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hypocapnia/demam

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Association between hypocapnia and febrile seizures.

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The purpose of this study is to determine whether hyperthermia-induced hyperventilation with subsequent hypocapnia is relevant to febrile seizures in children. This is only the second study to measure pCO2 and pH values in children with febrile seizures. This prospective case-control study enrolled

Association of Hypocapnia in Children with Febrile Seizures.

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Febrile seizure is a benign condition in children. Susceptibility genes associated with febrile convulsions have been identified, but the precise pathophysiologic mechanism that triggers febrile seizure is unclear. Using animal models, it has been demonstrated that hyperthermia causes

The influence of blood gas changes on hyperthermia-induced seizures in developing rats.

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Fever induces seizures in infants with febrile convulsions or epilepsy. Hyperpnea induced by fever may contribute to the induction of these seizures. In order to examine this possibility, we evaluated the effect of changes in arterial blood gas tension on hyperthermia-induced seizures in developing
OBJECTIVE To determine whether Labrador Retrievers participating in field trials develop respiratory alkalosis and hypocapnia primarily in conditions of high ambient temperatures. METHODS 16 Labrador Retrievers. METHODS At each of 5 field trials, 5 to 10 dogs were monitored during a test (retrieval

[A case of sarcoidosis presenting with high fever and acute respiratory failure].

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A 55-year-old man was admitted with complaints of remittent fever (39 degrees C) and dyspnea on exertion which began ten days previously. His family and past histories were non-contributory for diagnosis except his occupation as a stone mason for 26 years. The chest X-ray film taken on admission

Hyperthermia-induced cardiac arrest in dogs and monkeys.

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The pattern of dying from immersion hyperthermia was documented in 8 dogs, 9 rhesus monkeys and 12 pigtail monkeys. Under light general anesthesia and spontaneous breathing, the animals were immersed into water of 45 degrees C, which was subsequently adjusted to control brain (parietal epidural)

Cerebral oxygenation and hyperthermia.

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Hyperthermia is associated with marked reductions in cerebral blood flow (CBF). Increased distribution of cardiac output to the periphery, increases in alveolar ventilation and resultant hypocapnia each contribute to the fall in CBF during passive hyperthermia; however, their relative contribution

Human cardiorespiratory and cerebrovascular function during severe passive hyperthermia: effects of mild hypohydration.

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The influence of severe passive heat stress and hypohydration (Hypo) on cardiorespiratory and cerebrovascular function is not known. We hypothesized that 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q) would compromise blood flow velocity in the middle cerebral

Characteristics of hyperthermia-induced hyperventilation in humans.

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In humans, hyperthermia leads to activation of a set of thermoregulatory responses that includes cutaneous vasodilation and sweating. Hyperthermia also increases ventilation in humans, as is observed in panting dogs, but the physiological significance and characteristics of the hyperventilatory

Cerebrovascular and corticomotor function during progressive passive hyperthermia in humans.

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The present study examined the integrative effects of passive heating on cerebral perfusion and alterations in central motor drive. Eight participants underwent passive hyperthermia [0.5°C increments in core temperature (Tc) from normothermia (37 ± 0.3°C) to their limit of thermal tolerance (T-LIM;

[The current clinical spectrum of pulmonary thromboembolism].

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BACKGROUND. Mortality in pulmonary thromboembolism (PTE) decreases considerable when it is diagnosed early. The suspicion based on clinical and complementary data is essential for an early diagnosis. METHODS. Retrospective review of the clinical features in patients diagnosed of PTE in an Internal

Intraoperative events diagnosed by expired carbon dioxide monitoring in children.

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Expired carbon dioxide measurements (PeCO2) were used (1) to assess the adequacy of initial alveolar ventilation, and (2) to document intraoperative airway events and metabolic trends. Three hundred and thirty-one children were studied. Thirty-five intraoperative events were diagnosed by continuous

Impact of Secondary Insults in Brain Death After Traumatic Brain Injury.

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In addition to primary injury in severe head trauma, secondary systemic insults that aggravate the brain injury may result in fatal neurologic outcome. We aim to evaluate the correlation between brain death and secondary systemic insults in 100 patients with severe traumatic brain injury (TBI)

[Hierarchical strategy for treating elevated intracranial pressure in severe traumatic brain injury].

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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

[The internal environment and intracranial hypertension].

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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
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