High levels of<unk> s stimulate peripheral chemoreceptors and the central respiratory centers in the medulla causing increased ventilation and a respiratory alkalosis. The increased pH secondary to hyperventilation with respiratory alkalosis causes an increase in lipolysis and ketogenesis which causes the production of lactate and organic keto-acids (such as beta-hydroxybutyrate). The accumulation of these organic acids can cause an acidosis with an increased anion-gap as well as a decreased buffering capacity of the body.<unk>  toxicity also causes an uncoupling of oxidative phosphorylation and a decrease in citric acid cycle activity in the mitochondria. This decrease in aerobic production of adenosine triphosphate (ATP) is accompanied by an increase in anaerobic production of ATP through glycolysis which leads to glycogen depletion and hypoglycemia. The inefficient ATP production through anaerobic metabolism causes the body to shift to a catabolic predominant mode for energy production which consists of increased oxygen consumption, increased heat production (often manifesting as sweating), liver glycogen utilization and increased carbon dioxide production. This increased catabolism accompanied by hyperventilation can lead to severe insensible water losses, dehydration and hypernatremia. Acute aspirin or<unk> s overdose or<unk>  can cause initial respiratory alkalosis though metabolic acidosis ensues thereafter. The acid-base, fluid, and electrolyte abnormalities observed in<unk>  toxicity can be grouped into three broad phases: * Phase I is characterized by hyperventilation resulting from direct respiratory center stimulation, leading to respiratory alkalosis and compensatory alkaluria. Potassium and sodium bicarbonate are excreted in the urine. This phase may last as long as 12 hours. * Phase II is characterized by paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys. This phase may begin within hours and may last 12–24 hours. * Phase III is characterized by dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4–6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.
Salicylate poisoning
Sepsis
Tin poisoning
Myocardial infarction
Thallium poisoning
Psychomotor agitation
Sulfuric acid poisoning
Diabetic ketoacidosis