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At least 973 records · Page 54Linked to original sources
PubMed1986

Nasal vasomotor responses in man to breath holding and hyperventilation recorded by means of intranasal balloons.

Nasal vasomotor responses were recorded in conscious human subjects by means of water filled balloons. Hyperventilation caused an increase in intranasal balloon pressure associated with vasodilatation whereas breath holding caused a decrease associated with vasoconstriction. The amplitude of the nasal vasomotor response was influenced by the nasal cycle with the greatest response always observed on the congested or low airflow side of the nose. The results suggest that an elevated arterial level of carbon dioxide causes a pronounced vasoconstruction of the nasal blood vessels and that this response may be clinically relevant in controlling nasal bleeding.

Humans↗
PubMedDate not supplied

Refractoriness after hyperventilation-induced asthma.

It is still debated as to whether the bronchospasm induced by hyperpnoea in asthmatic subjects is followed by a period of refractoriness to a subsequent challenge. We studied, therefore, the effect of repeated challenges with eucapnic hyperpnoea in asthmatic subjects and compared it to that in normal subjects. Ten normal and 34 asthmatic subjects were challenged twice with a steady isocapnic hyperventilation (25 l X min-1 X m-2 BSA for 6 min) of dry air at room temperature. The interval between challenges was 30 min in the normal subjects and was 30-60 min in asthmatic subjects to allow for full recovery of FEV1 before the second challenge. In the normal subjects, neither the first nor the second challenge caused a detectable change in FEV1. In the asthmatic subjects, the fall in FEV1 was on average less marked at 5, 8 and 10 min after the second challenge than after the first one (p less than 0.05 by analysis of variance). Analysis of data from individuals showed partial to full refractoriness in 14 of the 34 subjects. In no instance was the fall in FEV1 significantly greater after the second challenge than after the first one. Thirteen other asthmatic subjects were challenged twice at a 30-60 min interval with stepwise increases in ventilation of dry air at room temperature until wheezing or chest tightness occurred or a ventilation of 50 l X min-1 X m-2 BSA was reached.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

The hyperventilation syndrome: a neurosis or a manifestation of magnesium imbalance?

It has been proven with clinical, psychological and electromyographic tests that the hyperventilation (HV) syndrome cannot be separated from so-called genuine tetany. Tetanic patients with and without HV are characterized by a significant hypocalcemia; but a significant hypomagnesemia is exclusively found in tetanic patients with HV attacks. Possible pathogenic mechanisms are discussed which may explain the HV attacks as a consequence of primary magnesium deficiency.

Adolescent↗
PubMed1985

Management of infants with severe respiratory failure and persistence of the fetal circulation, without hyperventilation.

The successful management of 15 infants suffering from persistence of fetal pulmonary circulation and in severe respiratory failure is presented. The treatment regimen focused on minimizing barotrauma. Infants were intubated nasotracheally and ventilated with intermittent mandatory ventilation. Peak inspiratory pressures were determined by the clinical assessment of chest excursion. Ventilator settings and fractional inspiratory oxygen (FiO2) were selected to maintain a PaO2 between 50 and 70 mm Hg; PaCO2 was not a controlling parameter and was allowed to increase as high as 60 mm Hg. Hyperventilation and muscle relaxants were not used. High ventilator rate was used in ten infants who required high inspiratory pressure to maintain chest excursion, with a favorable response in five. Tolazoline was given to 14 infants of whom ten showed an improvement in oxygenation; dopamine was given to three infants who were oliguric. All infants survived, and only one infant developed chronic lung disease which was defined by the infant's need for supplemental oxygen beyond 30 days of life.

Birth Weight↗
PubMed1976

Mechanism of post dialysis hyperventilation in patients with chronic renal insufficiency.

Several hypotheses have been put forward to explain postdialysis hypocapnia. Three were tested in this study: impairment of tissue oxygenation by dialysis (D)-induced alkalosis (Bohr effect), the D disequilibrium syndrome, and the loss of carbon dioxide (CO2) in D fluid. In 17 patients pre-DPCO2 was significantly correlated with plasma bicarbonate concentration (HCO3) and no disproportionate reduction of PCO2 was discernible. In 10 patients using a bath acetate concentration of 38 mEq/1 PCO2 was unchanged after D (35.4 versus 35.9 mm Hg before D), and was low relative to HCO3 whic increased from 21.2 to 28.0 mEq/1. After a dialysis using an acetate concentration of 25 mEq/1 HCO3 remained constant (20.4 versus 21.1 mEq/1 pre-D), whereas PCO2 fell from 35.3 to 30.8 mm Hg (P less than 0.001). Consequently PCO2 was again low relative to HCO3. Removal of CO2 by D fluid was excluded as a cause for low blood PCO2: addition of gaseous CO2 to the bath had no influence on arterial blood gases. Since post-D hypocapnia was not prevented when HCO3 was kept constant, it was concluded that post-D alkalosis cannot be the main reason for post-D hyperventilation, and that other factors related to the process of D are responsible.

Acetates↗
PubMed1979

[Hyperventilation and inhibitory synapses].

Injection of subconvulsive doses of strychnine blocking the inhibitory synapses significantly increases the reflex activity of the respiratory muscle evoked by stimulation of the sciatic nerve as well as by inhalation of hypercapnic gas mixture. Thus the inhibitory synapses prevent the extreme hypocapnia evoked by hyperventilation.

Animals↗
PubMed1983

[A reduction in the hyperventilation threshold by intravenous infusion of adrenaline in the treadmill exercise].

Seven healthy male subjects underwent a treadmill incremental work test in control conditions and during an intravenous epinephrine infusion (10 micrograms/min). At all exercise intensities, epinephrine increased heart rate, ventilation, respiratory quotient and plasma lactate levels without significant changes in oxygen consumption. Under epinephrine infusion, the "anaerobic threshold", considered as the critical intensity at which ventilation began to increase non linearly with oxygen consumption, appeared at a lower intensity and for a higher plasma lactate level than in control conditions. We conclude that the hyperventilation threshold does not necessarily reflect a muscular hypoxia. It could be due to an effect of catecholamines on peripheral chemoreceptors, maybe by alpha-adrenergic vasoconstriction in the carotid bodies.

Blood Pressure↗
PubMedDate not supplied

[Bronchial response to carbachol and isocapnic hyperventilation in asthma].

Bronchial challenge tests with carbachol and isocapnic voluntary hyperventilation (IVH) were performed in 15 asthmatics on two separate occasions. For the IVH test, the subject inhaled dry air at 20-21 degrees C; respiratory frequency and tidal volume were controlled in order to obtain various 3 min levels of ventilation; isocapnia was maintained by adding CO2 to the inspired air. Bronchial response was assessed by measuring airway conductance (Gaw) with a plethysmograph. Individual dose-response curves were constructed, allowing the calculation of two indices: the slope of the dose-response curve and the value of the minute-ventilation (V25, expressed as percent of predicted maximal minute-ventilation), or the dose of carbachol (D25) causing a 25% decrease in Gaw. There was no significant correlation between the slopes of carbachol and IVH dose-response curves and between the values of V25 and D25. These data demonstrate that the IVH and carbachol tests cannot be used indifferently to assess bronchial responsiveness.

Adolescent↗
PubMed1984

Comparison of ultrasonically nebulized distilled water and hyperventilation with cold air in asthma.

To assess the potential value of brief non-pharmacologic challenge tests in the measurement of bronchial responsiveness and to investigate whether the responses are induced by similar mechanisms, we carried out comparative five-minute inhalation challenges with ultrasonically nebulized distilled water and cold air hyperventilation in nine asthmatic subjects. Decrements in FEV1 following both challenges were closely correlated (r = 0.885) and ranged from 8% to 59% of baseline following challenge with the former and from 6% to 59% following the latter. Each method was therefore equally effective in demonstrating bronchial hyperresponsiveness. Moreover, the strong correlation between the responses to both challenges coupled with previous observations suggests that the two stimuli may act by similar mechanisms.

Administration, Intranasal↗
PubMed1983

Are exercise and isocapnic voluntary hyperventilation identical bronchial provocations?

There is a positive and direct relationship between the magnitude of heat lost from the respiratory tract, the degree of cooling of intrathoracic airways and the magnitude of the airway obstructive response that develops in asthmatic subjects following exercise. We explore the possibilities of the causal nature of this relationship, the potential mechanisms by which they may relate and attempt to focus on the controversies that still exist with regard to the equivalency of respiratory heat loss (RHL) produced by exercise and by isocapnic voluntary hyperventilation (VHV) in asthmatics.

Asthma↗
PubMed1980

Effect of 1% enflurane (Ethrane) anesthesia on cerebral blood flow and metabolism in neurosurgical patients during normo- and hyperventilation.

We have measured the CBF in ten neurosurgical patients. A first measurment was made during anesthesia with nitrous oxide 70% and a second with nitrous oxide 70% + 1% enflurane, both at a PaCO2 of 40 Torr. A third measurement was performed also with nitrous oxide + 1% enflurane, but at a PaCO2 of 30 Torr. We used the method of intracarotid 133Xe injection, with a gammacamera recording. In order to avoid any decrease of cerebral perfusion pressure, which might influence the CBF, an infusion of phenylephrine was used, if needed. At a constant PaCO2 of 40 Torr, there was no statistically significant difference in CBF with nitrous oxide + 1% enflurane compared to nitrous oxide alone. No change in cerebral vascular resistance was observed. When PaCO2 was lowered to 30 Torr, under 70% nitrous oxide + 1% enflurane, there was a 43% decrease in CBF (from a mean of 42 ml/100 G/min. to a mean of 24 ml/100 g/min.). Cerebral vascular resistance had an increase of 79%. In some instances, the decrease in CBF reached values around 20 ml/100 g/min. and in one case, even less. That level is generally considered to be the lowest acceptable limit in the conscious man, though not necessarily in the anesthetised one. Under hypocapnia, the cerebral arterio-venous oxygen difference increased, but the CMRO2 did not change. There were little differences in lactate and pyruvate cerebral metabolic rates, all values remaining within normal ranges. In conclusion, we believe that enflurane is a favorable anesthetic agent for neurosurgical operations at the concentration of 1%, CMRO2 is reduced, there is no significant effect on cerebral blood vessels, CBF and CVR do not change. However, a complementary use of hypocapnia may reduce CBF to dangerously low levels, if at the start, it shows already a pathological decrease and if hyperventilation is applied at a marked degree.

Adolescent↗
PubMed1980

Hyperventilation syndrome: report of case.

Hyperventilation is a common response to anxiety or threatening situations. In certain individuals, it is a mechanism for producing alarming physiologic and metabolic changes. The changes as well as the causes and treatment have been described.

Adolescent↗
PubMed1980

[Role of the pyramidal tract in the mechanism of dyspnea and hyperventilation].

Hypoxia evoked by mechanical asphyxia first of all disturbs the generation of potentials in pyramidal tract neurons. Hypoxic work, therefore, causes inadequate contraction of somatic muscles, a difficulty in work performance and respiratory discomfort. Concurrently, the disturbance of the pyramidal tract disinhibits the respiratory center of the brain stem with a result of excessive hyperventilation during hypoxic work.

Afferent Pathways↗
PubMedDate not supplied

[The use of hyperventilation for improving the visualization of glial tumors of the brain in magnetic resonance tomography using the contrast substance Gd-DTPA].

This study was undertaken to evaluate the influence of hyperventilation (HV) as a test on the image contrast of brain glial tumors in enhanced magnetic resonance (MR) imaging. HV was performed for 2 min (30 breaths/min) before intravenous injection of Gd-DTPA (Magnevist), Schering AG, Germany, in a dose of 0.1 mmol/kg. A total of 19 patients with glial tumors of the brain were examined. After the functional test, the image contrast of tumor tissue was compared with tumor contrast after the standard enhanced MR imaging. Nineteen patients with brain tumors were assessed. The tumor types were histologically verified in all cases (nine malignancy degree I-II astrocytomas, six malignancy degree III astrocytomas, three ependymomas, one malignant oligodendroglioma). MRI was performed on a Magnetom 42 SP-1.0 T. There was an increase in the image contrast of degree I-II astrocytomas neither after the standard enhanced MRI nor after it in the presence of HV. On the contrary, in 2 cases there was an opposite effect--the tumor contrast decrease after the functional test. Ependymomas showed patterns of increases in contrast intensity from 10 to 13% as compared with the enhanced standard MRI in all cases. In these conditions the intrinsic structure and boundaries of tumors became more distinguished. Cases with malignant astrocytomas and oligodendroglioma had contrast enhancement increases as well. It is concluded that in cases with degree I-II astrocytomas, the use of HV does not improve the visualization of lesions. In ependymomas and anaplastic astrocytomas, HV aids in more significantly assessing the intrinsic structure and the extent of tumorigenesis and it may be useful as a functional test to assess the anaplastic extent of glial tumors of the brain and as a procedure enabling the contrast agent to be used in smaller dosages.

Astrocytoma↗
PubMed1995

[Chronic hyperventilation syndrome. The role of respiratory re-training].

This study compares three non-pharmacological approaches to the chronic hyperventilation syndrome (CHS). Eighteen subjects were evaluated at the start of the study then one and 6 months after having received in a random fashion one of the following treatments: group I (teaching approach of one hour on the respiratory physiology of the CHS and on breathing techniques; n = 5); group II (same approach as in group I with breathing retraining of 8 sessions; n = 8); group III (same as group II with the addition of a modified Jacobson's progressive relaxation; n = 5). Whereas all three groups had a similar symptomatic score at the beginning of the study (although subjects of group III had in general higher scores and were symptomatic for a longer period), our results show that all subjects improved after 4 weeks, those in group II showing the greatest improvement (p < 0.05). This confirms the relevance of applied and repeated pedagogy in approaching subjects with the CHS.

Adolescent↗
PubMed1975

[Controlled hyperventilation with dead space (author's transl)].

We report on a new kind of ventilation-hyperventilation, whereby dead space is added between the patient and the respirator. This kind of ventilation is compared with positive end expiratory pressure ventilation together with intermittent sighs on 10 dogs. Over a period of 80 hours no respiratory or circulatory differences were found in the two groups. There also was no difference in clinical or anatomic histologic findings. It was demonstrated that dogs can be artificially ventilated for a much longer period than estimated. The findings of "respirator lungs" were only shown in an emphysema of the lungs.

Acidosis, Respiratory↗
PubMed1993

The grey area of effort syndrome and hyperventilation: from Thomas Lewis to today.

Lewis used the diagnosis 'effort syndrome' for subjects whose ability to make and sustain effort had been reduced by homeostatic failure. A major element was depletion of the body's capacity for buffering the acids produced by exercise. In his view this systems disorder was not to be regarded as a specific organ disease, and losing sight of the metabolic element would foster the invention of fanciful, unphysiological diagnoses. His views were dismissed because normal resting plasma bicarbonate levels were considered by others in that era to exclude serious depletion of the body's total capacity for buffering the effects of exertion. Today, effort syndrome is still a useful diagnosis for a condition of exhaustion and failure of performance associated with depletion of the body's buffering systems. Other elements associated with homeostatic failure are now recognised, principally emotional hyperarousal and hyperventilation. Their physiological interrelationships are described. Effort syndrome is amenable to recovery through rehabilitation, and it may be a mistake to treat chronic fatigue syndrome and unspecific illness without including it in the differential diagnosis.

Adaptation, Physiological↗