nyimalay wrote:
Net effect in most adult is either a respiratory alkalosis or a mixed respiratory alkalosis-metabolic acidosis .
The latter mixed pattern means acidosis (not alkalosis) with odd CO2 and HCO3 pattern.

pr20 wrote:
UW didn't mentioned about the specific time sequence but says that acute salicylate intoxication in adults causes mixed disorder with respiratory alkalosis and metabolic acidosis with PH on the acidic side.

cuadrado_g wrote:
This is my interpretation:

First: Resp Alkalosis: Direct stimulation ASA in respiratory centers...then Second: Metabolic Acidosis (Accumulation of Lactid Acid)...The starting problem is Resp Alkalosis so most of the time you will find the case in Alkalosis or in a Mixed Resp Alkalosis and Met Acidosis, the second case will have a slight alkalotic pH also, close to normal but alkalotic anyways; because the body never overcompensate or even compensate, the starting problem is reflected in the pH.

Acid-base abnormalities — A variety of acid-base disturbances can occur with salicylate intoxication. Salicylates stimulate the respiratory center directly, resulting in an early fall in the PCO2 and respiratory alkalosis [3,10,11]. An anion-gap metabolic acidosis then follows, due primarily to the accumulation of organic acids, including lactic acid and ketoacids [11,12]. (See "Approach to the adult with metabolic acidosis").

The net effect of these changes is that most adults have either a respiratory alkalosis or a mixed respiratory alkalosis-metabolic acidosis; pure metabolic acidosis is unusual in adults [11], but it may be seen in children who are brought to medical care soon after ingestion [10]. Acute respiratory acidosis is rare in the early stages of aspirin toxicity, but it may be seen in later stages of profound poisoning. Respiratory acidosis that occurs early in the course of aspirin poisoning should suggest coingestion with a respiratory depressant. Approximately one-third of adults who self-poison ingest one or more other medications, many of which are respiratory depressants [11]. (See "General approach to drug intoxication in adults").

This primary respiratory alkalosis contributes to the development of the anion gap acidosis by promoting lactic acid production to minimize the rise in pH. In experimental animals, lactate accumulation is minimal if the initial fall in PCO2 is prevented, but it gradually becomes more prominent as hypocapnia is allowed to occur [12]. Salicylic acid itself (mol wt 180) has only a minor effect on serum pH, since a plasma level of 50 mg/dL (3.6 mmol/L) represents a concentration that is less than 3 meq/L.

WaqasQureshi wrote:
The respiratory alkalosis starts in 30 minutes of overdose. The acidosis usually occurs after 3 hours to 4 hours

it depends upon the time when you see the pH.

It is alkalotic in the beginning and later after 4 hours or so it shifts towards acidemia. AFter 6 hours, its more acidic that is <7.35