The interpretation of perioperative lactate abnormalities in patients undergoing cardiac surgery

Abstract

Hyperlactataemia and lactic acidosis are commonly encountered during and after cardiac surgery. Perioperative lactate production increases in the myocardium, skeletal muscle, lungs and in the splanchnic circulation during cardiopulmonary bypass. Hyperlactataemia has a bimodal distribution in the perioperative period. An early increase in lactate levels, arising intraoperatively or soon after intensive care unit admission, is a familiar and concerning finding for most clinicians. It is highly suggestive of tissue ischaemia and is associated with a prolonged intensive care unit stay, a prolonged requirement for respiratory and cardiovascular support and increased postoperative mortality. Its presence should prompt a thorough search for potential causes of tissue hypoxia. In contrast, late-onset hyperlactataemia, a less well recognised complication, occurs 4 to 24 hours after completion of surgery and is typically associated with preserved cardiac output and oxygen delivery. Risk factors for late-onset hyperlactataemia include hyperglycaemia, long cardiopulmonary bypass time and elevated endogenous catecholamines. Although patients with this complication may have a longer duration of ventilation and intensive care unit length of stay than those with normolactataemia, an association with increased mortality has not been demonstrated. The discovery of late-onset hyperlactataemia should not delay the postoperative progress of an otherwise stable patient following cardiac surgery.