Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock

Kreymann, G.; Grosser, Sebastian; Buggisch, Peter; Gottschall, Claus; Matthaei, S.; Greten, H.

doi:10.1097/00003246-199307000-00015

Cited by 242 publications

(153 citation statements)

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“…Assuming that StO 2 was being measured accurately, this difference may have emerged due to impaired tissue oxygen consumption in sepsis, which correlates with the severity of sepsis. [19][20][21] This effect has also been observed by others. 22 These differences at lower ScVO 2 raise the possibility that adjunct measurement of StO 2 may be prognostic or have a role in the management of this patient subset.…”

Section: Discussionsupporting

confidence: 84%

Tissue Oxygenation Does Not Predict Central Venous Oxygenation in Emergency Department Patients With Severe Sepsis and Septic Shock

Napoli

Machan²,

Forcada³

et al. 2010

Academic Emergency Medicine

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Objectives: This study sought to determine whether tissue oxygenation (StO 2 ) could be used as a surrogate for central venous oxygenation (ScVO 2 ) in early goal-directed therapy (EGDT). Methods:The study enrolled a prospective convenience sample of patients aged ‡18 years with sepsis and systolic blood pressure <90 mm Hg after 2 L of normal saline or lactate >4 mmol, who received a continuous central venous oximetry catheter. StO 2 and ScVO 2 were measured at 15-minute intervals. Data were analyzed using a random coefficients model, correlations, and Bland-Altman plots.Results: There were 284 measurements in 40 patients. While a statistically significant relationship existed between StO 2 and ScVO 2 (F(1,37) = 10.23, p = 0.002), StO 2 appears to systematically overestimate at lower ScVO 2 and underestimate at higher ScVO 2 . This was reflected in the fixed effect slope of 0.49 (95% confidence interval [CI] = 0.266 to 0.720) and intercept of 34 (95% CI = 14.681 to 50.830), which were significantly different from 1 and 0, respectively. The initial point correlation (r = 0.5) was fair, but there was poor overall agreement (bias = 4.3, limits of agreement = )20.8 to 29.4).Conclusions: Correlation between StO 2 and ScVO 2 was fair. The two measures trend in the same direction, but clinical use of StO 2 in lieu of ScVO 2 is unsubstantiated due to large and systematic biases. However, these biases may reflect real physiologic states. Further research may investigate if these measures could be used in concert as prognostic indicators.ACADEMIC EMERGENCY MEDICINE 2010; 17:349-352 ª

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Section: Discussionsupporting

confidence: 84%

Tissue Oxygenation Does Not Predict Central Venous Oxygenation in Emergency Department Patients With Severe Sepsis and Septic Shock

Napoli

Machan²,

Forcada³

et al. 2010

Academic Emergency Medicine

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“…Kreyman et al [19] showed that energy expenditure decreases with severity of ill ness resulting in prevailing hypometabo lism in patients with severe sepsis and sep tic shock. One may speculate that a low er caloric intake by EN especially in the early phase of illness could be sufficient to maintain basal metabolism for survival and prevent metabolic stress.…”

Section: Discussionmentioning

confidence: 99%

Enteral nutrition is associated with improved outcome in patients with severe sepsis

Elke¹,

Kuhnt

Ragaller

et al. 2013

Med Klin Intensivmed Notfmed

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“…Patients in severe sepsis and septic shock display a 30% increase of oxygen consumption and baseline metabolism compared with normal basal values, but both are markedly reduced compared with "uncomplicated" sepsis (47). Once organ dysfunction develops, however, oxygen consumption and resting metabolic rate decrease, suggesting that, during multiple organ failure, patients seem to tolerate lower values of oxygen supply (48).…”

Section: Metabolic Changesmentioning

confidence: 99%

Molecular Events in the Cardiomyopathy of Sepsis

Flierl

Rittirsch

Huber‐Lang

et al. 2008

Mol Med

109

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Septic cardiomyopathy is a well-described complication of severe sepsis and septic shock. However, the interplay of its underlying mechanisms remains enigmatic. Consequently, we constantly add to our pathophysiological understanding of septic cardiomyopathy. Various cardiosuppressive mediators have been discovered, as have multiple molecular mechanisms (alterations of myocardial calcium homeostasis, mitochondrial dysfunction, and myocardial apoptosis) that may be involved in myocardial dysfunction during sepsis. Finally, the detrimental roles of nitric oxide and peroxynitrite have been unraveled. Here, we describe our present understanding of systemic, supracellular, and cellular molecular mechanisms involved in sepsis-induced myocardial suppression. SYSTEMIC, SUPRACELLULAR MECHANISMS Decreased Coronary Blood FlowOne of the first suggestions was that reduced coronary perfusion in the septic heart might be responsible for a setting of global cardiac ischemia. This hypothesis was soon abandoned after direct measurements of coronary blood flow were obtained, showing no reduced, but rather increased, coronary blood flow (22,23). In later studies, however, increased levels of plasma troponin were observed and correlated with the severity of myocardial depression during sepsis and septic shock (24). Myocardial necrosis could not be observed in patients who died from septic shock (3,25), however, raising the question whether increases in troponin were due to cytokine-induced, transient increases in cardiomyocyte membrane permeability to troponin. To date, this remains to be determined. Alterations of MicrovasculatureThere is now increasing evidence that sepsis and septic shock leads to changes of the myocardial microvasculature. In a canine model of endotoxemia, maldistribution of heterogeneous coronary blood flow has been reported (26). These findings might be caused by endothelial swelling and nonocclusive intravascular fibrin deposits in the microvasculature (27). In parallel, activated cardiomyocytes from septic mice promoted transendothelial migration and activation of circulating neutrophils into the interstitium (28) where these cells may augment the sepsis-induced intracardial inflammation, and contribute to an increased vascular leakage, which has been described to also impair cardiac function and compliance secondary to myocardial edema (29,30). Yet, studies have failed to confirm cellular hypoxia in a murine sepsis model (31). Cardiosuppressing Circulating Proinflammatory MediatorsAnother hypothesis suggested circulating myocardium-depressing factors as the cause of septic cardiomyopathy (32). Parrillo et al. (33) confirmed the existence of a cardiodepressant substance by incubating isolated rat cardiomyocytes with serum obtained from septic shock patients, leading to decreased amplitude and velocity of cardiomyocyte shortening. Levels of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and the complement anaphylatoxin, C5a, are known to be elevated in the circulation during sepsis an...

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Oxygen consumption and resting metabolic rate in sepsis, sepsis syndrome, and septic shock

Cited by 242 publications

References 0 publications

Tissue Oxygenation Does Not Predict Central Venous Oxygenation in Emergency Department Patients With Severe Sepsis and Septic Shock

Tissue Oxygenation Does Not Predict Central Venous Oxygenation in Emergency Department Patients With Severe Sepsis and Septic Shock

Enteral nutrition is associated with improved outcome in patients with severe sepsis

Molecular Events in the Cardiomyopathy of Sepsis

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