in this issue , gutierrez et al .   compared simultaneous measurements of blood lactate concentrations in the right atrium and pulmonary artery in critically ill patients . they found decreases in both blood lactate concentrations and venous blood oxygen saturation in gradients from the right atrium to the pulmonary artery . these gradients are presumably produced by mixing right atrial blood with coronary venous blood , which has lower lactate concentrations and blood oxygen saturation . more interestingly , in this study , the lactate gradient was inverted in three patients , suggesting myocardial ischemia , a condition associated with lactate release by the heart . blood lactate levels are typically elevated in hypoperfusion states when pyruvate can not enter the krebs cycle as the cellular oxygen supply becomes insufficient . the pyruvate is shunted to lactate through the enzyme lactate dehydrogenase , producing only two molecules of energy - rich atp for every two molecules of pyruvate ( from one molecule of glucose ) , compared with 38 molecules of atp for each glucose molecule through the aerobic mitochondrial process when sufficient oxygen is present . this causes the lactate to pyruvate ratio to increase ( the normal value is around 10:1 ) . once molecular oxygen is again available , assuming that mitochondrial function is preserved , the excess lactate is rapidly metabolized back through pyruvate into carbon dioxide and water via the krebs cycle . lactate in the blood is metabolized mainly by the liver ( 50% ) and kidney ( 20% ) . striated muscles , the heart and the brain can also metabolize lactate and , in some conditions , this clearance can be significant . traditionally , elevated blood lactate levels in hemodynamically unstable patients have been interpreted as reflecting acute circulatory shock . the speed at which lactate is cleared from the blood through vigorous resuscitation strongly correlates with ultimate outcome , including mortality and organ failure . the best chances of survival occur when resuscitation efforts result in lactate clearance to normal values within 12 to 24 h [ 4 - 6 ] . blood lactate concentration represents a global marker of tissue oxygenation but does not reflect loco - regional tissue oxygenation . the venoarterial lactate gradient on both sides of an organ can be used to detect regional hypoxia . de backer et al .   demonstrated that lung lactate production occurs in subjects with acute lung injury states but not in patients with normal lungs , cardiogenic pulmonary edema or pneumonia . other organs can also produce lactate and experimental studies suggest that the gut can produce lactate in sepsis , which is probably from anaerobic metabolism as the portal lactate to pyruvate ratio is increased . the investigation of splanchnic lactate turnover in humans is much more complicated as access to the portal vein is not possible outside the operating room . since the liver is usually able to clear this small amount of gut - produced lactate , splanchnic ischemia may go unsuspected . de backer et al .   reported that hepatosplanchnic lactate release is uncommon in patients with severe sepsis and is not related to arterial lactate concentrations , abdominal infection or signs of gut or liver dysoxia . inadequate myocardial performance , characterized by left ventricular systolic depression and diastolic dilatation , is a common and early complication of septic shock . a possible direct cardiac myocytotoxic effect of bacterial endotoxins or mediators ( e.g. cytokines or reactive oxygen species ) induced by the infectious process and produced by activated leukocytes , macrophages and endothelial cells   should be considered . studies in humans   strongly argue against a decrease in coronary blood flow in the pathogenesis of this sepsis - induced cardiac injury . however , a dysfunctional microcirculation that produces regional flow disturbances and abnormal tissue oxygenation is a hallmark of septic shock , and may cause relative ischemia in various organs , including the heart . moreover , regional myocardial ischemia may well be present in sepsis patients with identifiable coronary risk factors or coexistent coronary artery disease . in this context , the diagnosis of myocardial ischemia remains difficult in sedated and mechanically ventilated patients with sepsis . indeed , elevation of troponin can be detected in a variety of conditions other than acute myocardial ischemia , especially in critically ill patients with severe sepsis . the use of the right atrium to pulmonary artery lactate gradient reported by gutierrez et al . in this issue however , the amplitude of the lactate gradients reported in this study   is close to the measurement error of blood lactate concentrations provided by many blood gas analyzers . further studies are needed to confirm these results and to study the usefulness of this lactate gradient in the detection of myocardial ischemia in critically ill patients .
inadequate myocardial performance is a common complication of severe sepsis . 
 studies in humans strongly argue against a decrease in coronary blood flow in the pathogenesis of this sepsis - induced cardiac injury . 
 moreover , regional myocardial ischemia may well be present in sepsis patients with coexistent coronary artery disease . 
 nevertheless , the diagnosis of myocardial ischemia remains difficult in patients with sepsis , since elevation of troponin in these patients can be the result of a variety of conditions other than acute myocardial ischemia . 
 the use of the right atrium to pulmonary artery lactate gradient could perhaps help the clinician in detecting myocardial ischemia in patients with sepsis .