Ann Thorac Surg 2012;93:693-694. doi:10.1016/j.athoracsur.2011.09.026
© 2012 The Society of Thoracic Surgeons
Correspondence
How Much Is Safe: The Flow of Antegrade Cerebral Perfusion During Deep Hyperthermia Circulatory Arrest
Bingyang Ji, MD,
Jinping Liu, MD,
Xiaohua Wang, MD,
Cun Long, MD
Department of Cardiopulmonary Bypass, Chinese Academy of Medical Sciences, Peking Union Medical College, Fuwai Hospital and Cardiovascular Institute, 167 Beilishi Rd, Fuwai Dajie, Xicheng qu, Beijing 100037, People's Republic of China
(Email: dr.ji.cpb{at}gmail.com).
To the Editor:
We read with great interest the recent article by Jonsson and colleagues [1]. The purpose of this animal investigation was to define the ischemic threshold of antegrade cerebral perfusion (ACP) during deep hyperthermia circulatory arrest (DHCA) using magnetic resonance imaging (MRI) and spectroscopy. We congratulate them for their excellent experimental design in using MRI techniques and biomarkers to evaluate cerebral perfusion, metabolism, and damage to define low-flow ACP, which may provide more evidence for avoiding injury to the brain when using ACP during DHCA.
It is well documented that combined ACP with DHCA has been advocated in complex congenital and arch repairs in recent years [2]. However, several issues remain unresolved relating to optimal management of the standard set of variables associated with perfusion practice when contemplating the use of ACP during DHCA. Technical issues related to the use of hypothermic ACP, such as the perfusate temperature, pH management, flow rate and pressure used to selectively perfuse the brain, are still unresolved. Routine methods of evaluation will likely clarify many of these issues as experience and investigations continue. So far, it is difficult to define from existing literature what the optimal flow and ischemic threshold for ACP at low temperatures should be. However, clinicians may be able to monitor changes during ACP using various tools, such as transcranial Doppler and near-infrared spectroscopy.
In this particular study, the authors tried to determine the ischemic threshold during ACP using pig DHCA models. They concluded that, in this model, the ischemic threshold was approximately 6 mL · kg · min. We would like to make a few comments concerning several limitations in this experimental design that may have negatively affected the results of the investigation. First, how did the authors define the flow rate in the control group with 6 mL · kg · min? Although they may have maintained the same time between the two groups, the authors did not mention the length of time between each flow rate. Second, because the authors used four different ACP flow rates in every single model during DHCA, it is difficult to clarify whether the damage to the brain occurred under this flow rate. It is more probable that, once ACP commenced, cumulative brain damage occurred until ACP ended. Moreover, because four different flow rates were used in the same animal, investigating cerebral histology after ACP would not yield meaningful results. Another issue we think the authors should consider carefully in future studies is that most heart centers use pH state to control blood gas during clinical DHCA. They used α-stat to manage the blood gas; consequently, their results do not provide a meaningful point of reference for clinicians.
We congratulate the authors for their results in this animal study, and also we suggest that the authors optimize their design in the future clinical studies, continuing to improve current strategies on cerebral protection during aortic arch repair.
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References
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- Jonsson O, Morell A, Zemgulis V, et al. Minimal safe arterial blood flow during selective antegrade cerebral perfusion at 20° centigrade Ann Thorac Surg 2011;91:1198-1205.[Abstract/Free Full Text]
- Di Eusanio M, Schepens MA, Morshuis WJ, et al. Brain protection using antegrade selective cerebral perfusion: a multicenter study Ann Thorac Surg 2003;76:1181-1188.[Abstract/Free Full Text]
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