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Malignant lymphoma of the central nervous system presenting with central neurogenic hyperventilation. Case report.

The case is described of a 72-year-old woman who presented with a progressive right hemiparesis and central neurogenic hyperventilation. Pathological and radiological studies revealed diffuse infiltration of a malignant lymphoma into the entire central nervous system and the upper spinal cord. The authors review 12 cases of tumor-induced central neurogenic hyperventilation and discuss the pathophysiology of this condition.

Aged↗

Effect of body temperature on salicylate-induced hyperventilation.

Hyperventilation and hyperpyrexia occur simultaneously during acute salicylate intoxication. The present experiments were designed to investigate the stimulatory effect of increased body temperature on respiration in this pathological state. Acute salicylate intoxication was produced in mongrel dogs by intravenous infusion of 200 mg sodium salicylate/kg body weight, and the effect of body temperature on salicylate-induced hyperventilation was studied by comparing the respiration of hyperthermic animals with the respiration of animals maintained normothermic during acute salicylate intoxication by bathing them in cold water. The minute volume of ventilation increased greatly over control levels in both normothermic and hyperthermic animals, but this increment was much larger in hyperthermic animals. The increase in ventilation of normothermic animals can be explained as a rise in alveolar ventilation which results in hypocapnia despite large increases in carbon dioxide production and oxygen consumption during acute salicylate intoxication. The further augmentation of ventilation in hyperthermic animals can be explained as a rise in deadspace ventilation in response to increased body temperature during acute salicylate intoxication.

Animals↗

Hyperventilation in the dental chair.

An anxious patient may experience an uncontrollable increase in ventilatory effort, far in excess of the body's metabolic needs, to such a degree that profound changes are induced in the cardiovascular and neurological systems. This abnormal drive to breathe rapidly leads to a reduction in the tension of carbon dioxide in alveolar gas and arterial blood and to mild alkalosis. The outward expression of these disturbances can be alarming for both patient and dentist, but for the physiologist searching for underlying mechanisms it is intriguing. The cursory coverage of this subject in some textbooks and lecture courses is regrettable when one considers that hyperventilation is not uncommon in a dental patient. This article examines the causes, signs, symptoms and management of acute hyperventilation.

Dental Anxiety↗

[Central neurogenic hyperventilation associated with a pontine infarction].

Central neurogenic hyperventilation in patients with a normal level of consciousness is uncommon. This condition occurs in bilateral pontine tegmental lesions, particularly tumors such as CNS lymphomas and glioma, as well as traumatic lesions. The physiopathological mechanisms are unknown and no there is no effective treatment for this entity. We report a case of central neurogenic hyperventilation associated to a unilateral basal pontine infarction.

Brain Stem Infarctions↗

[Bicycle exercise test, Holter ECG monitoring and hyperventilation test in diagnosis coronary arteries stenosis in postmyocardial infarction patients].

To assess contribution of dynamic (vasospastic) stenosis to pathogenesis of anginal attacks in postmyocardial patients, 148 patients 15-4 months after the infarction were examined using bicycle exercise, Holter ECG monitoring and hyperventilation test (HVT). The relations between painless myocardial ischemia and vasospastic reactions in the course of hyperventilation were also studied. The ECG segment ST responded similarly in 97% of the patients. In positive HVT there was a slight rise in the heart rate and double product. Vasospastic reactions prevailed in the disease aggravation. Dynamic stenosis in postmyocardial patients is characterized by significant variability of ischemia threshold and total duration of ischemic episodes more than 30 minutes for 24 hours.

Adult↗

Hyperventilation-precipitated cerebrovascular accident in a patient with sickle cell anaemia.

Hyperventilation exercise during electroencephalography precipitated a recurrence of right hemiplegia and aphasia in a patient with Hb SS disease. Although recovery of function started within hours of the event, full recovery has not occurred six months after. Hyperventilation provocative test during electroencephalography should be discouraged in patients with sickle cell anaemia.

Adolescent↗

[Effect of hyperventilation on the cerebral blood flow and metabolism in patients with craniocerebral trauma].

Cerebral blood flow and metabolism were studied in 44 patients with acute severe craniocerebral injuries (contusions of the brain and removal of intracranial hematomas) with consciousness depression (moderate coma), hospitalized in intensive neurological care wards. Oxygen supply to the brain was repeatedly evaluated (acid-base status of the jugular vein blood, oxygen arterio-venous difference, oxygen extraction coefficient), oxymetry of the brain was repeatedly carried out, and vital functions were monitored over the entire period of disease. Cerebral blood flow was monitored by rheoencephalography, which helped timely detect the changes in cerebral blood flow in patients with craniocerebral injuries during different ventilation protocols used in intensive care. All studies were carried out during three stages: 1) initial stage, when the patients were brought to intensive neurological care wards after surgical intervention, and during normoventilation (paCO2 36-40 mm Hg; 2) moderate hyperventilation (paCO2 35-26 mm Hg); and 3) pronounced hyperventilation (paCO2 25-20 mm Hg). Specific changes in the cerebral blood flow during the acute period of craniocerebral injury were detected during different ventilation regimens in 2 groups of patients: group 1 with lethal outcomes and group 2 with positive changes.

Adult↗

Olanzapine-induced hyperventilation: case report.

Although olanzapine therapy has been associated with fewer extrapyramidal side effects than the traditional antipsychotic medications, reported side effects include dystonia, tardive dyskinesia, hypotension, diabetes mellitus, seizures and neuroleptic malignant syndrome. There are no previous published reports of hyperventilation associated with olanzapine therapy, but we present the case of a male patient who developed dyspnea and hyperventilation while taking olanzapine.

Adult↗

DaCosta's syndrome: chronic symptomatic hyperventilation.

In 1871, DaCosta published his observation of somatic symptoms preceded by significant hyperventilation. More than a century later, the hyperventilation syndrome remains a poorly defined but common clinical condition. Although familiar to most practitioners of medicine when it presents as an acute phenomenon, the diagnosis may go unrecognized in its chronic form. The ability of a chronic hyperventilatory state to mimic a life-threatening cardiopulmonary disease is not always appreciated.

Adult↗

[Correlations between external respiration function and the blood content of the immune system cells in hyperventilation ].

Relations between hyperventilation, hyperventilation syndrome (HVS) and bronchial asthma (BA) are not finally established. This study modelled HVS in 92 volunteers to investigate HVS effect on external respiration function (ERF), immune status and hormonal and amino regulation. HVS was found to induce significant shifts in regulating systems (adrenergic, cholinergic, serotoninergic, conticosteroids) function and to alter correlations between ERF and blood levels of immune cells carrying various CD- and HLA-DR markers. The HVS model can be used for the study of HV role in immunopathogenesis of BA.

Adrenal Cortex Hormones↗

['Hyperventilation syndrome': often an easy to treat panic disorder].

Three patients, 2 men aged 35 and 26 years and 1 woman aged 41 years, had acutely occurring attacks, accompanied by diverse somatic complaints, and were diagnosed with hyperventilation syndrome. They recovered only when the complaints were recognised and treated as a panic disorder. Hyperventilation and the decrease of CO2 in the blood do not explain the symptoms and complaints in patients with panic disorder, a psychiatric disorder with a good prognosis. Treatment consists of cognitive behavioural therapy or a selective serotonin re-uptake inhibitor in the case of panic disorder and of a combination of those two treatments in the case of panic disorder with agoraphobia. Breathing exercises can form part of the behavioural therapy but not because the disorder is due to faulty breathing habits.

Adult↗

The relative contributions of histamine and prostanoids to bronchoconstriction provoked by isocapnic hyperventilation in asthma.

It has been proposed that exercise provokes bronchoconstriction in asthma by inducing mast cell degranulation, and that this occurs secondary to the hyperpnoea of exercise causing hypertonicity of the airway lining fluid. We investigated the contribution of the mast cell products, histamine and prostaglandins, to the bronchoconstriction induced by isocapnic hyperventilation (ISH) using single doses of terfenadine, a specific histamine H1-receptor antagonist, and flurbiprofen, a potent cyclooxygenase inhibitor. We also investigated the effect of flurbioprofen in single dose on bronchial histamine reactivity. Eleven asthmatics took part in a two phase, double-blind, randomized study. In phase 1, subjects attended on three occasions and received either terfenadine 180 mg, flurbiprofen 150 mg, or placebo, prior to 6 min of ISH. The mean maximum percentage fall in forced expiratory volume in one second (FEV1) induced by ISH was 31.5(+/- 3.2)% following placebo, 29.7(+/- 4.4)% following flurbiprofen (NS), and reduced to 16.6(+/- 3.7)% following terfenadine (p less than 0.01). In phase 2, subjects received bronchial challenge with histamine following either flurbiprofen 150 mg or placebo. No significant change in bronchial reactivity following flurbiprofen was seen. We conclude that as administered in this study, flurbiprofen has no effect on baseline bronchial reactivity to histamine. The inhibitory effect of terfenadine indicates that histamine, probably from airway mast cells, makes an important contribution to bronchoconstriction induced by isocapnic hyperventilation, whereas prostaglandin release has no significant role.

Adolescent↗

Cortical activity during hypoxic hyperventilation.

This study seeks to determine the pattern of electroencephalogram changes during stimulatory ventilatory responses to acute progressive hypoxia. Electroencephalograms were recorded in the 10-20 electrode system during progressive poikilocapnic hypoxic tests based on the rebreathing routine. Healthy subjects were used for he study. A major finding was that hypoxia decreased the power spectra of the alpha activity. The decrease was surprisingly rapid and greater at mild hypoxic desaturation when pulmonary ventilation was about to pick up than during the maximum hypoxic hyperventilation. The possible relation of hypoxic decline in brain bioactivity to the manifestation of hypoxic hyperventilation remains to be elucidated in further studies.

Adult↗

Post-task changes in visual P300 and their reversibility through brief hyperventilation.

Long hours of continuous, mental task reportedly increase the average auditory P3 latency of the normal subjects significantly, a change that is thought to be related to mental fatigue. We have tried out several protocols of varying task difficulty and duration in an effort to study the onset of the assumed fatigue-related changes. The present study shows that changes in visual event-related potential occur in less than two minutes if the task is sufficiently rigorous. The changes occur both in latency and in amplitude. Moreover, the changes are reversible with a brief (30 second) period of hyperventilation. The changes were most marked at Fz. Following the difficult task, the P3 amplitude at Fz decreased from 8.588 micro/V +/- 0.966 to 5.800 microV +/- 0.795 and the P3 latency increased from 368 +/- 4 ms to 380 +/- 3. Following hyperventilation, the P3 amplitude at Fz reverted to 8.457 +/- 5 and the P3 latency reverted to 371 +/- 5 ms. These observations call for further investigations on the cause of the post-task changes and their quick reversibility.

Adult↗

Diagnostic tests of hyperventilation syndrome.

In 90 patients referred to the pulmonary function laboratory for evaluation of hyperventilation syndrome (HVS) and in whom somatic causes of the complaints had been excluded, we investigated the degree of concordance between three widely applied diagnostic methods: 1) the standardized Nijmegen questionnaire on major daily complaints; 2) the reproduction of the same symptoms during the hyperventilation provocation test (HVPT); and 3) the responses of end-tidal CO2 fraction (FETCO2) during the HVPT. In 86% of the patients a concordance was found between Nijmegen questionnaire (i.e. score of 24/64 or more) and symptom reproduction during HVPT (i.e. recognition of at least 2 major daily complaints). Based on these combined data we made a definite diagnosis of HVS in 37 patients, of non-HVS in 40 patients, and we retained only a possible HVS in 13 patients. Each of the 16 complaints in the questionnaire contributed significantly to the distinction between HVS and non-HVS patients, and a striking similarity in rank order of daily complaints and reproduced symptoms was found. The responses in FETCO, during HVPT had little additional diagnostic value. A spontaneous fall of at least 0.25% FETCO2 during the 5 min adaptation period before the HVPT, was most reliably correlated with the aforementioned diagnostic criteria of HVS: specificity 83%, sensitivity 57%, and accuracy 70%. Neither the 3 min FETCO2 ratio nor the 5 min FETCO2 ratio during recovery after the HVPT showed a good correlation with the other diagnostic criteria. The response of FETCO2 during HVPT did especially not provide additional useful diagnostic information in the 13 patients with only possible HVS.

Activities of Daily Living↗

[Central neurogenic hyperventilation in an awake patient with a primary cerebral lymphoma].

We described clinical and neuropathological findings of a case of primary cerebral lymphoma with central neurogenic hyperventilation (CNH). A 54-year-old awake woman with a primary cerebral lymphoma presented hyperventilation for two weeks. Arterial blood gas showed severe respiratory alkalosis; PH 7.603, PaCO2, 10.5 mmHg, PaO2 129.8 mmHg, HCO2 10.4 mmol/L, BE -8.0, O2SAT 98.9%. Rebreathing from a paper bag, and intravenous administration of diazepam and sodium bicarbonate failed to alter the respiratory pattern. Consecutive CAT scans indicated that CNH didn't occur when the tumor extensively invaded the cerebral cortex, cerebellum, thalamus and basal ganglia but was initiated when the lymphoma invaded the brain stem. Pathological study showed lymphoma cells invaded the cerebral cortex, cerebellum, thalamus and basal ganglia severely, and the brain stem moderately and recently. Contrary to the cases reported by Plum, Lange and Bateman, the lower medulla was also involved. Possible mechanisms for CNH are discussed in relation to the pathological findings and consecutive CAT scan findings.

Brain Neoplasms↗

Hyperventilation response to cold water immersion: reduction by staged entry.

Staged immersion of humans into cold water was investigated to determine whether the hyperventilation response could be reduced by this behavioral technique. A simple, two-stage procedure involving immersion to the waist for 30 s before full immersion to neck level was compared to non-staged immersion. For the staged immersion, maximum values of respiratory minute volume and respiratory frequency were significantly reduced by 35% and 38%, respectively, from the maxima observed for non-staged immersion. These results indicate that if staged immersion into cold water is possible, it can attenuate the hyperventilation response and, therefore, the probability of sudden drowning. We recommend that this knowledge be incorporated into teaching programs concerning cold water safety.

Adult↗

Isocapnic hyperventilation.

Eucapnic hyperventilation is probably the same expression of asthma as exercise-induced asthma. Some dispute exists about the refractory period after the two challenges. Some claims that an refractory period exists after exercise-induced asthma and some cannot find any refractory period. The changes in the ventilatory capacity of asthmatics following exercise and eucapnic hyperventilation are similar.

Asthma↗