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PubMedDate not supplied

Control of the end-tidal PCO2 in the hyperventilation syndrome: effects of biofeedback and breathing instructions compared.

Twenty chronic hyperventilation syndrome patients were assigned to biofeedback training to raise end-tidal PCO2 level or received a breathing exercise schedule for home practice. Both methods offered equal opportunity for improving end-tidal PCO2 significantly. Alleviation of complaints, however, was only noticeable in the biofeedback group. This may be due to the fact that improvement in the severity of the hyperventilation syndrome was not only significantly related to increase in end-tidal PCO2 but also to initial end-tidal PCO2 level and state of the ventilatory controlling system. A follow-up evaluation three months after the end of the therapy programs showed an unchanged end-tidal PCO2 level in both groups as compared with post-treatment evaluation, but a significant relapse in complaints in the biofeedback group. Implications of these findings are discussed in the final section of this paper.

Biofeedback, Psychology↗
PubMed1983

[Hyperventilation as a method of detecting atrioventricular conduction disorders in athletes].

A hyperventilation test, rationed with respect to respiratory rate and duration, was performed in 140 athletes under electrocardiographic control. During the test, one athlete developed an episode of sino-auricular block, and four showed a temporary second-degree Wenkebach--Samoilov A--V block. In three of those, resting ECG demonstrated decelerated atrioventricular conductivity which was combined with signs of myocardial dystrophy in two cases and with periodically recorded coronary sinus rhythm in one. Two athletes were under long-term dispensary observation. When repeated tests were negative, the block developed in response to hyperventilation preceded by obsidan administration.

Adolescent↗
PubMed1980

Hyperventilating the hypoventilator.

A 65-year-old man had chronic hypoventilation and was demonstrated to have primary neuromuscular disease with major involvement of the thoracic bellows. By use of accessory muscles, he was able to voluntarily hyperventilate and reduce his PCO2 to normal. Hyperventilation gases must be interpreted with care in neuromuscular disease; the ability to reduce PCO2 to normal range does not exclude neuromuscular disease as a cause of chronic respiratory failure.

Aged↗
PubMed1978

The effect of breath holding, hyperventilation, and exercise on nasal resistance.

A group of 51 patients was studied by a technique of active posterior rhinomanometry that assessed the influence of breath holding, hyperventilation, and exercise on nasal resistance. Breath hodling of 30 seconds or longer produced a decrease in nasal resistance in most of the subjects tested. Hyperventilation had variable effects on nasal resistance, and exercise consistently decreased nasal resistance. These observations are consistent with the proposed effect of chemoreceptor stimulation on nasal airway resistance.

Adolescent↗
PubMed1995

[Syncope and chest pain. Demonstration of the mechanism by the hyperventilation test].

Two patients admitted to hospital because syncope and chest pain are presented. In both patients, hyperventilation test caused severe myocardial ischaemia (ST segment elevation) and sudden development of presyncopal sustained ventricular tachycardia which immediately responded to intravenous nitroglycerin. The relationship between coronary vasospasm and sudden death secondary to polymorphic ventricular tachycardia is discussed. Also, the usefulness of the hyperventilation test to detect this problem and to monitor its therapeutic response is addressed.

Chest Pain↗
PubMed1995

Changes in mucociliary clearance during and after isocapnic hyperventilation in asthmatic and healthy subjects.

Hyperpnoea with dry air could lead to a reduction in depth and hyperosmolarity of the periciliary fluid layer (PFL) as a consequence of evaporative water loss. We investigated whether mucociliary clearance (MCC) is likely to be affected by dry air hyperpnoea, which also results in airway narrowing in asthmatics. MCC was measured by radioaerosol technique, for about 1 h, in 10 asthmatic and 8 healthy subjects on 3 separate days: 1) nasal resting breathing with ambient air; 2) isocapnic hyperventilation (ISH) with dry air; and 3) ISH with warm humid air. Analysis of the initial and post-intervention lung radioactivity for the whole right lung and for defined regions of interest showed that, compared to ISH with warm humid air and nasal resting breathing, MCC was reduced during and increased post-ISH with dry air in the whole right lung of both groups. The mean reduction in clearance (+/- 95% confidence interval (95% CI)) was -9.3% (-3.1 to -15.6%) and -3.6% (-2.0 to -9.1%), and the mean increase (+/- 95% CI) was 19.2% (11.8 to 26.6%) and 14.8% (7.1 to 22.5%), compared to warm humid air, in asthmatic and healthy subjects, respectively. However, regional analysis showed that the changes were present in all lung regions of the asthmatics, whilst only in the central region of the healthy subjects. The duration of the increased clearance rates post-ISH was also different in both groups. The changes in mucociliary clearance during and after isocapnic hyperventilation with dry air was probably related to the water content of the inspired air, causing transient changes in the periciliary fluid layer.

Adult↗
PubMed1995

[Hyperventilation test: a noninvasive screening test for coronary vasospasm].

3 patients with coronary vasospasms in different clinical situations are presented. One patient had typical Prinzmetal angina but coronary arteries without significant stenosis. One patient without typical angina pectoris showed sudden significant ST elevations on anterior and lateral ECG tracings accompanied by typical ischemic chest pain. At angiography, a 70% LAD stenosis was found without high degree lesions. One patient (aged 30 years) had a documented anterior infarction with angiographically normal coronary arteries. In all these cases coronary vasospasms were recognized as the underlying cause of the symptoms. All the patients were treated with calcium channel blockers and have been asymptomatic since. Currently available data comparing the diagnostic value of hyperventilation with other tests for coronary vasospasms, such as ergonovine or acetylcholine, are discussed. The hyperventilation test can be recommended as the first test in the work up of suspected vasospastic angina pectoris.

Adult↗
PubMed1995

[An analysis of the data from the neurophysiological examination of patients with bronchial asthma and hyperventilation].

Bronchial asthma (BA) patients with hyperventilation (HV) were examined by means of evoked cutaneous sympathetic potential (ECSP) and short-latency evoked stem potentials to acoustic stimulation (SLESP to AS). Measurements of these parameters allowed quantitation and differentiation of hyperventilation disorders in BA patients. The latter were divided into 4 groups: BA patients with HV syndrome (HVS), BA patients with functional HV (FHV), BA patients with spontaneous HV (SHV) and BA patients without HV. BA patients with HVS exhibited a significant increase of latent ECSP period and latent periods III and V SLESP to AS peaks. This evidences for vegetative neuropathy and dysfunction of the pons and mesencephalic brain compartments. In BA patients with FHV there was a longer latent period II of SLESP to AS peak indicating dysfunction of caudal brain stem. BA patients with SHV and without HV had no significant shifts.

Adolescent↗
PubMed1994

Non-specific airway responsiveness to hyperventilation of low doses of sulfur dioxide and cold air of non-smoking healthy volunteers of different ages.

We examined the effect of hyperventilation (HV) of sulfur dioxide (SO2)-air and cold air for 5 minutes on airway responsiveness of 37 (12 females and 25 males) healthy non-smoking volunteers of different ages. Body-plethysmographic measurements of airway resistance (Raw) and intrathoracic gas volume (ITGV) were performed before, 3, 10 and 20 mins. after the end of HV of SO2-air or cold air. Specific airway resistance (sRaw), product of Raw x ITGV, was used to evaluate the airway responsiveness. The mean (standard error) of percent changes of sRaw (delta %sRaw) were 121 (22), 45 (8) and 25 (4) at 3, 10 and 20 mins. after the end of HV of SO2-air. The corresponding values were 52 (8), 25 (5) and 19 (3) after HV of cold air. The differences in delta %sRaw between HV of SO2 and cold air were statistically significant (two sided t-test) for the 3 (p < 0.01) and 10 (p < 0.05) mins. values. Hyperventilation of SO2 and cold air produced delta sRaw above 100% in 14 (37.8%) and 5 (13.5%) volunteers, respectively. The difference in frequencies of delta sRaw above 100% between the HV of SO2 and cold air was statistically significant (p < 0.05, chi 2-Test). We observed a decreasing order of airway responsiveness with increasing age following HV of SO2 but not after cold air. We conclude that airway responsiveness to SO2 is poorly related to the response to cold air.

Adolescent↗
PubMedDate not supplied

Effect of venous hypercarbia and hyperventilation on myocardial contractility in canine haemorrhagic shock.

To study the effect of venous hypercarbia on myocardial contractility, haemorrhagic shock was produced in six healthy mongrel dogs by ex-sanguination of 15 ml of blood/kg body weight every 20 minutes till a loss of 45 ml/kg was achieved. After recording haemodynamic and respiratory parameters, the dogs were hyperventilated by positive pressure ventilation for 30 minutes and haemodynamic and blood gas parameters reassessed. During haemorrhagic shock, mean cardiac output decreased from 4.23 l min to 0.98 l min (p < 0.01), stroke index from 2.25 to 0.35 ml/kg (p < 0.05) and left ventricular stroke work index from 3.72 to 0.19 g. m/kg. The mean mixed venous pCO2 increased from 35 mmHg to 56.7 mmHg (p < 0.05). During hypoventilation, mixed venous pCO2 decreased to 40 mmHg (p < 0.05) and without any volume replacement, mean cardiac output increased 2.5 l min (P < 0.05), stroke index to 1.13 ml/kg (p < 0.05) and left ventricular stroke work index, and index of myocardial contractility, increased to 0.78 g.m/kg (p < 0.05). Thus, although hypovolaemia is the major cause of low cardiac output in haemorrhagic shock, this study shows that venous hypercarbia (which probably indicates tissue respiratory acidosis) further worsens circulatory failure by decreasing myocardial contractility. Hyperventilation improves cardiac functions and increases output by relieving tissue hypercarbia in spite of persistent hypovolaemia.

Animals↗
PubMed1993

[Influence of airway temperature and humidity of hyperventilation induced bronchoconstriction in rabbits].

It has been suggested that humidity and temperature of inspired air is important in determining the severity of hyperventilation induced bronchoconstriction (HIB). To investigate whether water loss or heat loss from airway plays more important role to induce HIB, we compared the effect of temperature and humidity of inspired air on HIB, in sensitized and non-sensitized rabbits. Inspired air containing 5% CO2 was conditioned to dry or humidified and to temperature of 9 degrees C or 25 degrees C during isocapnic hyperventilation. In sensitized rabbits, marked bronchoconstriction was observed when inspired air dry regardless of temperature. We conclude that 1) HIB is produced in sensitized rabbits and 2) humidity rather than temperature of inspired air is more important to induce HIB.

Animals↗
PubMed1993

Demonstration of focal brain ischemia induced by hyperventilation using Tc-99m HMPAO SPECT.

A case with vasospasm of the right anterior cerebral artery induced by hyperventilation is presented. Consecutive Tc-99m HMPAO brain SPECT studies at rest and during hyperventilation greatly contributed to the quantitative evaluation of focal perfusion decrease in conjunction with contrast angiography. This technique seems to be useful for the detection of alterations in regional brain perfusion during short duration intervention.

Adult↗
PubMed1995

[Clinical characteristics and outcome of 508 patients with hyperventilation syndrome].

The characteristics of hyperventilation syndrome (HVS) were studied in 508 patients who visited our hospital over 11 years. Information regarding symptoms and laboratory data was collected from the clinical records, and outcome was surveyed with a questionnaire mailed to all patients. Patients with acute HVS ranged in age from 5-85 years, and acute HVS was particularly prevalent among women in their late teens. Triggers of HVS included anxiety, nausea & vomiting, and fever due to the common cold. The primary symptoms were dyspnea and numbness, but these differed from the symptoms that appeared during a provoked attack, Half of the patients had no underlying disorder, but the others were suffering from neurosis, cardiovascular disorders, or other diseases. These characteristics of acute HVS did not differ from those seen in patients in whom the diagnosis of HVS was confirmed with arterial blood gas analysis. Half of the patients recovered without treatment, and the others underwent paper-bag rebreathing or intravenous infusion of sedatives. The prevalence of chronic HVS was 2% and almost all those patients were middle-aged women. In contrast, the questionnaire revealed that half of the patients had repeated HVS attacks. In 10% of the patients, these attacks persisted for more than 3 years. Many of these patients reported that they sighed frequently and felt air hunger while in remission. These findings were compatible with the criteria for chronic HVS. Therefore, it may be possible to diagnose HVS from symptoms alone, without hyperventilation provocation tests. In conclusion, these data underscore the importance of clinical symptoms in the diagnosis of HVS.

Adolescent↗
PubMed1997

[Isocapnic hyperventilation test adjusted to child's resting ventilation rate].

In order to validate an Isocapnic Voluntary Hyperventilation (IVH) test applicable to daily practice and to adapt the stimulus to height, 9 healthy and 15 asthmatic children performed a Resting Ventilation Rate (RVR)-corrected IVH. They performed a three-minute IVH with room temperature dry air achieving twice (IVH2) and three times (IVH3) their RVR. Mean Maximal Expiratory Flow (MEF) in the middle half of Forced Vital Capacity (FVC) (MEF25-75%) and mean MEF at 25% of FVC (MEF25%) are decreased in the asthmatic group 10 minutes IVH3 (p = 0.02 and < 0.002) compared to healthy group. Mean FEV1 of both group are not different. Comparing Forced Expiratory Flows variation after IVH to baseline intrasubject coefficient of variation, sensitivity of the test is 80% and specificity 100% when variations of MEF25-75% and MEF25% together with FEV1 variations are considered. This suggests an easy way to adapt an hyperventilation stimulus to size and emphasizes the utility of taking account of MEF25-75% and MEF25% in detecting non specific bronchial hyperreactivity in asthmatic children.

Adolescent↗
PubMedDate not supplied

[Changes in EEG induced by prolonged hyperventilation in humans].

The data obtained revealed a significant augmentation of the EEG slow-wave activity following a 32-minute hyperventilation in neurologically healthy subjects. In 43% of the subjects, on the 8th minute of the hyperventilation a generalised paroxysm of the delta-activity occurred.

Adult↗
PubMed1998

Functional MRI of the rat somatosensory cortex: effects of hyperventilation.

Functional mapping of the rat somatosensory cortex was performed with T2*-sensitized MRI using a forepaw electrical stimulation model in alpha-chloralose-anesthetized rats at 7 T under both normocapnia and mild hyperventilation-induced hypocapnia. A highly localized activation area, consistent with the known somatosensory cortical region, was detected in all seven animals studied during hypocapnia and in five of the same animals during normocapnia. Quantitatively, hypocapnia was found to significantly increase both the size of the fMRI activation area (3.4 +/- 0.6 mm2 versus 1.5 +/- 0.6 mm2 in normocapnia, mean +/- standard error, n = 7, P < 0.03) and the average fMRI signal intensity increase (3.4 +/- 0.6% versus 2.7 +/- 0.4%, n = 5, P < 0.05). The increased sensitivity of fMRI to functional activation may reflect a widened arterial-venous oxygenation difference resulting from an increased effective oxygen extraction during hyperventilation. The dependence of the fMRI response on the ventilation state underscores the need to control for physiological parameters in animal fMRI studies.

Afferent Pathways↗
PubMed1999

Hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity.

PURPOSE: In this study we examined whether normocapnia maintained by hyperventilation after lower limb tourniquet deflation prevents an increase in cerebral blood flow velocity. METHODS: Thirteen patients, undergoing elective orthopedic surgery, requiring a pneumatic tourniquet around the lower extremity, were divided into two groups. In group 1, ventilation was controlled at tidal volume of 10 mL x kg(-1) and respiratory rate of eight per minute after tourniquet release. In group 2, ventilation was controlled to maintain P(ET)CO2 between 30 and 35 mmHg after tourniquet release. Arterial blood pressure, heart rate, peak and mean middle cerebral artery (MCA) flow velocity, and arterial blood gas were measured every minute for ten minutes after tourniquet release. The MCA blood flow velocity was measured using Transcranial Doppler ultrasonography (TCD). RESULTS: In group 1, the maximum peak MCA flow velocity was 53+/-6 cm x sec(-1) (50%+/-6% increase compared with pre- release value), and achieved 3+/-0.4 min after tourniquet release. In group 2, there was no increase either in mean or peak MCA velocity after tourniquet release. CONCLUSIONS: Normocapnia maintained by hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity.

Blood Flow Velocity↗
PubMed1985

Comparison of deep and shallow endotracheal administration of dionosil in dogs and effect of manual hyperventilation.

The endotracheal route has been used as a second route of choice for administration of emergency drugs for several years; however, the optimal technique for administration of drugs by this route has not been clearly defined. One important aspect of technique involves the question of how distribution to the distal-most endobronchial tree is influenced by initial depth of endotracheally administered drug instillation and use of forced manual hyperventilation. This study demonstrates that depth of instillation of drugs administered by the endotracheal route may not be an important factor in the delivery of medications to absorptive sites in the lung. It appears, however, that forced manual hyperventilation is essential to assure bilateral and optimal distal delivery of endotracheally administered medications.

Animals↗