Background Increased oxygen extraction, the ratio of consumption to delivery, has been associated with poor outcome after surgery Oxygen consumption (VO2) can change in several ways in the perioperative period, but is seldom monitored directly in routine care This study investigates the effects of general anaesthesia on VO2 Methods We searched PubMed, EMBASE, and Cochrane Library 1946-2018 for studies including VO2 measurements before and after anaesthesia induction Quality was assessed by Cochrane risk of bias tool and NIH Quality Assessment tool for before-and-after studies Changes in VO2 after anaesthesia induction were pooled in a random effects model meta-analysis with standardized mean differences transformed to absolute changes of VO2 Changes in VO2 after surgical incision and after recovery from anaesthesia were analysed as secondary outcomes in the included studies Results Twenty-four studies including 453 patients were analysed for VO2 changes induced by anaesthesia Studies were published during 1969-2000 and mean age of patients ranged 28-70 years VO2 decreased after anaesthesia induction by -65 (-75; -55, 95% CI) mL min-1 and indexed VO2 (VO2I) by -33 (-38; -28, 95% CI) mL min-1 m-2  After surgical incision and in the post-operative period VO2 increased again Heterogeneity was considerable among the studies and the overall quality of evidence was very low Conclusions General anaesthesia probably reduces oxygen consumption but the effect estimate is uncertain Given the limited generalizability and low quality of the available evidence, new studies in modern perioperative settings and in today's older high-risk surgical patient populations are needed

The effects of general anaesthesia on oxygen consumption: A meta-analysis guiding future studies on perioperative oxygen transport

Con: Perioperative continuous monitoring of mixed venous oxygen saturation should not be routine in high-risk cardiac surgery

Resume La litterature concernant les effets des agents utilises pour la sedation sur la demande metabolique des patients en etat critique est relativement ancienne (dix a 20 ans) et de qualite assez moyenne. Il s’agit le plus souvent de travaux experimentaux ou d’etudes de cohortes. Le niveau de preuve est donc assez bas, correspondant le plus souvent a un « avis d’expert ». Difficile a quantifier avec precision, la baisse de la demande metabolique associee a l’utilisation des agents analgesiques et sedatifs est liee essentiellement a une diminution de la reponse neuroendocrine au stress. Cette reponse met en jeu prioritairement le systeme sympathique dont l’activite peut etre efficacement bloquee par les agents anesthesiques. D’autres facteurs peuvent intervenir, comme la diminution de l’activite motrice spontanee, la diminution du travail respiratoire et/ou la baisse de la temperature. La contribution relative de ces differents facteurs depend de la situation clinique du patient. Les effets propres des agents anesthesiques sur le metabolisme cellulaire sont limites et ne concernent que la composante fonctionnelle de ce metabolisme, principalement au niveau du cerveau et du cœur. Si le controle de l’activite sympathique peut s’averer benefique chez le patient en etat critique, le blocage complet de cette activite peut avoir des effets deleteres sur la balance en oxygene des tissus. En effet, le systeme sympathique constitue un des mecanismes majeurs d’adaptation en cas de diminution du transport d’oxygene, assurant la redistribution du flux sanguin restant, en fonction de la demande metabolique des tissus. L’inhibition complete de la reponse neuroendocrine au stress et donc du systeme sympathique empeche cette redistribution et aboutit a une baisse des capacites d’extraction en oxygene des tissus. Un desequilibre entre demande et apport d’oxygene peut apparaitre, avec developpement d’une hypoxie tissulaire. La mise en route d’une sedation chez le patient en etat critique implique donc une surveillance etroite du niveau de celle-ci. Lorsqu’une diminution de la demande metabolique est recherchee specifiquement, ou quand une sedation est envisagee chez un patient presentant un transport d’oxygene limite, les effets de la sedation sur le transport et la consommation d’oxygene devront egalement etre surveilles. Le choix des substances a utiliser dependra essentiellement des objectifs a atteindre. En ce qui concerne les agents intraveineux, il n’y a pas d’evidence de ce qu’une association de medicaments soit plus efficace qu’une autre afin de reduire la demande metabolique du patient.

Effets des agents sédatifs sur la demande métabolique

Epidemiological evidence has highlighted a strong relationship between cardiorespiratory fitness and surgical outcomes; specifically, fitter patients possess heightened resilience to withstand the surgical stress response. This narrative review draws on exercise and surgical physiology research to discuss and hypothesise the potential mechanisms by which higher fitness affords perioperative benefit. A higher fitness, as indicated by higher peak rate of oxygen consumption and ability to sustain metabolic homeostasis (i.e. higher anaerobic threshold) is beneficial postoperatively when metabolic demands are increased. However, the associated adaptations with higher fitness, and the related participation in regular exercise or physical activity, might also underpin the observed perioperative benefit through a process of hormesis, a protective adaptive response to the moderate and intermittent stress of exercise. Potential mediators discussed include greater antioxidant capacity, metabolic flexibility, glycaemic control, lean body mass, and improved mood. 

Physiological relationship between cardiorespiratory fitness and fitness for surgery: a narrative review.

Under normal conditions, oxygen consumption is independent of systemic oxygen delivery. When supply is reduced, the systemic oxygen extraction ratio increases until a critical limit is reached below which oxygen consumption (\( \dot{V}{{O}_{2}} \)) becomes limited by delivery. During surgery, anesthetic agents have complex effects on tissue oxygen balance since they can alter both oxygen supply (DO2) and oxygen demand. Since lactic acidosis is a sensitive marker of the development of tissue hypoxia, preoperative determination of blood lactate can help to detect inadequate tissue oxygenation during anesthesia. However, many factors such as perioperative glucose supply or sympathetic stimulation of glycolysis can interfere with lactate production and metabolism, so that the interpretation of preoperative blood lactate levels is sometimes difficult. Moreover, the precise effects of anesthetic agents on oxygen extraction capabilities of the tissues are not yet well defined. Alterations of oxygen extraction capabilities could lead to an abnormal dependency of oxygen consumption on oxygen supply. This review will focus on the effects of the most commonly used anesthetic agents on tissue oxygen supply-demand balance and their practical implications.

Jay L. Falk

Papers

Impaired oxygen utilization during anesthesia and surgery