Which metabolic disturbance is most likely to occur due to acute aspirin toxicity?

Acute aspirin toxicity leads to metabolic acidosis primarily due to its ability to cause increased production of organic acids and its effect on the respiratory system. When aspirin (salicylate) is ingested in toxic amounts, it prompts an initial respiratory alkalosis through hyperventilation, as it stimulates the brain's respiratory centers. This results in decreased carbon dioxide levels (hypocapnia) and an increase in blood pH.

However, as toxicity progresses, the metabolic effects dominate. Salicylates disrupt normal metabolic processes and can lead to the accumulation of lactic acid and other organic acids as a result of cellular metabolism being impaired. This accumulation drives the pH down, leading to metabolic acidosis.

In more severe cases, respiratory compensation may also occur, but the hallmark of acute aspirin toxicity is the development of metabolic acidosis due to the combination of increased acid production and confusion in metabolic regulation. Thus, the most common and clinically significant metabolic disturbance seen in acute aspirin toxicity is metabolic acidosis.