Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming

Stecker, Michael S.; Cheung, Albert T.; Pochettino, Alberto; Kent, Glenn P.; Patterson, Terry; Weiss, Stuart J.; Bavaria, Joseph E.

doi:10.1016/s0003-4975(00)02021-x

Cited by 95 publications

(60 citation statements)

References 8 publications

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“…It is frequently observed in deep general anesthesia (2). It is also observed in a range of pathological conditions including hypothermia (3)(4)(5), hypoxic-ischemic trauma/coma (6), and the so-called Ohtahara syndrome (7,8), a type of early infantile encephalopathy. These etiologies indicate that the burst suppression pattern represents a low-order dynamic mechanism that persists in the absence of higher-level brain activity.…”

mentioning

confidence: 99%

A neurophysiological–metabolic model for burst suppression

Ching

Purdon

Vijayan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

254

326

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Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.B urst suppression-an electroencephalogram (EEG) pattern in which high voltage activity (burst) and flatline (suppression) periods alternate systematically but quasiperiodically (almost periodic but with variations in inter-and intra-burst duration) (1)-is a state of profound brain inactivation. It is frequently observed in deep general anesthesia (2). It is also observed in a range of pathological conditions including hypothermia (3-5), hypoxic-ischemic trauma/coma (6), and the so-called Ohtahara syndrome (7,8), a type of early infantile encephalopathy. These etiologies indicate that the burst suppression pattern represents a low-order dynamic mechanism that persists in the absence of higher-level brain activity. Indeed, the fact that many different conditions produce similar brain activity suggests that there may be a common pathway to the state of brain inactivation and may indicate fundamental properties of the brain's arousal circuits (2).The basic features of the burst suppression phenomenon have been established through a variety of EEG studies that are reviewed in ref. 9. The two most notable of these features are the spatial homogeneity of bursts and the quasi-periodic nature of the suppression. Later research has been directed at describing the phenomenon in vivo and in the specific context of general anesthesia. In particular, the early work of Steriade et al. (10) helped establish the neural correlates of burst suppression, including the differential participation of cortical and subcortical cell types. More recent studies (11,12) have suggested that burst suppression is associated with enhanced excitability in cortical networks. These studies implicate extracellular calcium as a correlate for the switches between burst and suppression.Despite the findings of these studies, a unifying mechanism for burst suppression-one that explains its prevailing features and also accounts for its range of etiologies-has not been proposed. Indeed, the existing characterizations of burst suppression in pathological situations are highly limited. Computational models offer a means of synthesizing the availabl...

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mentioning

confidence: 99%

A neurophysiological–metabolic model for burst suppression

Ching

Purdon

Vijayan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

254

326

View full text Add to dashboard Cite

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“…Stecker and colleagues reported the patern of EEG electrocerebral activity during aortic arch operations requiring deep hypothermic circulatory arrest [12,18]. Between a nasopharyngeal temperature of 21.5 and 34.2°C, a majority of patients are found to have either lateralized, generalized, or bilateral independent periodic discharges, or transient and synchronous increases in EEG wave amplitude, against a background of continuous electrocerebral activity.…”

Section: Eeg Changes During Systemic Cooling and Rewarmingmentioning

confidence: 99%

“…The viewpoint is that maximal cerebral protection is achieved at temperatures suicient to induce electrocerebral inactivity on EEG, under the assumption that maximal suppression of cerebral metabolic activity is achieved at electrocerebral inactivity [2,11]. Stecker and colleagues reported that the process of cooling to electrocerebral inactivity produced a uniform degree of cerebral protection, independent of the actual nasopharyngeal temperature [12]. Consequently, many institutions have introduced intraoperative EEG to allow for the identiication of electrocerebral inactivity before initiating circulatory arrest [13][14][15][16], which leads to average minimum temperatures of less than 16°C [17,18].…”

Section: Introductionmentioning

confidence: 99%

Intraoperative Electroencephalography During Aortic Arch Surgery

Murashita¹

2017

Electroencephalography

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Since its introduction, deep hypothermic circulatory arrest has been widely used for cerebral protection during aortic arch surgery. The use of electroencephalogram plays an important role in intraoperative neurophysiologic monitoring. Systemic cooling to the point of electrocerebral inactivity has been thought to ensure optimal neuroprotection from the ischemic injury during circulatory arrest. Therefore, electroencephalogram can guide surgeons to induce deep hypothermic circulatory arrest at an optimal timing. In the meantime, along with the advent of adjunctive cerebral perfusion techniques, there is a certain trend that circulatory arrest is induced at higher degrees than traditional deep hypothermic approach, called moderate hypothermic circulatory arrest. The role of electroencephalogram in this approach has not been well established yet, but some studies suggested the importance of intraoperative electroencephalogram in this approach as well. Electroencephalogram is also utilized in emerging operative techniques called hybrid arch repair. To conclude, intraoperative use of electroencephalogram can greatly contribute to cerebral protection in the ield of aortic arch surgery, and surgeons should be familiar with its mechanism, indication, and interpretation.

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“…However, the optimal level of hypothermia is still debated. Studies based on electroencephalographic monitoring have shown that a median nasopharyngeal temperature of 18°C allows electrocortical silence (Stecker et al, 2001). Today, based on the results of several studies, HCCA at 18°C is considered safe for durations of up to 40 minutes (Griepp, 2001).…”

Section: Deep Hypothermic Circulatory Arrestmentioning

confidence: 99%