• Journal of Chest Surgery
• /
• v.30 no.8
• /
• pp.752-759
• /
• 1997

Profound hypothermia protects . cerebral function during total circulatory arrest(TCA) in the surgical treatment of a variety of cardiac and aortic diseases. Despite its importance, there is no ideal technique to monitor the brain injury from ischemia. Since 1994, we have developed compressed spectral array(CSA) of electroencephalography(EEG) and monitored cerebral activity to reduce ischemic injury. The purposes of this study are to analyse the efficacy of CSA and to establish objective criteria to consistently identify the safe level of temperature and arrest time. We studied 6 patients with aortic dissection(AD, n=3) or aortic arch aneurysm(n=3, ruptured in 2). Body temperatures from rectum and esophagus and the EEG were monitored continuously during cooling and rewarming period. TCA with cerebral ischemia was performed in 3 patients and TCA with selective cerebral perfusion was performed in 3 patients. Total ischemic time was 30, 36 and 56 minutes respectively for TCA group and selective perfusion time was 41, 56 and 92 minutes respectively for selective perfusion group. The rectal temperatures for flat EEG were between 16.1 and 22. $1^{\circ}C$ (mean: 18.4 $\pm$ 2.0): the esophageal temperatures between 12.7 and $16.4^{\circ}C$ (mean $14.7\pm1.6).$ The temperatures at which EEG reappeared $5~15.4^{\circ}C$ for esophagus. There was no neurological defic t and no surgical mortality in this series. In summary, the electrical cerebral activity Teappeared within 23 minutes at the temperature less than $16^{\circ}C$ for rectum. It seemed that $15^{\circ}C$ of esophageal temperature was not safe for 20 minutes of TCA and continuous monitoring the EEG with CSA to identify the electrocerebral silence was useful.

• Journal of Chest Surgery
• /
• v.29 no.12
• /
• pp.1360-1365
• /
• 1996

From September 1992 to May 1996, 38 patients ranging in age from 23 to 78, were operated for aortic dissection at Asan medical center There were 21 men and 17 women. The underlying aortic pathology were acute aortic dissection in 23, chronic aortic dissection in 15. Eight patients had Martian syndrome. In 34 cases of DeBakey type I, II patients, femoral artery and vein and/or right atrial auricle were used as cannulation site. With deep hypothermic c rculatory arrest (esophageal temperature 12 $\pm$ 2.5$^{\circ}C$) and retrograde cerebral perfusion of cold oxygenated blood through SVC, we replaced the ascending aorta and the part of arch if necessary. The mean duration of the total circulatory arrest time was 25 $\pm$ 1.7 mintstuts. In 4 cases of DeBakey type III patients, we replaced descending thoracic aorta or thoracoabdomlnal aorta without shunt or bypass under normothermia with an average 30: 1.5 minutesaortic cross clamp time. One death(2.6%) occurred on the twenty-second postoperative day owing to asphyxia related to ulcer bleeding. Postoperative complications were myocardial infarction with transient left peroneal palsy in 1 case, transient lower extremity weakness in 1 case and prolonged ventilatory support in 1 case. Two patients required reoperation due to retrograde extended dissection and aortic insufuciency. There was no late death with an average 25 months follow-up period.

• Journal of Chest Surgery
• /
• v.30 no.5
• /
• pp.471-478
• /
• 1997

Introduction: The use of rabbits as a cardiopulmonary bypass(CPB) animal model is extremely dif%cult mainly due to technical problems. On the other hand, deep hypothermic circulatory arrest(CA) is used to facilitate surgical repair in a variety of cardiac diseases. Although steroids are generally known to be effective in the treatment of cerebral edema, the protective effects of steroids on the brain during CA are not conclusively established. Objectives of this study are twofold: the establishment of CPB technique in rabbits and the evaluation of preventive effect of steroid on the development of brain edema during CA. Material '||'&'||' Methods: Fifteen New Zealan white rabbits(average body weight 3.5kg) were divided into three experimental groups; control CA group(n=5), CA with Trendelenberg position group(n=5), and CA with Trendelenberg position + steroid(methylprednisolone 30 mglkg) administration group(n=5). After anesthetic induction and tracheostomy, a median sternotomy was performed. An aortic cannula(3.3mm) and a venous ncannula(14 Fr) were inserted, respectively in the ascending aorta and the right atrium. The CPB circuit consisted of a roller pump and a bubble oxygenator. Priming volume of the circuit was approximately 450m1 with 120" 150ml of blood. CPB was initiated at a flow rate of 80~85ml/kg/min, Ten min after the start of CPB, CA was established with duration of 40min at $20^{\circ}C$ of rectal temperature. After CA, CPB was restarted with 20min period of rewarming. Ten min after weaning, the animal was sacrif;cod. One-to-2g portions of the following tissues were rapidly d:ssected and water contents were examined and compared among gr ups: brain, cervical spinal cord, kidney, duodenum, lung, heart, liver, spleen, pancreas. stomach. Statistical significances were analyzed by Kruskal-Wallis nonparametric test. Results: CPB with CA was successfully performed in all cases. Flow rate of 60-100 mlfkgfmin was able to be maintained throughout CPB. During CPB, no significant metabolic acidosis was detected and aortic pressure ranged between 35-55 mmHg. After weaning from CPB, all hearts resumed normal beating spontaneously. There were no statistically significant differences in the water contents of tissues including brain among the three experimental groups. Conclusion: These results indicate (1) CPB can be reliably administered in rabbits if proper technique is used, (2) the effect of steroid on the protection of brain edema related to Trendelenburg position during CA is not established within the scope of this experiment.

• Journal of Chest Surgery
• /
• v.33 no.6
• /
• pp.445-468
• /
• 2000

Background: Retrograde cerebral perfusion(RCP) is currently used for brain protection during aorta surgery, however, for the safety of it, various data published so far are insufficient. We performed RCP using pig and investiaged various parameters of cerebral metabolism and brain injury after RCP under deep hypothermia. Material and Method: We used two experimental groups: in group I(7 pigs, 20 kg), we performed RCP for 120 minutes and in group II (5 pigs, 20 kg), we did it for 90 minutes. Nasopharyngeal temperature, jugular venous oxygen saturation, electroencephalogram were continuously monitored, and we checked the parameters of cerebral metabolism, histological changes and serum levels of neuron-specific enolose(NSE) and lactic dehydrogenase(LDH). Central venous pressure during RCP was mainained in the range of 25 to 30 mmHg. Result: Perfusion flow rates(ml/min) during RCP were 130$\pm$57.7(30 minutes), 108.6$\pm$55.2(60 minutes), 107.1$\pm$58.8(90 minutes), 98.6$\pm$58.7(120 minutes) in group I and 72$\pm$11.0(30 minutes), 72$\pm$11.0(60 minutes), 74$\pm$11.4(90 minutes) in group II. The ratios of drain flow to perfusion flow were 0.18(30 minutes), 0.19(60 minutes), 0.17(90 minutes), 0.16(120 minutes) in group I and 0.21, 0.20, 0.17 in group II. Oxygen consumptions(ml/min) during RCP were 1.80$\pm$1.37(30 minutes), 1.72$\pm$1.23(60 minutes), 1.38$\pm$0.82(90 minutes), 1.18$\pm$0.67(120 minutes) in group I and 1.56$\pm$0.28(30 minutes), 1.25$\pm$0.28(60 minutes), 1.13$\pm$0.26(90 minutes). We could observe an decreasing tendency of oxygen consumption after 90 minutes of RCP in group I. Cerebrovascular resistance(dynes.sec.cm-5) during RCP in group I incrased from 71370.9$\pm$369145.5 to 83920.9$\pm$49949.0 after the time frame of 90 minutes(p<0.05). Lactate(mg/min) appeared after 30 minutes of RCP and the levels were 0.15$\pm$0.07(30 minutes), 0.18$\pm$0.10(60 minutes), 0.19$\pm$0.19(90 minutes), 0.18$\pm$0.10(120 minutes) in group I and 0.13$\pm$0.09(30 minutes), 0.19$\pm$0.03(60 minutes), 0.29$\pm$0.11(90 minutes) in group II. Glucose utilization, exudation of carbon dioxide, differences of cerebral tissue acidosis between perfusion blood and drain blood were maintained constantly during RCP. Oxygen saturation levels(%) in drain blood during RCP were 22.9$\pm$4.4(30 minutes), 19.2$\pm$4.5(60 minutes), 17.7$\pm$2.8(90 minutes), 14.9$\pm$2.8(120 minutes) in group I and 21.3$\pm$8.6(30 minutes), 20.8$\pm$17.6(60 minutes), 21.1$\pm$12.1(90 minutes) in group II. There were no significant changes in cerebral metabolic parameters between two groups. Differences in serum levels of NSE and LDH between perfusion blood and drain blood during RCP showed no statistical significance. Serum levels of NSE and LDH after resuming of cardipulmonary bypass decreased to the level before RCP. Brain water contents were 0.73$\pm$0.03 in group I and 0.69$\pm$0.06 in group II and were higher than those of the controls(p<0.05). The light microscopic findings of cerebral neocortex, basal ganglia, hippocampus(CA1 region) and cerebellum showed no evidence of cerebral injury in two groups and there were no different electron microscopy in both groups(neocortex, basal ganglia and hippocampus), but they were thought to be reversible findings. Conclusion: Although we did not proceed this study after survival of pigs, we could perform the RCP successfully for 120 minutes with minimal cerebral metabolism and no evidence of irreversible brain damage. The results of NSE and LDH during and after RCP should be reevaluated with survival data.