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PubMed1988

Local "inverse steal" induced by hyperventilation in head injury.

Hyperventilation is used routinely to reduce intracranial pressure in victims of severe head injury. In the clinical setting, the effects of hyperventilation on regional cerebral blood flow usually are not known. We describe a case in which hyperventilation resulted in local, paradoxic increases in cerebral blood flow (i.e., "inverse steal") associated with a reduction in intracranial pressure. Although the reduced intracranial pressure was thought to be beneficial, serial computed tomographic scans suggested that the inverse steal response could have promoted cerebral edema, resulting in secondary brain injury.

Brain Injuries↗
PubMed1999

Investigation of the most effective provocation test for patients with coronary spastic angina: usefulness of accelerated exercise following hyperventilation.

This study sought to compare the clinical usefulness of the hyperventilation plus cold stress test or the hyperventilation combined with accelerated exercise test with other single tests in patients with coronary spastic angina. The study examined 24 patients (23 men, mean age 66 years) with angiographically confirmed coronary spastic angina and less than 50% stenosis. Moreover, none had spontaneous ST segment elevation before the study. Under no medication for at least 24 h prior, 4 procedures were performed from 09.00 h to 11.00 h: (i) a hyperventilation test for 5 min (HV(5)); (ii) HV(5) combined with a cold stress test for the last 2 min (HV(5)+CS(2)); (iii) a treadmill exercise test based on Bruce's protocol (TM(3)); and (iv) a treadmill exercise test accelerated at 1 min intervals according to Bruce's protocol immediately after HV(5) (HV(5)+TM(1)). The rate of appearance of chest pain and ischemia-induced ECG changes due to HV(5)+TM(1) were significantly higher than the other 3 tests. HV(5)+CS(2) was not superior to HV(5) alone. The incidence of provoked ST segment elevation due to HV(5)+TM(1) was higher than with the other 3 procedures. Thus, in patients with coronary spastic angina, no spontaneous ST segment elevation and near normal coronary arteries, HV(5)+CS(2) was no more useful than HV(5) alone. It is recommended that the newly designed HV(5)+TM(1) combination test be used for documenting evidence of ischemia in patients with coronary spastic angina, low disease activity and near normal coronary arteries.

Acetylcholine↗
PubMed1991

The effect of body posture on exercise- and hyperventilation-induced asthma.

Recent studies have shown that swimming is of relatively low asthmogenicity, even under conditions of high respiratory heat (and/or water) loss (RHL). It has been suggested that the horizontal body position may contribute to swimming's low asthmogenicity. We studied the effects of upright and prone body postures on pulmonary function following exercise (EIA) and after nonexercise hyperventilation (HIA). Twelve asthmatic boys (aged 12 to 16 years) underwent two 8-min exercise sessions of shoulder flexion-extension and two 8-min isocapnic hyperventilation treatments, in a counterbalanced order, either while lying prone or standing upright. All tests were carried out in a climatic chamber at 10 +/- 1 degree C and 31 +/- 2 percent relative humidity. Minute ventilation (VE) was kept constant at a predetermined individual level during all treatments. No differences were observed in pulmonary functions between the prone and upright postures following either exercise (FEV1 = -20.5 +/- 18.7 percent vs -22.2 +/- 18.7 percent, respectively) or hyperventilation (FEV1 = -29.6 +/- 19.0 percent vs -29.7 +/- 20.2 percent). We conclude that body posture on land has no meaningful effect on the severity of bronchoconstriction in asthmatic children; however, in view of some conceivable physiologic benefits of the prone position in water, an interactive effect on swimming-induced asthma (SIA) of body posture and water immersion cannot be ruled out.

Adolescent↗
PubMed1995

The refractory period after eucapnic voluntary hyperventilation challenge and its effect on challenge technique.

To evaluate whether there is a refractory period (RP) after hyperventilation challenge, we compared the bronchoconstrictive response to repetitive eucapnic voluntary hyperventilation challenge with dry, room temperature air (EVH). The serial challenges were identical with 11 known asthmatics hyperventilating for 6 min at a target minute ventilation of 30 times their FEV1 measured before either challenge. There was a significant difference between the mean postchallenge fall in FEV1 to the initial EVH challenge (27.4 +/- 9.8%) and the response to the second EVH challenge (16.1 +/- 5.9%) (p = 0.0001), indicating refractoriness. We then evaluated whether 6 min of uninterrupted EVH challenge gives a similar bronchospastic response to that which results from an equivalent (by total minute ventilation) interrupted challenge of 2 min of EVH repeated three times. The mean post-challenge fall in FEV1 in response to this interrupted challenge was 18.9 +/- 10.6%, which was significantly different from the 27.4% fall in response to 6 consecutive minutes of EVH (p = 0.036). This study demonstrates that there is a refractory period after repeated EVH challenges and this refractoriness affects the response to interrupted, or dosed, EVH challenge.

Adult↗
PubMed2001

Usefulness of accelerated exercise following mild hyperventilation for the induction of coronary artery spasm : comparison with an acetylcholine Test.

STUDY OBJECTIVES: This study was performed to compare the results of accelerated exercise following mild hyperventilation and a standard acetylcholine (ACh) test for the induction of coronary artery spasm in patients with drug-induced coronary artery spasm. METHODS AND RESULTS: The subjects were 74 patients with angiographically confirmed coronary artery spasm who were examined using accelerated exercise (ie, exercise that was accelerated every minute according to the protocol of Bruce and Horsten) following mild hyperventilation and who were not receiving any medication. ACh was injected in incremental doses of 20 microg and 50 microg into the right coronary artery and incremental doses of 20 microg, 50 microg, and 100 microg into the left coronary artery. Positive coronary spasm was defined as > or =99% luminal narrowing. Accelerated exercise following a mild hyperventilation test was as useful for detecting evidence of ischemia as was an ACh test (48 patients [64.9%] vs 49 patients [66.2%], respectively; not significant). No difference was observed between ischemic changes on ECG as a result of the newly combined method and the occurrence of ACh-induced spasm. ACh-induced coronary vasospasm occurred in 61 patients (82.4%). In the remaining 13 patients, intracoronary administration of ergonovine provoked coronary spasms. No serious irreversible complications were detected as a result of this newly combined method. CONCLUSIONS: The effectiveness of our newly combined procedure is equivalent to that of an ACh test to diagnose patients with coronary artery spasm.

Acetylcholine↗
PubMed2005

Hyperventilation in head injury: a review.

The aim of this review was to consider the effects of induced hypocapnia both on systemic physiology and on the physiology of the intracranial system. Hyperventilation lowers intracranial pressure (ICP) by the induction of cerebral vasoconstriction with a subsequent decrease in cerebral blood volume. The downside of hyperventilation, however, is that cerebral vasoconstriction may decrease cerebral blood flow to ischemic levels. Considering the risk-benefit relation, it would appear to be clear that hyperventilation should only be considered in patients with raised ICP, in a tailored way and under specific monitoring. Controversy exists, for instance, on specific indications, timing, depth of hypocapnia, and duration. This review has specific reference to traumatic brain injury, and is based on an extensive evaluation of the literature and on expert opinion.

Brain↗
PubMed2004

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia.

The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), alpha-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O2) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxia-induced hyperventilation (595 +/- 49 for KYN, N = 7 and 525 +/- 84 ml kg-1 min-1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 +/- 0.2 for KYN and 34.7 +/- 0.4 masculine C for MCPG) compared to saline (912 +/- 110 ml kg-1 min-1 and 34.8 +/- 0.2 masculine C, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction.

Animals↗
PubMed2002

Is hyperventilation-induced nystagmus more common in retrocochlear vestibular disease than in end-organ vestibular disease?

Hyperventilation-induced nystagmus (HVIN) has previously been shown by the senior author to be common in patients with both acoustic neuromas and following resection. The recurrent study's aim was to examine if HVIN was specific for retrocochlear pathology. To test this, the incidence of HVIN in 24 patients with confirmed acoustic neuroma was compared with its incidence in 38 patients with end-organ vestibular disease (defined as a greater than 25% reduction in caloric testing). Hyperventilation was carried out for 90 seconds. The results showed that 58% of the acoustic neuroma group were positive for HVIN versus 18% of the end-organ group. This difference was very significant on chi-square testing (p < .002). Hyperventilation-induced nystagmus appears to be much more prevalent in retrocochlear pathology than in end-organ pathology.

Adult↗
PubMedDate not supplied

Comparison of isocapnic hyperventilation and histamine or methacholine inhalation for the assessment of airway responsiveness.

Several stimuli have been used to evaluate the degree of airway hyperresponsiveness in asthma. Each of these has possible advantages and disadvantages when compared to the other methods. The most widely used involves the inhalation of chemical bronchoconstrictors, most commonly histamine or methacholine. This paper contrasts these inhalation tests with airway challenges using isocapnic hyperventilation of dry air. Isocapnic hyperventilation uses a naturally occurring stimulus to provoke bronchoconstriction rather than a chemical stimulus and can be administered in a dose-response fashion. Therefore, isocapnic hyperventilation may be particularly useful in epidemiologic surveys. The maximal dose administered, however, is determined by the level of a subject's maximal voluntary ventilation: also the equipment needed to administer the challenge is relatively complex when compared to other methods. By contrast, histamine and methacholine inhalation tests require simple, inexpensive equipment and can be inhaled at high concentrations, which means that airway responsiveness can be measured even in many nonasthmatic subjects. However, at high inhaled concentrations, histamine has many more systemic side effects than methacholine. Once the factors known to influence the measurements of airway responsiveness are controlled, the measurements made with one method correlate well with all other methods. Therefore, the method chosen will often depend on the requirements of the study or clinical laboratory.

Asthma↗
PubMed1979

Effects on fetal breathing movements of maternal challenges. Cross-over study on dynamic work, static work, passive movements, hyperventilation and hyperoxygenation.

Ten women in the last trimester of a normal pregnancy were subjected to five different loads in a cross-over study. Fetal breathing movements (FBM), fetal heart rate (FHR), maternal heart rate (MHR), and mean arterial pressure (MAP), maternal transcutaneously measured pO2 (Tc-pO2), and the energy supply to the Tc-pO2 electrode were recorded continuously before, during, and after the load. Maternal capillary pH and pCO2 were measured at three representative time points. The immediate responses of the incidence of FBM to the different challenges were: increase after dynamic work (bicycle test); no change after static work (isometric muscle contraction) and passive movements; decrease after hyperventilation and hyperoxygenation. FHR was unaffected by all challenges. The FBM incidence varied in parallel with pCO2 after dynamic work and hyperventilation and inversely with the Tc-pO2 rise caused by hyperoxygenation. Maternal pH was increased after passive movements (no change in FBM) and after hyperventilation (decreased incidence of FBM), FBM seem to be more sensitive to environmental changes than is the FHR. Mechanical stimuli to the uterus were not responsible for the augmentation of FMB seen after the bicycle test. The present observations reveal the multifactorial nature of the regulation of FBM, and support the role of CO2 as a major stimulator of breathing movements also in prenatal life.

Adult↗
PubMed1982

Fetal response to voluntary maternal hyperventilation. A preliminary report.

Maternal hyperventilation can cause transient reduction in fetal oxygen tension. Fifty women with normal and high-risk pregnancies, between the 32nd and 43rd week, were voluntarily hyperventilated; in 33, fetal heart rate (FHR) acceleration or transient tachycardia were observed (reactive FHR). Of the 33 pregnancies the outcome was good in 30 (91%) as judged by the absence of perinatal death, no fetal distress in labor and no intrauterine growth retardation (IUGR). In 14 patients in whom there was no FHR response to maternal hyperventilation (non-reactive FHR), the outcome of pregnancy was significantly worse; one infant died neonatally, 10 were either chronically (IUGR), or acutely distressed. Only in 3 was the outcome good (21%). The study showed that there is good correlation between a "reactive" FHR and favorable neonatal outcome, and between a "non-reactive" FHR and an unfavorable neonatal outcome.

Apgar Score↗
PubMedDate not supplied

Auditory brainstem responses in Rett syndrome: effects of hyperventilation, seizures, and tympanometric variables.

This study examined the effects of tympanometric variables, stage of disease, hyperventilation, and seizures on the auditory brainstem response (ABR) in Rett syndrome (RS). Thirty-four female children with RS ranging in age from 2 years, 3 months to 15 years, 7 months participated in the study. ABRs and tympanograms were recorded from all of the subjects. When the ABR peaks were identifiable, interpeak latency intervals (IPLIs) for I-III, III-V, and I-V were computed for each waveform. The peaks (I, III, and V) and IPLIs were characterized as abnormal if either the peaks were absent or the latencies were greater than 2 SD from the normative data (obtained on female children). Analyses revealed significant prolongation of wave I latencies in Rett children with abnormal tympanograms. ABR wave III latencies were significantly affected by the presence of seizures and hyperventilation. The Pearson chi-square statistic revealed significant differences in the rate of wave III and V abnormalities due to the presence and degree of hyperventilation and the presence of seizures. Wave I abnormalities were also observed in the presence of normal middle ear function, suggesting the presence of sensorineural hearing impairment in some RS children. Clinical implications of these findings are discussed.

Acoustic Impedance Tests↗
PubMed2004

Every breath you take: hyperventilation and intracranial pressure.

Hyperventilation can rapidly lower ICP, but because it induces a consistent reduction in CBF and because the effects on ICP are transient, the only role that hyperventilation plays in the management of intracranial hypertension is in the management of acute elevations in ICP. In these circumstances, hyperventilation can be life-saving and can temporize until more definitive treatment of the intracranial hypertension can be undertaken.

Humans↗
PubMed1993

Association between asbestos-related pleural plaques and resting hyperventilation.

This study reports an association between pleural plaques and resting hyperventilation in a group of workers exposed to asbestos. Information on exposure level, pack-years of cigarette smoking, chest radiographs, ventilation parameters, single-breath diffusing lung capacity, and arterial gases were obtained for 344 workers. After the exclusion of 37 workers for isolated parenchymal fibrosis, combined pleuroparenchymal fibrosis, or diffuse pleural thickening, 55 subjects with isolated pleural plaques were evaluated against 252 no-plaque workers. A quantitative pleural score revealed mild pleural disease. Forty-four workers with plaques (80%) had hypocapnia induced by resting hyperventilation. The quantitative pleural score correlated significantly with the partial pressure of carbon dioxide in arterial blood (correlation coefficient = 0.7). A decrement in forced vital capacity was associated with plaques, whether controlled for age, smoking, and exposure or not. It was concluded that the resting hyperventilation observed in some asbestos-exposed subjects is related to the presence of mild pleural plaques and a restrictive disorder.

Adult↗
PubMed1978

[Hyperventilation test in coronary disease: a comparison with a bicycle ergometer exercise test. Report of 100 cases].

A hundred cases have been studied and divided into three categories:--60 normal subjects;--30 coronary subjects with a positive exercise test;--10 subjects with defective nervous control of the circulation; using the exercise test, we studied the effects of hyperventilation on repolarisation of the ventricle. In the normal subjects there was no ischaemic depression of the ST segment, but there were minor changes in repolarisation which affected the T wave in 73% of subjects and were essentially posterior in distribution. In the coronary subjects, we found three with ischaemic depression of the ST segment and one with ST elevation of 2.5 mm (6.7% of the coronary subjects). This last finding is evidence against the commonly held hypothesis that reproduction of ST depression by hyperventilation during the exercise test indicates a false positive test. In the patients with defective nervous control of the circulation, 9 had an ischaemic type of ST depression, either as a new feature or as a more severe one compared with that found at rest. The mechanism by which these depressions are produced has not been totally explained:--in the cases with defective nervous control of the circulation, it appears that latent increased sympathetic activity is increased by the hyperventilation;--in the coronary subjects, it may be caused by true ischaemia or by an associated defect in nervous control of the circulation.

Adult↗
PubMed1999

[The mechanism of breathing under the conditions of prolonged voluntary hyperventilation].

Effects of voluntary hyperventilation (2 h, 70-80% of maximal lung ventilation) on external breathing, gas exchange and blood circulation were studied in 12 healthy male volunteers. Hyperventilation was shown to change structure of the respiratory cycle as variation and expiration time were decreased. Indices of the external breathing did not reduce but, on the contrary, there was a significant increase in the alveolar ventilation and a reduction in the dead space ventilation. Considerable losses of carbon dioxide with the expired air were noted only during initial 10-15 min of intensive breathing. The angular coefficient for the most steep section of the CO2 loss curve ranged from 150 to 200 ml/min as a result of which the total CO2 deficit in this period (i.e. the CO2 release exceeds the O2 consumption) was about 2 l. Hereafter, the CO2 deficit did not virtually increase despite intensive functioning of the external breathing system. This became apparent from the regain of the respiratory coefficient, a significant and gradually growing CO2 ventilation coefficient. Values of PETO2 and PETCO2 remained stable throughout the experiment with quite substantial hypocapnia: up to 15-20 mm Hg. Thus, the cardiorespiratory system has a powerful defence mechanism to prevent exacerbation of hypocapnia despite intensive ventilation of the alveolar space. This mechanism comes into action at the very first minutes of hyperventilation, reaches maximal efficiency within 10-15 min and maintains this level during the whole period of investigation (about 2 h).

Adult↗
PubMed2000

Cerebral oxygenation at high altitude and the response to carbon dioxide, hyperventilation and oxygen. The Birmingham Medical Research Expeditionary Society.

Cerebral oxygenation is likely to be of critical importance in determining function at high altitude. The present study has used the technique of near-IR spectroscopy to monitor changes in cerebral regional oxygenation in response to inhaled carbon dioxide, hyperventilation and supplementary oxygen on ascent to 4680 m over 3 days. At sea level, inhaled CO(2) resulted in a significant rise in cerebral regional oxygenation [from mean 69.6% (S.D. 2.4% to 71. 1+/-2.3%; means+/-S.D.; P<0.001). At 4680 m, CO(2) increased regional cerebral oxygenation (63.8+/-2.5% to 65.9+/-2.2%; P<0.001) and also increased peripheral oxygen saturation (75.1+/-6.1% to 83. 6+/-4.0%; P<0.001). Voluntary hyperventilation resulted in improved peripheral oxygen saturation at 2770 m, 3650 m and 4680 m, whereas cerebral regional oxygenation was reduced at sea level and at 2770 m, unchanged at 3650 m and increased at 4680 m. Supplementary oxygen (6 1itres/min) at 4680 m resulted in greater improvements in peripheral oxygen saturation (76.7+/-7.9% to 98.1+/-1.5%; P<0.001) and cerebral regional oxygenation (64.6+/-3.3% to 70.6+/-2.9%; P<0. 001) than were found with CO(2) or hyperventilation. We conclude that attempts to increase CO(2) inhalation or ventilation at high altitude are likely to be beneficial for cerebral oxygenation in the short term.

Adult↗
PubMed1979

[Hyperventilation and oxygen supply of the myocardium. II. Effect of nitroglycerin and dipyridamole].

1. Voluntary hyperventilation during rest in the recumbent position induces a fall in H+ concentration, PCO2 and PO2 in mixed venous blood and in the blood of the coronary sinus. 2. If the breathing volume is increased during voluntary hyperventilation between 2- and 2.5 fold above the volume at rest, O2 uptake increases by only 6% but CO2 excretion rises by 66%. 3. Cardiac output decreases by 8% and the O2 extraction of the myocard increases by 12%. There is a quantitative relationship between arterial pH or PCO2 and changes in the systemic and coronary circulation. Blood pressure decreases in the pulmonary circulation. 4. Nitroglycerin during hyperventilation produces an additional reduction in cardiac output but no effect on the O2 extractions of the myocard. 5. With dipyridamol, the O2 extraction of the myocard is reduced and the PO2 in the blood of the coronary sinus increases. 6. In the case of severe coronary obstruction, the effect of dipyridamol can cause acute angina pectoris and left heart insufficiency due to poststenotic ischemis (steal syndrome).

Adult↗