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At least 289 records · Page 16Linked to original sources
PubMed2002

Voluntary hyperventilation into a simple mixing chamber relieves high altitude hypoxia.

Involuntary hyperventilation is a critical factor in acclimatization to a high altitude. Unacclimatized subjects do poorly when acutely exposed to high altitude. This may not be due to hypocapnia itself, but rather an associated symptom which inhibits hypoxic respiratory stimulation. In an unacclimatized individual, voluntary hyperventilation may greatly relieve hypoxia and may be an alternative to involuntary hyperventilation. However, subjects voluntarily hyperventilating may overventilate and become disabled from severe hypocapnia. A simple mixing chamber is described which makes voluntary hyperventilation easier, safer, and possibly more effective. A subject breathing into a mixing chamber was able to maintain an SaO2 of 90% at 20,000 ft.

Adult↗
PubMedDate not supplied

[Differential approach to the application of hyperventilation in acute period of severe brain injury in relation to cerebral circulation].

Seventeen patients with severe brain injury (Glasgow-8 Coma Scale 3-8 scores) complicated by traumatic subarachnoidal hemorrhage and severe cerebral hemodynamic disorders (hyperemia, vasospasm) were examined. Hyperventilation was performed in different phases of cerebral circulation under multiparametrical monitoring (intracranial pressure, cerebral perfusion pressure, jugular oximetry, Doppler study using the carotid compression test). The use of hyperventilation to eliminate intracranial hypertension in victims with brain hyperemia was shown to make cerebral circulation consistent with brain tissue oxygen demands and to improve the autoregulatory reserve of cerebral vessels. The application of hyperventilation to eliminate intracranial hypertension in vasospasm leads to a temporary reduction in intracranial pressure, but simultaneously causes cerebral circulatory changes that do not correspond to cerebral oxygen demands, as well as lowered cerebral perfusion pressure, which increases a risk for ischemic brain tissue lesion. This requires a strict rationale for the use of hyperventilation and for multiparametrical monitoring of cerebral functions, which includes jugular oximetry, Doppler transcranial study, and measurement of intracranial pressure throughout the hyperventilation period in order to prevent secondary brain lesion.

Adolescent↗
PubMed1989

[Use of controlled hyperventilation in the treatment of comatose patients with cranial injuries].

Controlled hyperventilation is a recognized method by which it is possible to reduce the intracerebral blood volume and thus the intracranial pressure (ICP). In the review, the physiological conditions involved in the regulation of ICP are illustrated, particularly in connection with acute cranial traumata and effect of controlled hyperventilation in these situations is discussed. Controlled hyperventilation is recommended in the hyperacute phase for all patients with cranial trauma prolonged impairment of consciousness (Glasgow Coma Scale less than 7 for more than 30 minutes) and other clinical evidence of expanding space-occupying intracranial process. Prolonged hyperventilation is recommended for younger patients as these have most frequently hyperaemia and retained CO2 reactivity and for patients with predominantly cortical lesions as assessed by CT scanning. Caution in the employment of hyperventilation is advised in elderly patients, severely traumatized patients and late in the course of cerebral trauma.

Adult↗
PubMed1983

Controlled hyperventilation in patients with intracranial hypertension. Application and management.

When elevated intracranial pressure (ICP) complicates the course of various forms of cerebral edema, the likelihood of survival with full recovery is greatly diminished. Controlled mechanical hyperventilation effectively lowers ICP in some patients by causing cerebral vasoconstriction. Improved survival occurs in patients with elevated ICP from head trauma and intracranial infection treated with hyperventilation; however, no benefit has been demonstrated in patients with increased ICP from strokes or hypoxic brain damage. Proper management of the hyperventilation requires knowledge of basic cerebral circulatory physiology. Arterial Paco2 tensions should be maintained between 25 and 30 mm Hg. Vasoconstrictive effects of hyperventilation diminish after 48 to 72 hours when renal mechanisms compensate for the respiratory alkalosis. When hyperventilation is discontinued, the Paco2 must be gradually returned to normal values, since sudden changes may cause a marked rise in ICP.

Brain↗
PubMed1999

Functional imaging of the visual cortex with bold-contrast MRI: hyperventilation decreases signal response.

Hypocapnia due to hyperventilation reduces cerebral blood flow and volume. To investigate the effects of hyperventilation on the regional signal response to visual activation using blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI), six volunteers were investigated during visual stimulation under normocapnia and hypocapnia conditions. Hyperventilation significantly decreased in visual cortex the BOLD MRI response to visual stimulation (3.97+/-0.5% [mean ( SD) in normocapnia vs. 0.77+/-0.7% in hypocapnia, P < 0.01]. In three of six subjects, functional signal changes were reduced to noise level. The reduced stimulus response during hyperventilation is probably due to a decreased overshoot in the blood oxygenation response. These results indicate that BOLD-contrast functional MRI is highly sensitive to pCO2 changes.

Adult↗
PubMed1997

The hyperventilation of cirrhosis: progesterone and estradiol effects.

Progesterone and estradiol are metabolized in the liver and are elevated in patients with cirrhosis. Progesterone stimulates ventilation by activating progesterone receptors in the central nervous system; estradiol may facilitate progesterone's actions by increasing progesterone receptors. This study evaluated whether progesterone and estradiol contribute to the respiratory alkalosis common in cirrhotic patients. Arterial blood gases and progesterone and estradiol levels were obtained in 50 patients with cirrhosis. Multiple linear regression revealed a statistically significant correlation between PaCO2 and progesterone and estradiol (r = .54, P < .05). Patients with severe hyperventilation (PaCO2 < or = 30 mm Hg) had statistically higher levels of progesterone and estradiol than did patients with mild hyperventilation (30 < PaCO2 < or = 35) or normal ventilation (PaCO2 > 35) (P < .05). Although the progesterone levels were two orders of magnitude lower than those associated with hyperventilation in pregnant patients, the increased ventilatory effect may be because of the altered blood-brain barrier (BBB) present in cirrhotic patients. Progesterone and estradiol appear to contribute to the hyperventilation in cirrhotic patients.

Adult↗
PubMedDate not supplied

Breath-holding in healthy and pulmonary-compromised populations: effects of hyperventilation and oxygen inspiration.

Suspension of respiration during end-expiration often is recommended to minimize body organ displacement between sequential image acquisitions. The purpose of this report is to evaluate techniques for end-expiratory breath-holding applicable to a pulmonary-compromised population. Eighty-seven consecutive outpatients with chronic pulmonary diseases and 31 healthy nonsmoking volunteers were recruited for the study. All subjects were asked to hold their breath in end-expiration while in the supine position (29 after breathing room air, 29 after hyperventilating room air for six breaths, and 29 after breathing O2 from a portable oxygen tank via nasal cannula until pulse-oximeter readings stabilized or reached 100%). Each volunteer was tested with all three methods. The mean length of time for a breath-hole on room air without hyperventilation was 9.2 seconds for the patients and 31.7 seconds for the volunteers. A breath-hold after hyperventilation of room air was timed at 12.3 seconds for the patients and 41.2 seconds for the volunteers, and after O2 administration, the breath-hold was 22.4 seconds for the patients and 60.9 seconds for the volunteers. No adverse effects occurred. The pulmonary-compromised patient can suspend respiration most successfully after O2 administration (P < .0001), whereas hyperventilation seems to be less beneficial. Nonpulmonary-compromised volunteers can hold their breath for longer periods of time.

Adult↗
PubMed1980

Hyperventilation and vertigo.

An electronystagmographic study was conducted on 19 normal subjects, in order to observe whether the subjective sensation of dizziness provoked by hyperventilation could be confirmed objectively by nystagmus. Each of them had two electronystagmograms, the first being a routine ENG and the second a repetition of the first, but with additional periods of 90 sec. of hyperventilation at certain precise pre-determined moments of the test. Hyperventilation was not shown to have significant effect on the slow phase of post caloric nystagmus; however, it increased significantly (p = 0.061) the number of positions in which nystagmus was elicited. Hyperventilation would have such an effect in producing a certain degree of cerebral hypoxia through cerebral vasoconstriction and the Bohr effect.

Adult↗
PubMed1997

In vivo measurement of regional brain metabolic response to hyperventilation using magnetic resonance: proton echo planar spectroscopic imaging (PEPSI).

A new rapid spectroscopic imaging technique with improved sensitivity and lipid suppression, referred to as Proton Echo Planar Spectroscopic Imaging (PEPSI), has been developed to measure the 2-dimensional distribution of brain lactate increases during hyperventilation on a conventional clinical scanner equipped with a head surface coil phased array. PEPSI images (nominal voxel size: 1.125 cm3) in five healthy subjects from an axial section approximately 20 mm inferior to the intercommissural line were obtained during an 8.5-min baseline period of normocapnia and during the final 8.5 min of a 10-min period of capnometry-controlled hyperventilation (end-tidal PCO2 of 20 mmHg). The lactate/N-acetyl aspartate signal increased significantly from baseline during hyperventilation for the insular cortex, temporal cortex, and occipital regions of both the right and left hemisphere, but not in the basal ganglia. Regional or hemispheric right-to-left differences were not found. The study extends previous work using single-voxel MR spectroscopy to dynamically study hyperventilation effects on brain metabolism.

Adult↗
PubMed1995

Effect of angiotensin converting enzyme inhibition on airway conductance during hypocapnic hyperventilation in normal subjects.

In nine normal subjects, specific airway conductance was measured by whole body plethysmography before and immediately after hypocapnic hyperventilation. This procedure, forced expiratory manoeuvres and arterial blood pressure measurements were carried out before and 4 h after placebo and the angiotensin converting enzyme inhibitor, enalapril, in a double-blind, randomized study design. Bronchoconstriction to hypocapnic hyperventilation was shown by a reduction in specific airway conductance on all occasions (P < 0.001). A reduction in mean blood pressure was obtained after enalapril compared to placebo (P < 0.05). No significant change attributable to enalapril was observed in any lung function measurement either at rest or immediately after hypocapnic hyperventilation, despite an expected enhancement of endogenous angiotensin converting enzyme activity by alkalosis. Inhibition of angiotensin converting enzyme revealed no effect of the endogenous activity of this enzyme on airway calibre either at rest or during the bronchoconstrictor response to hypocapnic hyperventilation.

Adolescent↗
PubMed1996

Cerebral hypoxia after hyperventilation causes "re-build-up" phenomenon and TIA in childhood moyamoya disease. A near-infrared spectroscopy study.

Near-infrared spectroscopy was used to monitor the sequential changes in the cerebral oxygenation state during and after hyperventilation in two children with moyamoya disease. Hyperventilation induced the build-up phenomenon and a decrease in the concentration of oxy-hemoglobin ([oxy-Hb]) and total hemoglobin ([t-Hb]). The termination of hyperventilation was followed by partial recovery of [oxy-Hb] and [t-Hb]. Subsequently, however, [oxy-Hb] and [t-Hb] decreased again and cytochrome oxidase was reduced. These impairments of the cerebral hemodynamics and oxygen metabolism were closely associated with the re-build-up phenomenon on EEG and with transient ischemic attacks (TIA). The present study implies that cerebral hypoxia after hyperventilation is closely related to the re-build-up phenomenon and ischemic attacks in children with moyamoya disease.

Anastomosis, Surgical↗
PubMed1976

[Effect of hyperventilation on cerebral blood flow and metabolism in man; continuous monitoring of arterio-cerebral venous glucose differences (author's transl)].

CBF decreases when arterial PCO2 is lowered by physiological, pathological or therapeutically induced hyperventilation. This is accompanied by an undelayed compensatory increase of oxygen-av-differences. Continuous monitoring of enzymatically determined glucose-av-differences of the brain during hyperventilation has for the first time shown that there is an undelayed fall of the cerebral venous glucose content, too. This indicates that the brain cells extract an augmented amount of glucose per ml blood during decreased CBF. Therefore glucose metabolism of the brain is not impaired during non-critical CBF reduction. However, when arterial PCO2 falls below 25 mmHg a detrimental effect on CBF and cerebral metabolism has to be expected. CBF will then decrease below the critical threshold for an undisturbed oxygen supply, and the respiratory alcalosis will lead to a disturbed oxygen delivery due to the Bohr-effect. As a consequence both of these factors will reduce the energy-yielding oxydative glycolysis and augment the little energy producing anaerobic glycolysis with a concomitant increase of lactate formation, resulting in a tissue and spinal fluid lactate acidosis. From our results it is therefore concluded that induced hyperventilation should be avoided, and that central hyperventilation in diseased states has to be considered as an additional threat to the brain.

Acidosis↗
PubMed1983

Effect of CO2-induced hyperventilation on carbon tetrachloride (CCl4) levels following acute CCl4 poisoning.

To study under standardized experimental conditions the effect of a CO2-induced hyperventilation therapy on carbon tetrachloride (CCl4) levels following acute CCl4 poisoning, rats received 2.5 ml CCl4/kg BW by gastric intubation and were subsequently either treated by CO2-induced hyperventilation or kept in an atmosphere containing air. Peak levels of CCl4 were observed in the fat, liver and blood 3-6 h after the intoxication and were found to be considerably lower in animals treated by CO2-induced hyperventilation compared to their respective controls. These data therefore strongly support the efficacy of the CO2-induced hyperventilation therapy for CCl4 intoxication.

Adipose Tissue↗
PubMed2004

Whole-brain vascular reactivity measured by fMRI using hyperventilation and breath-holding tasks: efficacy of 3D prospective acquisition correction (3D-PACE) for head motion.

Functional MR imaging (fMRI) study using hyperventilation and breath-holding task has been reported to be one of the non-invasive methods to examine whole-brain vascular reactivity. The purpose of this study was to evaluate the efficacy of a method for 3D prospective detection and correction of head motion (3D-PACE) in a study of whole-brain vascular reactivity using hyperventilation and breath-holding tasks. Eight healthy volunteers were scanned using an fMRI protocol of hyperventilation and breath-holding task blocks at 3 T in separate runs with and without 3D-PACE. In two subjects, two more runs with and without 3D-PACE were repeated. The mean total number of activated voxels +/- standard deviation was 26,405.3+/-1,822.2 in the run with 3D-PACE and 17,329.9+/-2,766.3 in the run without 3D-PACE ( P<0.05), although there is some intersubject variation regarding the effect of 3D-PACE. In the two subjects whose performed two more runs, the number of activated voxels were smaller in the run without 3D-PACE than even in the run with 3D-PACE performed later. We conclude that 3D-PACE is beneficial for fMRI studies of whole-brain vascular reactivity induced by hyperventilation and breath-holding.

Adult↗
PubMed2005

Predicting the response of intracranial pressure to moderate hyperventilation.

BACKGROUND: Hyperventilation may cause brain ischaemia after traumatic brain injury. However, moderate reductions in PaCO(2) are still an option in the management of raised intracranial pressure (ICP) under some circumstances. Being able to predict the ICP-response to such an intervention would be advantageous. We investigated the ability of pre-hyperventilation ICP and cerebrospinal compensatory reserve to predict the reduction in ICP achievable with moderate hyperventilation in head injured patients. METHODS: Thirty head injured patients requiring sedation and mechanical ventilation were investigated. ICP was monitored via an intraparenchymal probe and intracranial cerebrospinal compensatory reserve was assessed using an index (R(ap)) based on the relationship between mean ICP and its pulse amplitude. Measurements were made at a constant level of PaCO(2) during a 20-minute baseline period. The patients were then subjected to an acute decrease in PaCO(2) of approximately 1 kPa and, after an equilibration period of 10 minutes, measurements were again made at a constant level of PaCO(2) for a further 20 minutes. A multiple linear regression model, incorporating baseline PaCO(2), ICP, and R(ap) was used to identify the relevant predictors of ICP reduction. FINDINGS: Baseline ICP and R(ap) were both significant predictors of ICP-reduction (p=0.02 and 0.001 respectively) with R(ap) being the more powerful parameter. CONCLUSIONS: A model based on cerebrospinal compensatory reserve and ICP can predict the achievable ICP-reduction and may potentially be used to optimise patient selection and intensity of hyperventilation.

Adult↗
PubMed1982

The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina.

In 10 cases of Prinzmetal's angina in which episodes of myocardial ischemia were easily and reproducibly induced by hyperventilation, this test was performed 111 times, 41 times under control conditions and 70 times during treatment with one or more of the following drugs: phentolamine, isosorbide dinitrate, propranolol, verapamil, nifedipine and amiodarone. Seventeen of 18 negative tests performed under the influence of a long-acting drug coincided with total remission of the patient's anginal episodes when this drug was administered on a short- or long-term basis. No patient died or sustained infarction during a follow-up period of 10.9 months. A negative test was thus a good indication that the clinical response to the corresponding drug would be favorable. The electrocardiographic changes and chest pain provoked by hyperventilation occurred not when alkalosis was greatest (hydrogen ion [pH] change from 7.42 to 7.58, p less than 0.001), but when pH was approaching normal or control values. The onset of electrocardiographic changes occurred an average of 175 seconds after the end of hyperventilation and, in two cases, the time lag was as much as 480 and 705 seconds, respectively. This raises several questions regarding the true mechanism triggering coronary spasm under such conditions. The hyperventilation test appears to be a useful and safe procedure for selecting the best possible drug for long-term treatment of Prinzmetal's angina as well as for comparing the relative efficacy of different drugs.

Adult↗
PubMed1990

Usefulness of the hyperventilation test in stable exertional angina pectoris in selecting medical therapy.

To assess the prevalence of abnormal coronary vasoconstriction in stable exertional angina and to evaluate whether the presence of increased coronary tone may have therapeutic implications, we studied 83 consecutive patients with typical exertional angina, positive response to exercise stress testing and documented coronary artery disease. Abnormal coronary vasoconstriction was induced by a hyperventilation test in 16 patients (group I) while the remaining 67 had a negative response (group II). No differences were observed between the 2 groups with regard to clinical, exercise and angiographic data. All group I patients and 16 patients in group II repeated hyperventilation and exercise tests after the administration of dihydropyridine-type calcium antagonists (7 patients nifedipine, 9 patients felodipine). After treatment 15 of 16 group I patients had a negative response to the hyperventilation test. The total exercise duration was significantly increased (278 +/- 183 vs 554 +/- 248 seconds; p less than 0.001) with higher values of rate pressure product at peak exercise (168 +/- 47 vs 235 +/- 67 mm Hg x beats/min/100; p less than 0.0025). In group II no significant differences were observed between pre- and posttreatment values for total exercise duration (244 +/- 210 vs 308 +/- 243 seconds) and rate pressure product at peak exercise (170 +/- 46 vs 188 +/- 56 mm Hg x beats/min/100). These data show that the hyperventilation test can be used to select a subset of patients with stable exertional angina and detectable abnormal coronary vasoconstriction who will improve their exercise tolerance with coronary vasodilator treatment.

Angina Pectoris↗
PubMed1989

Behavioral treatment of angina-like chest pain in patients with hyperventilation syndrome.

The hyperventilation syndrome is present in as many as 50% of patients with non-cardiac chest pain. This study evaluated a behavioral treatment of this disorder in three adult females. They had long histories of chest pain and were documented to be free of coronary artery disease. Each subject met the DSM-III-R diagnostic criteria for an anxiety disorder. Following treatment, all subjects showed a marked decrease in the frequency and intensity of chest pain episodes and in the frequency of shortness of breath episodes. Two subjects maintained their progress at one-year follow-up. The results lend support to the efficacy of controlled breathing and relaxation training for the treatment of hyperventilation-related chest pain and to the inclusion of a hyperventilation provocation test in the diagnosis of the syndrome as well as its role in changing cognitions regarding cardiac status. Also discussed is the rationale for treating hyperventilation related chest pain in a medical care setting.

Anxiety Disorders↗