for the process of alkalosis observed after volume<unk> . One popular theory is that alkalosis is simply the loss of solvent volume without a proportional loss in bicarbonate concentration or increase in carbon dioxide concentration. This explanation may be especially appropriate for the very short term after volume loss. Another suggests that the alkalosis is due to renal compensatory mechanisms used to correct volume loss. Extracellular fluid (ECF) volume<unk>  is associated with decreased blood volume and decreased renal perfusion pressure. Three compensation mechanisms engage as a result: # renin secretion is increased, # production of angiotensin II is increased, and # secretion of aldosterone is increased. Increases in angiotensin II cause increased Na+–H+ exchange in the proximal tubule and increased HCO3− (bicarbonate) reabsorption in the proximal tubule due to increased luminal H+. Increased aldosterone secretion stimulates the H-ATPase of alpha-intercalated cells of the collecting duct, which causes 1) increased distal tubule H+ secretion, worsening the metabolic alkalosis, and 2) increased generation of "new" bicarbonate within these same cells, which will be reabsorbed. Additionally, increased aldosterone secretion causes increased collecting duct K+ secretion, in turn causing the hypokalemia seen with<unk> . Finally, it has been suggested that the term<unk> " is actually a misnomer, and that the alkalosis observed during volume<unk>  is actually attributable entirely to chloride depletion, which leads to a failure of pendrin, a chloride/bicarbonate exchanger in the collecting duct.
Contraction alkalosis
Metabolic alkalosis
Respiratory alkalosis
Hypercapnia
Respiratory acidosis
Acidosis
Normal anion gap acidosis
Metabolic acidosis