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Hyperventilation
Selected AbstractsHyperventilation and the Pitt-Hopkins syndromeDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 7 2008Robert Ouvrier MD FRACP No abstract is available for this article. [source] Topiramate-induced metabolic acidosis: report of two casesDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2001Chun-hung Ko MRCP FHKAM Medical Officer Two children who presented with symptomatic metabolic acidosis after being put on topiramate (TPM) are reported. The first patient was an 11-year-old male with refractory complex partial epilepsy who was put on TPM for 13 months. He developed hyperventilation 1 week after increasing the dose to 300mg/day. Arterial blood gas revealed hyperchloraemic metabolic acidosis with partial respiratory compensation: pH 7.36, PCO2 27.2 mmHg, bicarbonate 14.9 mEq/L, base excess -8.9 mmol/L. Hyperventilation and acidosis resolved after administration of sodium bicarbonate and reduction of the dose of TPM. The second patient was a female who developed increasing irritability at age 16 months and 21 months, each time associated with introduction of TPM and resolved promptly upon withdrawal of the drug. Venous blood gas taken during the second episode revealed pH 7.34, PCO2 37.4 mmHg, bicarbonate 20.4 mEq/L, base excess -4.2 mmol/L. The predominant mechanism of TPM-induced hyperventilation involves inhibition of carbonic anhydrase at the proximal renal tubule, resulting in impaired proximal bicarbonate reabsorption. The occurrence of hyperpnoea or mental status change in any patient who is on TPM should prompt an urgent blood gas sampling, with correction of the acid-base disturbances accordingly. [source] Hyperventilation and Epileptic SeizuresEPILEPSIA, Issue 12 2004S. Nizam Ahmed No abstract is available for this article. [source] Twenty Years of "Hyperventilation": What is the Arrhythmia Mechanism?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2001PEDRO BRUGADA M.D. [source] Intraoperative hyperventilation vs remifentanil during electrocorticography for epilepsy surgery , a case reportACTA NEUROLOGICA SCANDINAVICA, Issue 6 2010T. W. Kjaer Kjaer TW, Madsen FF, Moltke FB, Uldall P, Hogenhaven H. Intraoperative hyperventilation vs remifentanil during electrocorticography for epilepsy surgery , a case report Acta Neurol Scand: 2010: 121: 413,417. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Background,,, Traditionally, intraoperative intracranial electroen-cephalography-recordings are limited to the detection of the irritative zone defined by interictal spikes. However, seizure patterns revealing the seizure onset zone are thought to give better localizing information, but are impractical due to the waiting time for spontaneous seizures. Therefore, provocation by seizure precipitants may be used with the precaution that spontaneous and provoked seizures may not be identical. Objective,,, We present evidence that hyperventilation induced and drug induced focal seizures may arise from different brain regions in the same patient. Methods,,, Hyperventilation and ultra short acting opioid remifentanil were used separately as intraoperative precipitatants of seizure patterns, while recording from subdural and intraventricular electrodes in a patient with temporal lobe epilepsy. Two different ictal onset zones appeared in response to hyperventilation and remifentanil. Both zones were resected and the patient has remained essentially seizure free for 1 year. Furthermore, this is the first description of hyperventilation used as an intraoperative seizure precipitant in human focal epilepsy. [source] Topiramate-induced metabolic acidosis: report of two casesDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 10 2001Chun-hung Ko MRCP FHKAM Medical Officer Two children who presented with symptomatic metabolic acidosis after being put on topiramate (TPM) are reported. The first patient was an 11-year-old male with refractory complex partial epilepsy who was put on TPM for 13 months. He developed hyperventilation 1 week after increasing the dose to 300mg/day. Arterial blood gas revealed hyperchloraemic metabolic acidosis with partial respiratory compensation: pH 7.36, PCO2 27.2 mmHg, bicarbonate 14.9 mEq/L, base excess -8.9 mmol/L. Hyperventilation and acidosis resolved after administration of sodium bicarbonate and reduction of the dose of TPM. The second patient was a female who developed increasing irritability at age 16 months and 21 months, each time associated with introduction of TPM and resolved promptly upon withdrawal of the drug. Venous blood gas taken during the second episode revealed pH 7.34, PCO2 37.4 mmHg, bicarbonate 20.4 mEq/L, base excess -4.2 mmol/L. The predominant mechanism of TPM-induced hyperventilation involves inhibition of carbonic anhydrase at the proximal renal tubule, resulting in impaired proximal bicarbonate reabsorption. The occurrence of hyperpnoea or mental status change in any patient who is on TPM should prompt an urgent blood gas sampling, with correction of the acid-base disturbances accordingly. [source] Electroclinical Picture of Autosomal Dominant Nocturnal Frontal Lobe Epilepsy in a Japanese FamilyEPILEPSIA, Issue 1 2000Masatoshi Ito Summary: Purpose: Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is the first described partial epilepsy syndrome known to be due to a single gene mutation. We found a first Japanese ADNFLE family with a novel mutation of the neuronal nicotinic acetylcholine receptor (nAChR) ,4 subunit (CHRNA4) gene. The aim of this report is precisely to describe the electroclinical manifestations of ADNFLE in this family and to compare these findings with those of other families reported previously in the literature. Methods: Three affected family members were investigated electroclinically by close clinical observation, interictal EEG, video-EEG monitoring, magnetic resonance imaging, and single-photon-emission tomography. Information about other affected family members was obtained from either the spouse or the parents. Mutations within the CHRNA4 gene were examined in seven family members. Results: The clinical manifestations and diagnostic findings in the members of this family were consistent with ADNFLE. However, there were intrafamilial and interfamilial variations in clinical features. The seizures of the patients were brief tonic seizures, with hyperventilation in children and secondarily generalized tonic,clonic convulsions in adults. The onset of the children's seizures began in infancy and early childhood. The children's seizures were sometimes provoked by movement and sound stimulation, and did not respond to antiepileptic drugs. On the other hand, the adults' seizures disappeared spontaneously or were easily controlled with carbamazepine. Three children showed hyperactivity, and two children had mild mental retardation. All patients had impaired consciousness during their seizures and no auras. A novel missense mutation (c755C>T) in exon 5 of the CHRNA4 gene was found in four affected family members. Conclusions: The electroclinical pictures of a Japanese family with ADNFLE were basically the same as those of other families reported, but with slight differences. ADNFLE is probably not uncommon, and it is very likely that there are unidentified patients with this inherited disorder in Japan. [source] Arterial blood gas parameters of normal foals born at 1500 metres elevationEQUINE VETERINARY JOURNAL, Issue 1 2010E. S. HACKETT Summary Reasons for performing study: Arterial blood gas analysis is widely accepted as a diagnostic tool to assess respiratory function in neonates. To the authors' knowledge, there are no published reports of arterial blood gas parameters in normal neonatal foals at altitude. Objective: To provide information on arterial blood gas parameters of normal foals born at 1500 m elevation (Fort Collins, Colorado) in the first 48 h post partum. Hypothesis: Foals born at 1500 m will have lower PaO2 and PaCO2 than foals born at sea level due to low inspired oxygen and compensatory hyperventilation occurring at altitude. Methods: Sixteen foals were studied. Arterial blood gas analysis was performed within 1 h of foaling and subsequent samples were evaluated at 3, 6, 12, 24 and 48 h post partum. Data were compared to those previously reported in healthy foals born near sea level. Results: Mean PaO2 was 53.0 mmHg (7.06 kPa) within 1 h of foaling, rising to 67.5 mmHg (9.00 kPa) at 48 h post partum. PaCO2 was 44.1 mmHg (5.88 kPa) within one hour of foaling, falling to 38.3 mmHg (5.11 kPa) at 48 h. Both PaO2 and PaCO2 were significantly lower in foals born at 1500 m elevation than those near sea level at several time points during the first 48 h. Conclusions and potential relevance: Foals at 1500 m elevation undergo hypobaric hypoxia and compensatory hyperventilation in the first 48 h. Altitude specific normal arterial blood values are an important reference for veterinarians providing critical care to equine neonates. [source] EFNS guideline on the treatment of cerebral venous and sinus thrombosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2006K. Einhäupl Cerebral venous and sinus thrombosis (CVST) is a rather rare disease which accounts for <1% of all strokes. Diagnosis is still frequently overlooked or delayed due to the wide spectrum of clinical symptoms and the often subacute or lingering onset. Current therapeutic measures which are used in clinical practice include the use of anticoagulants such as dose-adjusted intravenous heparin or body weight-adjusted subcutaneous low-molecular-weight heparin (LMWH), the use of thrombolysis, and symptomatic therapy including control of seizures and elevated intracranial pressure. We searched MEDLINE (National Library of Medicine), the Cochrane Central Register of Controlled Trials (CENTRAL) and the Cochrane Library to review the strength of evidence to support these interventions and the preparation of recommendations on the therapy of CVST based on the best available evidence. Review articles and book chapters were also included. Recommendations were reached by consensus. Where there was a lack of evidence, but consensus was clear we stated our opinion as good practice points. Patients with CVST without contraindications for anticoagulation should be treated either with body weight-adjusted subcutaneous LMWH or dose-adjusted intravenous heparin (good practice point). Concomitant intracranial haemorrhage related to CVST is not a contraindication for heparin therapy. The optimal duration of oral anticoagulation after the acute phase is unclear. Oral anticoagulation may be given for 3 months if CVST was secondary to a transient risk factor, for 6,12 months in patients with idiopathic CVST and in those with ,mild' hereditary thrombophilia. Indefinite anticoagulation (AC) should be considered in patients with two or more episodes of CVST and in those with one episode of CVST and ,severe' hereditary thrombophilia (good practice point). There is insufficient evidence to support the use of either systemic or local thrombolysis in patients with CVST. If patients deteriorate despite adequate anticoagulation and other causes of deterioration have been ruled out, thrombolysis may be a therapeutic option in selected cases, possibly in those without intracranial haemorrhage (good practice point). There are no controlled data about the risks and benefits of certain therapeutic measures to reduce an elevated intracranial pressure (with brain displacement) in patients with severe CVST. Antioedema treatment (including hyperventilation, osmotic diuretics and craniectomy) should be used as life saving interventions (good practice point). [source] Effects of hyperventilation on fast goal-directed limb movements in spinocerebellar ataxia type 6EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001M.-U. Manto It has been shown previously that hyperventilation modifies the features of the nystagmus in cerebellar patients (Walker and Zee, 1999). It has been hypothesized that hyperventilation influences the oculomotor control through a metabolic effect on cerebellar calcium channels, which play a critical role in the firing behaviour of neuronal populations in the cerebellum. This hypothesis has been tested here by analysing fast goal-directed limb movements before and after hyperventilation in spinocerebellar ataxia type 6 (SCA-6), a disease associated with a polyglutamine expansion in the , 1-A voltage-dependent calcium channel. Cerebellar hypermetria associated with fast distal single-joint movements was found to be increased following hyperventilation in patients presenting SCA-6 but remained unchanged in patients with idiopathic late-onset cerebellar degeneration (ILOCA). This is a new provocative test to enhance distal dysmetria in SCA-6. The present results strengthen the hypothesis of Walker and Zee. It is suggested that hyperventilation enhances the defective calcium transfers in SCA-6, resulting in an impairment of the calcium influx in particular into Purkinje cells involved in the control of fast goal-directed voluntary movements. [source] Ventilatory control in humans: constraints and limitationsEXPERIMENTAL PHYSIOLOGY, Issue 2 2007Susan A. Ward Below the lactate threshold (,L), ventilation responds in close proportion to CO2 output to regulate arterial partial pressure of CO2. While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic ,coupling' between and . Above ,L, is driven down to constrain the fall of arterial pH by a compensatory hyperventilation, probably of carotid body origin. When requirements are high (as in highly fit endurance athletes), can attain limiting proportions. Not only does this impair gas exchange at these work rates, but there may be an associated high metabolic cost for generation of respiratory muscle power, which may be sufficient to divert a fraction of the cardiac output away from the muscles of locomotion to the respiratory muscles, further compromising exercise tolerance. [source] The Contribution of Chemoreflex Drives to Resting Breathing in ManEXPERIMENTAL PHYSIOLOGY, Issue 1 2001Safraaz Mahamed The contribution of automatic drives to breathing at rest, relative to behavioural drives such as ,wakefulness', has been a subject of debate. We measured the combined central and peripheral chemoreflex contribution to resting ventilation using a modified rebreathing method that included a prior hyperventilation and addition of oxygen to maintain isoxia at a PET,O2 (end-tidal partial pressure of oxygen) of 100 mmHg. During rebreathing, ventilation was unrelated to PET,CO2 (end-tidal partial pressure of carbon dioxide) in the hypocapnic range, but after a threshold PET,CO2 was exceeded, ventilation increased linearly with PET,CO2. We considered the sub-threshold ventilation to be an estimate of the behavioural drives to breathe (mean ± S.E.M. = 3.1 ± 0.5 l min,1), and compared it to ventilation at rest (mean ± S.E.M. = 9.1 ± 0.7 l min,1). The difference was significant (Student's paired t test, P < 0.001). We also considered the threshold PCO2 observed during rebreathing to be an estimate of the chemoreflex threshold at rest (mean ± S.E.M. = 42.0 ± 0.5 mmHg). However, PET,CO2 during rebreathing estimates mixed venous or tissue PCO2, whereas the resting PET,CO2 during resting breathing estimates Pa,CO2 (arterial partial pressure of carbon dioxide). The chemoreflex threshold measured during rebreathing was therefore reduced by the difference in PET,CO2 at rest and at the start of rebreathing (the plateau estimates the mixed venous PCO2 at rest) in order to make comparisons. The corrected chemoreflex thresholds (mean ± S.E.M. = 26.0 ± 0.9 mmHg) were significantly less (paired Student's t test, P < 0.001) than the resting PET,CO2 values (mean ± S.E.M. = 34.3 ± 0.5 mmHg). We conclude that both the behavioural and chemoreflex drives contribute to resting ventilation. [source] Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PETACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2010L. SCHLÜNZEN Background: Arterial carbon dioxide tension (PaCO2) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). Methods: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H215O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. Results: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO2 was decreased from 5.5 ± 0.7 to 3.8 ± 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. Conclusions: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia. [source] Salt stress and resistance to hypoxic challenges in the common carp (Cyprinus carpio L.)JOURNAL OF FISH BIOLOGY, Issue 3 2000G. De Boeck Long term exposure to brackish water (171 mm NaCl) affected the capacity of common carp Cyprinus carpio to deal with hypoxic conditions and the critical oxygen concentrations for oxygen consumption increased. In addition, regulation of ammonia excretion was lost. The cytosolic phosphorylation potential (the index of the energy status of a cell in terms of potential transferable phosphate groups) in the lateral muscle on the other hand remained relatively unaffected, indicating that oxygen transport to the tissues was not severely compromised. It appears that exposure to brackish water reduces the capacity of common carp to cope with hypoxic conditions mainly because of the high energetic cost of hyperventilation under conditions where energy stores are depleted, and not because of any impeded oxygen transport mechanisms. [source] Application of intensive care medicine principles in the management of the acute liver failure patientLIVER TRANSPLANTATION, Issue S2 2008David J. Kramer Key Points 1Acute liver failure is a paradigm for multiple system organ failure that develops as a consequence of sepsis. 2In the United States, systemic inflammatory response, sepsis, and septic shock are common reasons for intensive care unit admission. Intensive care management of these patients serves as a template for the management of patients with acute liver failure. 3Acute liver failure is attended by high mortality. Although intensive care results in improved survival, the key treatment is liver transplantation. Intensive care unit intervention may open a "window of opportunity" and enable successful liver transplantation in patients who are too ill at presentation. 4Intracranial hypertension complicates the course for many patients with acute liver failure. Initially, intracranial hypertension results from hyperemia, which is cerebral edema that reduces cerebral blood flow and eventuates in herniation. The precepts of neurocritical care,monitoring cerebral perfusion pressure, cerebral blood flow, and cortical activity,with rapid response to hemodynamic abnormalities, maintenance of normoxia, euglycemia, control of seizures, therapeutic hypothermia, osmotic therapy, and judicious hyperventilation are key to reducing mortality attributable to neurologic failure. Liver Transpl 14:S85,S89, 2008. © 2008 AASLD. [source] Brain edema in liver failure: Basic physiologic principles and managementLIVER TRANSPLANTATION, Issue 11 2002Fin Stolze Larsen MD In patients with severe liver failure, brain edema is a frequent and serious complication that may result in high intracranial pressure and brain damage. This short article focuses on basic physiologic principles that determine water flux across the blood-brain barrier. Using the Starling equation, it is evident that both the osmotic and hydrostatic pressure gradients are imbalanced across the blood-brain barrier in patients with acute liver failure. This combination will tend to favor cerebral capillary water influx to the brain. In contrast, the disequilibration of the Starling forces seems to be less pronounced in patients with cirrhosis because the regulation of cerebral blood flow is preserved and the arterial ammonia concentration is lower compared with that of patients with acute liver failure. Treatments that are known to reverse high intracranial pressure tend to decrease the osmotic pressure gradients across the blood-brain barrier. Recent studies indicate that interventions that restrict cerebral blood flow, such as hyperventilation, hypothermia, and indomethacin, are also efficient in preventing edema and high intracranial pressure, probably by decreasing the transcapillary hydrostatic pressure gradient. In our opinion, it is important to recall that rational fluid therapy, adequate ventilation, and temperature control are of direct importance to controlling cerebral capillary water flux in patients with acute liver failure. These simple interventions should be secured before more advanced experimental technologies are instituted to treat these patients. [source] Anesthesia for free vascularized tissue transferMICROSURGERY, Issue 2 2009Natalia Hagau M.D., Ph.D. Anesthesia may be an important factor in maximizing the success of microsurgery by controlling the hemodynamics and the regional blood flow. The intraanesthetic basic goal is to maintain an optimal blood flow for the vascularized free flap by: increasing the circulatory blood flow, maintaining a normal body temperature to avoid peripheral vasoconstriction, reducing vasoconstriction resulted from pain, anxiety, hyperventilation, or some drugs, treating hypotension caused by extensive sympathetic block and low cardiac output. A hyperdynamic circulation can be obtained by hypervolemic or normovolemic hemodilution and by decrease of systemic vascular resistance. The importance of proper volume replacement has been widely accepted, but the optimal strategy is still open to debate. General anesthesia combined with various types of regional anesthesia is largely preferred for microvascular surgery. Maintenance of homeostasis through avoidance of hyperoxia, hypocapnia, and hypovolemia (all factors that can decrease cardiac output and induce local vasoconstriction) is a well-established perioperative goal. As the ischemia,reperfusion injury could occur, inhalatory anesthetics as sevoflurane (that attenuate the consequences of this process) seem to be the anesthetics of choice. © 2008 Wiley-Liss, Inc. Microsurgery, 2009. [source] Decreased cortical inhibition and yet cerebellar pathology in ,familial cortical myoclonic tremor with epilepsy'MOVEMENT DISORDERS, Issue 16 2007Anne-Fleur van Rootselaar MD Abstract Cortical hyperexcitability is a feature of "familial cortical myoclonic tremor with epilepsy" (FCMTE). However, neuropathological investigations in a single FCMTE patient showed isolated cerebellar pathology. Pathological investigations in a second FCMTE patient, reported here, confirmed cerebellar Purkinje cell degeneration and a normal sensorimotor cortex. Subsequently, we sought to explore the nature of cerebellar and motor system pathophysiology in FCMTE. Eye movement recordings and transcranial magnetic stimulation performed in six related FCMTE patients showed impaired saccades and smooth pursuit and downbeat nystagmus upon hyperventilation, as in patients with spinocerebellar ataxia type 6. In FCMTE patients short-interval intracortical inhibition (SICI) was significantly reduced. Resting motor threshold, recruitment curve, silent period, and intracortical facilitation were normal. The neuropathological and ocular motor abnormalities indicate cerebellar involvement in FCMTE patients. Decreased SICI is compatible with intracortical GABAA -ergic dysfunction. Cerebellar and intracortical functional changes could result from a common mechanism such as a channelopathy. Alternatively, decreased cortical inhibition may be caused by dysfunction of the cerebello-thalamo-cortical loop as a result of primary cerebellar pathology. © 2007 Movement Disorder Society [source] How do anaesthesiologists treat malignant hyperthermia in a full-scale anaesthesia simulator?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2001T. i Gardi Background: Clinical malignant hyperthermia (MH) is rare and usually occurs unexpectedly. Prompt diagnosis and correct treatment is crucial for survival of the patient developing fulminant MH. The aims of the present study were to investigate whether anaesthesiologists could make a correct diagnosis of MH and to evaluate their treatment of fulminant MH in a simulator. Methods: Thirty-two teams (one anaesthesiologist/one nurse anaesthetist) were exposed to an event of clinical MH in a full-scale simulator. Their performance was videotaped for retrospective analysis of the treatment on the basis of the recommendations of the Danish Malignant Hyperthermia Register. Results: All 32 teams asked the surgeon to terminate the surgery as fast as possible, switched off the vaporiser and administered 100% oxygen. Although all intended to hyperventilate the patient, only 14 teams actually managed to perform the hyperventilation. Most problems were found in teams that switched to manual ventilation. All teams treated the patient with dantrolene, and symptomatic treatment was initiated by all even though some elements of the full treatment were lacking, possibly due to the limited time available. Conclusion: All teams diagnosed MH in the simulator satisfactorily. The surprising negative finding was that more than half of the participants failed to hyperventilate the "patient" although they intended to do so. This investigation shows that the problem in these teams' treatment of MH was more a question of practical management of the resources than lack of theoretical knowledge. [source] Management of critically ill children with traumatic brain injuryPEDIATRIC ANESTHESIA, Issue 6 2008GILLES A. ORLIAGUET MD PhD Summary The management of critically ill children with traumatic brain injury (TBI) requires a precise assessment of the brain lesions but also of potentially associated extra-cranial injuries. Children with severe TBI should be treated in a pediatric trauma center, if possible. Initial assessment relies mainly upon clinical examination, trans-cranial Doppler ultrasonography and body CT scan. Neurosurgical operations are rarely necessary in these patients, except in the case of a compressive subdural or epidural hematoma. On the other hand, one of the major goals of resuscitation in these children is aimed at protecting against secondary brain insults (SBI). SBI are mainly because of systemic hypotension, hypoxia, hypercarbia, anemia and hyperglycemia. Cerebral perfusion pressure (CPP = mean arterial blood pressure , intracranial pressure: ICP) should be monitored and optimized as soon as possible, taking into account age-related differences in optimal CPP goals. Different general maneuvers must be applied in these patients early during their treatment (control of fever, avoidance of jugular venous outflow obstruction, maintenance of adequate arterial oxygenation, normocarbia, sedation,analgesia and normovolemia). In the case of increased ICP and/or decreased CPP, first-tier ICP-specific treatments may be implemented, including cerebrospinal fluid drainage, if possible, osmotic therapy and moderate hyperventilation. In the case of refractory intracranial hypertension, second-tier therapy (profound hyperventilation with PaCO2 < 35 mmHg, high-dose barbiturates, moderate hypothermia, decompressive craniectomy) may be introduced, after a new cerebral CT scan. [source] Acrodermatitis Enteropathica-like Dermatosis Associated with Ornithine Transcarbamylase DeficiencyPEDIATRIC DERMATOLOGY, Issue 4 2007José C. Pascual M.D. Ornithine transcarbamylase deficiency is the most frequent urea cycle disorder. It is a hereditary-X-linked disease with over 150 mutations described (1).Ornithine transcarbamylase deficiency causes vomiting, lethargy, hyperventilation, and even death, mainly in the neonatal period (2). Ammonia, an extremely toxic molecule for the organism, is generated during protein catabolism and is accumulated in patients with this deficiency. Part of the treatment consists of a low-protein diet, to avoid hyperammonemia episodes, which can even have a fatal outcome. Patients can become deficient in several amino acids, either through the low-protein diet or directly through the primary enzyme deficiency; this in turn can cause an acrodermatitis enteropathica-like dermatosis. [source] Decreased blood flow of the left thalamus during somnolent episodes in a case of recurrent hypersomniaPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 3 2002IWAO NOSE md Abstract A 24-year-old male with recurrent hypersomnia associated with decreased blood flow in the thalamus on single photon emission computed tomography (SPECT) is reported. In the hypersomnolent period, the decrease of blood flow in the left thalamus was revealed in the SPECT and slow waves appeared sporadically or sometimes as a burst on the electroencephalogram (EEG). In a phase of insomnia in the convalescent period there were almost no slow waves in the resting EEG but many slow waves appeared on hyperventilation EEG and the power spectrum at this hyperventilation resembled the power spectrum at the resting EEG in the hypersomnolent period. In the remission period there was no abnormal data in these testings. [source] Monitoring asthma therapy using indirect bronchial provocation tests,THE CLINICAL RESPIRATORY JOURNAL, Issue 1 2007John D. Brannan Abstract Objectives:, Bronchial provocation tests that assess airway hyperresponsiveness (AHR) are known to be useful in assisting the diagnosis of asthma and in monitoring inhaled corticosteroid therapy. We reviewed the use of bronchial provocation tests that use stimuli that act indirectly for monitoring the benefits of inhaled corticosteroids. Data Source:, Published clinical trials investigating the effect of inhaled corticosteroids on bronchial hyperresponsiveness in persons with asthma were used for this review. Study Selection:, Studies using indirect stimuli to provoke airway narrowing such as exercise, eucapnic voluntary hyperventilation, cold air hyperventilation, hypertonic saline, mannitol, or adenosine monophosphate (AMP) to assess the effect of inhaled corticosteroids were selected. Results:, Stimuli acting indirectly result in the release of a variety of bronchoconstricting mediators such as leukotrienes, prostaglandins, and histamine, from cells such as mast cells and eosinophils. A positive response to indirect stimuli is suggestive of active inflammation and AHR that is consistent with a diagnosis of asthma. Persons with a positive response to indirect stimuli benefit from daily treatment with inhaled corticosteroids. Symptoms and lung function are not useful to predict the long-term success of inhaled corticosteroid dose as they usually resolve rapidly, and well before inflammation and AHR has resolved. Following treatment, AHR to indirect stimuli is attenuated. Further, during long-term treatment, asthmatics can become as non-responsive as non-asthmatic healthy persons, suggesting that asthma is not active. Conclusions:, Non-responsiveness to indirect bronchial provocation tests following inhaled corticosteroids occurs weeks to months following the resolution of symptoms and lung function. Non-responsiveness to indirect stimuli may provide a goal for adequate therapy with inhaled corticosteroids. Please cite this paper as: Brannan JD, Koskela H and Anderson SD. Monitoring asthma therapy using indirect bronchial provocation tests. The Clinical Respiratory Journal 2007;1:3,15. [source] The Rett Syndrome Behaviour Questionnaire (RSBQ): refining the behavioural phenotype of Rett syndromeTHE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 8 2002Rebecca H. Mount Background: Although physical features, including loss of hand skills, deceleration of head growth, spasticity and scoliosis, are cardinal features of Rett syndrome (RS), a number of behavioural features are also associated with the disorder, including hand stereotypies, hyperventilation and breath holding. No study has tested the specificity of these behavioural features to individuals with RS, compared to individuals with severe to profound mental retardation (SMR). Method: A novel checklist of characteristic RS behavioural and emotional features, the Rett Syndrome Behaviour Questionnaire (RSBQ), was developed to test the type and specificity of behavioural features of RS against those found in girls with SMR. Results: After controlling for the effects of RS-related physical disabilities, the RSBQ discriminated between the groups. Some aspects of the behaviours found to be specific to RS are included in the necessary or supportive RS diagnostic criteria, notably hand behaviours and breathing problems. Additional behavioural features were also more frequently reported in the RS than the SMR group, including mood fluctuations and signs of fear/anxiety, inconsolable crying and screaming at night, and repetitive mouth and tongue movements and grimacing. Conclusions: Full validation of the scale requires confirmation of its discriminatory power and reliability with independent samples of individuals with RS and SMR. Further delineation of the specific profile of behaviours seen in RS may help in identification of the function of the MECP2 gene and in improved differential diagnosis and management of individuals with RS. [source] Evaluation of a transportable capnometer for monitoring end-tidal carbon dioxideANAESTHESIA, Issue 10 2010T. Hildebrandt Summary We compared a small and transportable Capnometer (EMMAÔ) with a reference capnometer, the Siesta i TS Anaesthesia. During air-breathing through a facemask, both the EMMA (nine modules) and reference capnometer sampled expired gas simultaneously. A wide range of end-tidal carbon dioxide values were obtained during inhalation of carbon dioxide and voluntary hyperventilation. The median IQR [range] difference between all sets of carbon dioxide values (EMMA , reference) was ,0.3 (,0.6 to 0.0 [,1.7 to 1.6] kPa; n = 297) using new batteries, which was statistically significant (p = 0.04) and located to two of the nine EMMAs tested. Using batteries with reduced voltage did not influence the measurements. The 95% CI of the medians of the differences were ,0.4 to ,0.2. We conclude that the EMMA can slightly under-read the end-tidal carbon dioxide but is generally comparable with a free-standing monitor. The precision of the EMMAs was similar whether new batteries or batteries with reduced voltage were used. [source] Enhanced vascular responses to hypocapnia in neurally mediated syncopeANNALS OF NEUROLOGY, Issue 3 2008Lucy Jane Norcliffe-Kaufmann PhD Objective The susceptibility to suffer neurally mediated syncope and loss of consciousness varies markedly. In addition to vasodilatation and bradycardia, hyperventilation precedes loss of consciousness. The resultant hypocapnia causes cerebral vasoconstriction and peripheral vasodilatation. We postulate that more pronounced cerebral and peripheral vascular responses to reductions in arterial CO2 levels underlie greater susceptibility to neurally mediated syncope. Methods We compared vascular responses to CO2 among 31 patients with histories of recurrent neurally mediated syncope and low orthostatic tolerance and 14 age- and sex-matched control subjects with no history of syncope and normal orthostatic tolerance. Vascular responses to CO2 were calculated after all subjects had fully recovered and their blood pressures and heart rates were stable. We measured blood flow velocity in the middle cerebral artery (transcranial Doppler) and in the left brachial artery (brachial Doppler), and end-tidal CO2 during voluntary hyperventilation and hypoventilation (end-tidal CO2 from 21,45mm Hg), and determined the slopes of the relations. Results Hypocapnia produced a significantly greater reduction in cerebral blood flow velocity and in forearm vascular resistance in patients with neurally mediated syncope than in control subjects. Opposite changes occurred in response to hypercapnia. In all subjects, the changes in cerebral blood flow velocity and forearm vasodilatation were inversely related with orthostatic tolerance. Interpretation Susceptibility to neurally mediated syncope can be explained, at least in part, by enhanced cerebral vasoconstriction and peripheral vasodilatation in response to hypocapnia. This may have therapeutic implications. Ann Neurol 2007 [source] Sickle cell disease and electroencephalogram hyperventilationANNALS OF NEUROLOGY, Issue 1 2006Mara Prengler MD No abstract is available for this article. [source] CURRENT CONTROVERSIES IN THE MANAGEMENT OF PATIENTS WITH SEVERE TRAUMATIC BRAIN INJURYANZ JOURNAL OF SURGERY, Issue 3 2006Alexios A. Adamides Background: Traumatic brain injury is a major cause of mortality and morbidity, particularly among young men. The efficacy and safety of most of the interventions used in the management of patients with traumatic brain injury remain unproven. Examples include the ,cerebral perfusion pressure-targeted' and ,volume-targeted' management strategies for optimizing cerebrovascular haemodynamics and specific interventions, such as hyperventilation, osmotherapy, cerebrospinal fluid drainage, barbiturates, decompressive craniectomy, therapeutic hypothermia, normobaric hyperoxia and hyperbaric oxygen therapy. Methods: A review of the literature was performed to examine the evidence base behind each intervention. Results: There is no class I evidence to support the routine use of any of the therapies examined. Conclusion: Well-designed, large, randomized controlled trials are needed to determine therapies that are safe and effective from those that are ineffective or harmful. [source] Physiological Effects of a Novel Immune Stimulator Drug, (1,4)-,- d -Glucan, in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2009Ravishankar Koppada We investigated physiological and immunological effects of a low and a high dose of ,- d -glucan (0.5 and 10 mg/kg), in vivo, testing the hypothesis that intravenous administration of ,- d -glucan does not affect haemodynamic, respiratory, haematological, and immune responses in normal rats. Male rats (300,400 g) were anaesthetized, tracheostomized, and catheterized in one femoral artery and vein. The mean arterial blood pressure and heart rate were continuously recorded. The baselines for gas exchange, differential blood cell count, and plasma concentration of TNF-,, IL-1,, IL-4, IL-6, and IFN-, were determined. Rats were then randomly assigned to controls (n = 7), a low dose (0.5 mg/kg; n = 10), and a high dose (10 mg/kg; n = 7) of ,- d -glucan for a six 6 hr study period. Gas exchange, differential cell count, plasma concentration of TNF-,, IL-1,, IL-4, IL-6, and IFN-,, and mean arterial blood pressure values remained within physiological range. Intravenous administration of 10 mg/kg ,- d -glucan created tachycardia, associated with hyperventilation, and significant reductions in the blood haemoglobin and haematocrit concentrations. We suggest that these in vivo effects of ,- d -glucan should be considered for future clinical and/or experimental trials. [source] Intraoperative hyperventilation vs remifentanil during electrocorticography for epilepsy surgery , a case reportACTA NEUROLOGICA SCANDINAVICA, Issue 6 2010T. W. Kjaer Kjaer TW, Madsen FF, Moltke FB, Uldall P, Hogenhaven H. Intraoperative hyperventilation vs remifentanil during electrocorticography for epilepsy surgery , a case report Acta Neurol Scand: 2010: 121: 413,417. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Background,,, Traditionally, intraoperative intracranial electroen-cephalography-recordings are limited to the detection of the irritative zone defined by interictal spikes. However, seizure patterns revealing the seizure onset zone are thought to give better localizing information, but are impractical due to the waiting time for spontaneous seizures. Therefore, provocation by seizure precipitants may be used with the precaution that spontaneous and provoked seizures may not be identical. Objective,,, We present evidence that hyperventilation induced and drug induced focal seizures may arise from different brain regions in the same patient. Methods,,, Hyperventilation and ultra short acting opioid remifentanil were used separately as intraoperative precipitatants of seizure patterns, while recording from subdural and intraventricular electrodes in a patient with temporal lobe epilepsy. Two different ictal onset zones appeared in response to hyperventilation and remifentanil. Both zones were resected and the patient has remained essentially seizure free for 1 year. Furthermore, this is the first description of hyperventilation used as an intraoperative seizure precipitant in human focal epilepsy. [source] | ||||||||||||||||||||||||||||||||||