Hello,

Hyperlactatemia is often observed in post cardiac surgery along with hypoxemia and low output syndrome. Non-Hypoxic hyperlactatemia maybe due to Delayed Clearance, Renal or Hepatic dysfunction etc. But it is not mandatory to observe all the three in every individual.

Post surgery hyperlactatemia is mostly the consequence of excess lactate production, although a reduction of hepatic lactate clearance may contribute to the condition.

Lactate is a by product of anaerobic metabolism, it becomes elevated in hypoperfusion states when pyruvate cannot enter the Krebs cycle due to insufficient oxygen supply and is converted to lactate. Increased lactate production can be physiologic as a result of postprandial rest, postabsorptive rest, sustained submaximal exercise or catecholamine-stimulated glycolysis.

So Hyperlactatemia during the first 24 hours post surgery is associated with a prolonged ITU/ICU stay. Postoperative hyperlactatemia may be due to poor tissue perfusion and the body-buffering mechanisms are not able to compensate for the decreasing pH. The most frequent cause for secondary hyperlactatemia is the hypoperfusion and tissue hypoxia that are associated with significant cardiopulmonary compromise. Either systemic or regional hypoperfusion may result in hyperlactatemia.

Early postoperative measurable adverse effects, such as base deficit, maximal anion gap and bicarbonate levels, were significantly different between patients with postoperative hyperlactatemia and patients with low-normal lactatemia in the early postoperative period.

Intravenous injections of epinephrine, glycerol etc. are known to cause transient hyperlactatemia.

Hyperlactatemia can occur in the setting of adequate tissue perfusion, intact buffering systems, and adequate tissue oxygenation.

Lactic acidosis, on the other hand, is associated with major metabolic dysregulation, tissue hypoperfusion, the effects of certain drugs or toxins, and congenital abnormalities in carbohydrate metabolism. It also occurs as a result on markedly increased transient metabolic demand (eg, postseizure lactic acidosis). Congenital lactic acidosis is secondary to inborn errors of metabolism, such as defects in gluconeogenesis, pyruvate dehydrogenase, the tricarboxylic acid cycle, or the respiratory chain. These disorders generally reflect situations in which the disposal of pyruvate by biosynthetic or oxidative routes is impaired.

Lactic acidosis may not necessarily produce acidemia in a patient. The development of lactic acidosis depends on the magnitude of hyperlactatemia, the buffering capacity of the body, and the coexistence of other conditions that produce tachypnea and alkalosis (eg, liver disease, sepsis). Thus, hyperlactatemia or lactic acidosis may be associated with acidemia, a normal pH, or alkalemia.