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At least 19 recordsLinked to original sources

PubMed1987

Hypocapnic hyperventilation versus isocapnic hyperventilation with ambient air or with dry air in asthmatics.

The effects of three types of hyperventilation challenge tests (free hypocapnic, ambient air; controlled isocapnic, ambient air; controlled isocapnic, dry air), on FEV1 and on Raw were compared in 12 asymptomatic asthmatics. Controlled isocapnic hyperventilation of dry air as well as of ambient air caused bronchoconstriction lasting for more than 8 min, but the degree of bronchoconstriction was significantly greater with the former. Free hypocapnic hyperventilation of ambient air caused peak bronchoconstriction after 1 min, followed by a steady functional improvement; the values after 1 min were similar to those following isocapnic dry air hyperventilation, and values after 8 and 15 min were similar to those following isocapnic ambient air hyperventilation. The changes in Raw induced by the three types of hyperventilation were not influenced by a preceding full inspiration. In the eight subjects in whom the lung function had returned to within 10% of control after 30 min, identical duplicate hyperventilation challenge tests performed at that time demonstrated a significant, partial refractoriness for all tests. Thus the simple, free hypocapnic, hyperventilation test with ambient air was found to be as reliable as the more sophisticated controlled isocapnic tests.

Adult↗

PubMed1996

Double-blind placebo-controlled study of the hyperventilation provocation test and the validity of the hyperventilation syndrome.

BACKGROUND: Hyperventilation syndrome (HVS) describes a set of somatic and psychological symptoms thought to result from episodic or chronic hyperventilation. Recognition of symptoms during the hyperventilation provocation test (HVPT) is the most widely used criterion for diagnosis of HVS. We have investigated the validity of the HVPT and of the concept of HVS. METHODS: In a randomised, double-blind, crossover design, the ability of 115 patients with suspected HVS to recognise symptoms during the HVPT was compared with the ability to recognise symptoms during a placebo test (isocapnic overbreathing, with carbon dioxide levels maintained by manual titration). 30 patients who had positive results on the HVPT underwent ambulatory transcutaneous monitoring of pCO2 to ascertain whether they hyperventilated during spontaneous symptom attacks. FINDINGS: Of the 115 patients who underwent the HVPT and the placebo test, 85 (74%) reported symptom recognition during the HVPT (positive diagnosis HVS). Of that subset, 56 were also positive on the placebo test (false-positive), and 29 were negative on the placebo test (true-positive). False-positive and true-positive patients did not differ in symptom profile or in physiological variables. During ambulatory monitoring (15 true-positive, 15 false-positive) 22 attacks were registered. Transcutaneous end-tidal, pCO2 decreased during only seven. The decreases were slight and apparently followed the onset of the attack, which suggests that hyperventilation is a consequence rather than a cause of the attack. There were no apparent differences between false-positive and true-positive patients. INTERPRETATION: The HVPT is invalid as a diagnostic test for HVS. Hyperventilation seems a negligible factor in the experience of spontaneous symptoms. The term HVS should be avoided.

Adult↗

PubMed1987

The standardization of hyperventilation on EEG recording in childhood. I. The quantity of hyperventilation activation.

In thirty-seven children free of neurological symptoms, we attempted the standardization of hyperventilation on EEG. We also attempted to determine the quantity of hyperventilation activation necessary to produce equivalent degrees of EEG slowing at different ages. The respiratory rate (RR), total expiratory volume/min (VE), O2 consumption volume/min (VO2), expiratory CO2 volume/min (VCO2), tcpO2 and tcpCO2 were monitored before, during and after hyperventilation. The optimal conditions for adequate activation were found to be: a respiratory rate of 30/min, a 3-fold elevation of VE and a duration of 4 minutes. With this activation, the degree of EEG slowing was found to be nearly inversely proportional to the age (in the age range of 6 years to 17 years old). Therefore, this activation may be adequate and useful for evaluating the EEG development in childhood. As to the relationship between the appearance of EEG slowing and changes in respiratory factors, the pCO2 decrease and the cerebral blood flow decrease, which may be evoked by the pCO2 decrease, are the most fundamental factors that produce EEG slowing during hyperventilation. The difference in the response on hyperventilation between children and adults may be due to age-related CNS sensitivity to CO2 and/or cerebral vascular CO2 responsiveness.

Adolescent↗

PubMedDate not supplied

Prehospital hyperventilation after brain injury: a prospective analysis of prehospital and early hospital hyperventilation of the brain-injured patient.

BACKGROUND: The Brain Trauma Foundation's Guidelines for the Management of Severe Head Injury state that the use of prophylactic hyperventilation after traumatic brain injury (TBI) should be avoided because it can compromise cerebral perfusion. The objective of this study was to assess the prevalence of unintentional hyperventilation. METHODS: A prospective evaluation of all intubated trauma patients with a diagnosis of TBI was performed. Patients with signs of impending herniation were excluded. RESULTS: Forty patients were included in the study. The average Glasgow Coma Scale (GCS) was 6.3. Of these, 28 patients (70%) were unintentionally hyperventilated. Eleven (39%) of the hyperventilated patients died or were discharged in a persistent vegetative state. Of the remaining 12 patients who experienced normal ventilation, three patients (25%) died or were discharged in a vegetative state (p = ns) (Table 1). CONCLUSION: Hyperventilation was common after TBI. However, patients ventilated to a normal PaCO2 were significantly more acidotic. Prehospital personnel should undergo educational training after development of strict ventilation protocols for patients suffering TBI.

Adult↗

PubMedDate not supplied

Local blood flux in skin and muscle during voluntary hyperventilation in healthy controls and patients with hyperventilation syndrome.

Laser Doppler fluxmetry was used to analyze local blood flux in the anterior tibial muscle and the skin of the calf simultaneously during 3 min of hyperventilation. Examinations were performed in 10 controls and 10 patients with a hyperventilation syndrome in order to evaluate a possible different vascular response to the provocation test. During hyperventilation, mean muscle blood flux increased in both groups. In controls, flux augmented from 23.4 +/- 12.3 arbitrary units (AU) to 51.6 +/- 28.3 AU (p < 0.05) and in patients from 21.6 +/- 10.8 AU to 45.0 +/- 26.4 AU (p < 0.05). The changes of skin blood flux during hyperventilation were not significant. The flux response did not differ significantly in controls and patients. Using the laser Doppler technique we were able to confirm muscular vasodilatation previously reported during short-term hyperventilation. Possible mechanisms include release of vasoactive substances and/or a stimulation of the autonomic nervous system.

Adult↗

PubMed1975

[Artificial hyperventilation in head injury. I. Spontaneous hyperventilation and assisted ventilation (author's transl)].

The present study was desined to clarify the roles of artificial hyperventilation in management of the patients with cerebral injury. Here reported is the first part of the serial studies and concerned with general informations about hyperventilation. The measurements of PaCO2, minute ventilation volume (VE), dead space (VD), tidal volume (VT), cardiac output (by dye dilution method), oxygen consumption (by Fick' principle) and oxygen equilibrium were performed in the patients suffering from acute, severe head injury. And the effect of assisted ventilation on them were investigated (using pressure-limited respirator). 1. There was a common finding that marked and sustained increase in VE, VA (alveolar ventilation), and decrease in PaCO2 existed during the first week of injury. 97% of both VE and VA were above normal and mean value of PaCO2 was 29-33 mmHg. The syndrome of spontaneous hyperventilation was evidently more prominent in the nonsurvived group of patients. It was noteworthy that increased VE (or VA) was dependent neither on VD or pulmonary dysfunction nor on metabolic acidosis of arterial blood. The relation of VA to base excess in head injury was well contrasted to that of acute CO poisoning. 2. Assisted ventilation resulted in increased VT and decreased respiratory rate, and little change in VE. Consequently, PaCO2 changed only from 33.0 to 29.4 mmHg as a mean of entire series of patients. But when the influence affected by hypoxemic drive was subsided, a significant reduction of PaCO2 was disclosed following assisted ventilation. The assisted ventilation with pure oxygen was also associated with reduced cardiac output (from 6.0l/min to 5.3l/min), though the oxygen consumption changed variedly among the patients. 3. The fact was confirmed that both hypocapnea and alkalosis produced the left-sised shift of oxygen dissociation curve, decrease in P50 (P02 at 50% saturation of oxygen), and in addition, narrowed arterio-mixed venous oxygen difference. The changes of artero-mixed venous oxygen saturation difference which were calculated at 100 mmHg of PaO2 and 40mmHg of mixed venous PO2 were in a linear fashion with those of P50. Apart from the problems on injured brain, the beneficial and non-beneficial effects of hyperventilation were further discussed. The availability and inidcation of artificial hyperventilation should be precisely evaluated later, in a comprehensive manner with the subsequent studies (Part 2 and 3) on cerebral metabolism and intracranial pressure.

Brain Injuries↗

PubMed1990

Symptom reporting during voluntary hyperventilation and mental load: implications for diagnosing hyperventilation syndrome.

Hyperventilation is considered an important factor in the production of a variety of somatic symptoms. This complex of symptoms is called the Hyperventilation Syndrome (HVS). Recognition of symptoms during the hyperventilation provocation test (HVPT) is a widely used criterion for diagnosing HVS. The validity of this criterion is tested in the present study. Twenty-three patients suspected of HVS performed a HVPT (hyperventilation during 3 min) and a mental load task (Stroop Color Word Test; CWT). It appeared that about the same number of patients (61%) recognized symptoms during the HVPT as during the CWT (52%), despite severe hypocapnia in the first test and normocapnia in the second. Reporting of symptoms was significantly related to psychological state and trait measures (SCL-90 and STAI scores) and unrelated to the degree of hypocapnia. These data have far reaching consequences, as they not only undermine the validity of the HVPT, but also question the tenability of the concept of HVS.

Agoraphobia↗

PubMed1979

[Hyperventilation and airway resistance. Bronchial spasms after hyperventilation].

Airway resistance, FEV1.0 and lung volume were measured by body plethysmography before and after voluntary hyperventilation. In normal subjects, resistance increased to 130--140% of the initial value measured before hyperventilation. The same increase was observed in silicosis patients without chronic obstructive bronchitis. Asthmatic patients in an asymptomatic phase showed a rise in airway resistance to an average of 255% of the nearly normal initial values, and also a reduction in FEV1.0. In normal subjects and asthmatic patients, the administration of bronchodilators inhibits the rise in airway resistance induced by hyperventilation. The hyperventilation test can be used to identify increased susceptibility to bronchoconstriction.

Asthma↗

PubMed1999

Presence of hyperventilation in patients with asthma-like symptoms but negative asthma test responses: provocation with voluntary hyperventilation and mental stress.

BACKGROUND: A group of patients reporting asthma-like symptoms but with negative asthma tests has been identified. OBJECTIVE: The objective of this study was to determine whether hyperventilation might explain these symptoms and whether the tests could be used as diagnostic tools. METHODS: A hyperventilation provocation test (HVPT), a mental stress test, and the Word Color Conflict Test (WCCT) were performed on 10 patients with asthma-like symptoms, 10 patients with asthma, and 10 healthy subjects. End-tidal PCO 2 (PETCO2) was recorded 10 minutes after the HVPT and during the WCCT. Blood pressure, heart rate, and respiratory rate were also studied. The Nijmegen symptom questionnaire was used in the assessment of symptoms. RESULTS: After the HVPT, the PETCO2 values recovered most slowly in the study group, the difference being significant compared with the healthy group (P <.01). During the WCCT, the study group had the lowest PETCO2 values at the 10- and 15-minute measurements, the difference again being significant compared with the healthy group (P <.05). The study group more often experienced symptoms before the test than the group with asthma (P <.05) and the healthy group (P <.001). The study group recognized significantly more symptoms previously experienced during the HVPT than the group with asthma (P <.05) and the healthy group (P <.01) and during the WCCT than the healthy group (P <.05). The study group showed a negative correlation between the PETCO2 level and the number of symptoms after the HVPT at 8 (r = -0-72; P <.05) and 10 minutes (r = -0.76; P <.05) and after the WCCT (r = -0.59; P <.05). Blood pressure, heart rate, and respiratory rate showed small differences between the groups. CONCLUSION: Patients with asthma-like symptoms may experience hyperventilation when provoked. Mental stress might be 1 trigger factor. The HVPT and WCCT can be used as diagnostic instruments.

Adult↗

PubMed1991

Evaluation of the clinical usefulness of capnography curves during a hyperventilation provocation test in the diagnosis of hyperventilation syndrome.

We evaluated the diagnostic usefulness of capnography curves during and following a hyperventilation provocation test (HVPT) in the hyperventilation syndrome (HVS). The diagnosis of HVS was based on the Nijmegen questionnaire and on the reproduction of symptoms during HVPT. Capnography curves of 40 HVS patients, 40 non-HVS patients with psycho-somatic complaints and 26 healthy controls were analyzed. There was no difference in baseline end-tidal CO2-level (FETCO2) between the 3 groups. The spontaneous fall of FETCO2 during the adaptation phase was clearly different in HVS patients versus non-HVS patients or controls: -0.12 mmol/l (95% confidence limits -0.18 to -0.06) versus +0.01 mmol/l (95% confidence limits -0.04 to +0.16) (p = 0.002). The 3 minutes FETCO2 recovery ratio and the 5 minutes ratio were not significantly different between the groups. In conclusion, in this study the spontaneous fall of FETCO2 during the adaptation phase of the HVPT was the only valuable part of the capnography test to discriminate between HVS and non-HVS patients.

Carbon Dioxide↗

PubMed1964