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PubMed2000

Hyperventilation and asymptomatic chronic asthma.

BACKGROUND: We have consistently argued that mild asthma is an important underlying aetiological factor in patients with severe symptomatic hyperventilation. While hyperventilation has been demonstrated in acute asthma, there have been few studies in mild chronic asthma, and mechanisms are uncertain. METHODS: Twenty three currently asymptomatic chronically asthmatic patients (occasional use of bronchodilators, normal lung function, hyperresponsive to methacholine) were studied and 17 matched normal subjects acted as controls. Ventilation, pattern of breathing, arterial carbon dioxide and oxygen tensions (PaCO(2), PaO(2)), end tidal PCO(2) (PETCO(2)), standard lung function, airway responsiveness to methacholine, airway inflammation assessed by eosinophils in induced sputum, and psychiatric morbidity (Spielberger STAI-Y and Beck Depression Inventory) were measured. RESULTS: Despite the absence of current asthmatic symptoms, no clinical evidence of hyperventilation, and normal lung function in the patients with asthma, PaCO(2) and PETCO(2) were significantly (p<0.01) lower in the patients than in the control group (mean (SD) PaCO(2) 4.96 (0.43) kPa for patients versus 5.27 (0.38) kPa for controls (mean difference 0.31 kPa, 95% confidence interval (CI) 0.06 to 0.56, p<0.02)). PETCO(2) was very similar to PaCO(2) in both groups (mean (SD) PETCO(2) 4.89 (0.47) kPa for the patients and 5.28 (0.40) for the controls (mean difference 0.39 kPa, 95% CI 0.12 to 0.66, p<0.01)). There was no significant difference in ventilation or respiratory pattern between the two groups. The reduced PaCO(2) in the asthmatic patients correlated significantly with the concentration of methacholine provoking a fall in FEV(1) of more than 20% (PC(20)) (r = 0.56, p<0.01) but not with any aspect of lung function, eosinophil count, or anxiety/depression. CONCLUSION: Mild asymptomatic asthma is not associated with clinically significant hyperventilation but is associated with a significant reduction in both arterial and end tidal PCO(2) which relates to airway hyperresponsiveness rather than to the degree of airway obstruction or mucosal inflammation. Anxiety and depression appear not to be implicated.

Adolescent↗
PubMed1985

Hyperventilation-induced changes of the blood picture.

In a controlled study of 11 male volunteers the following changes (means +/- SD) were observed in venous blood during (D) and 75 min after (A) a period of 20 min of voluntary hyperventilation in comparison with before (B) hyperventilation (P values referring to the difference between D and B) erythrocyte count 5.18 +/- 0.17 X 10(6) (B), 5.70 +/- 0.21 X 10(6) (D) (P less than 0.001), and 5.18 +/- 0.16 X 10(6)/microliter (A); hemoglobin 15.7 +/- 0.6 (B), 17.2 +/- 0.7 (D) (P less than 0.001), and 15.8 +/- 0.6 g/dl (A); centrifuged hematocrit 46.6 +/- 1.0 (B), 50.4 +/- 1.7 (D) (P less than 0.001), and 47.0 +/- 1.8% (A). The platelets increased from 159 +/- 30 X 10(3) (B) to 205 +/- 40 X 10(3) (D) (P less than 0.001) and returned to 157 +/- 26 X 10(3)/microliter (A). The leukocytes (WBC) were 4,210 +/- 630 (B), 6,220 +/- 1,660 (D) (P less than 0.001), and 6,190 +/- 1,870/microliter (A) (P less than 0.002, as compared with B). The rise of WBC during hyperventilation was mainly due to a 83% increase of lymphocytes, whereas a 93% increase of neutrophil leukocytes accounted for the increased WBC 75 min posthyperventilation. The increase of the ratio of band forms to segmented neutrophils from 9 (B) to 19% (A) (P less than 0.01) indicates that band forms were released from the bone marrow. The results show that WBC and platelets can be mobilized by hyperventilation by as yet unidentified mechanisms.

Adult↗
PubMed1991

Human initial responses to immersion in cold water at three temperatures and after hyperventilation.

The present investigation was designed to examine the influence of water temperature and prior hyperventilation on some of the potentially hazardous responses evoked by immersion in cold water. Eight naked subjects performed headout immersions of 2-min duration into stirred water at 5, 10, and 15 degrees C and at 10 degrees C after 1 min of voluntary hyperventilation. Analysis of the respiratory and cardiac data collected during consecutive 10-s periods showed that, at the 0.18-m/s rate of immersion employed, differences between the variables recorded on immersion in water at 5 and 10 degrees C were due to the duration of the responses evoked rather than their magnitude during the first 20 s. The exception to this was the tidal volume of subjects, which was higher on immersion in water at 15 degrees C than at 5 or 10 degrees C. The results suggested that the respiratory drive evoked during the first seconds of immersion was more closely reflected in the rate rather than the depth of breathing at this time. Hyperventilation before immersion in water at 10 degrees C did not attenuate the respiratory responses seen on immersion. It is concluded that, during the first critical seconds of immersion, the initial responses evoked by immersion in water at 10 degrees C can represent as great a threat as those in water at 5 degrees C; also, in water at 10 degrees C, the respiratory component of this threat is not influenced by the biochemical alterations associated with prior hyperventilation.

Adult↗
PubMed1992

Prophylactic effects of dexamethasone in lung injury caused by hyperoxia and hyperventilation.

To determine if prophylactic corticosteroids would prevent acute lung injury caused by hyperoxia and barotrauma, 29 piglets (1.2 +/- 0.3 kg, 1-2 days of age) were studied. Ten piglets were hyperventilated [arterial PCO2 (PaCO2) 15-20 Torr] with 100% O2 for 48 h and compared with 10 piglets treated with the identical management but given 0.7 mg/kg of dexamethasone at time 0 and every 12 h for the 48-h study. Six piglets were normally ventilated (PaCO2 40-45 Torr) for 48 h with 21% O2 as an additional control group. Pulmonary function and tracheal aspirates were examined at time 0 and every 24 h. Bronchoalveolar lavage was performed for surfactant analyses at the conclusion of the study. In animals treated with hyperoxia and hyperventilation, lung compliance decreased 32% and tracheal aspirate polymorphonuclear leukocyte (PMN) chemotactic activity increased by 51%, cell counts by 204%, number of PMNs by 277%, elastase activity by 111%, and albumin concentration by 328% over 48 h (P less than 0.05). In contrast, dexamethasone-treated piglets had increases in only tracheal aspirate albumin concentration (206%) over the 48-h study. All cellular and biochemical variables were lower in dexamethasone-treated compared with hyperoxic hyperventilated piglets. Room air normal ventilation controls had only a 108% increase in tracheal aspirate albumin concentration noted. Despite quantitative differences in surfactant among the three groups, activity was unaffected. Results indicate that hyperoxia and hyperventilation for 48 h causes significant inflammatory changes and acute lung injury and that prophylactic high-dose dexamethasone significantly ameliorates this lung damage.

Animals↗
PubMed2002

Central dopamine modulates anapyrexia but not hyperventilation induced by hypoxia.

Hypoxia causes hyperventilation and decreases body temperature (T(b)) and metabolism [O(2) consumption (VO(2))]. Because dopamine (DA) is released centrally in response to peripheral chemoreceptor stimulation, we tested the hypothesis that central DA mediates the ventilatory, thermal, and metabolic responses to hypoxia. Thus we predicted that injection of haloperidol (a DA D(2)-receptor antagonist) into the third ventricle would augment hyperventilation and attenuate the drop in T(b) and VO(2) in conscious rats. We measured ventilation, T(b), and VO(2) before and after intracerebroventricular injection of haloperidol or vehicle (5% DMSO in saline), followed by a 30-min period of hypoxia exposure. Haloperidol did not change T(b) or VO(2) during normoxia; however, breathing frequency was decreased. During hypoxia, haloperidol significantly attenuated the falls in T(b) and VO(2), although hyperventilation persisted. The present study shows that central DA participates in the thermal and metabolic responses to hypoxia without affecting hyperventilation, showing that DA is not a common mediator of this interaction.

Animals↗
PubMed1987

Central neurogenic hyperventilation in a patient with medulloblastoma.

Central neurogenic hyperventilation is a rare but important cause of the frequently observed phenomenon of hyperventilation. Its diagnosis demands that primary respiratory or metabolic causes, as well as cerebrospinal fluid abnormalities, be ruled out. We hereby describe a patient whose attacks of hyperventilation were the presenting sign of her disease and might be consistent with the central neurogenic mechanism. This patient suffered from a medulloblastoma which compressed the pons. After removal of the tumor the hyperventilation attacks ceased.

Adult↗
PubMed1997

Sch 37224, an experimental antiallergy compound, inhibits the neuropeptide component of hyperventilation- and nicotine-induced bronchoconstriction in guinea pigs.

Sch 37224 is an experimental antiallergy compound that inhibits hyperventilation-induced bronchoconstriction (HIB) in guinea pigs and cold air bronchospasm in human asthmatics. HIB in guinea pigs may involve the release of tachykinins such as neurokinin A (NKA) and substance P (SP), and the action of Sch 37224 in this model may relate to inhibition of these neuropeptides. We studied the effect of Sch 37224 on the neuropeptide component of HIB that was enhanced in guinea pigs treated with the neutral endopeptidase inhibitors, thiorphan and phosphoramidon. Pulmonary resistance (RL) and dynamic lung compliance (CDyn) were measured in anesthetized, mechanically ventilated guinea pigs. RL and CDyn were measured at baseline (1 ml/100 g tidal volume and 50 breaths/min) and after a 10-min period of hyperventilation (1 ml/100 g, 150 breaths/min). Hyperventilation produced modest changes in RL (+41 +/- 12%) and CDyn (-12 +/- 3%) which were markedly enhanced by treatment with 3 mg/kg of either thiorphan or phosphoramidon (RL + 269 +/- 43% for thiorphan, + 292 +/- 63% for phosphoramidon and CDyn -65 +/- 3% for thiorphan, -51 +/- 13% for phosphoramidon). In the presence of thiorphan or phosphoramidon, the bronchospasm to hyperventilation was significantly reduced (> 70%) with 5 mg/kg, p.o., of Sch 37224. In other studies, the peptidergic (conducted in the presence of ipratropium bromide and phosphoramidon) bronchoconstrictor response to intravenous nicotine (1 mg/kg) was also inhibited by Sch 37224 (0.3-10 mg/kg, p.o.). However, Sch 37224 (5 mg/kg, p.o.) had no effect on the bronchoconstrictor response to intravenous NKA. These results indicate that Sch 37224 inhibits the neuropeptide component of HIB and nicotine in guinea pigs and this effect appears to be mediated by the inhibition of the release of tachykinins from airway C fibers.

Animals↗
PubMed1986

Hyperventilation syndrome: measurement of objective symptoms and subjective complaints.

In 303 subjects, amongst whom 250 patients suspected of suffering from the hyperventilation syndrome, lung functions were measured, a hyperventilation provocation test was performed and a questionnaire was taken. The subjects were subdivided into categories of nonhyperventilators, and 3 categories of hyperventilators, on the basis of objective measurable lung function parameters and the result of the provocation test. The outcome of the questionnaire in the various categories was evaluated. Some subjective complaints were related to age, sex, PaCO2 and lung function of the subjects. There was no clear correlation between PaCO2 and neurological signs. Hypoventilation after the provocation test occurred in only 5 subjects. No indications were found that hyperventilation might be an early sign of chronic obstructive lung disease.

Adolescent↗
PubMedDate not supplied

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral blood flow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induce hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paCO2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p less than 0.05). When paCO2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypocapnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.

Adenosine Triphosphate↗
PubMed1992

Cerebral blood flow velocity after hyperventilation-induced vasoconstriction in hypertensive patients.

BACKGROUND AND PURPOSE: The aim of our study was to evaluate by transcranial Doppler ultrasonography the dynamics of blood flow velocity changes in the middle cerebral artery during and after hypocapnia-induced vasoconstriction in untreated essential hypertensive patients. METHODS: Sixteen hypertensive patients (10 men and six women, 29-62 years of age) and 10 healthy control subjects (six men and four women, 30-62 years of age) were studied. Patients with mild-to-moderate essential hypertension (mean +/- SE blood pressure, 171/106 +/- 3/2 mm Hg) belonged to stage I or II of the World Health Organization classification. Mean blood flow velocity in the middle cerebral artery, arterial blood pressure, and end-tidal CO2 partial pressure were recorded at baseline, during 2-minute hyperventilation, and every 30 seconds up to 5 minutes after hyperventilation. RESULTS: End-tidal CO2 partial pressure values overlapped in the two groups throughout the study. Baseline values of mean blood flow velocity in hypertensive patients were similar to those in normotensive subjects (mean +/- SE values, 64.7 +/- 3.9 cm/sec versus 58.6 +/- 3.7 cm/sec). A similar fall in mean blood flow velocity was observed in hypertensive patients and normotensive subjects (43.2 +/- 2.8% versus 46.7 +/- 3.6%). Mean blood flow velocity reverted to baseline more quickly in hypertensive patients: 1.5 minutes after hyperventilation, mean blood flow velocity was 60.7 +/- 3.1% and 84.9 +/- 1.8% of control in normotensive subjects and hypertensive patients, respectively. No changes in arterial blood pressure were observed in either group throughout the study. CONCLUSIONS: This study demonstrates that the recovery of blood flow velocity in the middle cerebral artery after hyperventilation is faster in hypertensive patients than in normal subjects, thus providing further evidence that chronic hypertension is associated with changes in the dynamics of cerebral blood vessel reactivity.

Adult↗
PubMed1989

Duration of action of inhaled terbutaline at two different doses and of albuterol in protecting against bronchoconstriction induced by hyperventilation of dry cold air in asthmatic subjects.

Although several studies have examined the duration of the bronchodilator effect of several inhaled beta-2-adrenergic agents, the duration of the blocking effect on bronchial hyperresponsiveness, another key feature of asthma, has seldom been studied. We investigated this problem in eight adult asthmatic subjects who underwent hyperventilation tests with dry cold air on 4 different days. On the first day, five hyperventilation tests with assessment of the level of ventilation causing a 20% fall in FEV1 (PD20) were obtained to evaluate the within-day variability of the test. On the three other visits, after a baseline hyperventilation test, albuterol 200 micrograms, terbutaline 500 micrograms, and terbutaline 1,500 micrograms were administered in a double-blind, randomized way. Hyperventilation tests were carried out 1, 2, 4, and 6 h later. The blocking effect on the treatment days, as assessed by the differences in PD20 for each test compared with baseline PD20 for that day, was corrected for the within-day variability of the control day. There was a significant bronchodilator effect 1 h after administering the drug; it was equivalent for albuterol 200 micrograms (25.6 +/- 14.7%) and terbutaline 1,500 micrograms (21.7 +/- 13.5%) and significantly less for terbutaline 500 micrograms (14.1 +/- 10.0%). Complete or partial blockade on bronchial responsiveness was obtained in the majority (six to seven of eight) of the subjects 1 h after inhaling the bronchodilator, with progressive reduction in the effect later on. Four subjects still showed a blocking effect 6 h after terbutaline 1,500 micrograms was administered, one subject after terbutaline 500 micrograms, and no subjects after albuterol (chi square = 6.6, p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1985

Eucapnic voluntary hyperventilation of compressed gas mixture. A simple system for bronchial challenge by respiratory heat loss.

Eucapnic voluntary hyperventilation (EVH) of cold, dry air has been shown to be an effective stimulus for bronchoconstriction in people with reactive airways. The system for respiratory heat exchange (RHE) challenge can be greatly simplified from what is presently used. A relationship was derived which predicts that a single fraction of inspired CO2 (0.0489) will produce near normal alveolar CO2 over a wide range of voluntary hyperventilation. This relationship was verified in 19 normal subjects who performed a total of 110 periods of hyperventilation with minute ventilation (VE) randomly distributed between 40 and 105 L/min. The experimentally determined CO2 production of the voluntary hyperventilation was found to be 3.72 ml/min per L/min over a range of VE from 40 to 105 L/min. Next, a group of 10 patients with exercise-induced asthma (EIA) were challenged with a standard exercise protocol, ventilating ad libitum from a source of dry air at room temperature. On another day, the same pattern of VE, and hence RHE, was required of them using the simplified EVH scheme. The average decreases in forced expiratory volume in one second and specific airway conductance were 32 +/- 10% and 66 +/- 13%, respectively, after the exercise challenge, and 33 +/- 12% and 73 +/- 12% after EVH. The difference between corresponding mean values was not significant. We conclude that a simplified EVH challenge can be done using a single dry gas mixture without the need for cooling inspired gas or monitoring end-tidal fraction of CO2. This test can be used to identify and study patients with EIA without the requirement for an exercise challenge or the need for elaborate gas conditioning and monitoring equipment.

Adult↗
PubMed1994

Hyperventilation in patients who have sustained myocardial infarction after a work injury.

Patients who present with acute myocardial infarction after a work injury (AMI-WI) often report symptoms consistent with chronic hyperventilation which date back as far as the work injury itself, rather than to the AMI. The aim of the study was to test the hypothesis that hyperventilation significantly contributes to the symptoms of AMI-WI patients. The prevalence of hyperventilation was assessed by clinical capnography in 12 AMI-WI patients, 20 normal controls, 15 AMI patients whose AMI was conventional and not subsequent to a work injury (AMI-C) and 14 patients with post-traumatic stress disorder (PTSD). End-tidal carbon dioxide partial pressure (P(et)CO2) was measured at rest, after 1 min hyperventilation (FHPT), after recall of the relevant stressor (Think) and when the breathing was felt to be normal (MBIN). P(et)CO2 levels after FHPT were: 29.0 +/- 1.5 (mean +/- SD) mmHg for AMI-WI; 26.7 +/- 1.9 mmHg for PTSD; 32.1 +/- 4.1 mmHg for AMI-C and 33.7 +/- 1.4 mmHg for the controls (P < 0.05 and P < 0.01 for AMI-WI and PTSD, respectively, versus controls). After Think, the levels were 25.8 +/- 1.6 mmHg for AMI-WI, 24.6 +/- 1.4 mmHg for PTSD, 31.2 +/- 4.1 mmHg for AMI-C and 31.2 +/- 1.5 mmHg for normals (P < 0.05 and P < 0.01 for AMI-WI and PTSD, respectively, versus controls). For MBIN, values of P(et)CO2 were 26.8 +/- 1.7 mmHg and 26.7 +/- 1.5 mmHg for AMI-WI and PTSD versus 33.8 +/- 1.2 mmHg for normals, (P < 0.01 for both versus controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Accidents, Occupational↗
PubMed1990

Pseudoseizures caused by hyperventilation resembling absence epilepsy.

During the 4-year period, 1982-1986, 18 patients presented to the Children's Hospital, Camperdown, Sydney, with the following features: (1) Recurrent "absences" clinically indistinguishable from childhood absence epilepsy, (2) Normal clinical examination, (3) Electroencephalogram (EEG) demonstrating normal waking background and sleep activity. On hyperventilation, "absences" occurred, characterized on EEG by a marked build-up of paroxysmal slow-wave activity unassociated with evidence of epileptic activity. We designate these attacks "pseudoseizures caused by hyperventilation resembling absence epilepsy." Individual cases demonstrated a variety of other symptoms consistent with the hyperventilation syndrome. There was an identifiable environmental stress in 13 of the 18 cases. Follow-up of 13 patients after a mean period of 20 months revealed that only two children continued to have occasional absences, associated with a clear history of breathing up when upset. Treatment did not influence outcome. On repeat hyperventilation with EEG and respiratory monitoring, five of the 13 had pseudoseizures. There was no indication that susceptibility to these episodes was associated with an abnormal CO2 response. It is postulated that the occurrence of pseudoseizures is related to cerebrovascular immaturity and an excessive vasoconstrictor response to a given level of CO2.

Adolescent↗
PubMed1988

Hyperventilation in panic attacks. Ambulant monitoring of transcutaneous carbon dioxide.

Transcutaneous carbon dioxide monitoring has been used to investigate directly the frequency and role of hyperventilation during naturally occurring panic attacks in freely ambulant volunteers and patients. Illustrative preliminary data from healthy subjects and from four patients with panic attacks are presented. These confirm that some patients do hyperventilate during their attacks but indicate that some do not. The unreliability of traditional methods for identifying hyperventilators is demonstrated. These data indicate the potential of ambulant monitoring in research into hyperventilation and panic.

Adult↗
PubMed2000

Hyperventilation associated with quetiapine.

OBJECTIVE: To describe a case of hyperventilation associated with the administration of quetiapine. CASE SUMMARY: A 69-year-old African-American woman admitted to a psychiatric hospital for treatment of major depression with psychotic features was treated and successfully discharged with quetiapine, along with metronidazole and miconazole to treat bacterial/monilial vaginitis. Three days after discharge, the patient presented to a community hospital with shortness of breath and hyperventilation. The patient was admitted and treated for tachypnea and acute respiratory alkalosis. During this hospitalization, the patient was noted to have increased respiratory rate following the administration of quetiapine. DISCUSSION: Hyperventilation was reported during the clinical trials of quetiapine; however, this is the first published report to date. Serotonin is involved both centrally and peripherally in the regulation of respiration. A contributing factor in this case may have been the concomitant administration of metronidazole, which inhibits the cytochrome P450 enzyme (CYP3A4) also responsible for the metabolism of quetiapine. CONCLUSIONS: The development of hyperventilation and respiratory alkalosis was associated with the administration of quetiapine.

Aged↗
PubMed1991

Voluntary hyperventilation in obesity hypoventilation.

Arterial blood gas analysis was performed before and after 60 to 90 s of voluntary hyperventilation in 27 consecutive patients with occlusive sleep apnea syndrome (OSA) and daytime hypercapnia. The percentage of fall in PaCO2 from baseline was examined in relationship to age, body mass index, sleep-disordered breathing indices, and pulmonary function variables. In 14 subjects without airflow obstruction, only one individual could not voluntarily hyperventilate into the normal range, whereas 6 of 13 subjects with airflow obstruction could not hyperventilate to eucapnia. The average percentage of fall in PaCO2 was 16 mm Hg (SEM = 1.3 mm Hg). The percentage of fall in PaCO2 correlated significantly with FEV1/FVC ratio (r = 0.47, p = 0.01) and with FEV1 (r = 0.5, p = 0.008). Although the baseline PaCO2 did not correlate with FEV1, the posthyperventilation PaCO2 did (r = 0.54, p = 0.003). Voluntary hyperventilation studies herein suggest a predominant role for impairment of ventilatory control in the maintenance of hypercapnia in OSA since a fall of PaCO2 into the normal range can usually be obtained. The correlation between the percentage of fall in PaCO2 and spirometric measures of respiratory mechanics, as well as the inability of some subjects to normalize the PaCO2 voluntarily suggests an added role for respiratory mechanical impairment in obesity hypoventilation.

Adult↗
PubMed1996

Eucapnic voluntary hyperventilation as a bronchoprovocation technique: development of a standarized dosing schedule in asthmatics.

A variety of dosing schedules have been reported for the hyperventilation method of broncho-provocation testing. To evaluate the effect of challenge technique on the bronchoconstrictive response, we had 16 subjects perform eucapnic voluntary hyperventilation (EVH) with dry, room temperature gas using four different dosing schedules. The hyperventilation challenge dosages included the following: (1) a target minute ventilation (VE) of 20 x FEV1 for 6 min; (2) a target VE of 15 x FEV1 for 12 min; (3) an interrupted challenge with a target VE of 30 x FEV1 for 2 min repeated 3 times; and (4) a target VE of 30 x FEV1 for 6 min. Challenges 2, 3, and 4 gave identical absolute ventilatory challenges (identical factor FEV1 x minutes) but at different VE dosages or time. Challenges 1 and 4 were of identical length, but different target VE. The mean postchallenge fall in FEV1 was 16.6 +/- 10.9%, 11.0 +/- 8.1%, 19.6 +/- 9.9%, and 26.7 +/- 11.3% for challenges 1, 2, 3, and 4, respectively. The response to an identical EVH challenge (FEV1 x 30 for 6 min) was reproducible when performed on separate days. We conclude that the challenge technique used for hyperventilation testing will have a significant impact on the bronchoconstrictive response and must be taken into account when interpreting study results. Tests may be quantitatively comparable over a narrow range of challenge time and VE. We recommend that a 6-min uninterrupted EVH challenge using dry, room temperature gas at a target VE of 30 x FEV1 be adopted as the "standard" challenge.

Adult↗