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PubMed1992

Salmeterol protects against hyperventilation-induced bronchoconstriction over 12 hours.

To study the dose-response relationship of salmeterol for protection against a naturally occurring stimulus, isocapnic hyperventilation tests of cold air were done in 16 asthmatic patients. The subjects inhaled either 50 micrograms salmeterol, salbutamol 200 micrograms, or placebo in a double-blind, randomised, cross-over study. The FEV1 was measured prior to medication and the provocative ventilation (PV20) required to induce a 20% fall in FEV1 was calculated by linear interpolation from ventilation-response curves obtained 0.5, 4, 8, and 12 h after medication. Following salbutamol, the mean FEV1 were 4.11, 3.89, 3.58, and 3.55 l, with a significant difference from placebo up to 4 h. Following salmeterol, mean FEV1 values were 3.95, 4.10, 3.93, and 3.88 l, with a significant difference from placebo up to 12 h. The mean PV20FEV1 after salbutamol was 78.8, 58.5, 52.7, and 48.4 l.min-1, the 0.5 h value being significantly different from placebo. After salmeterol, the mean PV20FEV1 values were 84.6, 82.5, 67.8, and 65.8 l.min-1, with a significant difference from placebo up to 12 h. We conclude that, besides its long-lasting bronchodilating effect, salmeterol protects against hyperventilation-induced bronchoconstriction for at least 12 h.

Adult↗
PubMed1994

The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation.

Cerebral venous oxygen desaturation may occur when hyperventilation is employed during neurosurgical procedures. In this study, we examined the effect of arterial hyperoxia (PaO2 > 200 mmHg) on jugular bulb venous oxygen tension (PjvO2), saturation (SjvO2) and content (CjvO2) in 12 patients undergoing anaesthesia for neurosurgical procedures. Under stable anaesthetic conditions, the inspired oxygen fraction (FIO2) was varied to give four different levels of arterial oxygen tension (PaO2 100-200, 201-300, 301-400, and > 400 mmHg), at two levels of controlled hyperventilation (PaCO2(25) and 30 mmHg). In five patients, a transcranial Doppler probe was used to insonate the middle cerebral artery throughout the study period. Regression lines were constructed for each patient for the PjvO2, SjvO2 and the corresponding PaO2 for both levels of PaCO2 (all PjvO2-PaO2 and SjvO2-PaO2 regression lines r2 > 0.85, P < 0.0001). From these lines we calculated the PjvO2, SjvO2 and CjvO2 at PaO2 of 100, 250 and 400 mmHg, at each level of PaCO2 for each patient. At PaCO2 of 25 mmHg, hyperoxaemia increased PjvO2 (from 27.6 +/- 1.1 mmHg at PaO2 of 100 mmHg to 30.6 +/- 1.4 and 33.6 +/- 1.8 mmHg at PaO2 of 250 and 400 mmHg respectively) and SjvO2 (from 54 +/- 3% at PaO2 of 100 mmHg to 60 +/- 3 and 65 +/- 3% at PaO2 of 250 and 400 mmHg respectively, P < 0.05). Hyperoxaemia had a similar effect on SjvO2 and PjvO2 at a PaCO2 of 30 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1999

Effects of voluntary hyperventilation on cortical sensory responses. Electroencephalographic and magnetoencephalographic studies.

It is well established that voluntary hyperventilation (HV) slows down electroencephalographic (EEG) rhythms. Little information is available, however, on the effects of HV on cortical responses elicited by sensory stimulation. In the present study, we recorded auditory evoked potentials (AEPs) and magnetic fields (AEFs), and somatosensory evoked magnetic fields (SEFs) from healthy subjects before, during, and after a 3- to 5-min period of voluntary HV. The effectiveness of HV was verified by measuring the end-tidal CO2 levels. Long-latency (100-200 ms) AEPs and long-latency AEFs originating at the supratemporal auditory cortex, as well as long-latency SEFs from the primary somatosensory cortex (SI) and from the opercular somatosensory cortex (OC), were all reduced during HV. The short-latency SEFs from SI were clearly less modified, there being, however, a slight reduction of the earliest cortical excitatory response, the N20m deflection. A middle-latency SEF deflection from SI at about 60 ms (P60 m) was slightly increased. For AEFs and SEFs, the center-of-gravity locations of the activated neuronal populations were not changed during HV. All amplitude changes returned to baseline levels within 10 min after the end of HV. The AEPs were not altered when the subjects breathed 5% CO2 in air in a hyperventilation-like manner, which prevented the development of hypocapnia. We conclude that moderate HV suppresses long-latency evoked responses from the primary projection cortices, while the early responses are less reduced. The reduction of long-latency responses is probably mediated by hypocapnia rather than by other nonspecific effects of HV. It is suggested that increased neuronal excitability caused by HV-induced hypocapnia leads to spontaneous and/or asynchronous firing of cortical neurones, which in turn reduces stimulus-locked synaptic events.

Adult↗
PubMed1995

Nocturnal hyperventilation in pregnancy--reversal with nasal continuous positive airway pressure.

A 41-year-old mother with a twin pregnancy had disabling hyperventilation with severe nocturnal symptoms at 25 weeks' gestation. The nocturnal attacks were relieved with nasal continuous positive airway pressure, which she successfully used throughout the rest of the pregnancy. Nasal continuous positive airway pressure could be an option to control severe pregnancy-induced hyperventilation.

Adult↗
PubMed1982

The effects of hyperventilation; individual variability and its relation to personality.

Self-reported affective and somatic disturbances and heart rate changes resulting from a brief period of voluntary hyperventilation are presented and related to individuals' Eysenck Personality Questionnaire (E.P.Q.) scores. Considerable individual variability was observed in the effects of hyperventilation. Neuroticism was significantly correlated with affective but not self-reported somatic or objectively measured heart rate changes. Other possible determinants of observed variability and its possible relevance to the etiology of panic attacks are discussed.

Adult↗
PubMed1987

Panic disorder and agoraphobia: fear of fear or fear of the symptoms produced by hyperventilation?

Two versions of the fear-of-fear hypothesis of panic disorder are discussed. The fear-of-the-somatic-effects-of-fear version, which is distinguished from the classical conditioning version, is compared with the hyperventilation theory of panic disorder and agoraphobia. The fear-of-the-somatic-effects-of-fear hypothesis is criticized on the basis of its inability to explain adequately (a) the initiation of panic attacks, (b) the growth in intensity of panic attacks, and (c) the termination of panic attacks. The tenability of the hyperventilation theory is supported by evidence from programs of treatment derived from the basic assumptions of the theory.

Agoraphobia↗
PubMed1988

Panic attacks during sleep: a hyperventilation-probability model.

Panic attacks during sleep are analysed in terms of a hyperventilation theory of panic disorder. The theory assumes that panic attacks during sleep are a manifestation of severe chronic hyperventilation, a dysfunctional state in which renal compensation has led to a relatively steady state of diminished bicarbonate. Reductions in respiration during deep non-REM sleep lead to respiratory acidosis which triggers hyperventilatory hypocapnea and subsequent panic. A probability model designed to predict when during sleep panic attacks are likely to occur is supported by relevant data from studies of sleep and panic attacks. Implications for treatment are discussed.

Carbon Dioxide↗
PubMed1990

Elevated serum lactate following hyperventilation during glucose infusion in panic disorder.

Early investigators reported that patients with anxiety syndromes associated with panic attacks produced more lactate during exercise than control subjects. These studies suggested a metabolic difference between patients and controls. However, the possibility that patients were simply less fit than controls could not be excluded. In this study, serum lactate was measured in panic disorder patients in response to a metabolic challenge not involving exercise. Voluntary hyperventilation during iatrogenic hyperglycemia led to an increase in serum lactate. The increase in serum lactate was significantly greater in panic disorder patients than in controls. Hyperventilation provoked panic attacks in 4 of 8 patients and none in 6 controls. There was no evidence of a relationship between the increase in lactate or the associated decrease in phosphate and the level of anxiety produced by this procedure.

Adult↗
PubMed1980

Hyperventilation induced abnormalities in the electroencephalogram of children with Moyamoya disease.

Two cases of Moyamoya disease in children are presented. The EEG of each child demonstrated minimal abnormalities at rest. However, during 3 min of hyperventilation, the record developed rhythmic delta activity which persisted in excess of 5 min after termination of over breathing. This activity did not respond to glucose administration and was maximal in the areas correlating with the clinical symptoms. It appears to represent a physiologic correlate of an abnormal vascular response to hypocapnia. Although admittedly a non-specific response, the persistence of delta activity easily provoked by hyperventilation, the topographic correspondence to the ultimately demonstrated vascular anomaly, and the lack of response to glucose ingestion represent a combination of factors which, in the appropriate clinical setting, are distinctive and of diagnostic value. Currently, invasive arteriography is required for definitive diagnosis of Moyamoya. Improved selection of children for invasive studies may be accomplished by EEG screening.

Adolescent↗
PubMed1988

Changes in quantitative EEG and blood flow velocity due to standardized hyperventilation; a model of transient ischaemia in young human subjects.

A standardized hyperventilation (HV) procedure has been developed in which the end-tidal pCO2 was decreased to 2 kpa. In 24 young male subjects blood flow velocity and qEEG were studied before, during and after HV. This standardized hyperventilation procedure gave rise to a decrease in blood flow velocity to 40% of baseline value and highly significant qEEG changes in 3 derivations. Both relative and absolute band power estimates showed an increase in slow activity and a decrease in alpha and beta activity. The use of subtraction spectra led to a more precise and detailed presentation of these changes than the use of classical qEEG parameters. These changes were reproducible after 1 week. The effects found in the presented model of HV-induced ischaemia appeared to be twice as large as those found in a model of hypobaric hypoxia. The present model might be used to test the efficacy of anti-ischaemic drugs in young human subjects.

Adult↗
PubMed1991

Physical exercise and voluntary hyperventilation in childhood absence epilepsy.

The aim of this study was to compare the effects of a physical exercise test and of voluntary hyperventilation between controls and children with absence epilepsy. Eighteen children (6 controls and 12 epileptics) were studied during rest (R), a maximal physical exercise test (15 min; PE), recovery (REC) and voluntary hyperventilation (3 min; VHPV). EEG and ECG were recorded during the experiment; respiratory parameters were measured to quantify PE; plasma levels of pH, lactate, pyruvate, glucose and antiepileptic drugs were determined. A decrease in the number of absences was observed during PE whereas an increase was observed during VHPV. We found significant positive correlations between the number of children with absences, the total number of absences for each state, frequency of absences per minute and the corresponding mean plasma pH, which demonstrate that the lower the pH is, the fewer absences occur. On the other hand, there was no relationship between the number of absences and the values of other parameters. Relations between variations of the plasma value of the pH, and thus the probable cerebral value of pH, and neuronal excitability are discussed. Our results indicate that children who suffer absence epilepsy should not be discouraged from sport practice.

Adolescent↗
PubMed1991

Quantitative EEG changes under various conditions of hyperventilation in the sensorimotor cortex of the anaesthetized cat.

The effects on the EEG rhythms recorded from the sensorimotor cortex (post-sigmoid gyrus) of anaesthetized cats were studied under 4 conditions of artificial mechanical hyperventilation (HV) before and after cervical bilateral vagotomy. In animals with intact vagus nerves, using visual examination, EEG changes were only observed within the 2nd min during HV produced by increased stroke volume (delta V) with associated hypocapnia. Quantitative EEG (qEEG) showed that, for the same increase in minute ventilation and the same degree of hypocapnia, delta V induced a greater and earlier relative decrease (2nd min) in the power density of delta, theta and alpha bands, than increased pump frequency (delta F). The delta F tests produced a fall only in the theta band and within the 3rd min. With constant paCO2, transient modifications occurred only with delta V and were limited to the first 30 sec. In bivagotomized cats, moderate EEG responses to delta V plus associated hypocapnia persisted partly in the alpha band. Finally, no changes appeared with delta V or delta F when the vagus nerves were cut and paCO2 was maintained constant. The present data suggest strongly that, in anaesthetized cats, peripheral vagal afferents from the respiratory system play a major role in the EEG changes caused by artificial hyperventilation.

Animals↗
PubMed1985

A controlled study of a breathing therapy for treatment of hyperventilation syndrome.

A therapy directed toward slowing and regularizing the ventilatory pattern was compared with a partial-treatment, comparison procedure for individuals with somatic and psychological symptoms attributable to hyperventilation episodes (i.e. hyperventilation syndrome). Comparing repeated measures between a pretreatment baseline session and a post-treatment followup, we found that the experimental therapy, in contrast to the comparison procedure, produced a greater number of, and more extensive, improvements in psychological, symptom complaint and ventilatory dimensions. Results also suggest changes in central respiratory control mechanisms as a consequence of treatment.

Adult↗
PubMedDate not supplied

Apnea following hyperventilation in man.

To assess the incidence of posthyperventilation apnea (PHA), breathing patterns after active voluntary hyperventilation were determined during EEG recording by means of: (1) a thermocouple in 1060 patients; (2) a pneumotachograph coupled with a capnograph in 100 further patients. All the patients were randomly chosen. PHA of 12.6 +/- 0.48 occurred in only 18% of awake subjects and was not related to the magnitude of the lowering of end-tidal FECO2 during the test. PHA frequency increased when sleep followed hyperventilation and in patients with clinical or EEG evidence of cerebral pathology and seemed to be age-related. This study supports the hypothesis that in man a central neural mechanism closely linked to vigilance and connected with active breathing supplies sufficient neural facilitation to prevent the apnea consequent on the decrease in chemical humoral stimulation. Posthyperventilation sleep reduces this neural facilitation, allowing the lack of chemical stimulation to induce apnea. The high incidence of PHA reported in some studies might be due to a decrease in vigilance which was not detected by the usual behavioral or electroencephalographic tests.

Adolescent↗
PubMed1983

Progesterone-induced hyperventilation in the guinea pig.

Progesterone-induced hyperventilation has thus far not been reported in animals other than humans. Accordingly we investigated the effects of chronic progesterone treatment on ventilation in guinea pigs. Virgin female guinea pigs were divided into those treated with cholesterol as controls (C), progesterone (P), or estrogen plus progesterone (E&P). All hormones were administered in silastic capsules placed subcutaneously for 28 days. On day 28 arterial blood gases and respiratory rates were determined. Arterial pH was elevated in P- and E&P-treated animals compared with controls (7.43 +/- 0.04 and 7.43 +/- 0.03 vs 7.39 +/- 0.05, respectively, P less than 0.05). Arterial PCO2 was reduced in both progesterone-treated groups compared to controls (33.9 +/- 5.8 (P), 33.1 +/- 2.8 (E&P), 38.0 +/- 4.3 (C)), and was correlated with systemic progesterone concentrations in animals receiving E&P (r = -0.85, P less than 0.01) but not in animals receiving P alone (r = -0.07, P = N.S.). Arterial [HCO-3], PO2 and respiratory rates were not different between groups. We conclude that chronic progesterone administration produces hyperventilation in guinea pigs, and that estrogen facilitates this action of progesterone.

Animal Diseases↗
PubMed1983

Effects of PCO2 on respiratory pattern during thermal and exercise hyperventilation in domestic fowl.

The relationship between respiratory pattern and arterial PCO2 was investigated during hyperventilation induced by graded exercise and hyperthermia. Treadmill exercise was performed both in isothermic and hyperthermic conditions. Isothermic exercise was induced by spraying the birds with water before exercise at environmental temperatures of 18 +/- 2 degrees C. Hyperthermic exercise was performed in unsprayed birds at temperatures of 18 +/- 2 degrees C and 30 +/- 2 degrees C. During isothermic exercise there was no significant change in arterial PCO2 at moderate work loads and only a small drop in PCO2 at the heaviest work loads; ventilation was increased by coupled increases in tidal volume and respiratory frequency. During exercise in unsprayed birds rectal temperature rose progressively and arterial PCO2 fell progressively with work load. At each work load ventilation was higher and breathing was more rapid and shallow than during isothermic exercise. These effects were more pronounced during exercise at 30 +/- 2 degrees C than at 18 +/- 2 degrees C. When normal PCO2 was maintained during hyperthermic exercise, as a result of the administration of CO2-enriched air, polypnea was suppressed and the tidal volume-respiratory frequency relationship became identical to that observed during graded isothermic exercise. Maintenance of normal PCO2 in resting birds subjected to a gradual increase in environmental temperature also resulted in changes in respiratory pattern identical to those obtained during eucapnic exercise. It is concluded that, provided arterial PCO2 is held constant, the pattern of breathing is the same for hyperventilation induced by exercise or by body temperature increases.

Animals↗
PubMed1983

The release of surfactant in rat lung by brief periods of hyperventilation.

We investigated the release of surfactant-type phospholipids (S) using the isolated perfused rat lung (IPL). Following a 20 min equilibration period the lungs were hyperventilated for up to 15 min and then lavaged. Changing the peak inspired pressure (PIP) from 10 to 20 cm H2O rapidly increased the rate of release of S; this rate declined after 2 min. In contrast, doubling frequency of ventilation while maintaining the control tidal volume had no effect. The increase in alveolar S reflected release. rather than redistribution, and after 2 min amounted to about 8% of total S in lung tissue. Equivalent hyperventilation in an open-chested intact rat released significantly less S, suggesting possible tonic neurohumoral suppression in vivo. The release of S in the IPL was depressed by reducing temperature, but was not affected by hypoxia, 2,4 dinitrophenol, phenylephrine or dibutyrylguanosine 3',5'-cyclic monophosphate. We suggest that increasing tidal volume may directly distort the alveolar type II cell; each cell reacts to its own threshold distortion by releasing a pool of S in all-or-none fashion.

Animals↗
PubMed1989

Role of hyperventilation in hypoxia on lung growth in rats.

This study was conducted in an attempt to differentiate the contribution of hyperventilation, if any, from that of low PO2 on adaptive lung growth in response to hypoxia. Male albino rats were exposed to one of the following: (1) Room air for 7 days, as control; (2) 10% O2 in N2 for 7 days; (3) 10% O2 for 6 h, 1 day or 2 days and air for the remaining of 7 days; (4) 10% O2 for 2 days and 7% CO2 in air for 5 days; (5) air for 2 days and 7% CO2 for 5 days; or (6) 7% CO2 in air for 7 days. Lung growth was assessed by measuring the lung weight, lung air volume, lung DNA content and rate of DNA synthesis in lung explants. Hypoxia stimulated lung DNA synthesis even when administered for only 6 h, and the effects persisted for a few days after discontinuation of hypoxia. Hypercapnia did not stimulate DNA synthesis in lung. In 2 day hypoxic 5 day air rats the lung weight and lung DNA content increased, in 2 day air 5 day hypercapnic rats only the lung volume increased, and in 2 day hypoxic 5 day hypercapnic rats all parameters of lung growth, i.e., lung weight, DNA content and air volume increased as in 7 day hypoxic rats. The results suggest that adaptive or compensatory lung growth in hypoxia is brought about on one hand by the direct effect of low PO2 on lung cells, resulting in lung hyperplasia, and on the other hand by the mechanical stimulation of lung tissue by hyperventilation, causing lung distension.

Animals↗