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PubMed1993

Effect of inhaled amiloride on the bronchial response to methacholine and cold air hyperventilation challenges.

Inhaled amiloride has been recently demonstrated to have an effect on the decline of pulmonary function in patients with cystic fibrosis. Other diuretics have been demonstrated to provide protection against bronchoconstriction in asthmatic subjects. We report on the effect of inhaled amiloride on cold air hyperventilation challenge (CAHC) and methacholine challenge in asthmatics. We studied nine subjects with mild-moderate asthma in a double-blind, placebo-controlled, crossover study. Our results showed amiloride did not significantly protect against the bronchoconstriction induced by CAHC. Inhaled amiloride did not affect FEV1 in the hour after inhalation, and there was no significant difference between placebo or amiloride on the dose of methacholine causing a 20 percent fall in FEV1. Inhaled amiloride appears not to have a profile of action as previously seen with inhaled furosemide.

Administration, Inhalation↗
PubMed1996

Tracheobronchial constriction in asthmatics induced by isocapnic hyperventilation with dry cold air.

Although it is well known that isocapnic hyperventilation (IHV) with dry cold air produces airway constriction in asthmatic subjects, the site of airway narrowing is nuclear. To address this issue, we have quantified the tracheal and bronchial response to IHV with dry cold air in 15 patients with mild asthma and 7 healthy control subjects. We employed the acoustic reflection technique to evaluate changes in airway cross-sectional areas caused by IHV with dry cold air. Airway areas were measured during tidal breathing before and 5 to 10, 30, 60, and 90 min following cold air challenge. For analysis purposes, airway areas were divided into three anatomic segments: extrathoracic tracheal segment, intrathoracic tracheal segment, and main bronchial segment. These segments were assessed at a fixed volume below total lung capacity. Maximal and partial expiratory flow-volume curves were also obtained before each set of area measurements. In normal subjects, IHV with dry cold air caused no significant changes in FEV1, flow at 30% of the vital capacity in the partial curve (V30p), or airway areas. In asthmatics, at 5 to 10 min after challenge, we found that FEV1 decreased by 22 +/- 5% (mean +/- SEM) (p < 0.0001), V30p by 33 +/- 8% (p < 0.003), intrathoracic tracheal area by 10.7% +/- 2% (p < 0.03), and main bronchial area by 14 +/- 3% (p < 0.003). At 30 min, tracheal and main bronchial areas were returned to baseline levels; however, FEV1 and V30p were still significantly decreased, by 13 +/- 3% and 16 +/- 4%, respectively. We conclude that in asthmatics, IHV with dry cold air causes both tracheal and bronchial constriction, and that recovery seems to occur first in the central airways.

Acoustics↗
PubMed1997

Hypoxic ventilatory response and breathlessness following hypocapnic and isocapnic hyperventilation.

STUDY OBJECTIVES: To investigate the etiology of posthyperventilation (post-HV) hypoxemia following voluntary hyperventilation (VHV), we examined the effects of hypocapnic (hypo-CO2) and isocapnic (iso-CO2) VHV on the hypoxic ventilatory response (O2-response) and on the sensation of breathlessness during the O2-response. METHODS: O2-responses and visual analog scale (VAS) scores for estimating breathlessness in 10 normal subjects during the O2-response under iso-CO2 conditions and under hypo-CO2 conditions immediately following voluntary maximal HV of 3 min duration were examined. RESULTS: Although there was no significant difference in the post-HV ventilation levels following hypo-CO2 vs iso-CO2 VHV, the VAS scores at the start of the O2-response following hypo-CO2 VHV (30.2+/-24.2 mm) were significantly higher (p<0.05) than the VAS scores at the start of the O2-response following iso-CO2 VHV (13.7+/-8.4 mm). However, VHV did not have a significant effect on the O2-response at 2 min after the VHV when the arterial O2 saturation (SaO2) was below 90%. The nonsteady-state hypo-CO2 induced by VHV greatly attenuated the O2-response below 90% SaO2 and VAS scores at 70% SaO2. CONCLUSIONS: Elevated VAS scores immediately following the hypo-CO2 VHV, which might be independent of actual breathing levels, and the attenuation of the O2-response following the hypo-CO2 VHV were not due to input from lung and chest wall mechanoreceptors induced by the hyperpnea itself, but rather to the hypo-CO2 induced by hyperpnea.

Adult↗
PubMed2004

Field exercise vs laboratory eucapnic voluntary hyperventilation to identify airway hyperresponsiveness in elite cold weather athletes.

STUDY OBJECTIVE: For the 2002 Winter Olympic Games, athletes were required to submit objective evidence of asthma or exercise-induced bronchoconstriction (EIB) for approval to inhale a beta(2)-agonist. Eucapnic voluntary hyperventilation (EVH) was recommended as a laboratory challenge that would identify airway hyperresponsiveness (AHR) consistent with EIB. The objective was to compare the change in FEV(1) provoked by EVH with that provoked by exercise in cold weather athletes. DESIGN: Spirometry was measured before and for 15 min after challenges. The two challenges were performed in random order at least 24 h apart. SETTING: EVH was performed in the laboratory at 19 degrees C, and exercise took place in the field in the cold (2 degrees C, 45% relative humidity). PARTICIPANTS: Thirty-eight athletes (25 female subjects; median age, 16 years). INTERVENTIONS: For the EVH, athletes inhaled dry air containing 5% carbon dioxide for 6 min at a target ventilation equivalent to 30 times baseline FEV(1). Exercise was performed by cross-country skiing, ice skating, or running for 6 to 8 min. MEASUREMENTS AND RESULTS: AHR consistent with EIB was defined as >or= 10% fall in FEV(1) from baseline after challenge. Eleven athletes were exercise positive (EX+) [FEV(1) fall, 20.5 +/- 7.3%], and 17 athletes were EVH positive (FEV(1) fall, 14.5 +/- 4.5%) [mean +/- SD]. Of 19 subjects with AHR, 58% were identified by exercise and 89% were identified by EVH. EVH identified 9 of 11 subjects who were EX+ and a further 8 subjects with potential for EIB. The average ventilation during EVH was 28 times FEV(1). CONCLUSION: Performing EVH for 6 min in the laboratory had a greater chance of identifying AHR in these athletes compared with 6 to 8 min of field exercise in the cold. The EVH test will be useful to evaluate elite summer sports athletes whose widely different forms of exercise provide an "equipment" challenge to any laboratory.

Adolescent↗
PubMed1983

Endurance of hyperventilation in chronic airflow limitation.

The capacity to sustain an increase in ventilation (VE) sufficient to decrease the end-tidal partial pressure of carbon dioxide (PETCO2) by about 10 mm Hg was studied in six hypercapnic patients with moderate to severe chronic airflow limitation (CAL). Patients could continue such an increased VE for a finite time (range 5 to 54 minutes). During hyperventilation (H), ventilation was approximately doubled and represented 77.1 +/- 8.4 (mean +/- SE) percent of maximum voluntary ventilation, mean oxygen consumption (VO2) increased 44 percent (p less than 0.005) and mean inspiratory pleural pressure (Ppl) swings were 43.8 +/- 10.5 percent of maximum Ppl. Four patients achieved reductions of PETCO2 less than 10 mm Hg, and two patients achieved or exceeded the target decrease in PETCO2. The decrease in PaCO2 was correlated with the wasted ventilation ratios (VD/VT) during H, the greatest decrease in PaCO2 being related to the lowest VD/VT (p less than 0.05). Electromyographic (EMG) evidence of inspiratory muscle fatigue developed in four of the six patients during H. Five normal subjects achieved an equal or greater decrease in PETCO2, and none showed EMG evidence of inspiratory muscle fatigue. We conclude that, although impaired gas exchange limits the capacity to voluntarily reduce the PaCO2, the development of respiratory muscle fatigue in some patients with CAL may also contribute by limiting the capacity to sustain the substantial increase in respiratory muscle work done in the attempt.

Adult↗
PubMed1991

Central neurogenic hyperventilation in invasive laryngeal carcinoma.

We describe a patient with central neurogenic hyperventilation secondary to extension of a laryngeal tumor into the base of the brain, resulting in extrinsic compression of the medulla. Such an association has not been previously described. Unique features which distinguish this patient from previously reported cases are emphasized. Possible mechanisms involved in pathogenesis, as well as types of therapy, are outlined.

Alkalosis, Respiratory↗
PubMed1991

Caffeine consumption decreases the response to bronchoprovocation challenge with dry gas hyperventilation.

OBJECTIVE: To determine whether caffeine consumption affects bronchoprovocation challenge (BPC). DESIGN: A prospective, double-blind, placebo-controlled, randomized, crossover trial. PATIENTS: Eleven nonsmoking men, aged 18 to 42 years, with normal baseline spirometry and evidence of exercise-induced bronchospasm. INTERVENTION: On three separate test days, each individual received, in random order, either placebo, 5 mg/kg caffeine, or 10 mg/kg caffeine, and then underwent BPC with eucapnic voluntary hyperventilation (EVH). RESULTS: Caffeine (10 mg/kg) significantly reduced bronchoconstriction compared to placebo (p = 0.02). The reduction in bronchoconstriction correlated with the serum level of caffeine (p = 0.014). CONCLUSIONS: Caffeine decreases bronchoconstriction due to EVH. Caffeine should be eliminated from diet prior to BPC.

Adolescent↗
PubMedDate not supplied

Changes in human nasal resistance associated with exercise, hyperventilation and rebreathing.

The nasal resistance to airflow determined in four subjects for periods of up to 7 hr. Cyclic changes in the resistance of each nasal passage were demonstrated in 13 or 24 experiments. After exercise on the cycle ergometer the total nasal resistance decreased and this change in nasal resistance was found to be directly related to the work rate. After oral rebreathing, the total nasal resistance decreased, and after hyperventilation the total nasal resistance increased. These changes in resistance are believed to be caused by changes in arterial pCO2 and mediated by the autonomic innervation of the nasal vasculature.

Adult↗
PubMed1995

Hyperactive VOR and hyperventilation after whiplash injury.

Otoneurological and respiratory tests were performed on 32 patients after whiplash injury caused by a rear-end car collision. Oculomotor and cervico-ocular test results were generally normal. In a significantly large number of case, the vestibulo-ocular reflex (VOR) was hyperactive (n = 17; 53%) and the respiratory test results were typical of the hyperventilation syndrome (HVS) (n = 12; 38%). Hyperactive VOR and the HVS occurred significantly more often in combination (n = 7; 22%) than could be accounted for by combined false positivity. Most of the significant findings were due to high relative frequencies in the women. The hyperactive VOR might have been the result of plastic adaptation to limited head mobility secondary to neck pain. Behavioural and emotional distress might offer alternative explanations for both the hyperactive VOR and HVS.

Adult↗
PubMed1971

The effect of passive hyperventilation on intraventricular pressure in the dog.

The effectiveness of passive hyperventilation in reducing intracranial pressure was studied in mongrel dogs by varying the levels of end-tidal pCO2 and airway pressure, and comparing the positive-negative and positive-atmospheric pressure. It has been shown that there is a point beyond which reduction of pCO2 does not affect cerebral blood flow. The present study demonstrates that another limiting factor is the degree of positive or negative airway pressure. Positive airway pressure impedes venous drainage, thereby increasing intracranial pressure. This increase could only partly be offset by applying negative expiratory airway pressure, since it was found that excessive negative airway pressure (greater than static recoil pressure of the lung) may trap air in alveoli. An optimal range of positive and negative airway pressures is defined.

Animals↗
PubMed1990

Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation.

Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.

Acute Disease↗
PubMed2001

Hyperventilation and loss of hemolymph Na+ and Cl- in the freshwater amphipod Gammarus fossarum exposed to acid stress: a preliminary study.

The effect of acidification on the acid-sensitive species Gammarus fossarum was investigated in the laboratory. The results showed that as mortality increased, mean hemolymph chloride and sodium concentrations decreased rapidly. Concomitantly, organisms hyperventilated during the first 24 h and then started to hypoventilate. These results demonstrated that exposure to acid stress in the acid-sensitive species G. fossarum led to ion-regulatory and respiratory failure as previously reported in fish and crayfish exposed to acid stress.

Animals↗
PubMed2000

Persistent, progressive hypophosphataemia after voluntary hyperventilation.

Hyperventilation (HV) and respiratory alkalosis are associated with hypophosphataemia, although the extent and duration of HV required to produce changes in serum phosphate levels are not known. We sought to characterize the effects of HV, with or without dextrose loading, on serum phosphate levels and other biochemical parameters. HV was monitored by controlling the end-tidal partial pressure of carbon dioxide (PETCO(2)). The effect of dextrose was studied because infusion of a glucose load is known to promote a fall in serum phosphate via stimulation of glycolysis. Eight healthy volunteers were enrolled in four study protocols: (1) HV for 20 min to a PETCO(2) of 25-30 mmHg (mild); (2) HV for 20 min to a PETCO(2) of 15-20 mmHg (severe); (3) mild HV with intravenous dextrose loading, and (4) dextrose loading alone. Periodic measurements of serum phosphate, venous pH, serum 2,3-diphosphoglycerate (2,3-DPG) and other parameters were made. Serum phosphate fell during HV and continued to decline after cessation of HV. Dextrose loading alone caused a fall in serum phosphate that continued for at least 30 min after cessation of the infusion (P<0.0002). HV combined with dextrose resulted in a greater decline in serum phosphate than either variable alone (P=0.003). The maximal decline in serum phosphate occurred in severe HV, with a mean decrease of 0.38 mmol/l at 20 min after cessation of HV (P<0.0001). Serum phosphate was still significantly lowered compared with baseline at 90 min after cessation of HV (P=0.001). Other significant changes seen with HV included a decrease in serum glucose (P<0.01), a decrease in serum potassium (P<0.05) and an increase in venous pH (P<0.007). Serum 2, 3-DPG levels did not change significantly in any study protocol. Thus relatively mild acute HV produces significant changes in serum phosphate. In both mild and severe HV this effect is progressive after cessation of HV. This phenomenon has not been shown before, and may have significant clinical implications.

Adult↗
PubMed2000

The role of cough and hyperventilation in perpetuating airway inflammation in asthma.

Air flowing through a pipe exerts frictional stress on the walls of the pipe. Frictional stress of more than 40 N/m2 (velocity equivalent of air 113 m/s) is known to cause acute endothelial damage in blood vessels. The frictional stress in airways during coughing may be much greater, however, since the velocity of air may be as high as speed of sound in air. We suggest that high levels of frictional stress perpetuate airway inflammation in airways which are already inflamed and vulnerable to frictional stress-induced trauma in patients with asthma. Activities associated with rapid ventilation and higher frictional stress (e.g. exercise, hyperventilation, coughing, sneezing and laughing) cause asthma to worsen whilst activities that reduce frictional stress (Yoga 'Pranayama', breathing a helium-oxygen mixture and nasal continuous positive airway pressure) are beneficial. Therefore control of cough may have anti-inflammatory benefits in patients with asthma.

Asthma↗
PubMed2001

[Hyperventilation syndrome: evaluation of voluntary hypoventilation programs in two rehabilitation centers].

PURPOSE: The effectiveness of a voluntary hypoventilation technique was assessed in two rehabilitation centers in patients with hyperventilation syndrome. METHODS: In the first center, 55 patients participated in an open program determining themselves the frequency and number of their consultations. In the second center 158 patients participated in a 10-week program that imposed five 60-min sessions. RESULTS: In the first center, the patients participated in 4.8 30-min sessions over a 6.1 week period. Their cardinal complaints had declined by 48% (range 14% to 67% depending on the type of complaint) at the end of the program. In the second center the patients experienced an improvement in their comfort of life (less sleep disorders, fatigability, symptoms of severe hypocapnia), increasingly so with each new session, those having completed the program reaching a 62% improvement. DISCUSSION: Due to the strong correlation observed between the clinical improvement (with a longer interval between acute episodes) and the quality of patient participation the beneficial effect of these voluntary hypoventilation rehabilitation programs cannot be attributed solely to the psychological effect of patient care.

Adult↗
PubMedDate not supplied

Central neurogenic hyperventilation with primary cerebral lymphoma: a case report.

We report a case of a bright, alert patient with central neurogenic hyperventilation (CNH) associated with cerebral malignant lymphoma. CNH is a syndrome comprising normal or elevated arterial oxygen tension, decreased arterial carbon dioxide tension, and respiratory alkalosis in the absence of cardiac or pulmonary disease that stimulates a compensatory hyperpnea. A-72-year-old man with recurrent central nervous system lymphoma presented with hyperpnea. showing a respiratory rate over 30 per minute. He was fully awake and conscious. Routine laboratory studies and chest X-ray were normal, but arterial blood gas examination on room air showed respiratory alkalosis, regardless of wakefulness or sleep. Pulmonary infarction was denied by pulmonary flow scintigram. Rebreathing from a paper bag, intravenous administration of diazepam, and oxygen inhalation failed to alter the respiratory pattern. Brain MRI demonstrated two mildly enhanced lesions within the left side of the medulla oblongata and right side of the pons. CNH is rare in patients with normal consciousness. It seems to be caused by brainstem injury that includes the respiratory center.

Aged↗
PubMed2002

Moyamoya syndrome: impaired hemodynamics on ECD SPECT after EEG controlled hyperventilation.

BACKGROUND AND PURPOSE: Ischemic symptoms in children with Moyamoya syndrome are typically provoked by hyperventilation (HV) and are accompanied by the "re-build-up" phenomenon in EEG. The value of scintigraphic detection of HV-provoked perfusion deficits remains to be elucidated. PATIENTS AND METHODS: In seven children with Moyamoya syndrome regional cerebral blood flow was assessed by 99mTc-ethyl-cysteine-dimer (ECD) single photon emission computed tomography (SPECT) after HV and under baseline conditions to identify ischemia prone regions. RESULTS: Regional marked hypoperfusion after HV was found in all patients. Predominant perfusion deficits were detected in the frontal lobes. CONCLUSION: ECD SPECT is a potential tool for the preoperative evaluation of cerebral hemodynamics and for monitoring angiosurgical therapies in Moyamoya disease.

Adolescent↗
PubMed2004

[Hyperventilation syndrome in bronchial asthma, essential hypertension and organic neurosis. Clinical picture and external respiration function].

The external respiration function was studied in 100 patients with hyperventilation syndrome (HVS) divided into 3 groups: 40 patients with HVS and bronchial asthma (group 1) consisting of 15 males and 25 females (age median--45 years, 25 percentile--37 years, 75 percentile--53 years); 39 patients with HVS and essential hypertension (group 2) consisting of 8 males and 31 females (age median 49, 25 percentile--40 years, 75 percentile--57 years); 21 patients with HVS without concurrent somatic diseases of group 3 (7 males, 14 females, age median 45 years, 25 percentile--28 years, 75 percentile--45 years). It is shown that different disorders of pulmonary ventilation correspond to different clinical manifestations of HVS. Thus, in bronchial obstruction (group 1) HVS manifests with "weak respiration", in restrictive pulmonary disorders (group 2) HVS manifests as "heavy respiration", in high parameters of bronchial permeability (group 3)--"shallow respiration".

Asthma↗