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Core body temperature is normally tightly regulated to within a few tenths of a degree. The major thermoregulatory defences in humans are sweating, arteriovenous shunt vasoconstriction, and shivering. The core temperature triggering each response defines its activation threshold. General anaesthetics greatly impair thermoregulation, synchronously reducing the thresholds for vasoconstriction and shivering. Neuraxial anaesthesia also impairs central thermoregulatory control, and prevents vasoconstriction and shivering in blocked areas. Consequently, unwarmed anaesthetised patients become hypothermic, typically by 1–2°C. Hypothermia results initially from an internal redistribution of body heat from the core to the periphery, followed by heat loss exceeding metabolic heat production. Complications of perioperative hypothermia include coagulopathy and increased transfusion requirement, surgical site infection, delayed drug metabolism, prolonged recovery, shivering, and thermal discomfort. Body temperature can be reliably measured in the oesophagus, nasopharynx, mouth, and bladder. The standard-of-care is to monitor core temperature and to maintain normothermia during general and neuraxial anaesthesia.

Mortality in the month following surgery is about 1000 times greater than anesthesia-related intraoperative mortality, and myocardial injury appears to be the leading cause. There is currently no known safe prophylaxis for postoperative myocardial injury, but there are strong associations among hypotension and myocardial injury, renal injury, and death. During surgery, the harm threshold is a mean arterial pressure of about 65 mmHg. In critical care units, the threshold appears to be considerably greater, perhaps 90 mmHg. The threshold triggering injury on surgical wards remains unclear but may be in between. Much of the association between hypotension and serious complications surely results from residual confounding, but sparse randomized data suggest that at least some harm can be prevented by intervening to limit hypotension. Reducing hypotension may therefore improve perioperative outcomes.

Each year, cardiac complications occur within 30 days after major noncardiac surgery in more than 10 million people worldwide; postoperative mortality is 1.5%. Enhanced patient monitoring and measurement of natriuretic hormone and troponin levels may improve outcomes. Although major noncardiac surgery has the potential to improve the quality and prolong the duration of a patient’s life, surgery may also precipitate complications such as death from cardiac causes, myocardial infarction or injury, cardiac arrest, or congestive heart failure. 1 In this article, we review what is known about the epidemiology and mechanisms of perioperative cardiac complications (i.e., from induction of anesthesia to within 30 days after surgery), preoperative methods of predicting these complications, perioperative cardiac interventions, and postoperative monitoring. Epidemiology and Mechanisms of Perioperative Cardiac Complications Worldwide, more than 200 million adults undergo major noncardiac surgery each year, 2 , . . .

PurposeCurrent guidelines recommend maintaining a mean arterial pressure (MAP) ≥ 65 mmHg in septic patients. However, the relationship between hypotension and major complications in septic patients remains unclear. We, therefore, evaluated associations of MAPs below various thresholds and in-hospital mortality, acute kidney injury (AKI), and myocardial injury.MethodsWe conducted a retrospective analysis using electronic health records from 110 US hospitals. We evaluated septic adults with intensive care unit (ICU) stays ≥ 24 h from 2010 to 2016. Patients were excluded with inadequate blood pressure recordings, poorly documented potential confounding factors, or renal or myocardial histories documented within 6 months of ICU admission. Hypotension exposure was defined by time-weighted average mean arterial pressure (TWA-MAP) and cumulative time below 55, 65, 75, and 85 mmHg thresholds. Multivariable logistic regressions determined the associations between hypotension exposure and in-hospital mortality, AKI, and myocardial injury.ResultsIn total, 8,782 patients met study criteria. For every one unit increase in TWA-MAP < 65 mmHg, the odds of in-hospital mortality increased 11.4% (95% CI 7.8%, 15.1%, p < 0.001); the odds of AKI increased 7.0% (4.7, 9.5%, p < 0.001); and the odds of myocardial injury increased 4.5% (0.4, 8.7%, p = 0.03). For mortality and AKI, odds progressively increased as thresholds decreased from 85 to 55 mmHg.ConclusionsRisks for mortality, AKI, and myocardial injury were apparent at 85 mmHg, and for mortality and AKI risk progressively worsened at lower thresholds. Maintaining MAP well above 65 mmHg may be prudent in septic ICU patients.

Three linked clinical observations prompted our current understanding of perioperative heat balance. The first was the extraordinarily rapid decrease in core temperature after induction of general anesthesia which led to an understanding of redistribution hypothermia. The second was the linear reduction in core temperature during the subsequent 2–3 h which led to an understanding of anesthetic effects on metabolic heat production and factors that influence cutaneous heat loss. And the third was the observation that core temperature reaches a plateau at about 34.5 °C which led to the understanding that thermoregulatory vasoconstriction re-emerges when patients become sufficiently hypothermic, and that arteri-venous shunt constriction constrains metabolic heat to the core thermal compartment. •The rapid decrease in core temperature after induction of general anesthesia led to an understanding of redistribution hypothermia.•The linear reduction in core temperature during the subsequent 2–3 h led to an understanding of metabolic heat production and cutaneous heat loss.•The core temperature plateau at about 34.5 °C led to the understanding that anesthetized patients are not poikilothermic, and that arteri-venous shunt constriction constrains metabolic heat to the core thermal compartment.

In a pragmatic trial, more than 30,000 patients requiring blood transfusion were randomly assigned to receive blood after short-term storage or long-term storage. In-hospital mortality did not differ significantly between the two groups. Red-cell transfusion is one of the most common medical interventions. 1 Blood is stored for up to 42 days before transfusion. Biochemical, structural, and functional changes during storage may reduce oxygen delivery to tissues, and the release of extracellular vesicles and cell-free DNA during storage may cause a hypercoagulable state. 2 Observational studies have suggested that prolonged blood storage is associated with an increased risk of cardiovascular events. 3 Randomized, controlled trials have not shown harm in transfusing red-cell units with a longer duration versus a shorter duration of storage. However, most of these trials have been restricted to high-risk populations and have . . .

Cardiopulmonary bypass initiates a systemic inflammatory response syndrome that is associated with postoperative morbidity and mortality. Steroids suppress inflammatory responses and might improve outcomes in patients at high risk of morbidity and mortality undergoing cardiopulmonary bypass. We aimed to assess the effects of steroids in patients at high risk of morbidity and mortality undergoing cardiopulmonary bypass. The Steroids In caRdiac Surgery (SIRS) study is a double-blind, randomised, controlled trial. We used a central computerised phone or interactive web system to randomly assign (1:1) patients at high risk of morbidity and mortality from 80 hospital or cardiac surgery centres in 18 countries undergoing cardiac surgery with the use of cardiopulmonary bypass to receive either methylprednisolone (250 mg at anaesthetic induction and 250 mg at initiation of cardiopulmonary bypass) or placebo. Patients were assigned with block randomisation with random block sizes of 2, 4, or 6 and stratified by centre. Patients aged 18 years or older were eligible if they had a European System for Cardiac Operative Risk Evaluation of at least 6. Patients were excluded if they were taking or expected to receive systemic steroids in the immediate postoperative period or had a history of bacterial or fungal infection in the preceding 30 days. Patients, caregivers, and those assessing outcomes were masked to allocation. The primary outcomes were 30-day mortality and a composite of death and major morbidity (ie, myocardial injury, stroke, renal failure, or respiratory failure) within 30 days, both analysed by intention to treat. Safety outcomes were also analysed by intention to treat. This study is registered with ClinicalTrials.gov, number NCT00427388. Patients were recruited between June 21, 2007, and Dec 19, 2013. Complete 30-day data was available for all 7507 patients randomly assigned to methylprednisolone (n=3755) and to placebo (n=3752). Methylprednisolone, compared with placebo, did not reduce the risk of death at 30 days (154 [4%] vs 177 [5%] patients; relative risk [RR] 0·87, 95% CI 0·70–1·07, p=0·19) or the risk of death or major morbidity (909 [24%] vs 885 [24%]; RR 1·03, 95% CI 0·95–1·11, p=0·52). The most common safety outcomes in the methylprednisolone and placebo group were infection (465 [12%] vs 493 [13%]), surgical site infection (151 [4%] vs 151 [4%]), and delirium (295 [8%] vs 289 [8%]). Methylprednisolone did not have a significant effect on mortality or major morbidity after cardiac surgery with cardiopulmonary bypass. The SIRS trial does not support the routine use of methylprednisolone for patients undergoing cardiopulmonary bypass. Canadian Institutes of Health Research.