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

Previous retrospective studies report a core body temperature cooling rate of 3 degrees C/h during avalanche burial. Hypercapnia occurs during avalanche burial secondary to rebreathing expired air, and the effect of hypercapnia on hypothermia during avalanche burial is unknown. The objective of this study was to determine the core temperature cooling rate during snow burial under normocapnic and hypercapnic conditions. We measured rectal core body temperature (T(re)) in 12 subjects buried in compacted snow dressed in a lightweight clothing insulation system during two different study burials. In one burial, subjects breathed with a device (AvaLung 2, Black Diamond Equipment) that resulted in hypercapnia over 30-60 min. In a control burial, subjects were buried under identical conditions with a modified breathing device that maintained normocapnia. Mean snow temperature was -2.5 +/- 2.0 degrees C. Burial time was 49 +/- 14 min in the hypercapnic study and 60 min in the normocapnic study (P = 0.02). Rate of decrease in T(re) was greater with hypercapnia (1.2 degrees C/h by multiple regression analysis, 95% confidence limits of 1.1-1.3 degrees C/h) than with normocapnia (0.7 degrees C/h, 95% confidence limit of 0.6-0.8 degrees C/h). In the hypercapnic study, the fraction of inspired carbon dioxide increased from 1.4 +/- 1.0 to 7.0 +/- 1.4%, minute ventilation increased from 15 +/- 7 to 40 +/- 12 l/min, and oxygen saturation decreased from 97 +/- 1 to 90 +/- 6% (P < 0.01). During the normocapnic study, these parameters remained unchanged. In this study, T(re) cooling rate during snow burial was less than previously reported and was increased by hypercapnia. This may have important implications for prehospital treatment of avalanche burial victims.
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PMID:Hypercapnia increases core temperature cooling rate during snow burial. 1466 May 14

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

Elevation of the i.c.v. injection dose of TSKY from 4 to 8 microg increased the movement activity of rats; in EEG theta- and beta-rhythms were enhanced and alpha-rhythm was suppressed. On the contrary, after treatment of 15 microg the rats fell into sleepy-like state; theta- and beta2-rhythms suppression, delta-, alpha- and beta1-rhythms were increased. Exposure under hypoxia-hypercapnia conditions reduced body temperature of mice to 18-19 degrees C, and maintain this state about 3-4 h after transferring into conventional gas medium. Preliminary cooling mice were administrated with TSKY that at dose 100 microg intraperitonally induced a prolonged hypothermia up to 12 h. Analogous injection without cooling raised mice temperature by 1.2 degrees C during about 2 h.
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PMID:[The effects of artificial analogue peptide TSKY isolated from the brain of hibernating ground squirrels in rats and mice]. 1582 26

In North America and Europe around 140 persons die every year due to avalanches, approximately 35 in North America, 100 in the European Alps, and 5 in other parts of Europe. Most of the victims are skiers and snowboarders. This article outlines the specific pathophysiology of avalanche burials, such as hypoxia, hypercapnia, and hypothermia and also other factors which influence survival. Strategies to minimize the mortality due to avalanches and the on-site treatment of buried persons are discussed. Finally, possibilities to reduce the number of avalanche deaths are pointed out.
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PMID:[Avalanche emergencies. Review of the current situation]. 1650 39

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

Cardiac arrest is a common disease in the United States, and many patients will die as a result of the neurological damage suffered during the anoxic period, or will live in a neurologically debilitated state. When cardiopulmonary-cerebral resuscitation results in the return of spontaneous circulation, intensive care is required to optimize neurological recovery. Such "brain-oriented" therapies include routine care, such as positioning and maintenance of volume status; optimization of cerebral perfusion, with the use of vasopressors if needed; management of increased intracranial pressure with agents such as hypertonic saline; assuring adequate oxygenation and avoiding hypercapnia; aggressive fever control; intensive glucose control, with the use of an insulin drip if needed; and management of seizures if they occur. To date, no neuroprotectant medications have been shown to improve neurological outcome. Induced moderate therapeutic hypothermia is utilized as a neuroprotective maneuver. Future treatment options and advanced monitoring techniques are also discussed. Further study to optimize neuroprotective strategies when treating patients who survive cardiac arrest is needed.
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PMID:Postresuscitative intensive care: neuroprotective strategies after cardiac arrest. 1696 40

Myxedema coma is the term given to the most severe presentation of profound hypothyroidism and is often fatal in spite of therapy. Decompensation of the hypothyroid patient into a coma may be precipitated by a number of drugs, systemic illnesses (eg, pneumonia), and other causes. It typically presents in older women in the winter months and is associated with signs of hypothyroidism, hypothermia, hyponatremia, hypercarbia, and hypoxemia. Treatment must be initiated promptly in an intensive care unit setting. Although thyroid hormone therapy is critical to survival, it remains uncertain whether it should be administered as thyroxine, triiodothyronine, or both. Adjunctive measures, such as ventilation, warming, fluids, antibiotics, pressors, and corticosteroids, may be essential for survival.
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PMID:Myxedema coma. 1712 41

The cooling of Wistar rats up to 15-19 degrees C under a condition hypoxia-hypercapnia increased the radioresistance with a dose reduction factor (DRF) of 1.4. To elucidate the mechanisms of hypothermia radioprotective effect was evaluated the functional state of rat neocortex using a electroencephalogram (EEG) as well as was studied the lipid composition of neocortex under the conditions of both normothermia and hypothermia. At 19-20 degrees C the activity within a wide range of frequencies in EEG was suppressed; the nonregular slow waves were recorded against a background of "silence". The reduction of EEG spectrum with increasing temperature began with the low frequencies. At 26-28 egresC the contribution of theta-rhythm (an indicator of brain activity level) in EEG reaches the normothermia value, from this point the rat brain starts to functionate as a whole system. At normothermia the similarity of neocortex lipid composition in nonhibernators (rats) and hibernators (ground squirrels) mammalians was noted. The difference is only in a higher content of phosphatidylinositol in rats. Rats falling into hypothermia state as well as ground squirrels into torpor is followed by a decrease of cholesterol content and the absence of significant changes of the phospholipid composition in neocortex tissues.
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PMID:[The effect of hypothermia on the rat radioresistance]. 1732 99

Cardiopulmonary resuscitation does not end with restoration of spontaneous circulation; rather, it must be continued with the application of all the measures that allow organ function to be maintained. The initial goal of hemodynamic treatment is to achieve normal blood pressure for the patient's age by means of fluids and/or vasoactive drugs. The aim of respiratory treatment is to normalize ventilation and oxygenation without causing further lung injury, avoiding hyperoxia and hyperventilation as well as hypoxia and hypercapnia. Neurological stabilization aims to reduce secondary brain damage, by avoiding hypertension and hypotension, maintaining normal ventilation and oxygenation, and treating hyperglycemia, agitation and seizures. Although no specific studies in children are available, data from adults have shown that early moderate hypothermia attenuates brain damage secondary to cardiorespiratory arrest, without increasing complications. After the arrest, the need for analgesia and/or sedation must be considered. The process of transportation to the pediatric intensive care unit (PICU) requires the following steps: stabilizing the patient, checking for and stabilizing fractures and external wounds, ensuring a stable airway and intravenous lines, assessing the need for nasogastric and bladder tubes, taking blood samples for analyses, contacting the PICU and informing the staff about the child's condition, choosing the optimal vehicle for transportation according to the child's condition and the distance, checking pediatric equipment and medications, selecting experienced staff and, finally, maintaining close surveillance and monitoring during transportation.
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PMID:[Post-resuscitation stabilization and transportation]. 1734 Jul 87

The objective of the treatment of intracranial hypertension is to decrease intracranial pressure (ICP) while maintaining cerebral blood flow (CBF). Despite numerous treatments, none of them associates total efficiency and security. Systemic secondary cerebral injuries, which are responsible for cerebral ischemia, lead us to administer non specific treatments in order to optimize CBF and cerebral oxygenation. Thus, the goals are: 1) to maintain cerebral perfusion pressure> or =70 mmHg; 2) to control metabolic status by preventing hyperglycaemia, anaemia and hyperthermia; 3) to maintain normoxia and normocapnia (hypercapnia increases ICP and hypocapnia decreases CBF). Beside the neurosurgical evacuation of extra- and intraparenchymatous haematomas, osmotherapy and cerebrospinal fluid (CSF) evacuation are the two specific treatments of intracranial hypertension. Osmotherapy consists in an administration of a hypertonic solution which induces a decrease in cerebral water and finally in ICP. Mannitol (20%), which is the reference, associates osmotic and rheologic effects, and decreases CSF production too. Recent data conduct us to administer larger doses, between 0.7 and 1 g/kg in 15 minutes. Hypertonic saline solution associates osmotic effects and plasma volume loading. Thus, this solution is particularly appropriate in severe head injury with arterial hypotension. CBF evacuation decreases rapidly ICP without any major side-effect. Until now, there is no proof of a superior efficiency of a treatment for intracranial hypertension compared to another. Considering their mechanism of action, all of them are efficient but potentially dangerous too. Indeed, the choice between treatments depends on data which are issued from the multimodal monitoring. General non specific treatments are always necessary. Specific treatments are indicated if ICP is above 20-25 mmHg. Maintaining cerebral perfusion pressure represents the first therapeutic goal. If intracranial hypertension persists, evacuation of CBF or osmotherapy may be advocated. In case of refractory intracranial hypertension, it may be useful to deepen neurosedation. Controlled hypocapnia and barbiturates remain a third line therapy providing to monitor and maintain an appropriate CBF and cerebral oxygenation. Controlled hypothermia and decompressive craniectomy must be individually discussed.
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PMID:[Hierarchical strategy for treating elevated intracranial pressure in severe traumatic brain injury]. 1785 Oct 25


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