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Deep hypothermic circulatory arrest (DHCA) came about as an extension and unification of the work being done in the 1950s in cardiopulmonary bypass (Gibbon), systemic hypothermia (Bigelow), and aortic surgery (Debakey, Cooley, Crawford). Successful intracardiac surgery was based on the use of cardiopulmonary bypass (CPB); however, some procedures (eg, aortic arch surgery) could not be performed with standard CPB cannulation because of an inability to perfuse the cerebrum. Bigelow's work in the animal lab demonstrated that moderate hypothermia could be protective in cases in which CPB was halted for up to 10 minutes.1 The earliest use of DHCA in adult cardiac surgery has been accredited to Niazi and Lewis in 1958.2 Initially, DHCA was performed topically without the assistance of CPB; however, it soon became apparent that at hypothermic temperatures the heart would fibrillate or slow to a stop. Rewarming also proved to be quite difficult because of poor circulatory function during hypothermia. Many of these issues were improved on with the coordination of CPB with DHCA by the physiologist Gollan and the continued development and improvement of pump oxygenators and heat exchangers.3 Extensive work on the metabolic aspects of DHCA were studied and put into clinical practice by Griepp and others in the 1970s, leading to safe and reliable techniques that have been adopted by many into general practice.


Currently, DHCA in adult cardiac surgery is used in ascending aortic and aortic arch replacements for aneurysmal disease, dissections, and extensive aortic calcifications (porcelain aorta). Circulatory arrest has also been described for resection of complex inferior vena cava (IVC) and cardiac tumors and pulmonary thromboendarterectomies, and has been widely adopted in congenital heart surgery for the repair of complex congenital lesions.


The adult human brain is the organ most susceptible to ischemic injury. Under normal conditions, cerebral autoregulation matches cerebral blood flow (CBF) to cerebral oxygen consumption and cerebral metabolic activity (CMRO2) under a wide range of cerebral perfusion pressures.4 Yet, despite the effectiveness of cerebral autoregulation at normal physiologic perfusion pressures, the duration of cerebral ischemic tolerance at normothermia is approximately 5 minutes, making irreversible damage imminent unless adjunct perfusion methodologies or alternative strategies are employed to decrease the cerebral metabolic requirement.


The brain consumes 20% of the total body oxygen consumption, with 40% of its energy used in the preservation of cellular integrity and 60% in the transmission of nerve impulses.5 Because the brain does not have the ability to store oxygen, CMRO2 is a true index of brain metabolic activity and has been the variable of interest in studies attempting to determine the effectiveness of hypothermia in providing cerebral protection. For example, studies have demonstrated that a 10°C reduction in body temperature reduces CMRO2 by a factor of four4 (Fig. 14-1). This exponential decrease in metabolic rate differs from the linear reduction in CBF that occurs with hypothermia6; a discrepancy that ...

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