| dc.description.abstract | Introduction The impact of anesthetic depth on hemodynamics has always been suspected to be a potentially pivotal factor in determining perioperative outcome, albeit with little systematically garnered evidence to support that assertion. Several studies have emerged in the last 5 years providing important hypothesis generating data that highlight the possible relationships between depth of anesthesia, hypotension, and 30-day mortality – coined the “triple low” hypothesis. Here, we review the evidence that may support these relationships and re-examine the data on the basis of basic scientific and clinical research, which suggests a plausible deleterious interaction between hemodynamic alterations and depth of anesthesia. Impact of anesthetic depth on neuro-cardiovascular control Before considering patient-centered data, it is worth revisiting the role of anesthesia and the perioperative period (Figure 26.1) in modulating central and peripheral neuro-cardiovascular control. Several studies – that can only be conducted in laboratory models – have confirmed the impact of anesthesia on central neural control of cardiovascular function by assessing how anesthesia affects physiologic function in decerebrate preparations. These experiments reveal several important neurophysiologic features of anesthesia of direct relevance to the interpretation of linking depth of clinical anesthesia to hemodynamic changes. First, anesthetic agents unequivocally reduce blood pressure and heart rate in decerebrate preparations. However, the same anesthetic agents tested profoundly alter various baro- and chemoreflex responses, at much lower anesthetic dose. Thus, the hemodynamic effects observed under general anesthesia may not be solely due to central depressant effects of anesthesia. There is a wealth of evidence that even low levels of various anesthetic agents impair peripheral neural function, including the detection of hypoxia and hypercapnia by the peripheral chemoreceptors. These physiologic changes impact profoundly on a range of hemodynamic responses, as explored extensively in both human and animal laboratory models. A range of physiologic responses may therefore be altered under anesthesia, that occur independently of excessive anesthetic depth and/or central integration of neural afferent information. Second, peripheral neural function may be altered via anesthetic and non-anesthetic mechanisms. For example, neuromuscular blockade may affect the measurement of depth of anesthesia. Similarly, higher levels of spinal blockade are positively correlated with bispectral index values in elderly patients. While high spinal anesthesia predictably decreases systolic blood pressure, bispectral index values also decrease, despite concomitantly preserved cardiac output. | en_US |
