Second, exchange for another anion such as Cl - or HCO 3 - facilitates lactate transport across the cell membrane. By this mechanism lactate uptake by the cell e. In contrast, lactate efflux will increase during alkalemia, resulting in an increase in lactate levels during systemic alkalemia [6]. The increase in lactate levels during alkalemia could also be related to the stimulation of phosphofructokinase in these conditions, resulting in increased glycolysis and thus increased lactate production.
Although a decrease in each of the components can cause a decrease in DO 2 , decreases in hemoglobin levels and arterial oxygen saturation are usually accompanied by compensatory increases in cardiac output so that DO 2 can be maintained to meet oxygen demand [8] and thus generally do not result in tissue hypoxia [9].
When this compensatory mechanism fails, DO 2 will decrease more rapidly in these conditions [10]. When DO 2 falls below a critical level, oxygen demand can no longer be met and oxygen consumption starts to fall coincided with an increase in blood lactate levels Fig. This phenomenon supply dependency has been demonstrated during experimental decreases in hemoglobin levels, arterial oxygen saturation and cardiac output [].
For obvious reasons, effects of lowering DO 2 to critical levels in humans are not well studied. In patients and healthy volunteers, acute decreases in hemoglobin levels are met by compensatory increases in cardiac output to maintain tissue oxygen delivery [8]. In patients with increased blood lactate levels, oxygen consumption fell immediately when DO 2 was lowered [14]. Ronco et al [16] also showed that lowering DO 2 below a critical level resulted in a decrease in oxygen consumption and a rise in blood lactate levels.
In critically ill patients, Vincent et al [17] showed that oxygen consumption increased only in patients with increased blood lactate levels when DO 2 was increased by the infusion of dobutamine. Interpretation of increased blood lactate levels in patients with sepsis can be difficult [7]. However, in the early phase of septic shock, increased blood lactate levels have also been associated with the presence of supply dependency and thus tissue hypoxia [18].
Should we therefore conclude that in clinical practice, increased blood lactate levels should be regarded as an indicator of the presence of tissue hypoxia [19]? In the absence of cellular hypoxia, dysfunction of the PDH enzyme complex also results in an increase in pyruvate levels Fig. Increased aerobic glycolysis increases intracellular pyruvate levels when there is no need for increased ATP production i.
Protein breakdown results in an increased amino acid disposal that may increase pyruvate levels in the process of gluconeogenesis Fig. Increased lactate production in the absence of cellular hypoxia has been documented in clinically relevant experimental settings sepsis, chatecholamine treatment and in patients [21,22].
Dysfunction of the PDH enzyme has been documented in experimental and clinical sepsis and could also be related to the decreased lactate clearance in septic patients. In addition, decreased blood flow decreased delivery of lactate to liver and kidney could influence lactate clearance. Finally, persistent cellular hypoxia in the presence of a hemodynamically stable condition could be related to decreased clearance Fig.
Plasma levels of lactate not only result from the production of the molecule but also from its clearance. Lactate clearance occurs predominantly in the liver and kidney, whereas during hyperlactatemia muscles also metabolize lactate. Decreased lactate clearance rather than increased production could be an important cause of increased blood lactate levels in septic patients following hemodynamic stabilization [23].
However, also in patients following cardiac surgery and in patients with liver dysfunction, clearance of blood lactate is deranged [24,25]. The relationship between lactate and hydrogen ion concentration is far from straightforward. Although the relationship between lactate levels and indices of metabolic acidosis are reasonable in low-flow states, the production of unmeasured ions, the presence of renal dysfunction and the arterial p CO 2 simply influenced by manipulating the mechanical ventilator are probably related to the weak-to-absent correlation between arterial pH, base excess or base deficit and lactate levels in the general intensive care population and patients with sepsis in particular [27,28].
Groeneveld et al [29] already showed that despite similar lactate levels, patients with septic shock had a lower arterial pH than patients with non-septic shock. In this study the severity of sepsis, as related to ultimate survival, also influenced the relationship between lactate level and arterial pH.
From the above we can conclude that increased blood lactate levels with or without concomitant acidosis reflect a complex metabolic disturbance in which increased aerobic and anaerobic production and decreased clearance are important elements.
Furthermore, the importance of these elements differs in different disease states. It is therefore no surprise that the reflection of such a complex metabolic disturbance is not met by clinical signs of critical illness, including the classical signs of shock [30].
Also, other laboratory abnormalities, usually coinciding critical illness, do not reflect blood lactate levels or changes in blood lactate levels [28,31]. In addition, a given level of oxygen delivery or oxygen consumption also cannot predict the presence of oxygen supply dependency or increased blood lactate levels [32]. This underlines the importance of measuring lactate levels rather than estimating them from other biochemical variables.
When first described Gaglio , the measurement of lactate levels required the collection of mL blood and took several days to complete. In , Broder and Weil [33] were the first to use a photospectrometric method to measure lactate levels in whole blood, decreasing turnaround time substantially. With this they set a trend in the monitoring of blood lactate levels in critically ill patients.
The labor-intensive aspect of the early measurement technique limited the widespread use, as results were usually available long hours after therapeutic decisions had to be made. Using a device like this can simultaneously provide information on hemoglobin levels, oxygen saturation and blood lactate levels.
Recently a handheld device using a reflective photometry method has been introduced and validated in emergency department patients [34] and ICU patients [35].
With this handheld device blood lactate measurements can be made using one drop of whole blood, and results are available within 60 seconds. This relatively cheap and easy-to-perform method can be used for rapid lactate measurements in emergency situations [36]. In the intensive care unit, blood drawn from an arterial line is usually used to measure blood lactate levels.
However, mixed venous blood can also be used to measure blood lactate levels in critically ill patients [37,38]. When capillary or peripheral venous blood is used, damming of blood and muscle activity should be avoided [39].
Collected blood samples should be stored on ice and measurements of blood lactate levels should be performed rapidly when metabolism of red and white blood cells is not stopped by the addition of e. Lactate monitoring needs to be incorporated into an interventional and therapeutic plan in order for the patient to benefit from these measurements.
Could such an easily obtainable parameter of complex abnormalities then be used to assign patients to an interventional plan? More specifically, could lactate levels be used to identify patients that would benefit from intensive care admission?
For this, lactate levels should be related to risk of morbidity and mortality from a disease state that is best managed in an intensive care unit. For more than 25 years, blood lactate levels have discriminated patients with less morbidity from patients with more morbidity and survivors from non-survivors in many forms of surgical interventions, trauma and critical illness [33,]. Also, most patients with increased lactate levels have a high risk of compromised vital organ functions [2]. In addition, limited clearance of lactate in patients without circulatory failure is still related to increased mortality in patients with sepsis [46].
Although the relationship between lactate and acidosis is complex, the combination of increased lactate levels and acidosis bears a high mortality [44]. Some studies showed that in specific patient groups, lactate levels were better predictors of survival and development of organ failure than complex scoring systems like APACHE II [47].
In a recent study, Smith et al [48] showed that blood lactate levels could discriminate patients with high risk of morbidity and mortality from patients with relative low risk. The portability of the lactate measuring devices, the ease and speed of the measurements could thus be important factors in the clinical utility of lactate levels as indicators for intensive care admission. Correction of hyperlactatemia by increasing the metabolism of pyruvate and hence lactate has no significant effect on mortality in critically ill patients.
Dichloroacetate enhances the activity of the pyruvate dehydrogenase complex, thus decreasing blood lactate levels. Both experimental and clinical studies have shown that administration of dichloroacetate decreases blood lactate levels during sepsis and septic shock [49,50,50]. However, in a recent controlled clinical trial patients , administration of dichloroacetate in critically ill patients with hyperlactatemia and metabolic acidosis had no significant effect on hemodynamics and survival [51].
Also correction of the metabolic acidosis accompanying hyperlactatemia has not been shown to improve hemodynamics, tissue hypoxia and survival in critically ill patients [52,53]. The mainstay of therapy in patients with increased blood lactate levels is improvement of tissue oxygen delivery.
This is usually accomplished by increases in DO 2. Fluid resuscitation, hemoglobin substitution and maintenance of arterial oxygen saturation are frequently used to improve tissue oxygen delivery. However, fluid resuscitation and inotropes to increase cardiac output have consistently been found to improve tissue oxygen delivery in patients with tissue hypoxia and thus remain the mainstay of therapy in these circumstances []. Few studies have prospectively studied the effect of using lactate levels to guide therapy.
Blow et al [59] vigorously resuscitated trauma patients with persistent hyperlactatemia to normalize blood lactate levels. Patients who failed to normalize lactate levels within 24 hours had a poor outcome whereas with patients in whom blood lactate levels returned to normal within 24 hours outcome was improved when compared with a historic control group.
Similar findings have been reported by others. A measurement of blood lactate should be part of the evaluation of every critically ill patient unless the diagnosis is obvious and immediate intervention surgery is necessary like in ruptured aneurysm. Especially in the early stages of critical illness, increased blood lactate levels indicate tissue hypoxia and insufficient compensatory mechanisms. A sad but illustrative case will clarify this. A young trauma victim was admitted to our emergency department with fractures of his upper and lower legs.
He was conscious, adequate and oriented in time, place and persons. Blood was drawn for routine evaluation including a blood lactate level. An echo of the abdomen was immediately performed and showed no abnormalities. CPR was ineffective and the patient died in the ER.
Despite his adequate conscious and stable hemodynamics this patient was running out of compensatory mechanism and from this lactate level it was clear that something dramatic was about to happen. In addition to the initial measurement of blood lactate levels, subsequent measurements inform the treating physician on the adequacy of the resuscitation [61].
Persisting increased blood lactate levels or a failure to decrease lactate levels should be followed by increasing oxygen delivery. This could be accomplished by increasing cardiac output [62,63] or microcirculatory blood flow with vasodilating agents like prostacyclin [64] or nitroglycerin [65]. In postoperative care we measure lactate levels routinely and increase oxygen delivery whenever lactate levels rise above 2. Increased blood lactate levels serve well as a marker of a complex metabolic derangement related to increased production, decreased clearance or a combination of both.
Clinicians should understand these complex processes, appreciate the usefulness and the limitations of monitoring blood lactate levels. Measurements of blood lactate levels should never replace a complete clinical evaluation. Rather, adding lactate measurements to clinical judgment and easily obtainable clinical variables enhances its predictive power [66,67]. The presence of increased blood lactate levels, especially in combination with acidosis, should urge the clinician to restore a probable imbalance between oxygen demand and oxygen delivery to the tissues, as this is the most frequent cause of increased blood lactate levels.
Increased lactate levels have been consistently associated with morbidity and mortality in a wide range of disease states for many years. Therefore the presence of increased blood lactate levels should prompt the clinician to initiate both diagnostic and immediate therapeutic actions and intensive care admission should be considered.
May contain information that is not supported by performance and intended use claims of Radiometer's products. See also Legal info. Radiometer and acutecaretesting. Sustainable threshold values are the most common assessment outcome and are used by endurance athletes primarily.
To determine sustainable lactate levels, subjects perform exercise at incremental loads, for 12 to 15 minutes, while having blood drawn in droplets either from a finger or earlobe.
A stationary bicycle, a personal bike and stationary trainer or a treadmill are typically used. The test starts with an easy-moderate work load which is maintained for a minutes. OBLA is the point at which lactate begins to accumulate in the blood at an accelerated rate. To determine peak, tolerated or clearance lactate levels involves other maximal effort tests and will not be reviewed in this document.
Lactate values cannot be used in every-day training but follow-up lactate values can be used as a measure of progress. Other information such as lactate endurance levels lactate values at a given heart rate or power output can also be tested and compared to subsequent tests.
One of the better ways to incorporate this information into training is to use the OBLA data to establish field time trail parameters. Once those are established the time trails can be re-assessed periodically to determine improvements in the field with lab reassessments used to establish new training parameters. All rights reserved. NursingCenter Blog. Continuing Education More. Elevated Lactate — Not just a marker for sepsis and septic shock.
Share this on. You may also want to review the following resource Sepsis Guidelines and Protocols: Providing Care to Patients Lactate is an organic molecule produced by most tissues in the human body, with the highest production found in muscle. The body normally produces energy by way of aerobic metabolism, which requires oxygen to break down carbohydrates, amino acids, and fats.
Via glycolysis, glucose is converted into pyruvate, which enters the Krebs cycle to produce oxygen and adenosine triphosphate ATP or energy. In this pathway, pyruvate is metabolized by the enzyme lactate dehydrogenase LDH into lactate. Lactate can be measured from both venous and arterial blood.
Serum samples should be processed within 15 minutes to avoid falsely elevated results. If processing cannot occur within this time frame, the sample should be kept on ice. Hyperlactatemia and lactic acidosis may occur with an increase in lactate production, a decrease in lactate clearance, or a combination of both.
Alternately, in Type B lactic acidosis, the etiology may be related to toxic-induced impairment of cellular metabolism, local hypoperfusion i.
0コメント