Lactate is a molecule produced continuously by the body, serving a normal role in metabolism. It is a byproduct of converting glucose into energy, especially when demand is high or oxygen is limited, such as during strenuous exercise. Hyperlactemia is the term used to describe an excessive amount of lactate in the bloodstream, defined by a persistent elevation above the normal resting level of less than 2 millimoles per liter (mmol/L). This signifies an imbalance between lactate production and clearance.
Defining Elevated Lactate Levels
Lactate production occurs primarily through anaerobic glycolysis, a metabolic pathway activated when cells cannot meet energy needs through oxygen-dependent metabolism. During this process, glucose is converted to pyruvate, which is then rapidly converted to lactate when oxygen is scarce. This conversion allows the cell to quickly generate a small amount of energy and recycle necessary cofactors.
Under normal conditions, the body efficiently manages this lactate load. The liver is the main organ responsible for clearing lactate from the blood, converting it back into glucose through the Cori cycle. The kidneys also contribute to lactate clearance, metabolizing approximately 30% of the total load. Hyperlactemia occurs when lactate production dramatically exceeds the capacity of the liver and kidneys, or when clearance mechanisms are impaired.
Clinically, a lactate level between 2 and 4 mmol/L is considered hyperlactemia, which may occur without causing significant changes to the blood’s acidity. This elevation acts as a warning sign, indicating underlying metabolic stress or tissue hypoperfusion that requires investigation. A normal resting lactate level is typically less than 1.0 mmol/L.
Underlying Causes and Contributing Factors
Causes of elevated lactate are clinically categorized into two main groups, reflecting whether the root issue is insufficient oxygen delivery or a metabolic problem. The most common and severe form is Type A hyperlactemia, which is directly linked to inadequate oxygen supply to the body’s tissues (tissue hypoxia or hypoperfusion). This oxygen debt forces cells to rely heavily on anaerobic metabolism, leading to lactate overproduction.
Type A causes include all forms of shock, such as septic shock, cardiogenic shock from heart failure, or hypovolemic shock from major blood loss. In these situations, blood flow and oxygen delivery to vital organs are compromised, and the resulting tissue distress drives the lactate level upward. Other Type A causes include cardiac arrest or regional ischemia, such as a blocked artery.
Type B hyperlactemia occurs when there is no apparent lack of oxygen delivery, but the body produces too much lactate or cannot clear it effectively. This category involves underlying diseases or external factors that disrupt normal cellular metabolism. Liver failure is a primary Type B cause because the liver’s ability to convert lactate back to glucose is compromised.
Certain medications can interfere with cellular processes, leading to a Type B elevation. Other conditions, such as malignancies, diabetic ketoacidosis, or severe thiamine deficiency, can create metabolic dysfunction that overwhelms the body’s ability to handle the lactate load. Even extreme muscle activity, like a seizure or intense exercise, can temporarily cause Type B hyperlactemia due to rapid production.
Medications associated with Type B hyperlactemia include:
- The diabetes drug metformin
- Some antiretroviral therapies for HIV
- Excessive doses of adrenaline-like medications
When Hyperlactemia Becomes Lactic Acidosis
Hyperlactemia becomes lactic acidosis when the persistently high lactate level causes a significant drop in the blood’s pH. This occurs because lactate is produced as part of lactic acid, which quickly dissociates in the blood, releasing hydrogen ions. The body’s buffering systems, primarily bicarbonate, are overwhelmed by the influx of these hydrogen ions.
Lactic acidosis is typically defined as a lactate concentration greater than 4 mmol/L accompanied by a blood pH below 7.35. Below this pH threshold, the acidic environment can interfere with enzyme function and impair the performance of organs, including the heart. Untreated, severe lactic acidosis can lead to multi-organ dysfunction and is associated with a poor prognosis.
Symptoms of severe lactic acidosis are often related to the underlying cause. The acidosis itself can manifest as rapid, deep breathing, which is the body’s attempt to expel carbon dioxide and raise the blood pH. As the condition worsens, patients may experience confusion, altered mental status, and a rapid heart rate as the body tries to compensate for poor circulation. The level of lactate serves as a marker of the severity of the underlying illness.
Treatment Focus and Recovery
The treatment strategy for hyperlactemia is centered on identifying and resolving the underlying cause, as attempting to lower the lactate level directly without addressing the source is generally ineffective. For Type A hyperlactemia, the primary goal is to restore adequate oxygen delivery and tissue perfusion. This often involves aggressive fluid administration to correct low blood volume and the use of vasopressors to maintain blood pressure and circulation. In cases of septic shock, this includes the rapid administration of antibiotics to treat the infection.
For Type B causes, treatment involves discontinuing any offending medications or treating the specific metabolic derangement, such as providing thiamine supplementation for deficiency. Serial measurements of the lactate level are used to monitor the effectiveness of these interventions. A falling lactate concentration indicates that the treatment is successfully resolving the metabolic stress.