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Triple low, double low: it's time to deal Achilles heel a single deadly blow.

Since the report by Monk and colleagues of an association between a cumulative duration of the bispectral index (BIS) <45 and postoperative mortality there has been debate regarding the plausibility that relatively excessive anaesthetic depth is deadly. It is not surprising that this premise has ignited a scientific controversy and that anaesthetists are both intellectually and emotionally vested in its resolution. If this hypothesis were indeed true, the concentration of (volatile) anaesthetic promoting death would be within what is currently considered the therapeutic window. Furthermore, if a minor increase in anaesthetic administration were truly fatally injurious, we would expect to see a marked increase in mortality with general compared with regional anaesthesia. Also, since some clinicians administer more anaesthesia than others, we would predict that these variations would manifest as differences in postoperative morbid and mortal outcomes. And yet, differences in major adverse outcomes, based on anaesthetic technique or individual anaesthetists, have not been apparent in several studies. The crude notion that the deeper the anaesthesia, the more harmful the consequences does not resonate with many clinicians. It is more intellectually palatable to entertain the view that an increase in mortality is reflective of patient vulnerability or indicative of increased sensitivity to anaesthetic agents. The B-Unaware Study Group found that the cumulative time with BIS <45 was associated with postoperative mortality following cardiac surgery, but surprisingly the duration of BIS <45 was not associated with increased volatile anaesthetic exposure. Nor did increased volatile anaesthetic exposure predict mortality. Given the dissociation between BIS <45 and total volatile anaesthetic exposure, the B-Unaware Study Group hypothesized the relationship between low BIS and 1-year mortality to be an epiphenomenon of an underlying patient condition or operative factor that remains to be elucidated. Subsequently Sessler and colleagues, based on a large observational cohort, reported that the cumulative duration of concurrent BIS <45, mean arterial pressure (MAP) <75 mm Hg, and minimum alveolar concentration (MAC) <0.8 was highly predictive of postoperative death. They termed this the ‘triple low’ condition and also reported that cumulative durations of any ‘double low’ condition (MAC and MAP, MAP and BIS, or MAC and BIS) portended mortality. In this issue of the British Journal of Anaesthesia, Maheshwari and colleagues examined the association between the BIS and MAP double low and postoperative mortality in patients undergoing cardiac surgery. After adjusting for co-variables and multiple comparisons, prolonged cumulative concurrence of double low (defined as BIS <43 and MAP <75 mm Hg and either BIS <37 or MAP <69 mm Hg) was associated with increased 30-day mortality and a composite outcome of in-hospital mortality and morbidity. The definition of double low used in the study was not based on a physiological motivation (e.g. autoregulation boundary), nor was it prespecified based on the seemingly logical thresholds of MAP <75 mm Hg and BIS <45, which had been previously proposed as optimal. Rather, the double low was derived using arbitrary statistical rules from the data. The definition of double low used in this study was BIS and MAP less than their mean values and either BIS or MAP less than 1 SD below the mean values of these parameters in this population. It is conceptually useful to consider the ‘low’ MAP and BIS parameters more critically. There is broad agreement that intraoperative hypotension can be directly injurious and can harm any organ in the body through impaired perfusion. There has been debate concerning the threshold for harm, with evidence suggesting that a MAP <55–60 mm Hg is often associated with organ injury. However, a generic ‘safe’ arterial pressure boundary will be unsafe for many patients, including some of those with elevated venous pressure, coronary artery disease,