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At least 523 records · Page 29Linked to original sources
PubMed2000

Effects of alcohol on the response to hyperventilation of participants high and low in anxiety sensitivity.

BACKGROUND: Previous research suggests that high levels of anxiety sensitivity (AS; fear of anxiety symptoms) may constitute a risk factor for alcohol abuse. The present study evaluated the hypothesis that high AS levels may increase risk for alcohol abuse by promoting a heightened sober reactivity to theoretically relevant stressors and heightened sensitivity to alcohol's emotional reactivity dampening effects, which would negatively reinforce drinking in this population. METHODS: One hundred and two undergraduate participants (51 high AS, 51 low AS) with no history of panic disorder were assigned to either a placebo, low-dose alcohol, or high-dose alcohol beverage condition (17 high AS, 17 low AS per beverage condition). After beverage consumption and absorption, participants underwent a 3 min voluntary hyperventilation challenge. RESULTS AND CONCLUSIONS: High-AS/placebo participants displayed greater affective and cognitive reactivity to the challenge than low-AS/placebo participants, which indicated increased fear and negative thoughts (e.g., "losing control") during hyperventilation among sober high AS individuals. Dose-dependent alcohol dampening of affective and cognitive reactivity to hyperventilation was observed only among high-AS participants, which suggested that high-AS individuals may be particularly sensitive to alcohol-induced reductions in their degree of fear and negative thinking in response to the experience of physical arousal sensations. In contrast, dose-dependent alcohol dampening of self-reported somatic reactivity was observed among both high- and low-AS participants. We discuss implications of these results for understanding risk for alcohol abuse in high-AS individuals, as well as directions for future research.

Adult↗
PubMedDate not supplied

[Hyperventilation syndrome and reflexologic methods of its correction].

Acupuncture has been studied for possibility to be used for correction of hyperventilation disorders. Diagnostics of hyperventilation syndrome (HVS) was carried out on the basis of data of clinical, laboratory and functional methods. Acupuncture was carried out using the first (strong) variant of classical inhibitive procedure of acupuncture. It was shown that reflex therapy decreased electroencephalographic characters of dysrhythmia and exaltation and paroxysmal activity as well as inter-hemisphere asymmetry in patients with HVS. Parallel with a decrease in the degree of negative subjective sensations, minute respiratory volume, non-informity of regional ventilation were observed to decrease and partial oxygen pressure in alveolar air--to increase. The positive results of reflex therapy of HVS indicate that it is possible to correct hyperventilation disorders using no pharmacotherapy.

Acupuncture Therapy↗
PubMed1959

Hyperventilation syndrome: a clinical and physiological evaluation.

There is a chronic hyperventilation syndrome which is much more common, of greater medical significance and far more difficult to diagnose than the better-known acute hyperventilation attack. This chronic syndrome tends to mimic grave organic disease with which it frequently is associated or superimposed. Studies on 250 patients with chronic hyperventilation patterns revealed the rapidity with which biochemical and physiological changes can occur and the characteristics of the resultant symptoms and signs, with particular reference to the heart and lungs. Once the diagnosis is suspected and appropriately confirmed, it is possible to "cure" over 70 per cent of such patients by means of simple therapeutic measures.

Chronic Disease↗
PubMed2003

Effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation.

Pressor response to laryngoscopy and tracheal intubation includes rises in blood pressure and heart rate. This response may be harmful in the presence of cerebral or myocardial diseases. Although different preventive measures have been developed the choice of the agent or method has not been defined clearly. Hypocapnia is commonly used in anesthesia practice for different indications. It depresses the cardiovascular system and lowers the cardiac output. This study investigated the effect of controlled hyperventilation on the pressor response to laryngoscopy and tracheal intubation in three groups of healthy adult patients with different levels of end tidal CO2. The blood pressure and heart rate were recorded during induction of general anesthesia before and after laryngoscopy and tracheal intubation. The pressor responses to laryngoscopy and tracheal intubation in hypocapnic and normocapnic groups were comparable. Moderate degrees of controlled hyperventilation caused relatively more fluctuation in blood pressure during induction of anesthesia. It can be concluded that controlled hyperventilation has no beneficial effect upon the pressor response to laryngoscopy and tracheal intubation.

Adult↗
PubMed1992

[The effects of sevoflurane/halothane anesthesia during normo- and hyperventilation on the energy metabolism of the cat brain].

Energy metabolism of the cat brain was studied using phosphorous-31 nuclear magnetic resonance (31P-NMR) during sevoflurane/halothane anesthesia with normo- and hyperventilation. Under normocapnia, the findings associated with abnormal energy metabolism were not observed at concentration of sevoflurane/halothane up to 2 MAC. Meanwhile under hypocapnia by hyperventilation, the value of phosphocreatine began to decrease at and below 20 mmHg of PaCO2 (2 MAC sevoflurane) and 30 mmHg of PaCO2 (2 MAC halothane) respectively. These abnormal findings of brain metabolism were limited to the cases with cerebral blood flow (CBF) of less than a half of control state (nonanesthetized and normoventilated), and they were normalized with increased CBF by the vasoconstrictor, metaraminol. From the above data, it was concluded that the deteriorated energy metabolism by hyperventilation was due to decrease in CBF with hypotension and there was no direct effect on cerebral metabolism with less than 2MAC of both sevoflurane and halothane.

Anesthesia, Inhalation↗
PubMed2005

[The effects of hyperventilation upon spinal dorsal horn neuronal single-unit activities under nitrous oxide anesthesia].

BACKGROUND: The purpose of this study is to investigate the effects of hyperventilation upon spinal dorsal horn neuronal single-unit activities under nitrous oxide anesthesia. METHODS: Eight decerebrated spinal cats with laminectomy were maintained with oxygen and pancuronium bromide. Following the control period of normocapnia, 50% nitrous oxide was administered for 30 minutes after a hypocapnia period of 20-25 mmHg for 20 minutes. The recoveries of activities followed with normocapnia and pure oxygen administration. The changes of spontaneous and evoked activities by the pinching were investigated every 5 minutes after control study. RESULTS: Inhalation of 50% nitrous oxide suppressed the WDR neuronal activities and with hyperventilation the suppressions significantly increased. CONCLUSIONS: These results were compatible with clinical reports on the effectiveness of hyperventilation as a maintenance method under N2O anesthesia.

Anesthesia, Inhalation↗
PubMed1992

[Hyperventilation syndrome: current advances].

The hyperventilation syndrome has been described for half a century but clearly remains underdiagnosed. Its acute manifestation is easily diagnosed ("the tip of the iceberg") but its recognition in numerous subtle forms requires a particular degree of alertness on the part of the clinician ("the hidden part of the iceberg"). The incidence of this syndrome in the general population varies according to different authors as between 6-11% and may mimic diverse organic disorders. The physiological consequences of hyperventilation are reviewed as well as their contribution in the clinical picture. The aetiology of the syndrome and its links with organic pathology or psychiatric disturbances continues to be debated. Is hyperventilation the expression of abnormal respiratory function or a preferred manifestation of anxiety? This article discusses and reviews the variety of tests which enable the presumptive diagnosis to be confirmed. The response to the proposed treatments is generally excellent when one takes account of the numerous possible options. These include comportmental therapies such as respiratory re-education, the utilisation of betablockers and psychotrophic drugs or psychotherapy.

Bronchial Provocation Tests↗
PubMed2007

[Severe hyperventilation as a differential diagnosis of acute coronary syndrome].

We report a case where a 30-year-old, otherwise healthy female was admitted to hospital with symptoms of hyperventilation, including chest discomfort and an abnormal ECG showing ST depressions and T-wave inversions. The ECG changes disappeared spontaneously during the next 24 hours as the patient was calmed down. A few weeks after discharge, the ECG changes were partially reproduced during a six-minute hyperventilation test. It is worth remembering that severe hyperventilation can cause ECG changes similar to those seen in acute coronary syndrome.

Acute Disease↗
PubMed1991

Hyperventilation does not increase alveolar surfactant phospholipids in the anesthetized rat.

Pulmonary distension elicits an increase of the surfactant secretion. Effects of hyperventilation on this same secretion are less precise since they were observed under particular experimental conditions. We report a study of the effects of hyperventilation on the phospholipid content of alveolar lining fluid in the rat. One hour's hyperventilation induced by addition of a dead space to the tracheal cannula of anesthetized rats did not affect the phospholipid content of broncho-alveolar lavage fluid collected in situ immediately after killing. Phospholipid content (4.82 +/- 1.39 mg.g-1 dry lung weight) did not differ significantly from that in anesthetized spontaneously breathing rats (4.00 +/- 1.09 mg.g-1 dry lung weight). Furthermore, phospholipid content was not found to increase in animals maintained at 37 degrees C for 20 min (4.43 +/- 1.30 mg.g-1 dry lung weight) or 60 min (3.55 +/- 0.88 mg.g-1 dry lung weight) after killing. In conclusion the constancy of phospholipid content can be due either to a normal secretion or to a hypersecretion with a concomitant removal.

Animals↗
PubMedDate not supplied

[Study of bronchial reactivity using dry, cold air and eucapnic hyperventilation].

The paper is concerned with diagnostic value provocation test with cold dry air and eucapnic hyperventilation for testing bronchial reactivity. Forty healthy subjects, 90 patients with bronchial asthma, 20 with chronic bronchitis, 2 with sarcoidosis, 14 with pollenosis, one with mucoviscidosis and 22 with dispnoa or long-lasting dry cough were tested. The total of 149 provocations have been carried out in patients and 40 in healthy subjects. Airways resistance after provocation with cold dry air and eucapnic hyperventilation in patients with bronchial asthma is increased over 100% in 13 (14%), over 200% in 12 (13%), over 300% in 25 (26%) and over 500% in 40 (47%) patients. Less intensive asthmatic attack was provoked in 14 (15%), moderate attack in 18 (20%) and severe attack in 58 (65%) patients with asthma. Provocation time lasted from 2 to 9.9 min. Inspired air temperature ranged from -23 degrees C to -26 degrees C. Airway resistance was measured before and after provocation by means of Bronchoscreen. Central airway resistance was increased in 2 patients, peripheral resistance in 78, and both resistances in 10 patients with bronchial asthma. The results pointed out that provocation with cold dry air and eucapnic hyperventilation resulted in bronchial hyperreactivity exclusively in patients with bronchial asthma, and the test was positive in 100% of patients with bronchial asthma.

Adolescent↗
PubMed1990

[Hyperventilation syncopes of a psychogenic nature].

As many as 61 patients with neurogenic syncopes were examined. Of these, 46 demonstrated well-defined signs of the hyperventilation syndrome within the structure of the clinical manifestations. The remaining 15 patients had no disorders indicated. The control group comprised 18 healthy persons. Thorough analysis of factors provoking syncopal, pre- and postsyncopal conditions, studies into the psychic and vegetative spheres including the respiratory system--all this made it possible to define a number of features characteristic of patients entering the groups under study. It has been shown that hyperventilation bears the function of the leading factor in the pathogenesis of vegetative disorders. In addition to chronic hyperventilation sequels, those disorders entail the occurrence of syncopal conditions. During treatment, of paramount importance is the correction of the impaired respiratory pattern, the reduction of neuromuscular excitability along with the use of psychotropic and vegetotropic remedies.

Adolescent↗
PubMed1990

Hyperventilation.

Physicians' and specialists' continued failure to recognise, diagnose and treat adequately the majority of hyperventilators is a disgrace. Hyperventilation Syndrome (H.V.S.), incorrectly labelled myalgic encephalomyelitis (M.E.), is the latest example of the profession's incompetence. Reasons for failure to teach doctors about H.V. are discussed followed by its incidence, and the tendency for patients to gravitate to Specialist Departments where general history and a complete physical examination have become more perfunctory as sophisticated tests have multiplied. Signs which should alert a clinician's suspicion are listed, which if present should lead to a series of suggested facilitating questions. Controversial aspects of tests to confirm diagnosis are discussed, and also recent work on the relationship of panic attacks to hyperventilation and vice versa. The need for understanding and how to elicit the typical psychopathogenesis is stressed. Lastly, a form of management is described which requires combined competent physiotherapy and competent psychological management. The latter involves uncovering the underlying psychopathology and then helping the patient resolve early loss or alienation which when reawakened by further losses or anticipated loss or surrogates, precipitate symptomatic H.V.

Adult↗
PubMed1989

Parameters of the wave M in 398 patients with tetanic syndrome proved with positive ischemic or hyperventilation tests.

398 patients with clinical signs of tetanic syndrome were examined. Their ischemic and/or hyperventilation tests were positive. The parameters of the wave M were analysed i.e. latency, amplitude, duration, shape and strength of stimulus. The signs of higher irritability of the peripheral nervous system were found out in women; they diminished during age. The ratio between men and women was 1:3.6. The significant differences were determined between the groups of negative and positive tests. In the group of positive tests we noticed the dependence of the wave M on the positivity of ischemic, hyperventilation tests, on amount of multiplets during the ischemic test, on the seasons of year and on the course of the period of years (1970-1974 and 1975 to 1978). The highest irritability was determined in the subgroup of hyperventilation tetany and in the subgroup with cramps provoked during ischemic tests.

Adult↗
PubMed1989

Hyperventilation clinical practice.

There is uncertainty about the diagnosis and definition of the hyperventilation syndrome. We prefer to regard hyperventilation (or hypocapnia with which it is synonymous) as a physiological response to abnormally increased respiratory "drive", which can be caused by a wide range of organic, psychiatric and physiological disorders, or a combination of these. This review outlines a clinical scheme for the diagnosis and assessment of hyperventilation and its causes.

Adult↗
PubMed1978

Theoretical considerations on the potential hazards of hyperventilation during anaesthesia.

The purpose of this paper is to evaluate the effect of hyperventilation on cerebral oxygenation. The best estimate of cerebral oxygenation is cerebral venous PO2 (PVO2). PVO2 has been considered in relation to PaCO2 during normoxaemia. In order to compare the effects of hyperventilation with the effects of hypoxaemia, PVO2 has also been considered in relation to PaO2 when PaCO2 is constant. The results indicate that the low PaCO2 values which may be seen in the operating room with manual ventilation have the same effect on cerebral oxygenation as severe hypoxaemia. It is emphasized that the brain is better protected against threats to cerebral oxygenation, e.g. hypotension, if PaCO2 is kept close to normal during anaesthesia. During neurosurgical anaesthesia the advantages of excessive hyperventilation must be weighed against the threat it poses to oxygenation in healthy areas of the brain.

Anesthesia↗
PubMed1988

[Changes in the brain bioelectrical activity and in the ACTH content of the blood plasma during voluntary hyperventilation in malignant neoplasm patients].

A 3-5-min spontaneous hyperventilation caused normalization of initially altered electroencephalogram and inactivation of hypothalamic structures in 14 patients with malignant tumors, as well as negative dynamics of bioelectrical brain activity and activation of diencephalic area in 6 healthy subjects. In hyperventilation ACTH plasma concentration increased 13-fold on average (from 14.2 +/- 12.1, to 185 +/- 82 pg/ml) in normal subjects and 2.4-fold (from 45.5 +/- 19.8 to 110 +/- 17 pg/ml) in oncological patients. It is assumed that changes in hypothalamo-hypophyseal reactivity in patients with malignant neoplasias can be associated with generalized intracellular metabolic acidosis, partially, compensated by gas alkalosis in the plasma due to hyperventilation.

Acid-Base Equilibrium↗
PubMed1988

[Effects of maternal hyperventilation and oxygen inhalation during labor on fetal blood-gas status].

The effects of maternal hyperventilation and oxygen inhalation on fetal blood-gas status were studied in 54 fetuses, vaginally delivered of mothers without medical and obstetrical complications. The cases were divided into four groups according to MA (maternal arterial) pH and PCO2 values and by respiring either oxygen or room-air as follows. Group N: pH less than 7.5, PCO2 greater than 23 mmHg (normoventilation), without maternal oxygen inhalation, group H: pH greater than 7.5, PCO2 less than 23 mmHg (hyperventilation), without oxygen inhalation, group NO: pH less than 7.5, PCO2 greater than 23 mmHg, with oxygen inhalation and group HO: pH greater than 7.5, PCO2 less than 23 mmHg, with oxygen inhalation. Umbilical venous (UV) PO2 (27.8 mmHg: mean), SO2 (60.8%) and CO2 (oxygen content, 12.4 ml/dl), and umbilical arterial (UA) PO2 (17.9 mmHg), SO2 (35.6%) and CO2 (7.3 ml/dl) values in group H were significantly lower than those in group N. The fetal oxygenation in group HO was similar to that in group N, and the fetal oxygen values in group NO were significantly higher than those in the other groups. The fetuses in groups H and HO tended to respiratory alkalosis. The UV oxygen values had negative correlations with MA pH and positive correlations with the MA PCO2 value in both oxygen and no-oxygen groups. There was no significant correlation between maternal and fetal PCO2 values, and higher fetal oxygen extraction (41%: mean) in group H. These facts suggest that severe maternal respiratory alkalosis due to hyperventilation may lead to a disorder in placental circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

CO2 response and pattern of breathing in patients with symptomatic hyperventilation, compared to asthmatic and normal subjects.

We studied six patients with symptomatic hyperventilation, using new techniques to quantify baseline variability of respiratory variables, and to assess CO2 sensitivity around the control point using a stimulus not detectable by the subject. We compared them with six normal subjects and six patients with mild asthma. Symptomatic hyperventilators had normal mean ventilation and end-tidal carbon dioxide tension (PETCO2) at rest. Asthmatic subjects had higher ventilation and lower PETCO2. Symptomatic hyperventilators had a larger number of sighs and abnormally wide fluctuations in baseline for inspiratory time, expiratory time, and PETCO2. These could not be explained by an abnormal ventilatory response to a transient CO2 input; the transient response near the control point was undoubtedly normal.

Adult↗