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PubMed1994

Oxygen desaturation following voluntary hyperventilation in normal subjects.

To investigate the severity of oxygen desaturation following voluntary hyperventilation (VHV) in normal subjects and its possible relation to chemoresponsiveness, we examined respiration following VHV in 16 normal male subjects. Monitoring was performed according to the standard polysomnography protocol including measurements of arterial oxygen saturation (SaO2) and transcutaneous PCO2 (PtcCO2). The subjects hyperventilated voluntarily for 3 min, and were then observed for more than 15 min. They hyperventilated again for another 3 min, and were followed again for more than 15 min. Eleven subjects fell into non-REM sleep after VHV, and their mean lowest SaO2 was 67.6 +/- 13.0% (n = 15 trials in 11 subjects, mean +/- SD). Falling asleep during hypocapnia caused desaturation, and periodic breathing was invariably observed soon after. The difference between the PtcCO2 during non-REM sleep with stable breathing and the PtcCO2 when the SaO2 was 90% following VHV was defined as the delta PtcCO2 (90). The delta PtcCO2 (90) and hypoxic ventilatory response (HVR) were positively and significantly correlated (r = 0.73, p < 0.01). While the subjects were awake, the mean lowest SaO2 was 73.5 +/- 17.4% (17 trials in 12 subjects). Remaining awake induced oxygen desaturation in some subjects but not in others. In one subject, desaturation during the waking state was caused by hypoventilation, not by central apnea. In the seven subjects whose respiration following VHV was monitored during the waking state in one trial and during the sleeping state in another trial, plots of the PtcCO2-SaO2 relationship for the waking state were generally positioned above those made for the sleeping state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Interaction of hyperventilation and arousal in the pathogenesis of idiopathic central sleep apnea.

Central apneas during sleep may arise as a result of reduction in PaCO2 below the apnea threshold. We therefore hypothesized that hyperventilation and arousals from sleep interact to cause hypocapnia and subsequent central apneas in patients with idiopathic central sleep apnea (ICSA). Accordingly, the relationships among preapneic ventilation, arousal from sleep, and the onset and duration of subsequent central apneas were examined during Stage 2 non-REM sleep in eight patients with ICSA (mean +/- SEM, 45.4 +/- 4.7 central apneas and hypopneas/h of sleep). During Stage 2 sleep, all episodes of periodic breathing with central apneas were triggered by hyperventilation. Minute ventilation (VI) was greater (6.3 +/- 0.7 versus 5.4 +/- 0.8 L/min, p < 0.05) and mean transcutaneous PCO2 (PtcCO2) was lower (37.8 +/- 1.3 versus 38.9 +/- 1.6 mm Hg, p < 0.05) during periodic breathing than during stable breathing. VI during the ventilatory phase of the periodic breathing cycle increased progressively with increasing grades of associated arousals from Grade 0 (no arousal) (10.3 +/- 1.4 L/min) to Grade 1 (EEG arousal) (12.6 +/- 1.6 L/min) to Grade 2 (movement arousal) (14.1 +/- 1.6 L/min, p < 0.01). There was a corresponding progressive increase in central apnea length following the ventilatory period from no arousal (14.1 +/- 2.0) to EEG arousal (16.4 +/- 1.8) to movement arousal (18.1 +/- 2.0 s, p < 0.01). We conclude that arousals and hyperventilation interact to trigger hypocapnia and central apneas in ICSA.

Aged↗
PubMed1998

Responsiveness to mannitol in asthmatic subjects with exercise- and hyperventilation-induced asthma.

We investigated airway responsiveness to mannitol, a new hyperosmolar challenge, in persons hyperresponsive to airway drying. We studied 36 asthmatic subjects, 18 to 40 yr of age, responsive to exercise (n = 23) and eucapnic hyperventilation (n = 28) defined by a 10% fall in FEV1. Fifteen subjects performed both challenges. All subjects performed a challenge with dry powder mannitol, encapsulated and delivered via a Dinkihaler until a 15% decrease in FEV1 was documented or a cumulative dose of 635 mg was delivered. All subjects responsive to eucapnic hyperventilation and all but one subject responsive to exercise were responsive to mannitol. Sixty-nine percent of subjects had a positive response to mannitol after less than 155 mg (6 capsules) and 94% less than 320 mg (10 capsules). The provoking dose of mannitol required to cause a 15% fall in FEV1 (PD15) was related to the severity of the response to exercise (Pearson's correlation coefficient [rp] = 0.68, p < 0.01) and eucapnic hyperventilation (rp = 0.68, p < 0.01) in subjects who were not taking inhaled corticosteroids. The mean (+/- SD) maximum percent fall in FEV1 after mannitol was 24.4 +/- 6.2% and recovery to bronchodilator occurred within 10 min in most subjects. The mannitol test is simple, inexpensive, faster to perform than hyperpnea with dry air and could become an office-based test. Further studies are now required to determine the sensitivity of mannitol to identify exercise-induced asthma in a random population.

Adolescent↗
PubMed2000

Heparin inhibits eicosanoid metabolism and hyperventilation-induced bronchoconstriction in dogs.

Inhalation of heparin, an anticoagulant, attenuates exercise- induced asthma (EIA) in human subjects. The purpose of this study was to determine if heparin inhibits hyperventilation-induced bronchoconstriction (HIB) in a canine model of EIA, and if its mode of action involves the inhibition of eicosanoid mediator production and release. We used a wedged bronchoscope technique to measure baseline peripheral airway resistance (Rp). We then performed either a 2-min or 5-min dry air challenge (DAC) by temporarily increasing from 200 to 2,000 ml/min the flow of 5% CO(2) in air used to ventilate a wedged sublobar segment. We compared HIB before and 60 min after aerosol treatment with either bacteriostatic water (BW) or heparin. We found that (1) heparin had no effect on baseline Rp, (2) BW did not alter the response to DAC, and (3) heparin reduced HIB by approximately 50-60%. On the basis of bronchoalveolar lavage fluid (BALF) cell analysis, heparin and BW caused acute infiltration of macrophages and eosinophils, and heparin increased the number of erythrocytes recovered immediately after DAC. Despite these acute inflammatory effects initiated prior to DAC, BALF mediator analyses revealed that pretreatment with heparin either attenuated or abolished hyperventilation-induced leukotriene, prostaglandin, and thromboxane release. Thus, our data provide direct evidence that inhaled heparin inhibits eicosanoid mediator production and release caused by hyperventilation with dry air, and significantly attenuates HIB.

Administration, Inhalation↗
PubMed2001

Repeated hyperventilation causes peripheral airways inflammation, hyperreactivity, and impaired bronchodilation in dogs.

Winter athletes have an increased incidence of asthma, suggesting that repetitive hyperventilation with cold air may predispose individuals to airways disease. We used a canine model of exercise-induced hyperpnea to examine the effects of repeated hyperventilation with cool, dry air (i.e., dry air challenge [DAC]) on peripheral airway resistance (Rp), reactivity, and inflammation. Specific bronchi were exposed to a single DAC on five consecutive days. Rp and Delta Rp to aerosolized histamine, intravenous histamine, or hypocapnia were measured daily. Bronchoalveolar lavage fluid (BALF) was obtained on the fifth day. Rp increased from 0.70 +/- 0.08 to 1.13 +/- 0.22 cm H(2)O/ml/s (n = 25) 24 h after the first DAC, rose to 1.49 +/- 0.24 cm H(2)O/ml/s by Day 3, and remained elevated throughout the remainder of the protocol. Repeated DAC increased reactivity to hypocapnia and intravenous histamine. Intravenous salbutamol failed to reduce Rp as effectively in challenged airways (111% of Day 1 baseline) as in naive airways (54% of baseline). Repeated DAC caused increased BALF neutrophils, eosinophils, and sulfidopeptide leukotrienes. We conclude that repeated DAC causes peripheral airways inflammation, obstruction, hyperreactivity, and impaired beta-agonist-induced relaxation. This suggests that other mechanisms in addition to increased smooth muscle tone may contribute to the development of repetitive hyperventilation-induced bronchial obstruction and hyperreactivity.

Airway Resistance↗
PubMed2002

Heparin inhibits hyperventilation-induced late-phase hyperreactivity in dogs.

Inhalation of heparin attenuates hyperventilation-induced bronchoconstriction in humans and dogs. The purpose of this study was to determine whether heparin inhibits the late-phase response to hyperventilation, which is characterized by increased peripheral airway resistance (RP), eicosanoid mediator production, neutrophilic/ eosinophilic inflammation, and airway hyperreactivity (AHR) at 5 h after dry air challenge (DAC). Fiberoptic bronchoscopy was used to record RP and airway reactivity (DeltaRP) to aerosol and intravenous histamine before and 5 h after DAC. Bronchoalveolar lavage fluid (BALF) cells and eicosanoid mediators were also measured approximately 5 h after DAC. DAC of vehicle-treated bronchi resulted in late-phase airway obstruction (approximately 120% increase over baseline RP), inflammation, increased BALF concentrations of leukotriene (LT) C(4), LTD(4), and LTE(4) and prostaglandin (PG)D(2), and AHR. Pretreatment with aerosolized heparin attenuated late-phase airway obstruction by approximately 50%, inhibited eosinophil infiltration, reduced BALF concentrations of LTC(4), LTD(4), and LTE(4) and PGD(2), and abolished AHR. We conclude that heparin inhibits hyperventilation-induced late-phase changes in peripheral airway function, and does so in part via the inhibition of eosinophil migration and eicosanoid mediator production and release.

Administration, Inhalation↗
PubMed2004

Hyperventilation with cold versus dry air in 2- to 5-year-old children with asthma.

UNLABELLED: Cold air challenge (CACh) has been shown to discriminate between children with asthma and healthy young children. Hyperventilation with dry room-temperature air is a simplified alternative. We compared responsiveness in young children with asthma between two standardized, single-step protocols: dry air challenge (DACh) performed as 6 minutes of eucapnic hyperventilation with dry room-temperature air and CACh as 4 minutes of hyperventilation. Response was measured as specific airway resistance by whole-body plethysmography and expressed as change from baseline in numbers of within-subject SDs (SDw). The challenge sequence was randomly assigned. A comparator challenge was performed 1 hour later if the first challenge gave a change of 3 SDw or more. Forty 2- to 5-year-old children with asthma were included. Responsiveness to cold versus dry air showed significant, but weak, correlation (r(2) = 0.34, p < 0.0001), but responsiveness to CACh exceeded DACh (7.6 vs. 5.4 SDw, p < 0.02). CACh seemed to induce reduction in response to the following DACh (p < 0.01), whereas no such reduction was seen after DACh. CONCLUSION: Responsiveness to CACh exceeded responsiveness to DACh, and CACh seemed to induce refractoriness in contrast to DACh, probably because of the additional stimulus from airway cooling. This finding suggests CACh as the preferred method of challenge.

Air↗
PubMed1985

Intraairway thermal profiles during exercise and hyperventilation in normal man.

When large volumes of air are inhaled at rapid rates of ventilation, substantial segments of the tracheobronchial tree become involved in the conditioning process and the inspirate does not reach body conditions of temperature and humidity until it passes well into the peripheral bronchi. To determine if the manner in which ventilation is elevated is an important factor in producing this response, we measured the temperature of the airstream at six points in the tracheobronchial tree from the pharynx to the subsegmental bronchi during 5 min of exercise and voluntary hyperventilation in seven normal subjects while they inhaled frigid air. Minute ventilation and respiratory frequency were recorded at minute intervals and intrathoracic temperatures were measured continuously. With both forms of hyperpnea, airway temperature fell dramatically, and there were no significant differences between exercise and hyperventilation. These results demonstrate that the thermal events that occur within the lung during short, moderately intense degrees of exercise can be readily simulated by voluntary hyperventilation when ventilation and inspired air conditions are matched. Our data also indicate that this form of exercise does not result in an increase in airstream temperature and raise the possibility that the bronchial blood supply may be determined by the local thermal needs of the airways to recover heat and water independent of, at least moderate, increases in cardiac output.

Adult↗
PubMed1993

Carbon dioxide hypersensitivity, hyperventilation, and panic disorder.

OBJECTIVE: The purpose of this article is to offer a comprehensive, data-based explanation of the relationship between hyperventilation and panic disorder linking CO2 hypersensitivity, cognitive/behavioral factors, and the respiratory effects of antipanic pharmacologic and psychological treatments. METHOD: The authors conducted a computerized search of MEDLINE for relevant articles. RESULTS: Some panic patients have a chronic, subtle respiratory disturbance. Acute hyperventilation is neither necessary nor sufficient for panic to occur. Respiratory abnormalities in panic patients may adaptively aim at coping with a hypersensitive CO2 chemoreceptor system. Pharmacologic panicogens also stimulate the respiratory system, causing hyperventilation. Triggering this hypersensitive respiratory control mechanism may incite panic. Antipanic medications may reset the receptor threshold. Misattribution and catastrophic interpretation of somatic symptoms or the sense of loss of control may contribute to panic symptoms. Behavioral interventions such as desensitization or breathing retraining may block the full-blown attack. Cognitive strategies through cognitive control of respiration may supplement and accentuate these interventions. CONCLUSIONS: Panic disorder may be due to an inherently unstable autonomic nervous system, coupled with cognitive distress.

Alkalosis, Respiratory↗
PubMed1997

Basilar artery response to hyperventilation in panic disorder.

OBJECTIVE: The purpose of this study was to measure the response of basilar artery blood flow to hyperventilation in patients with panic disorder. METHOD: Transcranial Doppler ultrasonography was used to measure basilar artery flow during rest and after hyperventilation in 16 patients with panic disorder and eight normal comparison subjects. The subjects rated their dizziness at each phase. RESULTS: The patients with panic disorder demonstrated greater reduction in flow rates and greater increases in dizziness than the normal comparison subjects. CONCLUSIONS: The greater basilar artery sensitivity to hyperventilation shown by panic disorder patients suggests a possible mechanism for the development of neurological symptoms during panic attacks.

Adult↗
PubMed2003

Cerebrovascular response to cognitive tasks and hyperventilation measured by multi-channel near-infrared spectroscopy.

We assessed the cerebral blood volume response in the bilateral frontal area in 10 healthy subjects during the design fluency task, verbal fluency task, and hyperventilation measured by 24-channel near-infrared spectroscopy. Oxygenated and total hemoglobin increased during the design fluency task and verbal fluency task and decreased during hyperventilation bilaterally, while deoxygenated hemoglobin did not change. The test-retest reliability examined in five subjects was acceptable to assess the cerebrovascular response to cognitive tasks and hyperventilation.

Adult↗
PubMed1986

Physiological responses to psychological challenge under hypnosis in patients considered to have the hyperventilation syndrome: implications for diagnosis and therapy.

Thirty patients who were considered to have the hyperventilation syndrome on clinical grounds (history and observation) were referred for testing: 29 patients completed a forced hyperventilation provocation test, and 28 underwent hypnosis during which time a psychological challenge was introduced which was meaningful to each individual patient. In 19/27 of these patients the PetCO2 fell by an average of 18.2 mmHg and persisted spontaneously for more than three minutes. In 10 normal controls studied in a similar fashion there was an average fall of 5 mmHg. The difference in response between responders and controls/non-responders was highly significant (P less than 0.001). A review of the literature is presented for comparison. It is considered that a psychological challenge under hypnosis may have important implications for diagnosis and therapy in some patients considered to have the hyperventilation syndrome.

Adult↗
PubMed1988

The 'think test': a further technique to elicit hyperventilation.

Hyperventilation can undermine cardiovascular homeostasis by generating autonomic imbalance, sympathetic dominance, hypokalaemia, and intracellular alkalosis with calcium ion shifts. The role of hyperventilation in episodic disorders such as arrhythmia and coronary vasospasm can be difficult to identify if the patient does not present in an attack and so a provocation challenge is required. Today, the standard challenge is the forced hyperventilation provocation test (FHPT). A capnograph enables the resting end-tidal PCO2 to be compared with the level 3 min after the period of overbreathing. We report the use of a patient-specific challenge. After the FHPT, the subject is invited to close his eyes and think about the circumstances of an attack, feelings and sensations experienced (breathing is not mentioned) or topics that were seen to disturb the rhythm of breathing when the medical history was taken. A fall of end-tidal PCO2 of 10 mmHg or more lasting at least one minute was taken as a positive response. Out of 57 patients with cardiovascular symptoms suggesting a hypocapnic influence, resting hypocapnia (end-tidal PCO2 = 30 mmHg) was present in 3 (5%). Of the remaining 54, the FHPT was positive in 16 (30%) and the 'think test' in 33 (61%). This suggests that patient-specific stimulation has advantages over an unspecific challenge in testing for episodic hypocapnia.

Adult↗
PubMed2003

Behavioral influences and physiological indices of ventilatory control in subjects with idiopathic hyperventilation.

Idiopathic hyperventilation has been defined as a respiratory-related psychophysiological complaint. This study attempted to clarify relationships between psychological and physiological variables in this condition. Participants demonstrated increased anxiety, depression, and symptoms consistent with hyperventilation. This was associated with a reduced peripheral chemosensitivity (isocapnic hypoxic rebreathe; -0.84 +/- 0.5 min-1.%O2(-1)), which was normalized with experimentally increased pCO2. Resting CO2 sensitivity was close to normal (2.1 +/- 1.0 min-1.mmHg-1). Breath hold time was significantly reduced versus controls (20.4 s +/- 12 s vs. 63 s +/- 31 s), and resting PETCO2 was correlated with the anxiety score. Also, the ventilatory response to moderate intensity exercise was augmented (vs. controls). The normalcy of pulmonary and chemoreceptor responses suggests that psychological factors may initiate this hyperventilation, which may become a conditioned response with an increased drive to breathe.

Anxiety↗
PubMed1998

Effect of nitric oxide synthase inhibitor on allergen- and hyperventilation-induced bronchoconstriction in guinea-pigs.

To elucidate the role of endogenous nitric oxide (NO) in allergen- (AIB) and hyperventilation-induced bronchoconstriction (HIB), the effects of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on AIB and HIB were studied in guinea-pigs. In the AIB group, 21 anaesthetized guinea-pigs, actively sensitized with 1% ovalbumin, were challenged with aerosolized 0.1% ovalbumin solution under mechanical ventilation. In the HIB group, 14 guinea-pigs were challenged with hyperventilation (tidal volume of 12 mL x kg(-1) at 150 breaths x min(-1) with 21% O2 and 5% CO2 dry gas) for 5 min. In both groups, lung resistance (RL) was measured using a pressure-volume-sensitive body plethysmograph, with or without L-NAME pretreatment (8 mg x kg(-1) i.v. followed by 2 mg x kg(-1) x min(-1) i.v.). The NO precursor, L-arginine was injected at a rate of 15 mg x kg(-1) x min(-1) after L-NAME injection (10 mg x kg(-1)) in the AIB group. The results were as follows. In the AIB group, the maximal RL change was significantly potentiated by pretreatment with L-NAME. This potentiating effect of L-NAME was reversed by L-arginine. In the HIB group, the pretreatment with L-NAME had no effect on increases in RL. These findings suggest that endogenous nitric oxide may play an important role in the modulation of allergen-, but not hyperventilation-induced bronchoconstriction in guinea-pigs.

Airway Resistance↗
PubMed1990

Central neurogenic hyperventilation: pharmacologic intervention with morphine sulfate and correlative analysis of respiratory, sleep, and ocular motor dysfunction.

Central neurogenic hyperventilation (CNH), for which there is no effective therapy, can eventually result in respiratory fatigue and death. This report describes a patient with CNH due to a brainstem anaplastic astrocytoma who also exhibited disturbances of sleep and ocular motor function. The CNH responded clinically to morphine sulfate and methadone. Analysis of ventilatory response to CO2 before and after morphine demonstrated a depression of ventilatory response (49 to 53% of baseline) and occlusion pressure response (35 to 50% of baseline) to CO2, with a requirement for high doses of naloxone (10 mg IV) to reverse the effect. Polysomnography revealed sustained hyperventilation, elevated O2 saturation, and low end-tidal CO2 throughout all stages of non-rapid eye movement (NREM) sleep, and absence of rapid eye movement (REM) sleep. Ocular motor evaluation disclosed absence of horizontal and reflexive saccades with compensatory head thrusts. Correlation of the clinical and physiologic data with the MRI abnormalities suggested that the lesion responsible for CNH in this patient might reside in the medial tegmental parapontine reticular formation. Since recurrent episodes of hyperventilation responded in a sustained fashion to IV and oral opiates, this treatment may warrant consideration in other patients with CNH.

Adult↗
PubMed1999

The effect of hyperventilation on downbeat nystagmus in cerebellar disorders.

Hyperventilation can affect nystagmus in patients with vestibular disorders. However, the effects on nystagmus in patients with cerebellar disease have not been systematically studied. Using the magnetic field search coil technique, we studied the effects of hyperventilation on nystagmus in a series of cerebellar patients. In four of eight patients, hyperventilation produced an increase in the slow-phase velocity of downbeat nystagmus. We speculate that this effect may be mediated through metabolic effects on cerebellar calcium channels.

Adult↗
PubMed2001

Chronic dyspnea and hyperventilation in an awake patient with small subcortical infarcts.

A 79-year-old woman presented with chronic dyspnea and hyperventilation. There was no evidence of pulmonary disease. Hyperventilation persisted during sleep and after high-dose administration of a narcotic. A head MRI revealed bilateral medial thalamic infarctions. Central neurogenic hyperventilation was diagnosed in this alert patient. The case may illustrate a role for the thalamus in regulating ventilation, but another small infarct not visible on MRI also could be responsible.

Aged↗