From tissue perfusion to metabolic marker: assessing organ competition and co-operation in critically ill patients?

1999 ◽  
Vol 25 (9) ◽  
pp. 890-892 ◽  
Author(s):  
X. M. Leverve
2005 ◽  
Vol 33 ◽  
pp. A126
Author(s):  
Jacqueline Wu ◽  
Olusola Soyemi ◽  
Matthias Walz ◽  
Ye Yang ◽  
Babs Soller ◽  
...  

CHEST Journal ◽  
2013 ◽  
Vol 143 (6) ◽  
pp. 1799-1808 ◽  
Author(s):  
Nasirul J. Ekbal ◽  
Alex Dyson ◽  
Claire Black ◽  
Mervyn Singer

2019 ◽  
Vol 47 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Patrick J. Gleeson ◽  
Ilaria Alice Crippa ◽  
Wasineenart Mongkolpun ◽  
Federica Zama Cavicchi ◽  
Tess Van Meerhaeghe ◽  
...  

2016 ◽  
Vol 63 (2) ◽  
pp. 41-47
Author(s):  
Jelena Velickovic ◽  
Guillaume Thiery ◽  
Dejan Velickovic ◽  
Goran Rakic ◽  
Krstina Doklestic ◽  
...  

Many critically ill patients with stabilized hemodynamics die with signs of multiorgan failure. One of the reasons is the derangement of microcirculation and tissue perfusion. It has been shown that microcirculatory distress left uncorrected for 24 hours is single independent predictor of mortality in sepsis. Serum lactate is the only indicator of microcirculatory changes that is monitored routinely in all critically ill patients. It has been widely believed that hyperlactatemia in sepsis is marker of tissue hypoxia and indicates the existence of oxygen debt resulting from tissue hypoperfusion and anaerobic glycolysis. Attempts to correct hyperlactatemia by delivering supranormal oxygen amounts have failed in septic patients. The term ?shock? lactate refers to hyperlactatemia originating from oxygen debt. Human studies failed to demonstrate the relationship between hyperlactatemia and tissue hypo-perfusion in the late phase of sepsis. Adrenergic stimulation in sepsis and accelerated aerobic glycolysis have been proposed as a likely mechanism of hyperlactatemia. Both exogenous and endogenous catecholamines are correlated with septic hyperlactatemia. Aerobically generated lactate mediated by cytokines is called ?stress? lactate and may serve as a marker of hypermetabolism rather than tissue hyperperfusion. Many studies and guidelines recommend targeting resuscitation to normalize lactate in septic patients. These recommendations need to be taken with reserve. Since lactate serves, under stress, as a source of energy and can be used as a fuel for oxidation as well as for glucose production, attempts to normalize lactate might be even harmful. Although high lactate clearance, due to a correction of oxygen debt contributes to a better prognosis in sepsis, the unusual complexity of lactate makes it almost impossible to make an unambiguous therapeutic decision, when comes to a lactate-guided treatment in sepsis.


1994 ◽  
Vol 28 (11) ◽  
pp. 1273-1284 ◽  
Author(s):  
Joseph F. Dasta ◽  
Brian L. Erstad

OBJECTIVE: To discuss the limitations of conventional monitoring techniques of shock and examine more recent monitoring techniques that are used to titrate therapies to attain supranormal oxygen transport goals. DATA SOURCES: Review articles and investigations published since 1973. STUDY SELECTION: Articles were selected if they examined the monitoring or treatment of shock. Emphasis was placed on finding investigations involving humans that used innovative methods to assess and treat inadequate tissue perfusion. DATA EXTRACTION: Data were extracted primarily from original investigations and review articles published in or translated into English. DATA SYNTHESIS: The conventional monitoring of shock often fails to detect inadequate tissue perfusion, which may lead to inadequate resuscitation of patients, resulting in increased morbidity and mortality. Attainment of supranormal values for oxygen transport variables has been associated with improved outcomes, especially in patients with hypovolemic shock or septic shock. Additionally, interventions used to increase these variables to supranormal values have resulted in improved survival in high-risk preoperative patients with hypovolemic or septic shock, but not in severely ill postoperative patients with multiple complications. CONCLUSIONS: Efforts to increase oxygen transport variables to supranormal values cannot be recommended routinely for all critically ill patients. Preoperative patients in early stages of hypovolemic or septic shock may benefit from therapies titrated to achieve supranormal goals, but patients in later stages of illnesses may be harmed by such attempts. Questions remain regarding how quickly and how long the oxygen transport variables should be elevated. The most effective and least toxic therapeutic interventions for increasing the variables need to be determined.


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