Blood Gas Analysis


significant inverse relationship with mortality (p=0.04). The investigators found an approximately 11% decrease likelihood of mortality for each 10% higher lactate clearance. Finally, patients with a lactate clearance ≥10% had a lower 30- and 60-day mortality rate compared with patients with a <10% lactate clearance (37.5 versus 67.7% and 42.5 versus 71.0%), respectively, (p=0.004 and p=0.007, respectively).21


This is


consistent with efforts emphasizing the importance of recognizing high lactate as a sign of tissue hypoperfusion and initiating treatment in the earliest hours of severe sepsis presentation.8,22–24


Lactate and Early Goal-directed Therapy EGDT8,23


and implementation of sepsis bundles24 for the early


management of severe sepsis and septic shock has become the standard of care in the ED and ICU. Rivers et al.8


demonstrated that


interventions that adjusted cardiac perfusion to balance oxygen delivery with oxygen demand provided significant benefits with respect to outcome in patients with severe sepsis and septic shock. This study compared in-hospital mortality rates in patients randomized to EGDT or standard therapy in the first six hours of care. Parameters of central venous oxygen saturation, lactate concentration, base deficit, and pH were monitored during the first six hours of resuscitation and the following interval (seven to 72 hours) to determine the efficacy of the two therapies and in-hospital mortality. The two patient groups were similar in risk factors at baseline (lactate levels, APACHE II scores, and perfusion parameters). During the seven- to 72-hour interval, the patients assigned to EGDT has a significantly improved central venous oxygen saturation (mean ± standard deviation [SD]) 70.4 ± 10.7% compared with 65.3 ± 11.4% in the group assigned to standard care (p=0.009). EGDT was associated with a lowering of lactate concentration (3.0 ± 4.4 versus 3.9 ± 4.4mEq/l; a lowering of base deficit (2.0 ± 6.6 versus 5.1 ± 6.7mEq/l; and a higher pH (7.40 ± 0.12 versus 7.36 ± 0.12 than patients receiving standard care.


Additionally, during the same period, APACHE II scores were significantly improved, indicating less severe organ dysfunction in the patients assigned to EGDT than in those assigned to standard therapy; (13.0 ± 6.3 versus 15.9 ± 6.4; p<0.001).8


Subsequently, guidelines for


protocolized management of severe sepsis and septic shock have incorporated measurement of lactate as soon as possible on arrival, as a primary indicator of tissue hypoperfusion, and initiation of treatment when lactate is ≥4mEq/l, even in patients who are not hypotensive. However, these authors state that “although lactate concentration may lack precision as a measure of tissue metabolic status, elevated levels in sepsis support aggressive resuscitation.”22,24


Is Lactate Reliable?


While hyperlactatemia is thought to be an indication of the metabolic stress response, energy failure, and impaired organ perfusion, it can be present under stable oxygenation and hemodynamic conditions.25,26 Additionally, elevated lactate concentrations can be found irrespective


1. 2.


3. Duke T, Dysoxia and lactate, Arch Dis Child, 1999;81:343–50.


Weil MH, Afifi AA, Experimental and clinical studies on lactate and pyruvate as indicators of the severity of acute circulatory failure (shock), Circulation, 1970;41:989–1001. Mizok BA, Falk JL, Lacic acidosis in critical illness, Crit Care


4. Med, 1992;20:80–93.


Khosravani H, Shahpori R, Stelfox HT, et al., Occurrence and adverse effect on outcome of hyperlactatemia in the critically ill, Crit Care, 2009;13:R90.


5. De Backer, Lactic Acidosis, Int Care Med, 2003;29:699–702. This was evident in the study by Revelly et al.6 evaluating the


mechanisms leading to hyperlactatemia in patients with severe sepsis or cardiogenic shock. In these patients, elevated lactate levels were related to increased production from increased glucose turnover from concomitant hyperglycemia and not impaired lactate clearance. Therefore, treatment aimed at correction of hyperglycemia and tissue perfusion could result in decreased lactate levels and improved patient outcomes.6,27


Summary


Hyperlactatemia occurs in nearly half of all patients admitted to the ICU, and presentation with or development of hyperlactatemia is associated by significantly increased mortality. While there are multiple factors that may contribute to high lactate production or low lactate clearance, lactate levels have been found to increase the risk for death directly and proportionately. Currently, elevated lactate levels of ≥4mEq/l, if recognized at any time, stimulates EGDT, but evidence suggests a lower lactate threshold should be established for resuscitation to be most effective.


In modern ICUs the frequent measurement of lactate using blood glucose analyzers is useful in identifying patients at increased risk for death and serve as an early marker of a potentially reversible state. While lactate measurement as an optimal guide to the end-point of resuscitation remains controversial, it is superior to other markers of resolution of tissue hypoxia and hypoperfusion. This evidence holds true for all patients with severe sepsis or shock regardless of the underlying pathology. Consideration for future research should be given to:


• • •


whether the serum lactate threshold used to prompt EGDT need be adjusted downward;


whether serum lactate should be measured prior to arrival to the ED to take advantage of the golden hours and optimize resuscitation; and


whether serum lactate should be used to risk stratify patients in the ED and ICU to determine which patients would potentially benefit most from aggressive resuscitation strategies. n


6. 7.


Revelly JP, Tappy L, Martinez A, et al., Lactate and glucose metabolism in severe sepsis and cardiogenic shock, Crit Care Med, 2005;33(10):2235–40.


Manikis P, Jankowski S, Zhang H, et al., Correlations of serial blood lacate levels to organ failure and mortalilty after


of the presence of lactic acidosis, and may precede clinical signs which appear at a critical stage.25


In fact, elevated lactate may be the only


indication of tissue hypoxia and anaerobic glycolysis when blood pressure, cardiac output, and urine output are within clinically acceptable ranges. Levraut et al.26


demonstrated that a combination of


low lactate production and low clearance could mask abnormal lactate metabolism in septic patients with normal or near normal lactate levels. In this prospective observational study the investigators found that when lactate levels were the same in survivors and non-survivors, production and clearance were higher in sepsis survivers at 28 days.26 Under these circumstances, lactate production and low lactate clearance could be the expression of very different metabolic situations with opposing effects on prognosis.


54


US RESPIRATORY DISEASE


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84