Hyperlactatemia: An Update on Postoperative Lactate

Abstract

While hyperlactatemia in postoperative cardiac surgery patients was once believed to solely reflect hypoperfusion, either from the accumulated “oxygen debt” during bypass or ongoing inadequate perfusion, our understanding of lactate generation, clearance, and management has evolved. A contemporary understanding of lactate balance is critical to the management of the postoperative patient with hyperlactatemia. In this review, we summarize the current understanding of lactate metabolism in pediatric patients following cardiac surgery and highlight two types of hyperlactatemia: type A, which is secondary to inadequate oxygen delivery and tissue hypoxia, and type B, which in postoperative pediatric cardiac surgery patients largely reflects increased glycolysis driven by the stress response. Both types may coexist; thus, it is imperative that providers first assess the patient for evidence of hypoperfusion. In patients with evidence of adequate perfusion, a type B component is often associated with a concomitant balanced (normal anion gap) metabolic acidosis and hyperglycemia. These patients will benefit from a more nuanced approach to their type B hyperlactatemia, as many will have a benign course and may be managed expectantly.

Impact of hepatopathy in pediatric patients after surgery for complex congenital heart disease

“…In addition, the postoperative peak lactate level as another indicator for LCOS was shown to be a risk factor for hepatopathy in our analysis. This observation is interesting in so far as the liver contributes about 60% to lactate metabolism [32].…”

Risk factors associated with prolonged postoperative intensive care unit stay in total anomalous pulmonary venous connection

“…Since the blood supply of lung only comes from a small number of bronchial arteries, and the coronary arteries is without blood during CPB, such technical characteristics determine the possibility of in su cient perfusion in lung and heart tissue. In addition, despite bypass delivering adequate calculated tissue perfusion for a given patient, variable in ammatory, microcirculatory, and mitochondrial responses during hypothermia and CPB likely contribute to elevated lactate [10]. For above reasons, adequate myocardial protection, shorten CPB and aortic clamped time may help decrease intraoperative lactate level.…”

The Status of An Inversely Coupled Oxic/Sulphidic Oscillator (OSO) in the Whole Body Chemocline Will Determine Clinical Unfolding in Systemic Inflammatory Response Syndrome (SIRS)* of Any Aetiology

“…Hyperlactemia, a feature of both post surgical SIRS [27] and sepsis [28] could be indicative of either inadequate oxygen delivery or an inability to use oxygen. H2O2 may favour aerobic glycolysis as a less energetic but less catabolic pathway designed to aid recovery [29].…”