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

It is important to know the effects of anaesthetics on cerebral blood flow and cerebral metabolism to enable appropriate selection of agents for the brain injured patient. Thiopental possesses favourable cerebrovascular and metabolic properties but has not been shown to improve outcome in head injured patients. Propofol has properties similar to thiopental. Its rapid metabolism as well as its ability to reduce intracranial pressure and its antiemetic properties render it a very favourable drug. Despite controversies surrounding the effects of short-acting narcotics on intracranial pressure, they continue to be used because they provide stable haemodynamic conditions when used with care. Isoflurane is currently advocated as the best inhalational agent for neuroanaesthesia because of its lesser effects on cerebral blood flow and intracranial pressure. The effects of nitrous oxide on cerebral blood flow and intracranial pressure appear to vary according to the background anaesthetic used. Nitrous oxide is still widely used in most neuroanaesthetic practices, as its effects can be blunted by barbiturates, narcotics and/or hypocapnia. There is no convincing human study on the cerebral protective properties of anaesthetic agents although mild hypothermia has been shown experimentally to offer significant protection against global and focal ischaemia.
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PMID:Cerebrovascular and cerebral metabolic effects of commonly used anaesthetics. 771 Feb 26

In the absence of reliable data, this work was performed to estimate the dose-effects function of carboxyhemoglobin (HbCO) on behavior in humans. Meta analysis is the quantitative analysis of the combined findings of a number of research reports. By meta analysis, an HbCO-behavior dose-effects function was estimated for rats and corrected for effects of hypothermia (which accompanies acute HbCO increases in rats but not in humans). By use of pulmonary function models and blood gas equations, equivalent HbCO values were calculated for data in the literature on hypoxic hypoxia and behavior. Another meta analysis was performed to fit a dose-effects function to the equivalent HbCO data and to correct for the behavioral effects of hypocapnia (which usually occurs during hypoxic hypoxia but not with HbCO elevation). The two extrapolations agreed closely and indicated that, for healthy sedentary persons, 18-25% HbCO would be required to produce a 10% decrement in behavior. Confidence intervals are computed to characterize the uncertainty. Frequent reports of lower-level effects are discussed.
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PMID:Behavioral effects of carbon monoxide: meta analyses and extrapolations. 800 76

Choreoathetosis developed in three patients after cardiopulmonary bypass with hypothermia. None had significant hypotension or hypoxemia; all had hypocapnia and respiratory alkalosis during the rewarming period. We postulate that hypocapnia-induced cerebral vasoconstriction may have contributed to ischemic damage in focal central nervous system areas.
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PMID:Choreoathetosis after surgery for congenital heart disease. 817 61

Based on a model of acute carbon monoxide (CO) poisoning in rats with an occluded left carotid artery, we have evaluated the effects of normobaric oxygen (NBO2) and hyperbaric oxygen (HBO2) on mortality and morbidity. After exposure to 2,700 ppm CO in air for 1 h, the rats were grouped and treated with air (group 1, untreated controls, in a previous study), 100 kPa O2 for 4 h (group 2), 300 kPa normoxia (group 3, pressure controls), and 300 kPa O2 (group 4) for 1 h, respectively. NBO2 started immediately, whereas HBO2 began 35 min after the end of the CO exposure. At the termination of the exposure, the four groups suffered identical levels of poisoning as indicated by the degrees of hypothermia, hypocapnia, drop in mean arterial pressure, and acidosis. Up to 48 h after the end of the CO exposure, mortalities were 76, 58, 75, and 17 in groups 1-4, respectively. The neurologic morbidities, indicated by abnormal motor behaviors and edema in the left cerebral hemispheres, were 84, 67, 83, and 42% in groups 1-4, respectively. Compared to the normoxic treatments, the HBO2, but not the NBO2, significantly reduced the mortality and the neurologic morbidity. HBO2 was also significantly better than NBO2 in increasing surviving time and survival rate. The results support the value of HBO2 in improving short-term outcome of acute CO poisoning in this rat model.
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PMID:Normobaric and hyperbaric oxygen treatment of acute carbon monoxide poisoning in rats. 917 69

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

Cardiopulmonary bypass (CPB) is one of the major tools of cardiac surgery. However, no clear data are available for the ideal value of sweep gas flow to oxygenator during CPB. The aim of this study was to determine the best value for sweep gas flow during CPB. Thirty patients undergoing isolated CABG were randomly and equally allocated into three groups. Sweep gas flow to oxygenator was kept at 1.35 l/min/m2 in group 1, 1.60 l/min/m2 in group 2, and 2.0 l/min/m2 in group 3. All patients were operated on under the same anaesthetic regime and surgical techniques. Samples for blood gas analysis were collected at T1: before CPB; T2: 5 min after the initiation of CPB; T3: just before rewarning; and T4: at the end of rewarming. Five minutes after the initiation of CPB (T2), pCO2 decreased significantly in groups 2 and 3 compared to group 1 (p < 0.02). With the addition of hypothermia (T3), the changes in the pH and pCO2 became more profound and, in this period, the levels in group 3 patients outranged the physiologic limits, with pCO2 and pH values being 28 +/- 3 mmHg and 7.50 +/- 0.04, respectively. At the end of the rewarming period (T4), in spite of increased carbon dioxide production, pCO2 values were below the physiologic limits in groups 2 and 3. We conclude that sweep gas flow to the oxygenator should be kept between 1.35 and 1.60 l/min/m2 during CPB to avoid hypocapnia, which results in alkalosis and has hazardous effects on lung mechanics, cerebral blood flow, and the cardiovascular system.
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PMID:Adjustment of sweep gas flow during cardiopulmonary bypass. 1224 39

Sevoflurane and propofol have been widely used as anesthetic agents for neurosurgery. Recent evidence has suggested that the influence of these anesthetics on cerebral oxygenation may differ. In the present study, the authors investigated jugular bulb oxygen saturation (SjO2) during propofol and sevoflurane/nitrous oxide anesthesia under mildly hypothermic conditions. After institutional approval and informed consent, 20 patients undergoing elective craniotomy were studied. Patients were randomly divided to the group S/N2O (sevoflurane/nitrous oxide/fentanyl anesthesia) or the group P (propofol/fentanyl anesthesia). After induction of anesthesia, the catheter was inserted retrograde into the jugular bulb and SjO2 was analyzed. During the operation, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. SjO2 was measured at normocapnia during mild hypothermia and at hypocapnia during mild hypothermia. There were no statistically significant differences in demographic variables between the groups. During mild hypothermia, SjO2 values were significantly lower in group P than in group S/N2O. The incidence of SjO2 less than 50% under mild hypothermic-hypocapnic conditions was significantly higher in group P than in group S/N2O. These results suggest that hyperventilation should be more cautiously applied during mild hypothermia in patients anesthetized with propofol and fentanyl versus sevoflurane/nitrous oxide/fentanyl.
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PMID:Jugular bulb oxygen saturation under propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild hypothermia in neurosurgical patients. 1467 62

During eupnoea, rhythmic motor activities of the hypoglossal, vagal and phrenic nerves are linked temporally. The inspiratory discharges of the hypoglossal and vagus motor neurones commence before the onset of the phrenic burst. The vagus nerve also discharges in expiration. Upon exposure to hypocapnia or hypothermia, the hypoglossal discharge became uncoupled from that of the phrenic nerve. This uncoupling was evidenced by variable times of onset of hypoglossal discharge before or after the onset of phrenic discharge, extra bursts of hypoglossal activity in neural expiration, or complete absence of any hypoglossal discharge during a respiratory cycle. No such changes were found for vagal discharge, which remained linked to the phrenic bursts. Intracellular recordings in the hypoglossal nucleus revealed that all changes in hypoglossal discharge were due to neuronal depolarization. These results add support to the conclusion that the brainstem control of respiratory-modulated hypoglossal activity differs from control of phrenic and vagal activity. These findings have implications for any studies in which activity of the hypoglossal nerve is used as the sole index of neural inspiration. Indeed, our results establish that hypoglossal discharge alone is an equivocal index of the pattern of overall ventilatory activity and that this is accentuated by hypercapnia and hypothermia.
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PMID:Uncoupling of rhythmic hypoglossal from phrenic activity in the rat. 1536 82

Trauma is the leading non-obstetric cause of maternal death. Optimal management of the pregnant trauma patient requires a multidisciplinary approach. The anaesthetist and critical care physician play a pivotal role in the entire continuum of fetomaternal care, from initial assessment, resuscitation and intraoperative management, to postoperative care that often involves critical care support and patient transfer. Primary goals are aggressive resuscitation of the mother and maintenance of uteroplacental perfusion and fetal oxygenation by the avoidance of hypoxia, hypotension, hypocapnia, acidosis and hypothermia. Recognizing and understanding the mechanisms of injury, the factors that may predict fetal outcome, and the pathophysiological changes that can result from trauma, will allow early identification and treatment of fetomaternal injury. This in turn should improve morbidity and mortality. A framework for the acute care of the pregnant trauma patient is presented.
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PMID:The pregnant trauma patient. 1596 Mar 98

The ventilatory responses to immersion and changes in temperature are reviewed. A fall in skin temperature elicits a powerful cardiorespiratory response, termed "cold shock," comprising an initial gasp, hypertension, and hyperventilation despite a profound hypocapnia. The physiology and neural pathways of this are examined with data from original studies. The respiratory responses to skin cooling override both conscious and other autonomic respiratory controls and may act as a precursor to drowning. There is emerging evidence that the combination of the reestablishment of respiratory rhythm following apnea, hypoxemia, and coincident sympathetic nervous and cyclic vagal stimulation appears to be an arrhythmogenic trigger. The potential clinical implications of this during wakefulness and sleep are discussed in relation to sudden death during immersion, underwater birth, and sleep apnea. A drop in deep body temperature leads to a slowing of respiration, which is more profound than the reduced metabolic demand seen with hypothermia, leading to hypercapnia and hypoxia. The control of respiration is abnormal during hypothermia, and correction of the hypoxia by inhalation of oxygen may lead to a further depression of ventilation and even respiratory arrest. The immediate care of patients with hypothermia needs to take these factors into account to maximize the chances of a favorable outcome for the rescued casualty.
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PMID:Respiratory responses to cold water immersion: neural pathways, interactions, and clinical consequences awake and asleep. 1671 16


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