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PubMed1998

Subjective symptoms and breathing pattern at rest and following hyperventilation in anxiety and somatoform disorders.

The purpose of the present study was to investigate the diagnostic specificity of bodily symptoms and respiratory behavior at rest and after a hyperventilation provocation test (HVPT) in patients that were either grouped according to the DSM classification or diagnosed as suffering from hyperventilation syndrome. Nine hundred three anxiety and somatoform patients, showing symptoms supposedly caused by psychogenic hyperventilation, and 170 healthy subjects, were studied. Breathing pattern and end-tidal CO2 concentration were recorded during breathing at rest and following a HVPT. Subjective symptoms in daily life and after HVPT were measured. A principal-components analysis was performed on both the symptoms and breathing variables and their specificity levels were compared in the two classifications of patients. Some symptoms in daily life were grouped together with the same symptoms after the HVPT, other symptoms were not. This suggests that the HVPT elicited partly specific symptoms, and partly reproduced the symptoms experienced in daily life. Similar findings were observed with respect to the breathing variables. Patients with panic differed from other patients with anxiety disorders by an increased level of symptoms and a FETCO2 decline at rest. The HVPT may be informative for diagnosis because it provokes some of the typical somatic and psychological symptoms, and it identifies the breathing instability that is characteristic of both patients with HVS and with anxiety. The same symptoms and breathing variables characterized the patients, whatever their classification. Overall, the specificity of breathing variables is rather low.

Adult↗
PubMed2005

[Primary central nervous system lymphoma presenting with central neurogenic hyperventilation. A case report and review of the literature].

INTRODUCTION: Central neurogenic hyperventilation (CNH) in an awake patient is a rare entity. OBSERVATION: We report here a 54-year-old patient who developed central neurogenic hyperventilation as the initial presentation of a primary central nervous system lymphoma located in the brainstem. CONCLUSION: The patient's hyperventilation resolved completely with chemotherapy for primary CNS lymphoma. Most of the cases reported in the literature are related to a diffuse tumor of the brainstem with an intriguing overrepresentation of primary CNS lymphoma. The pathogenesis of CNH is discussed.

Brain Stem Neoplasms↗
PubMed1986

Controlled study of respiratory responses during prolonged measurement in patients with chronic hyperventilation.

The respiratory responses of 17 patients with chronic hyperventilation but without demonstrable organic disease (group H) to various manoeuvres were compared with those of 21 healthy controls (group C). The responses were tested according to a 60 min protocol in which periods of rest were replaced by exercise, voluntary hyperventilation (VHV), reading, and CO2 inhalation. 5 patients with severe resting hypocapnia were investigated overnight during sleep. Chronic hyperventilation was of two types--persistent or provoked by exercise or VHV. It was due to modest increases in tidal volume and respiratory frequency but was generally not conspicuous. End-tidal PCO2 levels were gradually corrected to near normal during sleep but not by inhalation of CO2.

Adult↗
PubMed1999

Mental stress test is an effective inducer of vasospastic angina pectoris: comparison with cold pressor, hyperventilation and master two-step exercise test.

BACKGROUND: Cold pressor, hyperventilation and exercise stress tests were usually used for inducing an angina attack in patients with vasospastic angina pectoris. We induced vasospastic angina attack using the mental calculation stress test, and compared the results with those using other stress tests. SUBJECTS AND METHODS: Subjects were 29 patients with vasospastic angina pectoris. Their ages were 60.8+/-8.4 years. Coronary vasospasm was induced by an acetylcholine infusion test during coronary angiography. The mental stress test was performed as follows; after memorizing six digits numbers, they repeated these numbers in reverse for 5 min, and performed serial subtraction of 17 from 1000 for 5 min. Blood pressure, heart rate and ECG were recorded every 1-5 min during the mental stress test. The serum concentrations of epinephrine and norepinephrine were measured before and during the mental stress test. We compared these results with those obtained using cold pressor, hyperventilation and the Master two-step exercise stress test. RESULTS: (1) Eight of the 29 patients (28%) showed ischemic ST-T change, which was caused by the mental stress test. (2) The increase in norepinephrine was greater in patients with an ST-T change than without an ST-T change (0.11+/-0.06 vs. 0.04+/-0.04 ng/ml, P<0.01). (3) The incidence of the ST-T change caused by the mental stress test (28%) was similar to the cold pressor test (27%) and greater than that caused by the hyperventilation test (13%). The incidence of ST-T change caused by the Master two-step test was 55%. CONCLUSIONS: The mental stress test is an effective inducer of vasospastic angina attack, and attack may be induced by neurohumoral vasoconstrictive reflex and/or increased left ventricular afterload.

Acetylcholine↗
PubMed1989

Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients.

It is traditional practice to treat acute hyperventilation (thought to be due to anxiety) by having patients rebreathe into a brown paper bag. The author reports three cases in which this treatment, erroneously applied to patients who were hypoxemic or had myocardial ischemia, resulted in death. This clinical experience motivated a study of the effects of paper bag rebreathing in normal volunteers. Subjects deliberately hyperventilated to an average end-tidal CO2 concentration of 21.6 (SD, 3.2) mm Hg and then continued to hyperventilate into a no. 4 Kraft brown paper bag containing the calibrated sensors for a Hewlett-Packard 47210A capnograph and a Teledyne TED 60J digital oxygen monitor. Fourteen men and six women with an average age of 36 years (SD, 6.1) were tested. Results are reported as mm Hg. After 30 seconds of rebreathing, mean change in O2 from room air was -15.9 (SD, 4.6) and mean CO2 was 38.7 (SD, 6.2); at 60 seconds, -20.5 (6.0) and 40.2 (6.4); at 90 seconds -22 (6.8) and 40.5 (6.4); at 120 seconds -23.6 (6.8) and 40.7 (6.5); at 150 seconds -25.1 (1.2) and 41 (7.3); and at 180 seconds -26.6 (8.4) and 41.3 (7.5). A few subjects achieved CO2 levels as high as 50, but many never reached 40. The mean maximal drop in O2 was 26 (8.8); seven subjects had drops in oxygen of 26 mm Hg at three minutes, four had drops of 34 mm Hg, and one had a drop of 42 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Opioid peptide modulation of circulatory response to hyperventilation in humans.

After hyperventilation, systolic blood pressure (SBP) significantly decreased in 10 subjects (group 1), did not change in eight (group 2) and increased in 15 (group 3). Diastolic blood pressure and heart rate increased in all groups. The decrease in SBP was associated with a decrease in plasma catecholamines and increase in beta-endorphin, whereas the increase in SBP was accompanied by an increase in catecholamine and Met-enkephalin levels. Naloxone abolished the hyperventilation-induced SBP and catecholamine decrease only in group 1. These findings show an activation of the endogenous opioid system after hyperventilation and the role of beta-endorphin in reducing SBP in response to the test.

Adult↗
PubMed2001

A review of psychological factors/processes affecting anxious responding during voluntary hyperventilation and inhalations of carbon dioxide-enriched air.

Despite advances in our understanding of the nature of anxiety-related responding during periods of elevated bodily arousal, it is not necessarily evident by what psychological mechanisms anxiety is produced and maintained. To address this issue, researchers have increasingly employed biological challenge procedures to examine how psychological factors affect anxious responding during elevated bodily arousal. Of the challenging procedures, hyperventilation and inhalations of carbon dioxide-enriched air have been among the most frequently employed, and a relatively large body of literature using these procedures has now accumulated. Unfortunately, existing reviews do not comprehensively examine findings from hyperventilation and inhalations of carbon dioxide studies, and only rarely the methodological issues specific to these studies. To address these issues, we review the voluntary hyperventilation and carbon dioxide-enriched air literature in order to identify the primary methodological issues/limitations of this research and address the extent to which psychological variables influence anxious responding to such challenges. Overall, we conclude challenge research is a promising paradigm to examine the influence of psychological variables in anxious responding, and that such work will likely be enhanced with greater attention to psychological process issues.

Anxiety Disorders↗
PubMed2002

Transcutaneous PCO(2) monitoring with hyperventilation during phonation in vocal cord paralysis.

OBJECTIVE: Hyperventilation during phonation is one of the causes of fatigue in-patients with vocal disorders. METHODS: The transcutaneous (tc) PCO(2) during phonation in 8 normal subjects and 12 patients with unilateral vocal cord paralysis was measured. Cases were further divided into two groups by the degree of the tcPCO(2) decrease during phonation. Patients with a tcPCO(2) decrease less than 3.4 mmHg during phonation were classified as group 1 (G1). Patients with a tcPCO(2) decrease larger than or equal to 3.4 mmHg during phonation were classified into group 2 (G2). RESULTS: The average changes in tcPCO(2) in the G1 cases was not significantly different from that in normal subjects. The decrease in tcPCO(2) during phonation in the six G2 cases was 10.7+/-6.2 mmHg, and was significantly different from that in normal subjects (P<0.01, t-test). The decrease of tcPCO(2) during phonation in both G1 and G2 cases improved significantly after surgical treatment. Easy fatigability during phonation in two G1 cases and five G2 cases improved. CONCLUSIONS: The decrease in tcPCO(2) during phonation in cases of unilateral vocal cord paralysis is well correlated with easy fatigability. It is clinically useful to classify cases into two groups using the criteria of a less than 3.4 mmHg or larger than or equal to 3.4 mmHg decrease in tcPCO(2). These results also suggest that hyperventilation is one major cause for easy fatigability during phonation in cases with unilateral vocal cord paralysis. TcPCO(2) changes during phonation are useful in evaluating hyperventilation and the effect of treatment.

Adult↗
PubMed1999

Re-evaluation of the hypoxia theory as the mechanism of hyperventilation-induced EEG slowing.

To determine whether the well-accepted hypoxia theory accounts for hyperventilation-induced electroencephalogram (EEG) slowing, the authors monitored changes in cerebral oxygenation and end-tidal concentrations of carbon dioxide in 67 patients with epilepsy (age range = 5-12 years) during the hyperventilation activation test in a routine EEG examination. Relative concentration changes in cerebral oxygenated, deoxygenated, total hemoglobin, and oxidized cytochrome oxidase were measured by near-infrared spectroscopy in the frontal region. In all patients, except one who demonstrated EEG slowing, total and oxygenated hemoglobin decreased, and cytochrome oxidase was not reduced. EEG slowing occurred intermittently in 22 patients and was not synchronous with changes in either the cerebral oxygenation or end-tidal concentration of carbon dioxide. The degree of EEG slowing was diminished or the slow waves disappeared abruptly within 1 second after the cessation of hyperventilation in 22 patients when both the cerebral oxygenation and end-tidal concentration of carbon dioxide were still at low levels. The findings during the recovery periods do not confirm the hypoxia theory. It is thus supposed that more subtle mechanisms are the cause of EEG slowing.

Brain↗
PubMed1996

Hyperventilation during bronchial challenges in asthmatics: reproducibility and assessment of contributing factors.

Among asthmatics, the ventilatory response is heterogeneous during bronchial challenge. This study aimed to investigate the reproducibility of the response and to assess possible causes for hyperventilation. Repeated bronchial histamine and methacholine challenges (HiCh/MeCh) were performed in 10 asthmatic adolescents. Ventilation was monitored by respiratory inductive plethysmography (RIP), in order to minimally affect the spontaneous breathing pattern. FEV1 and the volume of trapped gas (measured as the volume of air mobilized by five maximal breaths after a multiple breath nitrogen washout to 2% N2), were used to assess mainly central and peripheral airways obstruction, respectively. When FEV1 had decreased by at least 20%, mean inspiratory flow (VTI/TI) increased by 21% and minute ventilation (V'I) by 21% and 23% during HiCh and MeCh, respectively (both P < 0.05). No correlation was found between the magnitude of the ventilatory response and either: the degree of FEV1 decline, the increase in gas trapping, SaO2 decline or the increase in dyspnoea score. Histamine challenge after beta 2-agonist pre-treatment was associated with increased ventilatory drive in one patient despite the absence of bronchial obstruction, indicating that histamine might directly stimulate afferent airway nerves which cause hyperventilation. The intra-individual variability of the ventilatory response (increase in V'I and VTI/TI) was more than 100% of the mean ventilatory response, while the variability of the bronchomotor response was about 25% of the mean bronchomotor response. Thus, during induced bronchial obstruction in asthmatics, the occurrence of hyperventilation and its intensity are not related to either the degree of central or peripheral airways obstruction, or to the degree of dyspnoea. The reproducibility of the ventilatory response is poor. The ventilatory response appears to be the result of a complex interaction between several afferent stimuli and central ventilatory control.

Administration, Inhalation↗
PubMed1996

Hyperventilation during exercise: independence on exercise-induced bronchoconstriction in mild asthma.

Ventilatory gas exchange during exercise was compared in patients with mild asthma (11 females and 11 males), hyperventilation syndrome (HVS, 11 females), and healthy subjects (11 females and 11 males) in order to assess hyperventilation during exercise and its association with exercise-induced bronchoconstriction. The asthmatics showed decreased working capacity and decreased maximal oxygen consumption, with no evidence of limitation due to impairment of ventilatory capacity. Ventilatory equivalents for CO2 and O2 (VE/VCO2 and VE/VO2) at rest did not differ between the controls and asthmatics, but they were significantly elevated in HVS. In female asthmatics, ventilatory equivalents during exercise were significantly (P < 0.05) elevated compared with those of healthy subjects; in female controls, VE/VCO2 was 30.1 +/- 3.3 at low exercise and 27.4 +/- 6.5 at maximal exercise. In female asthmatics, the corresponding figures were 34.9 +/- 6.1 and 36.7 +/- 5.3. Furthermore, VE/VCO2 individually related to percent of maximal oxygen consumption (VO2max) was significantly increased in female asthmatics both at low and high VO2. The highest ventilatory equivalents were obtained in HVS, 41.7 +/- 6.7 and 43.9 +/- 0.9, respectively. Significant exercise-induced bronchoconstriction (decrease of FEV1 > 15%) was found in 50% of the asthmatics. The ventilatory equivalents did not correlate with exercise-induced changes in FEV1 (r2 < 0.3). Mild exercise-induced hyperventilation which was observed in mild female asthmatics, did not appear to be related to exercise-induced bronchoconstriction.

Adult↗
PubMed1990

Nocturnal panic: response to hyperventilation and carbon dioxide challenges.

To examine the role of ventilatory response in nocturnal panic, subjects experiencing nocturnal panic were compared with those who experienced daytime panic attacks only. In particular, measures of chronic hyperventilation (baseline pCO2) and CO2 hypersensitivity (response to ventilatory challenges) were assessed. Subjective and psychophysiological measures were obtained during baseline, forced hyperventilation, and carbon dioxide inhalation phases of a standardized laboratory-based assessment. The groups did not differ with respect to subjective or physiological measures or to the frequency with which panic occurred during the assessment. The results do not lend support to models that emphasize central CO2 hypersensitivity and chronic hyperventilation as primary mechanisms underlying nocturnal panic.

Acid-Base Equilibrium↗
PubMed2002

Hyperventilation-induced high-amplitude rhythmic slowing with altered awareness: a video-EEG comparison with absence seizures.

PURPOSE: Hyperventilation-induced high-amplitude rhythmic slowing (HIHARS) in children may be associated with clinical episodes of altered awareness. The presence of automatisms has been proposed as a distinguishing feature that helps to differentiate absence seizures from nonepileptic causes of decreased responsiveness. This retrospective, controlled, video-EEG study compared the clinical characteristics of episodes of HIHARS with loss of awareness with those of absence seizures. METHODS: The database of a tertiary Children's Hospital was searched for patients studied between April 1993 and April 1997 who had at least one episode of HIHARS with loss of awareness. The absence control group was obtained by selecting the next patient, after an HIHARS study subject, who met the following criteria: (a) had at least one absence seizure occurred during hyperventilation in the EEG recording, and (b) had a diagnosis of idiopathic generalized epilepsy. The video-EEG and medical histories of all patients were reviewed and summarized. RESULTS: We reviewed video-EEG recordings of 77 episodes of HIHARS with loss of awareness from 22 children and 107 absence seizures during hyperventilation from 22 children. Eye opening and eyelid flutter were seen more frequently in absence seizures, whereas fidgeting, smiling, and yawning occurred more frequently during HIHARS episodes. Arrest of activity, staring, and oral and manual automatisms were observed in both groups. CONCLUSIONS: Automatisms are common in both HIHARS and absence seizures. Yawning, smiling, and particularly fidgeting occur more commonly and eye opening and eyelid flutter less commonly in HIHARS. However, episodes of HIHARS with loss of awareness clinically mimic absence seizures, and these conditions can be distinguished reliably only by EEG.

Awareness↗
PubMed1980

Clomipramine treatment of hyperventilation syndrome.

Six patients suffered from a hyperventilation syndrome for 3.4 +/- 1.2 years. They had a lowered PAco2 at rest and an abnormal CO2 response curve. During the entire period they had received unsuccessful treatment with anxiolytics, and had also undergone behaviour therapy for the last 1 -- 2 years without success. Both treatments were discontinued and the patients were placed on clomipramine, 25 mg t.i.d. for 9 months. Their anxiety and hyperventilation attacks diminished after one month of clomipramine, and their fear of attacks an their phobias subsided after two months. Eighteen months after clomipramine therapy had been initiated, they were feeling well without medication. The possible mode of action of clomipramine on the hyperventilation syndrome via central serotonergic mechanism is discussed.

Adult↗
PubMed1991

Chronic respiratory alkalosis. The effect of sustained hyperventilation on renal regulation of acid-base equilibrium.

BACKGROUND: In normal subjects, chronic hyperventilation lowers plasma bicarbonate concentration, primarily by inhibiting the urinary excretion of net acid. The quantitative relation between reduced arterial carbon dioxide tension (PaCO2) and the plasma bicarbonate concentration in the chronic steady state has not been studied in humans, however, and the laboratory criteria for the diagnosis of chronic respiratory alkalosis therefore remain undefined. We wished to provide such reference data for clinical use. Moreover, because chronic hyperventilation paradoxically lowers blood pH still further in dogs with metabolic acidosis, we desired to study the effect of chronic hypocapnia on the plasma bicarbonate concentration (and blood pH) in normal human subjects in whom acidosis had been induced with ammonium chloride. METHODS: Under metabolic-balance conditions, we used altitude-induced hypobaric hypoxia to produce chronic hypocapnia in nine normal young men, five of whom received ammonium chloride daily to cause metabolic acidosis (the mean [+/- SE] steady-state plasma bicarbonate level in these five was 12.0 +/- 0.5 mmol per liter). RESULTS: For each decrease of 1 mm Hg (0.13 kPa) in the PaCO2, the plasma bicarbonate concentration decreased by 0.41 mmol per liter in the subjects who started with a normal plasma bicarbonate concentration and by 0.42 mmol per liter in the subjects with acidosis. In contrast to the findings in previous studies of dogs, hypocapnia increased blood pH similarly in both groups; the blood hydrogen ion concentration decreased by about 0.4 nmol per liter for every decrease of 1 mm Hg (0.13 kPa) in PaCO2. CONCLUSIONS: These results provide reference data for the diagnosis of chronic respiratory alkalosis in humans. Although chronic hypocapnia decreased plasma bicarbonate levels similarly in normal subjects with acidosis and without acidosis, the percent reduction in PaCO2 was always greater than the corresponding percent reduction in the plasma bicarbonate concentration. Therefore, as was not true of the response in dogs, the subjects' blood pH always increased with hyperventilation, regardless of the initial plasma bicarbonate concentration.

Acid-Base Equilibrium↗
PubMed1990

Hyperventilation. Benign symptom or harbinger of catastrophe?

Hyperventilation is a common feature of many acute clinical conditions that can be benign or potentially catastrophic. The symptoms accompanying hyperventilation are diverse and non-specific, reflecting a physiologic state of hypocapnia secondary to alveolar overventilation. Results of arterial blood gas analysis confirm hypocapnia and may lead to identification of the clinical cause, with pH or PaO2 measurements indicating acid-base abnormalities or hypoxemia. Treatment should be directed at correcting the underlying clinical condition. In patients whose hyperventilation is caused by anxiety states, anxiolytic drug therapy in the acute phase should be followed by education, reassurance, retraining to change breathing patterns, and psychotherapy.

Adult↗
PubMed2000

Characterization of respiratory exposure to and effects of cold-air hyperventilation in guinea pigs.

The purpose of this study was to characterize the respiratory effects of single and repeated controlled exposures to clean warm humid and cold dry air in a new model of anesthetized, mechanically ventilated guinea pigs, and to compare findings with known effects in humans. Intratracheal air (T(tr)) and retrotracheal tissue (T(oe)) temperatures and peak expiratory airflow (PEF), tidal volume (V(T)), heart rate, and blood pressure of hyperventilating animals were measured continuously. Four consecutive 10-min exposures to warm humid air (n = 7) produced slight airway warming and minimal lung function changes during the exposure. In a single 10-min exposure to cold dry air (n = 39), T(tr) decreased from (means +/- SEM) 36.1 +/- 0.3 degrees C to 26.3 +/- 0.3 degrees C (Delta = -9.8 +/- 0.4 degrees C) and T(oe) from 36.4 +/- 0.2 degrees C to 35.5 +/- 0.2 degrees C (Delta = -0.9 +/- 0.1 degrees C). PEF and V(T) decreased in response to airway cooling with maximal decrements within the first 2-4 min from the beginning of the exposure period. The maximal decrease in PEF was from 21.7 +/- 0.3 ml s(-1) to 15.9 +/- 0.5 ml s(-1) (Delta = -26.7%) and that in V(T) from 5.2 +/- 0.1 ml to 4.2 +/- 0.1 ml (Delta = -19.2%) (p <.05 for both changes). The decreases in lung functions attenuated significantly during the course of the 10-min exposure to cold dry air, indicating adaptation. Consequently, the decrements in PEF and V(T) at 5, 7.5, and 10 min were significantly smaller than those at 3 min. In four consecutive 10-min exposures to cold dry air (n = 15), there were no statistically significant differences in T(tr) or T(oe) decreases between the exposure periods. The largest decreases in the lung function parameters were during the first exposure period, whereas there were significantly smaller responses during the second and third exposure periods (p <.05). Thus, a highly reproducible airway cooling and an immediate bronchoconstriction were produced in response to cold dry air hyperventilation in guinea pigs. During the course of cold-air exposure and in repeated exposures, there was a significant attenuation of the bronchial response, which resembled the refractoriness of the asthmatic airways to repeated hyperventilation of cold or warm dry air. The present guinea pig model seems to be well suited for production of complementary animal data on the pathophysiological effects of cold dry air on the tracheobronchial airways.

Adaptation, Physiological↗
PubMed1995

Hyperventilation reverses the nitrous oxide-induced increase in cerebral blood flow velocity in human volunteers.

Because hypocapnia is routine during general anaesthesia for intracranial procedures, we have compared, in 13 healthy volunteers, the effect of normocapnia (PE'CO2 5.3 kPa) and hypocapnia (PE'CO2 3.3 kPa) on mean blood flow velocity in the middle cerebral artery (Vmca) during normoventilation and hyperventilation with air and with 50% nitrous oxide in oxygen. After replacement of air with 50% nitrous oxide in oxygen, there was an increase in mean Vmca during normoventilation (air: mean 68.23 (SD 16.98) cm s-1 vs nitrous oxide in oxygen: 90.69 (20.41) cm s-1; P < 0.01), whereas during hyperventilation mean Vmca values were similar regardless of the inhaled gas mixture (air: 43.46 (9.97) cm s-1 vs nitrous oxide in oxygen: 41.69 (8.08) cm s-1. Our data suggest that the nitrous oxide-induced increase in mean Vmca can be blocked by hyperventilation.

Adult↗