Abstract

Since the pioneering report by Griepp in 1975, the use of deep hypothermia for cerebral and visceral organ protection has ushered in the modern era of safe and effective operation on the aortic arch during circulatory arrest (1). In large part due to advanced circulatory management strategies, the number of proximal aorta and arch replacements have increased each year since 2005, with over 10,000 operations reported to the Society of Thoracic Surgeons National Database in 2009 alone (2). However, despite these advances, neurologic complications remain a sobering limitation of arch repair, with national rates of major neurologic morbidity ranging between 3-5% for elective arch repairs and 9-13% for non-elective repairs (2). In addition, visceral organ injury such as renal failure requiring dialysis occurs in 3-6% of patients (2), highlighting the need for additional investigation into methods for ischemic end-organ protection during circulatory arrest. The concept of using hypothermia to temporarily reduce the oxygen and metabolic requirements of hypoxic tissues is intuitive and supported by decades of laboratory, translational, and clinical science. Nonetheless, the optimal temperature for hypothermic circulatory arrest (HCA) during arch surgery remains unclear and is confounded by a myriad of other clinical variables that are also without consensus, such as location of temperature measurement, cannulation site, perfusion rates, rapidity of cooling and rewarming, anesthetic and pharmacologic adjuncts, selective cerebral perfusion technique, and use of intraoperative electroencephalographic (EEG) neuromonitoring to guide cooling. As a result, HCA strategies vary considerably, even between respected high-volume centers, and are often dictated as much by dogma and tradition as by evidence. Maximal suppression of the cerebral metabolic rate of oxygen consumption occurs at EEG isoelectricity, or electrocerebral inactivity (ECI) (3,4), with modern aortic surgeons traditionally aiming to achieve this level of metabolic suppression through the use of ‘profound’ or ‘deep’ hypothermia. Although cooling below 18 °C was initially thought necessary to achieve ECI (3,4), more recent studies have shown that ECI can occur anywhere between 10 and 27 °C in human subjects (Figure 1) (5-7). As a result, many experienced centers, including our own, employ neurophysiologic intraoperative monitoring with EEG to precisely detect ECI prior to the initiation of circulatory arrest (6,8-10). Cooling to ECI by EEG ensures maximal suppression of cerebral metabolic activity prior to circulatory arrest, while minimizing perfusion time and hypothermic injury by avoiding excessive cooling (5). Figure 1 Cumulative (A) nasopharyngeal temperature and (B) cooling time required to achieve electrocerebral inactivity (ECI) in a series of 325 adult patients who underwent thoracic aortic surgery at Duke University Medical Center with deep hypothermic circulatory ... However, as early as 1983, concerns over the physiologic consequences of profound temperature reductions led some to advocate lesser degrees of hypothermia with circulatory arrest (11). Initial concerns focused primarily on bleeding complications thought to result from hypothermia-induced coagulopathy, as well as increased systemic inflammatory response from the prolonged perfusion times required for cooling and rewarming (11,12). More recently, concerns over subtle neurocognitive deficits caused by hypothermic neuronal injury have been raised (13-15), despite reports documenting complete neurocognitive preservation following deep HCA (16). In light of these theoretic concerns along with the advent of cerebral protection strategies, an increasing number of centers now employ ‘moderate’ or even ‘mild’ degrees of systemic hypothermia coupled with selective antegrade cerebral perfusion (SACP) (12,17-21). Although the benefits of SACP with HCA appear well established (10), there remains a lack of objective data demonstrating the superiority, or even non-inferiority, of moderate hypothermia with SACP in comparison to deep hypothermia with SACP, particularly pertaining to visceral organ and spinal cord protection (9). In the present article, we provide a brief overview of the history and evidence that shapes the current controversy regarding the optimal temperature for central nervous system and visceral organ protection with HCA employed during aortic arch repair. We conclude that, given the limitations of existing retrospective observational data, a multi-center randomized trial is needed to directly compare deep and moderate HCA and provide high-quality evidence-based guidelines for this critically important component of aortic arch repair.

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