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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

The role of perfusion pressure and flow during cardiopulmonary bypass with moderate hypothermia and hemodilution in the development of new postoperative renal or clinically apparent cerebral dysfunction was examined in 504 adults. Cardiopulmonary bypass flow was targeted at greater than 40 mL.kg-1.min-1 and pressure at greater than 50 mm Hg. Flows and pressures less than target occurred in 21.6% and 97.1% of patients, respectively. Fifteen patients (3.0%) suffered new renal and 13 (2.6%) new central nervous system dysfunction. Low pressure or flow during cardiopulmonary bypass, expressed in absolute values or in intensity-duration units, were not predictors of either adverse outcome. Multivariate analysis identified use of postoperative intraaortic balloon counterpulsation (p less than 10(-6], excessive blood loss in the ICU (p less than 10(-4], need for vasopressors before cardiopulmonary bypass (p less than 10(-4], postoperative myocardial infarction (p less than 10(-3], emergency reoperation (p less than 0.002), excessive postoperative transfusion (p less than 0.02), and chronic renal disease (p less than 0.03) as independent predictors of postoperative renal dysfunction. Independent predictors of postoperative central nervous system dysfunction were cardiopulmonary resuscitation in the intensive care unit (p less than 10(-6], intracardiac thrombus or valve calcification (p less than 0.02), and chronic renal disease (p less than 0.03). Age greater than 65 years (40.7% of patients) did not predict either outcome. We conclude that failure of the native circulation during periods other than cardiopulmonary bypass rather than the flows and pressures considered here is the major cause of renal and clinically apparent central nervous system dysfunction after cardiac operations.
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PMID:Role of perfusion pressure and flow in major organ dysfunction after cardiopulmonary bypass. 224 82

The relation between cerebral blood flow and oxygen consumption was studied in six children during cardiac operations with profound hypothermia. A combination of topical cooling and core cooling was used to reduce the nasopharyngeal temperature to 15 degrees C. The alpha-stat principle for pH management was used. Blood flow and oxygen consumption decreased significantly with temperature. At a nasopharyngeal temperature of 15 degrees C, blood flow was reduced to 25% of the awake level, corresponding to 34% of the asleep value obtained 15-30 min after intubation. Oxygen consumption decreased to 25% of the asleep value. During stable profound hypothermia, venous saturation in the jugular bulb was at the same level as 15 min after intubation (70%). Markedly lower values were observed during topical cooling, and particularly during rewarming (down to 21%), indicating a mismatch between cerebral blood flow and oxygen consumption. The speed of rewarming correlated with the fall in venous oxygen saturation (rs = 0.82, P less than 0.05). It is suggested that periods of cerebral blood flow/metabolic mismatch during topical cooling and rewarming may explain postoperative cerebral dysfunction after deep hypothermic procedures. A moderate speed of rewarming is advocated.
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PMID:Is cerebral blood flow/metabolic mismatch during rewarming a risk factor after profound hypothermic procedures in small children? 262 83

We sought to determine whether pentobarbital (PB) coma compromises the use of evoked potentials (EPs) in the assessment of brain dysfunction and of the prognosis of severely head-injured patients. Therefore, the effects of therapeutic PB on somatosensory (SEPs, BSEPs), visual (VEPs), and auditory (BAEPs) evoked potentials recorded from 20 patients early after injury were analyzed. Seventeen head-injured patients served as controls. EP studies were obtained shortly after admission (Mean Day 2, PB present) and approximately 2 weeks after injury (Mean Day 15, PB absent). The mean serum level of PB in the treatment group was 1.9 mg/100 ml. The drug effect was assessed by comparisons between the PB and the control groups. Statistical analyses were based on differences observed between two studies in the same patient. Analyses of covariance (F tests) were performed on data from all modalities. Wave form complexity was minimally affected by the drug. Middle and long latency components of the SEP were depressed by PB, and latencies of BSEP peaks and the early components of the SEP were delayed. The amplitude of some VEP peaks was reduced by PB. The BAEP was not significantly altered. All of the observed effects of PB were determined to be due to the hypothermia exhibited by PB-treated patients (mean temperature, 36.1 degrees C), which was not seen in the control group (mean, 37.8 degrees C). It is concluded that, with appropriate interpretation, EPs can be used to monitor brain function in head-injured patients when PB therapy is used.
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PMID:Effects of therapeutic pentobarbital coma on multimodality evoked potentials recorded from severely head-injured patients. 687 43

We present the case of a patient who had rupture of a pulsatile assist device (PAD) accompanied by massive air embolism, and the treatment that brought it to a successful outcome. After rupture of the skin of the PAD balloon, a massive amount of air was injected into the ascending aorta. The patient was placed in Trendelenburg position and cooled in deep hypothermia with cardiopulmonary bypass. He was given 1 gm of methylprednisolone intravenously, and the aortic valve replacement and double vein bypass graft were performed. After completion of the operation, the patient was partially rewarmed to 30 degrees C central temperature and transported by ambulance to a hyperbaric chamber where he was compressed to 6 atmospheres absolute 9 hours after the accident with clinical signs of severe brain dysfunction. The patient recovered completely and was discharged from the hospital on the tenth postoperative day.
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PMID:Massive arterial air embolism due to rupture of pulsatile assist device: successful treatment in the hyperbaric chamber. 731 94

This study was designed to demonstrate the changes in brain metabolism/function, and to clarify the reason for assessing brain dysfunction during cardiopulmonary bypass (CPB) with systemic hypothermia. Fifteen patients, who received high-dose fentanyl anesthesia, for cardiac surgery under CPB were analysed concerning systemic hemodynamics, brain oxygen extraction, internal jugular venous oxygen saturation (SjVO2), glucose uptake, and compressed spectral array EEG for brain function. Internal jugular venous temperature decreased from 35.4 +/- 1.0 degrees C (mean +/- SD) at pre-CPB, to 22.3 +/- 1.6 degrees C during CPB. Systemic oxygen delivery decreased by 43% (P < 0.01) with coincided decrease in brain oxygen extraction by 31% (P < 0.01) during CPB. SjVO2 rose from 64.5 +/- 6.3% of pre-CPB level to 78.7 +/- 2.2% during CPB (P < 0.01). Glucose uptake decreased 71% during CPB (P < 0.01). EEG frequency slowed down from 9.0 +/- 0.6 Hz of pre-CPB level to 3.5 +/- 0.3 Hz during CPB (P < 0.01). No patient showed neurological complications during and after surgery. The predictable changes in the variables during brain ischemia/hypoxia may be increase in oxygen extraction, decrease in SjVO2, inhibition of metabolism and low EEG activity. During CPB, EEG activity exhibited identical trend as during ischemia/hypoxia, while the changes in brain oxygen extraction and SjVO2 did not. In conclusion, detection of brain dysfunction by monitoring brain oxygen metabolism or EEG is controversial during CPB using hypothermia.
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PMID:[Clinical assessment of brain oxygen metabolism and function during cardiopulmonary bypass with induced hypothermia]. 774 82

A patient with Stanford type A acute aortic dissection who developed severe cerebral dysfunction after surgery using retrograde cerebral perfusion through the superior vena cava was examined. The patient was able to regain normal brain function with no neurological deficit. Postoperative venography taken through the superior vena cava showed the presence of competent venous valves at the venous angles. This suggests that the valves interrupted cerebral perfusion, decreasing blood flow to less than that required. After consideration of the possible causes of brain damage incurred during surgery for aortic aneurysm using retrograde cerebral perfusion, it was concluded that this patient was able to recover normal brain function because the surgery was performed under profound hypothermia.
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PMID:Cerebral death-like conditions after aortic aneurysm surgery using retrograde cerebral perfusion. 807 26

Neuropsychologic impairment in patients undergoing cardiopulmonary bypass may be associated with cerebral blood flow changes arising from different management protocols for carbon dioxide tension during bypass. Seventy patients having coronary artery bypass grafting were randomized to either pH-stat or alpha-stat acid-base management during cardiopulmonary bypass with a membrane oxygenator. In each patient, cerebral blood flow (xenon 133 clearance), middle cerebral artery blood flow velocity (transcranial Doppler sonography), and cerebral oxygen metabolism (cerebral metabolic rate and cerebral extraction ratio) were measured during four phases of the operation: before bypass, during bypass (at hypothermia and at normothermia), and after bypass. A battery, of neuropsychologic tests were also conducted before and 6 weeks after the operation. During hypothermic (28 degrees C) bypass, cerebral blood flow was significantly (p < 0.001) greater in the pH-stat group (41 mlx100 gm(-1)xmin(-1); 95% confidence interval 39 to 43 mlx100 gm(-1)xmin(-1)) than in the alpha-stat group (24 mlx100 gm(-1)xmin(-1); confidence interval 22 to 26 mlx100 gm(-1)xmin(-1)) at constant pressure and How. Arterial carbon dioxide tensions were 41 mm Hg (40 to 41 mm Hg) and 26 mm Hg (25 to 27 mm Hg), respectively; pH was 7.36 (7.34 to 7.38) and 7.53 (7.51 to 7.55), respectively. Middle cerebral artery flow velocity was significantly (p < 0.05) reduced in the alpha-stat group to 87% (77% to 96%) of the prebypass value, whereas it was significantly (p < 0.05) increased (152%; 141% to 162%) in the pH-stat group. Cerebral extraction ratio for oxygen demonstrated relative cerebral hyperemia during hypothermic (28 degrees C) bypass in both the pH-stat and alpha-stat groups (0.12 [0.11 to 0.14] and 0.25 [0.22 to 0.28], respectively); however, hyperemia was significantly more pronounced in the pH-stat group, indicating greater disruption in cerebral autoregulation. Neuropsychologic impairment criteria of deterioration in results of three or more tests revealed that a significantly (Fisher's exact test, p = 0.02) higher proportion of patients in the pH-stat group fared poorly than in the alpha-stat group at 6 weeks (17/35, 48.6% [32% to 65.1%], and 7/35, 20% [6.7% to 33.2.2%], respectively). In conclusion, patients receiving alpha-stat management had less disruption of cerebral autoregulation during cardiopulmonary bypass, accompanied by a reduced incidence of postoperative cerebral dysfunction.
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PMID:Alpha-stat acid-base regulation during cardiopulmonary bypass improves neuropsychologic outcome in patients undergoing coronary artery bypass grafting. 908 Nov 17

The effectiveness of monitoring somatosensory evoked potentials (SEPs) intraoperatively to detect brain damage early remains controversial. To assess the diagnostic accuracy of this modality, a study was conducted between 1991 and 1994, recording SEPs in 287 consecutive patients undergoing cardiac and aortic surgery using cardiopulmonary bypass (CPB) with moderate hypothermia or deep hypothermic circulatory arrest. From P1 to N2 of the SEPs occurring within 50 ms latency in response to electrical stimulation of the median nerve were recorded over the contralateral postcentral cortex at 5-min intervals using a Neuropack-2 (Nihon Koden, Tokyo, Japan). Normal SEPs were recovered in 247 patients postoperatively; however, 2 of these patients had suffered a cerebral infarction and 1, a transient stroke intraoperatively, demonstrating a false-negative incidence of 1.2%. On the other hand, three different types of abnormal SEPs were recorded postoperatively. P1 and N1 absence, probably caused by a subcortical lesion, was observed in 4 patients; P2 and N2 absence, probably caused by a cortical lesion, was observed in 8 patients; and a flat SEP, representing diffuse damage, was observed in 2 patients. Among these 14 patients with abnormal SEPs, 7 showed no neurologic disturbance at all, demonstrating a false-positive incidence of 50%. Thus, we concluded that when normal SEPs are recovered during weaning from CPB, the incidence of brain damage could be predicted at below 5%. Conversely, when abnormal SEPs are demonstrated, the incidence of brain dysfunction impeding a return to active life is estimated to be about 70%.
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PMID:Continuous monitoring of short-latency somatosensory evoked potentials during cardiac and aortic surgery. 872 17

The significance of mild-hypothermia as a treatment of brain ischemia-induced neuronal cell death was investigated by measurement of hippocampul excitatory amino acids, brain lactate and energy-charge just after 10 min of transient forebrain ischemia in a rat model with four vessels occluded. After 10 min of ischemia, cerebral circulation was restored. At that time, in the control group transient increases of hippocampul aspartate and glutamic acid levels were observed. Furthermore, brain lactate levels were also elevated but the energy-charge was reduced. These significant changes were observed in the non-isoflurane anesthesia and mild-hypothermia rats (control group). However, in rats with treatment of either isoflurane or mild-hypothermia, the excessive amount of amino acids and the significant fluctuation of brain metabolic/energy pathway seen in the control group were suppressed. Particularly, in the combined treatment group, these increased and decreased phenomena induced by brain ischemia were significantly inhibited. In a group of pre- and post-treatment of mild-hypothermia, the maximum peak of lactate was significantly less than that seen in the control group, although the sustained increased level of lactate was detected. These results indicate that the combined treatment with isoflurane anesthesia and mild-hypothermia is a suitable treatment for the brain dysfunction induced by ischemia and that the sustained hypothermia may help restore brain lactate levels after brain ischemia because of the lasting anaerobic metabolism.
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PMID:[Changes in brain metabolites under combined mild-hypothermia and isoflurane anesthesia in rat with temporal brain ischemia]. 1079 19


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