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PubMed1988

Hyperventilation with hypoproteinemia.

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.

Acid-Base Equilibrium↗
PubMed1986

Hyperventilation and aerophagia: a negative report.

Aerophagia is described as a frequent symptom in the hyperventilation syndrome. However, this has never been substantiated. In this study the extent of air swallowing was estimated from the size of the gastric air-bubble on the chest X-ray, in a group of 62 hyperventilators and in a group of 62 normals. No differences were found between the mean amounts of gastric air in the two groups. Women in both groups seemed to swallow more air than men. The amount of air was not related to the time of the day (meals). In 15 hyperventilators the subjective complaints of upper abdominal discomfort and of chest pain were quantified: no correlation was found with the amount of gastric air.

Abdomen↗
PubMed1986

Correlation of methacholine-induced non-specific bronchial reactivity and cold air hyperventilation challenge.

The degree of bronchoconstriction seen with cold air hyperventilation challenge was determined in 48 adult subjects with known degrees of methacholine-induced bronchial reactivity. The degree of bronchial reactivity as determined by the cold air hyperventilation challenge significantly correlated with the non-specific bronchial reactivity determined by a methacholine inhalation challenge. Cold air hyperventilation challenge can accurately confirm the presence of reactive airway disease.

Adult↗
PubMed1984

Analysis of hyperventilation response in asthmatics.

We have tested seven young adult asthmatics (17-35 years) with two different tests of airway reactivity, i.e., treadmill exercise test and isocapnic hyperventilation test. To estimate the level of respiratory heat loss we standardized environmental conditions so that during these tests patients inhaled compressed air of 23 degrees and 0% of R.H. The level of ventilation during these tests thus determined the respiratory heat loss. It was found that five out of seven tested patients showed dose-response-like relationships between a change in FEF 25-75% (or FEV1) and minute ventilation as measured during exercise or voluntary hyperventilation (r = -.80 to -.97). However, in two patients this relationship could not be established. These two patients had the lowest baseline pulmonary function of the whole group, and by definition they had the most hyperreactive airways. When the change in pulmonary function observed after three to six minutes of isocapnic hyperventilation (both at the same level of minute ventilation) were compared it was found that the six minute test caused only slightly greater changes (P less than 0.01) than the three minute test. It is concluded that in asthmatics the relationship between a decrease in pulmonary function and respiratory heat loss varies among patients.

Adolescent↗
PubMed1981

Hyperventilation syndrome in children and adolescents: long-term follow-up.

Records of 34 hyperventilating children aged 18 years or younger seen at the Mayo Clinic over a 25-year period were reviewed. Five different clinical subtypes were identified. Evaluation and treatment varied considerably. At follow-up, 40% were still hyperventilating as adults, and many had signs and symptoms of chronic anxiety. Hyperventilation in childhood can be a signal that the child is experiencing severe anxiety, which may persist into adulthood.

Adolescent↗
PubMed1980

Asthma hyperventilation and emotion.

Hyperventilation in asthmatic subjects causes airways obstruction as demonstrated by a fall in the Forced Expiratory Volume in one second. Clinically, measurements of blood gases during asthmatic attacks have shown that asthmatic subjects, who hyperventilate have a blood carbon dioxide level below normal unless ventilatory failure occurs. Two methods of demonstrating that asthmatic subjects hyperventilate on the thought of asthma were employed. 1. Chronic asthmatic subjects had their respiratory minute volume measured during relaxation and at the recall of an asthmatic attack. The mean minute volume rose from 10.1 litres when relaxed to 13.5 litres when recalling an asthmatic attack (p < .025). 2. Asthmatic volunteers had their respiratory minute volume measured during relaxation and on the hypnotic suggestion of anger, fright and asthma and pleasurable excitement, both in the conscious state and under hypnosis. The data were statistically treated by an analysis of variance. All emotion resulted in a significant increase in minute volume at the 0.1 level of significance.

Aged↗
PubMed1995

[Chronic hyperventilation syndrome].

Hyperventilation syndrome is a frequent, but poorly understood clinical entity. The clinical expression is a rich combination of respiratory, cardiac and neurological signs which can simulate various organic diseases. Hypocapnia remains the primum movens for most authors although the relationship with psychiatric situations, in particular in anxious patients, is increasingly emphasized. The diagnosis is currently based on the elimination of diseases associated with hyperventilation, then on Nijmegen's questionnaire and is confirmed by the reproduction of the same clinical picture in a voluntary hyperventilation test. Respiratory function tests offer little information. Treatment is based on combining rehabilitation therapy focused on the diaphragm and on relaxation. Specialized care may be needed in psychiatric patients.

Chronic Disease↗
PubMed1994

[The hyperventilation syndrome in children].

Hyperventilation syndrome is not a rare disorder present primarily in children, but in adolescents too. It points to anxiety in children with or without family problems. The clinical picture is polymorphous and often without a clear connection with hyperventilation. That is why it is necessary for the physician to be aware of this problem in practice. The diagnosis is made on the basis of clinical picture and hyperventilation provocative test, when one expects this disorder might occur. We have reported five cases of children with this syndrome, with a special review concerning clinical picture and the way which led to the confirmation of diagnosis.

Adolescent↗
PubMedDate not supplied

Hyperventilation and dizziness: case reports and management.

Dizziness is a common symptom in patients presenting to an otorhinolaryngologist. Hyperventilation accounts for up to 5% of cases with dizziness and is a contributory factor in a further 20% of cases. Six cases of dizziness due to hyperventilation are presented to illustrate the author's simple management policy. A high index of suspicion in the absence of an organic cause of dizziness and a simple provocation test will identify these cases. Management is aimed at demonstrating resting hypocapnia, investigations to exclude organic causes of hyperventilation and rehabilitation in collaboration with a clinical psychologist ensures the appropriate treatment for the dizziness and can avoid the development of chronic somatisation behaviours.

Adult↗
PubMed1994

[Effects of hyperventilation upon the spinal pain modulating system (third report)].

The purpose of this study is to investigate the mechanisms of the effect of hyperventilation on the spinal pain modulating system by using phentolamine. Under enflurane anaesthesia, cats received mid-collicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was changed to induce hypocapnia of PCO2 20-25 mmHg. After activities were well suppressed, phentolamine 0.5 mg with normal saline 1.0 ml was injected on the spinal cord. Changes of firings were investigated. When normocapnia was resumed, recovery followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Phentolamine significantly antagonized the suppressive effects of hyperventilation upon the activities of WDR cells. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to adrenergic pain modulating system.

Action Potentials↗
PubMed1994

[The role of parasympathetic nerve on hyperventilation-induced bronchoconstriction in sensitized rabbits].

We have demonstrated that hyperventilation-induced bronchoconstriction (HIB) is observed in sensitized rabbits, and that histamine may play a role in HIB. To investigate the role of parasympathetic neurotransmission in HIB, the effects of atropine and vagotomy on HIB were examined. Japanese white rabbits were sensitized with ovalbumin. They were then anesthetized and paralyzed with pancuronium, and then mechanically ventilated (TV: 7 ml/kg, RR: 40/min). The rabbits were divided into the following three groups: I) control group (n = 7), II) atropine-treated group (n = 6), III) bilateral vagotomy group (n = 6). Hyperventilation was performed at TV: 7 ml/kg, RR: 120/min for 15 min in dry room air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and at 0, 5, 15 and 30 minutes after hyperventilation. RL increases significantly at 5 minutes in group 1, but this change was significantly less marked in groups 2 and 3. However Cdyn was not significant change in each group. We conclude that parasympathetic neurotransmission may play an important role in HIB of sensitized rabbits.

Animals↗
PubMed1993

[The dynamic function of the motor apparatus of the respiratory system during maximal voluntary hyperventilation under hypoxia and hypercapnia].

The working ability in the course of hyperventilation can be divided into three stages: the adaptation, stable working ability, the fatigue. Hypoxia decreased the duration and intensity of voluntary hyperventilation. During hypercapnia, the hyperventilation is more intensive and shorter. The data obtained suggest a co-operation of one's own will and chemoreceptor stimuli under hypoxia and hypercapnia.

Adolescent↗
PubMed1994

[The effects of hyperventilation upon the spinal pain modulating system (second report)].

The purpose of this study is to investigate the effect of hyperventilation on the spinal pain modulating system by using naloxone. Under enflurane anaesthesia, cats were prepared with midcollicular decerebration and lumbar laminectomy. The spinal cord was transected at T12-L1. WDR cells, responding primarily to noxious peripheral stimuli, were sampled with a microelectrode at the depth of 2,000 microns from the cord dorsum. Following the control period, ventilation was adjusted to produce hypocapnia of PCO2 20-25 mmHg. After activities of WDR cells were well suppressed, naloxone 0.1 mg.kg-1 was given intravenously. Changes of firings of WDR cells were investigated. Returning to normocapnia, recovery of firings was followed. Hypocapnia of PCO2 20-25 mmHg significantly suppressed the activities of WDR cells. Naloxone significantly antagonized the suppressive effects of hyperventilation upon the activity of WDR cell. Our results suggest that the hyperventilation has suppressive effects on single-unit activity of WDR cell and the mechanisms of those suppressive effects are related to pain modulating system by endogenous opiates.

Action Potentials↗
PubMed1977

Hearing under stress: II. Effect of hyperventilation and hypercapnia on speech discrimination.

Changes in the ability to discriminate speech from a eucapnic state to hyperventilation and hypercapnia were investigated. Standard speech audiometric techniques were employed to determine the speech reception threshold and the speech discrimination values, while respiratory conditions were varied and measured utilizing a mixed-gas breathing method. Respiratory parameters were similar to those encountered in aircraft personnel who experience oxygen/pressure system malfunction. The results of the study suggest no significant change in the speech reception threshold while in a hyperventilated or hypercapnic state. The speech discrimination results, however, suggest a significant performance decrement while in a state of hyperventilation.

Auditory Perception↗
PubMedDate not supplied

[Transcranial Doppler ultrasonography and hyperventilation test in assessment of cerebral vasoreactivity after ischemic stroke].

In 36 patients 3 month after ischaemic stroke in regions supplied by MCA (Middle Cerebral Artery) physical examination, CT scanning and blood flow velocity recordings in ICA (Internal Carotid Artery) and MCA were performed. In both MCA blood flow velocity was measured in resting state and after 30 sec. of hyperventillation. The control group consisted of 40 healthy volunteers. In the control group blood flow decrease after hyperventillation was nearly equal in both hemispheres (38% in right and 37% in the left hemisphere). In studied group in the symptomatic hemisphere blood flow reduction was 21%. Vasoreactivity in the opposite hemisphere was similar to that in control group (35% decrease). The results suggest that vasoreactivity diminution is a local phenomenon limited to the infarcted area. Hyperventilation test, despite its simplicity, seems to be sufficient for screening vasoreativity.

Adult↗
PubMed1996

[Hyperventilation and cold pressor stress echocardiography for diagnosis of vasospastic angina : report of five cases].

Two-dimensional echocardiography was used for diagnosing coronary vasospasm during the cold pressor stress test immediately after hyperventilation in five patients with suspected vasospastic angina. The test consisted of hyperventilation for 6 min and cold water pressor for 2 min under continuous electrocardiographic and echocardiographic monitoring. Coronary angiography with intracoronary injection of acetylcholine was performed in all patients within 1 month after the stress test. During the stress test, new asynergies of both the anterior and inferior walls were seen in three of the five patients, and new asynergy of the anterior wall in the other two patients. All acetylcholine induced coronary artery spasms occurred at the same locations as the new asynergies provoked by the stress test. In three patients, wall motion abnormality occurred earlier than ST segment elevation, and the other two patients had no ST changes. Chest pain was induced in three patients and delayed in comparison to electrocardiographic and echocardiographic changes. Echocardiographic monitoring during the stress test could detect spasms unaccompanied by either ST segment changes or chest pain, and could detect multivessel coronary spasms. Hyperventilation and cold pressor stress echocardiography may be used for the diagnosis of vasospastic angina.

Acetylcholine↗
PubMed1977

[Diagnosis of hyperventilation for elimination of false-positive results of physical exercise test].

The study was conducted in 55 patients with cardiac pains. Electrocardiography was used successively prior to, during and following physical exercises, followed by Seldinger selective coronary angiography, and electrocardiography prior to, during and following hyperventilation tests. In 2 of 55 patients the result of the exercise test was interpreted as false-positive, since the coronary angiography demonstrated intact vessels, and during hyperventilation ECG recorded a decreased ST segment. To avoid false-positive results in patients with suspected angina pectoris the physical exercises tests can be considered positive only in cases in which hyperventilation caused no ECG changes typical for angina pectoris.

Adult↗
PubMed1996

[The possibility of the occurrence of hyperventilation apnea and loss of consciousness].

In work influence of various temporary modes of free hyperventilation of the lungs was investigated, usually used by the sportsmen before diving on reduction of the contents of CO2 in exhaling air of healthy men-divers. Attention was paid to the opportunity of occurrence of posthyperventilation apnea and loss of consciousness. It is shown, that washing away CO2 from organism at hyperventilation is limited. Hyperventilation (their depth and frequency was chosen arbitrary), spent during 60, 120, 180, 360 seconds causes in healthy trained men apnea and loss of consciousness.

Adult↗