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lactate

Definition (1):
  • Hyperlactatemia occurs when lactate produrction exceeds lactate consumption. It also signifies the addition of a number of protons equivalent to the number of excess lactate ions, regardless of the prevailing acid-base status. The major causes have been divided into disorders associated with tissue hypoxia (type A) and disorders in which tissue hypoxia is absent (type B).
(Patho)physiology (1):
  • The reaction integral to the generation or consumption of lactate is: pyruvate + NADH + H+ <-> lactate + NAD+.
  • In tissue hypoxia, lactate is overproduced and underutilized as a result of impaired mitochondrial oxidation. Hyperlactatemia can also result from aerobic glycolysis, an effective, albeit inefficient, mechanism for rapid generation of ATP (in sepsis, severe asthma, extensive trauma, cardiogenic or hemorrhagic shock, severe heart failure and pheochromocytoma). Aerobic glycolysis and tissue hypoxia are not mutually exclusive; under certain circumstances, both can contribute to hyperlactatemia.
  • Drugs that impair oxidative phosphorylation, such as antiretroviral agents and profolol, can augment lactic acid production and on rare occasions cause severe lactic acidosis.
Measurements:
  • An elevated serum anion gap, particularly a value >30 mmol/l, can provide supportive evidence. Correction of the anion gap for the effect of serum albumin can improve its sensitivity, but serum anion gap lacks sufficient sensitivity or specificity to serve as a screening tool for lactic acidosis (1).
  • The lower limit of the normal range for the blood lactate level, 0.5 mmol/l, is consistent among clinical laboratories, but the upper limit can vary substantially (1.0-2.2 mmol/l) (2,3).
  • Lactate can be measured in arterial or venous blood, since the values are virtually interchangeable (2).
  • In patients with severe circulatory compromise, central venous blood more accurately reflects the acid-base status of tissues that does arterial or peripheral venous blood (2). However, it remains unproven whether monitoring central venous blood gases in patients with severe hypoperfusion improves clinical outcomes. Monitoring of arterial blood gases is, of course, required for assessing pulmonary gas exchange (1).
Treatment:
  • Supporting the circulation and ventilation: acidemia blunts the response to catecholamines, thereby increasing the required dose. High doses of catecholamines can aggravate hyperlactatemia by reducing tissue perfusion or overstimulating the beta2-adrenoceptor (1). The opinions differ regarding which solution should be favored (4).
  • Improving the microcirculation.
  • Initiating cause-specific measures.
  • Base administration: the absence of evidence that bicarbonate therapy is beneficial has been attributed primarily to two adverse events that occur with its administration: intracellular acidification due to the accumulation of carbon dioxide after bicarbonate infusions and a pH-dependent decrease in levels of ionized calcium, a modulator of cardiac contractility. Other buffers have been developed to minimize carbon dioxide generation. Only THAM (tris-hydroxymethyl aminomethane) is currently available for clinical use (1).
  • Goals of Therapy (1):
    • Hemodynamic: mean arterial blood pressure 65-70 mmHg, heart rate <100/min, central venous pressure 8-12 mmHg, pulmonary wedge pressure 12-15 mmHg in patients receiving mechanical ventilation, urine output >0.5 ml/kg/h.
    • O2 delivery: hemoglobin level >7g/dl (but can vary on the basis of cardiovascular status of patient), arterial O2 saturation >=92%, central venous O2 saturation >=70%.
    • Acid-base measures: arterial blood pH >7.2, PaCO2 appropriate for [HCO3-] (in lung-protective ventilation, PaCO2 is maintained at hypercapnic levels).
Future risks:
  • There is a dose-response relationship between lactate levels and mortality: the higher the level, the greater the risk of death (2).
References:
  1. Jeffrey A. Kraut et al. Lactic Acidosis. N Engl J Med. 2014;371(24):2309-2319: full text.
  2. O. Kruse et al. Blood lactate as a predictor for in-hospital mortality in patients admitted acutely to hospital: a systematic review. Scand J Trauma Resusc Emerg Med. 2011;19(74): full text | pdf.
  3. DA del Portal et al. Emergency department lactate is associated with mortality in older adults admitted with and without infections. Acad Emerg Med. 2010;17:260-8: full text | pdf.
  4. FJ Gennari. Intravenous fluid therapy: saline versus mixed electrolyte and organic anion solutions. Am J Kidney Dis. 2013;62:20-2: full text | pdf.