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

There were presented operative technique and clinical results of extracorporeal circulation (ECG) with patients lungs utilization, instead of routinely applied artificial blood oxygenators. Auto-oxygenation method was applied in 12 patients with coronary artery disease treated by coronary artery bypass grafting (CABG). Operative procedure differs from the traditional one in two additional cannulations of pulmonary artery and left atrium. Two peristaltic pumps and incorporated in circulation blood reservoirs. Polystan 892910 allows for temporary substitution of cardiac function without lung disconnection. Lungs functioning during surgery do not render it difficult. Hypothermia enables to decrease respiration rate and tidal volume with no effect on physiological blood oxygenation and CO2 exhalation. Method assessment was based on results comparison with those obtained in patients treated by traditional method using bubble oxygenators-Venotherm 5,000. PO2, PCO2, platelets number and hemolysis extent were assessed before, in 10, 30, 60 min of ECG and just after it. Platelets activity and influence of the method on hemostatic disorders were evaluated based on clotting time by Ivy. Additionally hemostatic disorders were assessed by thoracic blood drainage volume calculated from the moment of protamine administration to drainage tubes withdrawal in average 18 hours after surgery. Laboratory parameters characteristically changing during ECG were also estimated. It was proved, that auto-oxygenation diminished negative effects of ECG. Increased platelets number, faster normalization of clotting time and decreased postoperative drainage were stated in the auto-oxygenation group. Postoperative drainage in this group was 260 +/- 60 ml in comparison with 800 +/- 100 ml of the control group. Authors consider that pulmonary function remaining during ECG positively affects on postoperative hemostasis. This method can be helpful in surgical management of coronary artery disease, especially in patients with primary coagulation disorders.
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PMID:[Personal observations with application of auto-oxygenation techniques in the surgical management of coronary disease]. 208 71

Eighty-six patients undergoing coronary artery bypass graft (n = 63) or intracardiac (n = 23) surgery were randomly assigned with respect to the target value for PaCO2 during cardiopulmonary bypass. In 44 patients the target PaCO2 was 40 mmHg, measured at the standard electrode temperature of 37 degrees C, while in 42 patients the target PaCO2 was 40 mmHg, corrected to the patient's rectal temperature (lowest value reached: mean 30.1, SD 1.9 degrees C). Other salient features of bypass management include use of bubble oxygenators without arterial filtration, flows of 1.8-2.4 l.min-1.m-2, mean hematocrit of 23%, and mean arterial blood pressure of approximately 70 mmHg, achieved by infusion of phenylephrine or sodium nitroprusside. Neuropsychologic function was assessed with series of tests administered on the day prior to surgery, just before discharge from the hospital (mean 8.0, SD 5.8 days postoperatively, n = 82), and again 7 months later (mean 220.7, SD 54.4 days postoperatively, n = 75). The scores at 8 days showed wide variability and generalized impairment unrelated to the PaCO2 group or to hypotension during cardiopulmonary bypass. At 7 months no significant difference was observed in neuropsychologic performance between the PaCO2 groups. Regarding cardiac outcome, there were no significant differences between groups in the appearance of new Q-waves on the electrocardiogram, the postoperative creatine kinase-MB fraction, the need for inotropic or intraaortic balloon pump support, or the length of postoperative ventilation or intensive care unit stay. These findings support the hypothesis that CO2 management during cardiopulmonary bypass at moderate hypothermia has no clinically significant effect on either neurobehavioral or cardiac outcome.
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PMID:A randomized study of carbon dioxide management during hypothermic cardiopulmonary bypass. 235 31

To evaluate the effects of 5% carbon dioxide (CO2) administration for hypothermic circulatory arrest, neurological evaluation and pathological studies were carried out on the canine brain. Twenty-two dogs were assigned to five groups: Group 1: Three dogs without hypothermia were sacrificed as the control group. Group 2: Nine dogs were subjected to surface hypothermia (20 degrees C) under deep ether anesthesia with 100% oxygen (O2) and hyperventilation. Circulatory arrest time was 30 min in Group 2A and 60 min in Group 2B. Group 3: Ten dogs were surface cooled (20 degrees C) under deep ether anesthesia with a 95% O2 and 5% CO2 mixture. Thirty minutes of circulatory arrest was instituted in Group 3A and 60 min in Group 3B. Dogs in Groups 2 and 3 were surface rewarmed and kept alive until they were sacrificed electively 6 or more months later. Results were as follows: (i) Postoperative neurological disturbance was detected in only two dogs in Group 2B. (ii) The percentage of damaged nerve cells among the total nerve cells counted in the cerebral cortex of the frontal lobe was significantly greater in Groups 2A (22.4%), 2B (30.1%), 3A (19.6%), and 3B (22.2%) compared with Group 1 (7.1%). (iii) The number of glia cells per nerve cell in the cerebellar dentate nucleus was significantly higher in Group 2B (27.2) than in Groups 1 (11.8), 2A (16.7), 3A (17.9), and 3B (18.6). (iv) The number of Purkinje cells in a 10-mm length of the cerebellum was markedly reduced to 89 in Group 2B compared with 122, 134, and 117 in Groups 1, 2A, and 3A, respectively. In conclusion, the results of quantitative pathological brain analysis reflected the incidence of postoperative neurological disturbance and suggested that the administration of 5% CO2 could prolong the time limit for circulatory arrest.
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PMID:The effects of 5% carbon dioxide on the quantitative analysis of long-term pathology of the brain after surface hypothermia. 210 59

During surgery under pentobarbital sodium anesthesia, 20 rats had heat exchange devices implanted into their abdominal cavity. After recovery, 14 rats underwent two sets of trials, one in which body core temperature (Tbc) was lowered to 34.5-35.5 degrees C and another in which Tbc was raised to 40.5-41.5 degrees C. Rats breathed air and hypoxic (15, 11, and 7% O2 in N2) and hypercapnic (2, 4, and 6% CO2 in air) gas mixtures. Respiratory responses were measured using a barometric method and compared with data from the same rats breathing the gas mixtures at normal Tbc (37.5-38.5 degrees C) before surgery. The six remaining rats served as controls (Tbc unchanged). Lowering Tbc increased respiration in air, whereas heating had no effect. Hypothermia and severe hypoxia combined to inhibit respiration when compared with breathing air at lowered Tbc or low O2 at normal Tbc. The CO2 response slope became steeper when Tbc was raised, suggesting an increased CO2 sensitivity. Possible sites for the hypothermia-hypoxia interaction and the hyperthermia-hypercapnia interaction are discussed.
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PMID:Body temperature effects on hypoxic and hypercapnic responses in awake rats. 211 31

In ten lightly anaesthetized dogs breathing spontaneously, we studied diaphragmatic force generation (Pdi 10, 30, 100 Hz and single twitch) and ventilatory control (P 0, 1, Vt/Ti and respiratory frequency). We found CO2 retention proportional to hypothermia (Fig. 3). The TP was not changed while VMxA and VMxD decreased (Table 1). High frequency fatigue and low frequency potentiation were found (Fig. 1, 2). These changes do not explain CO2 retention which correlated with fall in central drive (P 0, 1, Vt/Ti, Fig. 3, 4) and respiratory timing (respiratory frequency, Fig. 4).
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PMID:[Diaphragmatic strength and ventilatory control in experimental hypothermia]. 213 Feb 40

Cardiac arrests (CA) occurring during anaesthesia and recovery can be classified into three groups: CA not related to anaesthesia (NACA), CA related to anaesthesia (ACA), whether partially (PACA) or totally (TACA). In the French survey, NACAs were three times more frequent than ACAs. Nearly 25% of ACAs occurred at induction and consisted mainly in TACAs. Another quarter of ACAs occurred during maintenance and consisted mainly in PACAs. About 50% of ACAs occurred after the end of anaesthesia and had the highest mortality rate. Cardiac arrest corresponds to the status of a heart unable to generate the minimum aortic blood flow required for functioning of vital organs. For the brain, a zero-blood flow of more than 4 seconds results in coma. Consequently CA exists when the time interval between two subsequent efficient systoles is greater than 4 seconds. Anaesthetic agents can result in CA by 1) overdose (absolute, relative), 2) anaphylactoid/anaphylactic reactions, 3) specific effects (acetylcholine-like effect, hyperkalaemia and malignant hyperthermia for succinylcholine; vagal effect of vecuronium and atracurium; cardiotoxicity of bupivacaine) and 4) drug interaction. In hypoxic CA, severe neurologic impairment often still exists at the time of onset of CA. The anaesthesia machine and controlled ventilation can induce CA by hypoxic ventilation, overdose of anaesthetic vapour, excessive CO2 reinhalation, hypoventilation, disconnection, excessive pressure in airways. Cardiac hypothermia can be a cause of CA as well as a cause of unsuccessful CPR. Massive infusion of unwarmed fluids and IPPV with unheated gases generate a temperature gradient within the heart which may result in severe arrhythmias and CA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac arrest during anesthesia and recovery period]. 214 88

During the last decade several studies of cerebral blood flow (CBF) and metabolism in the acute phase of head injury have been published. It is the aim of this review to describe the dynamic changes in CBF, cerebral metabolic rate of oxygen (CMRO2), cerebral autoregulation (CA), and reactivity to PaCO2 and barbiturate (metabolic reactivity) in the acute phase after severe head injury and to discuss the therapeutical consequences with reference to prolonged artificial hyperventilation, hypothermia, barbiturate sedation, and mannitol therapy. On the basis of present knowledge concerning cerebral circulation and its regulation, the author reviews the literature concerning methodology for experimental and clinical CBF measurements and regulation of CBF and cerebral oxygen uptake. Emphasis is placed on studies of the effect of body temperature (hypothermia) as a therapeutic tool in the control of cerebral metabolism, blood flow, and intracranial pressure. Although hypothermia significantly reduces cerebral metabolism and blood flow, the effect of hypothermia on cerebral blood flow, metabolism, ICP, and outcome after acute head injury has never been investigated in clinically controlled studies. Experimental and clinical studies concerning sensitivity of CBF for changes in PaCO2 are reviewed. The normal CO2 reactivity defined as absolute (delta CBF/delta PaCO2) and relative (% change CBF/delta PaCO2) or delta in CBF/PaCO2 mm Hg are mentioned. In awake normocapnic man the relative CO2 reactivity averages 4%/mm Hg and the absolute CO2 reactivity 2ml/mm Hg. Uncontrolled prospective studies show a therapeutic effect of artificially prolonged hyperventilation on outcome. Only one preliminary controlled study indicates that the outcome is poorer and recovery prolonged. Nevertheless, in the acute phase of HI, artificial hyperventilation is used routinely for control of intracranial hypertension and during the intensive care management of the patients. The steal and inverse steal phenomena are reviewed. Although of considerable theoretical interest these phenomena are without clinical significance in patients with head injury, unless clinical CBF measurements are performed. The frequency of the inverse steal phenomenon in studies of rCBF with a 16-channel Cerebrograph (intraarterial approach) is found to be about 10%. During prolonged hyperventilation experimental studies and clinical studies of apoplexy show an adaptation of CBF and CSF-pH and bicarbonate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. 227 29

Organ culture of murine thyroid allografts in hyperbaric oxygen (95% O2 at 25 psi, 37 degrees C) for 48 hr, results in prolonged allograft survival. Endocrine tissues can be cultured at 37 degrees C--however, this method may not be applicable to vascularized organs at normothermia. The aim of this study was to apply hyperbaric oxygen culture (HOC) under organ preservation conditions (hypothermia, UW solution) that have been shown to be successful in clinical organ transplantation. B10BR/SGSNJ murine thyroid lobes were transplanted beneath the kidney capsule of C57BL/10J recipients. Thyroids were cultured in Eagle's MEM at 37 degrees C (controls) and at 5 degrees C, under hyperbaric conditions (95% O2:5% CO2, 25 psi). Alternatively, thyroids were cultured in UW solution (+/- allopurinol/GSH) at 5 degrees C, for up to 7 days. Graft survival was determined 21 days posttransplant by 125I uptake and by histology. In Eagle's MEM, HOC at 37 degrees C/48 hr and 5 degrees C/7 days, resulted in 93% and 20% allograft survivals, respectively. In UW solution (- allopurinol/glutathione [GSH]), HOC at 5 degrees C/7 days resulted in 83% allograft survival: immunoperoxidase staining showed a decrease of MHC class I alloantigen expression. Oxygen free radical scavenger (allopurinol/GSH) addition to the UW solution diminished this effect and suggested an oxygen free radical-mediated mechanism in immunoalteration. These results demonstrate that HOC for 7 days reduced the antigenicity and immunogenicity of murine thyroid grafts under conditions that simulate organ preservation. Hypothermic hyperbaric oxygen culture conditions require testing in a higher animal species and in vascularized grafts to determine if this method can be applied to whole-organ transplantation.
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PMID:Prolonged survival of murine thyroid allografts after 7 days of hyperbaric organ culture in the UW preservation solution at hypothermia. 233 13

With the pH-stat acid-base regulation strategy during hypothermic cardiopulmonary bypass (CPB), carbon dioxide (CO2) is generally administered to maintain the partial pressure of arterial CO2 at a higher level than with the alpha-stat method. With preserved CO2 vasoreactivity during CPB, this induction of "respiratory acidosis" can lead to a much higher cerebral blood flow level than is motivated metabolically. To evaluate CO2 vasoreactivity, cerebral blood flow was measured using a xenon 133 washout technique before, during, and after CPB at different CO2 levels in patients who were undergoing coronary artery bypass grafting with perfusion at either hypothermia or normothermia. The overall CO2 reactivity was 1.2 mL/100 g/min/mm Hg. There was no difference between the groups. The CO2 reactivity was not affected by temperature or CPB. The induced hemodilution resulted in higher cerebral blood flow levels during CPB, although this was counteracted by the temperature-dependent decrease in the hypothermia group. After CPB, a transient increase in cerebral blood flow was noted in the hypothermia group, the reason for which remains unclear. The study shows that manipulation of the CO2 level at different temperatures results in similar changes in cerebral blood flow irrespective of the estimated metabolic demand. This finding further elucidates the question of whether alpha-stat or pH-stat is the most physiological way to regulate the acid-base balance during hypothermic CPB.
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PMID:Cerebral vasoreactivity to carbon dioxide during cardiopulmonary perfusion at normothermia and hypothermia. 259 9

The effects of arterial alphastat regulation on brain intracellular pH (pHi) and several phosphate metabolites were assessed in anesthetized rats during hypothermia (28.6 +/- 0.2 degrees C) and normothermia (36.2 +/- 0.2 degrees C) by using 31P high-field (8.5 T) nuclear magnetic resonance (NMR). There were significant differences in pHi and metabolite ratios at the two temperatures under conditions of equal minute ventilation. During hypothermia, the brain pHi was 0.09 U higher, the phosphocreatine-to-inorganic phosphate (PCR/Pi) ratio 49% larger, and Pi-to-ATP 20% lower than at normothermia. These changes were fully reversible on warming the animal. The change in brain pHi/temperature was -0.011U/degrees C (95% confidence interval -0.007 to -0.016). The brain's ability to regulate its pHi and phosphate metabolism during hypercapnic acid-base stress was studied by using 10% CO2 ventilation. Hypothermic rats showed a larger fall in brain pHi (0.145 +/- 0.01 U, 7.15-7.01) with 10% CO2 than normothermic rats (0.10 +/- 0.02 U, 7.06-6.96). Similarly ventilated rats had a larger fall in arterial pH with 10% CO2 at hypothermia (0.36 +/- 0.04 U) than normothermia (0.24 +/- 0.01 U), so the delta brain pH/delta arterial pH was the same at both temperatures. The brain PCr-to-Pi ratio decreased approximately 20% during 10% CO2 breathing in both hypothermic and normothermic animals. Brain pHi and metabolite ratios returned to base line 30-50 min after CO2 washout in both groups. In summary, lowering body temperature while maintaining constant ventilation leads to changes in brain pHi and metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothermia on rat brain pHi and phosphate metabolite regulation by 31P-NMR. 260 61


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