Stress and inflammatory response after beating heart surgery versus conventional bypass surgery: the role of thoracic epidural anesthesia.
Cardiac surgery elicits a cascade of stress responses mediated by the release of various cytokines and stress hormones [Roth-Isigkeit 1998]. Apart from the stress induced by the surgical process, cardiopulmonary bypass (CPB) has been documented to play a major role in the perioperative stress response seen following cardiac surgery [Butler 1993, McBride 1995, Hall 1997]. The imbalance in pro- and anti-inflammatory responses may affect outcome in cardiac surgery patients [Casey 1993, McBride 1995, Menasch 1995]. Contact of blood with the CPB circuit, along with hypoperfusion of various organs prior to and during CPB, may aggravate this stress response and contribute to adverse outcomes in the perioperative period [Casey 1993, Menasch 1995, Tonnesen 1996]. Splanchnic hypoperfusion that occurs in cardiac surgery patients [Landow 1991] can result in increased permeability of the gut mucosal barrier, resulting in endotoxemia and release of proinflammatory cytokines. Lungs and kidneys play a role in sequestrating the proinflammatory cytokines and, in the presence of hypoperfusion, may be damaged by these cytokines [Gilliland 1999, Liebold 1999, Gormley 2000]. Avoiding CPB may reduce this stress response. Anesthetic techniques such as thoracic epidural analgesia (TEA) that improve splanchnic perfusion [Moore 1995, Kapral 1999, Ai 2001] may have a role in improving patient outcome. It is further known that ischemic myocardium can be a major source of proinflammatory cytokines [Wan 1999a]. The cardiac sympathetic block resulting from TEA has been shown to reduce ischemia reperfusion injury [Blomberg 1989, Blomberg 1990, Liem 1992a, Liem 1992b, Liem 1992c, Kirno 1994, Stenseth 1994]. Beating heart surgery done without the aid of CPB significantly attenuates cytokine and stress response [Brasil 1998, Fransen 1998, Gu 1998, Wan 1999b, Ganapathy 1999a, Ganapathy 2000a]. There is reduced renal dysfunction following beating heart surgery [Ascione 1999], which may be related to reduced proinflammatory cytokine surge. Thoracic epidural analgesia inhibits intraoperative cortisol as well as catecholamine surge but does not add further to the reduction in cytokine response [Ganapathy 1999b].
Ganapathy
S
S
Departments of Anesthesiology and Perioperative Medicine, London Health Sciences Centre, University Campus, University of Western Ontario, Canada. sganapat@uwo.ca
Murkin
J M
JM
Dobkowski
W
W
Boyd
D
D
D000767:Anesthesia, Epidural; D002315:Cardiopulmonary Bypass; D016207:Cytokines / Q000097:blood; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D013312:Stress, Physiological / Q000378:metabolism*; D019616:Thoracic Surgical Procedures; D016896:Treatment Outcome
D016207:Cytokines; D018836:Inflammation Mediators