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PubMed1990

Comparative effects of volume history on bronchoconstriction induced by hyperventilation and methacholine in asthmatic subjects.

The aim of this study was to find out if bronchodilatation following deep inspiration can be induced by the inhalation of a "natural" stimulus (hyperventilation of cold dry air), and if the effect is similar to that induced by methacholine. After baseline assessment of lung resistance (RL), 10 asthmatic subjects were asked to inhale cold dry air for 3 min. RL was monitored continuously for 3-4 min, at which time subjects were asked to take a fast deep inspiration. After recovery, the manoeuvre was repeated and RL was reassessed. The manoeuvre was then repeated a third time. After functional recovery, progressive doses of methacholine were inhaled until the increase in RL was comparable to that obtained after hyperventilation (56 +/- 16% and 65 +/- 24%, respectively, mean +/- SD, NS). The same deep inspiration manoeuvre was repeated three times with recovery as after hyperventilation of cold dry air. Maximum changes in RL were not significantly different after each of the three manoeuvres for either type of bronchoconstriction. The mean fall in RL was 14.2 +/- 9.9% after hyperventilation and 16.4 +/- 10.5% after methacholine. There was a satisfactory correlation (r = 0.80, p less than 0.01) between the bronchodilatation after deep inspiration for both types of stimuli. We conclude that the bronchodilator effect of deep inspiration is no different using either a pharmacological stimulus (methacholine) or a "natural" stimulus (hyperventilation of unconditioned air). These results show that assessing the response to hyperventilation with manoeuvres requiring deep inspiration, forced expiratory volume in one second (FEV1) may alter airway tone in a way similar to pharmacological stimuli.

Asthma↗
PubMed1987

Hyperventilation-induced changes in periodic oscillations in forehead skin blood flow measured by laser Doppler flowmetry.

Rhythmic oscillations in forehead skin blood flow were studied with the laser Doppler technique in thirteen healthy subjects. During voluntary hyperventilation, a three-fold increase in relative amplitude of the spontaneous rhythmic oscillations in forehead skin blood flow was observed, whereas mean blood flow decreased by 15%. During hyperventilation, the relative amplitude of the oscillations was on average 36% of the mean blood flow value. The mean incidence of the oscillations increased significantly, from 68% of the measuring time before, to 96% of the measuring time during hyperventilation. The oscillation frequency was not affected by hyperventilation. Before, during and after hyperventilation the average oscillation frequency was 0.140 Hz (8.4 min-1), 0.145 Hz (8.7 min-1) respectively. The application of heat or a local anaesthetic to the skin attenuated the relative amplitude of the oscillations in forehead skin blood flow during hyperventilation as well as before and after.

Adult↗
PubMed1987

[Bronchial provocation tests using hyperventilation].

The appearance of an asthmatic crisis in the minutes following physical exercise is common in symptomatic asthma. Exercise induced asthma (EIA) is linked to hyperventilation; voluntary isocapnic hyperventilation is capable of triggering a crisis. It is well established at present that EIA and post-hyperventilation asthma (HIA) are triggered by a rise in heat and water loss by the airways, which is inherent in hyperventilation. The respective role of water loss and cooling the airways are uncertain but one tends to think at the present time that the primary stimulus is the variation in osmolality of the liquid lining the epithelium. However, a relationship between the quantity of energy dissipated in the airways and the severity of EIA or HIA exists, although it is less tight than was once thought. This is perhaps not surprising, as the intermediary mechanisms connecting the stimulus to the response of the airways are poorly understood. All in all physical exercise and isocapnic hyperventilation of dry air and possibly cold air are useful and equivalent non-specific bronchial provocation tests, if only the ventilation and physical properties of the inhaled air are the same. Hyperventilation lends itself better than exercise to establishing dose-effect curves linking bronchial response to minute ventilation. Recommendations concerning the interruption of drugs, the measurement of the response and the assessment of the results are the same as with other non specific bronchial provocation tests with irritant substances or pharmacological agents.

Asthma, Exercise-Induced↗
PubMed1995

[Effects of a beta 2-agonist, sodium cromoglycate, and an anticholinergic agent on hyperventilation-induced bronchoconstriction in sensitized rabbits].

Hyperventilation can induce bronchoconstriction in ovalbumin-sensitized rabbits. To investigate the roles of the beta-receptor parasympathetic nervous system and of chemical mediators in hyperventilation-induced bronchoconstriction (HIB), the effects of a beta 2-agonist, of sodium cromoglycate, and of an anticholinergic agent on HIB were studied. Rabbits were divided to four groups and treated as follows. Group 1: Control (n = 7, 0.9% saline); Group 2: Procaterol (n = 4, 50 micrograms/l); Group 3: Sodium cromoglycate (n = 4, 10 mg/ml); and Group 4: Ipratropium bromide (n = 6, 1 mg/ml). Each drug was inhaled for 1 min via an ultrasonic nebulizer. Then, for the eucapnic hyperventilation challenge, sensitized rabbits were mechanically hyperventilated for 15 min (120 breaths/min, tidal volume = 7 ml/kg) with dry air containing 5% CO2 at room temperature. Total lung resistance and dynamic compliance were measured before, and 0, 5, 15, and 30 min after hyperventilation. The mean percent change in resistance measured 5 min after the hyperventilation was +49% in group 1, -6% in group 2, +23% in group 3, and +1% in group 4. The changes in groups 2 and 4 were significantly less than in group 1 (p < 0.05). In conclusion, HIB is mainly caused by bronchial smooth muscle constriction, and chemical mediators and the parasympathetic nervous system may play important roles in the development of HIB in sensitized rabbits.

Acetylcholine↗
PubMed1995

[Electrolyte changes during and after voluntary hyperventilation].

Paresthesia and tetanic finger cramps during hyperventilation-induced respiratory alkalosis are believed to derive from a pH-dependent decrease of ionized serum calcium. In the study reported here, ionized serum calcium, total calcium and total protein were measured during a three-minute hyperventilation period in ten volunteers. During hyperventilation finger paresthesias appeared in all probands without proof of any significant change in ionized serum calcium (1.26 +/- 0.05 mmol/l at the end of the three-minute hyperventilation period). Total protein increased as a consequence of hyperventilation-induced transient hemo-concentration. Paresthesias and tetanic finger cramps during the three-minute hyperventilation could not be related to changes of ionized serum calcium; however the other electrolytes, i.e. sodium, magnesium, potassium, chloride, phosphate and bicarbonate, showed, with the exception of sodium, significant changes.

Adult↗
PubMed1993

[Hyperventilation: not a cause of panic attacks].

OBJECTIVE: To investigate the importance of hyperventilation in the pathogenesis of panic attacks. DESIGN: Descriptive. SETTING: The Jelgersma Outpatient Clinic at Oegstgeest and the University Hospital Leiden, the Netherlands. METHOD: In 57 psychiatric patients with a panic disorder and 96 somatic patients with unexplained somatic complaints suggestive of hyperventilation, a Hyperventilation Provocation Test (HVPT) was conducted. Of the somatic patients, 33 had recently experienced a panic attack. During the test, various physiological and symptom criteria for the Hyperventilation Syndrome were assessed. Several measures for concomitant psychopathology were collected as well. RESULTS: No significant differences were found in physiological criteria for the Hyperventilation Syndrome between psychiatric patients with a panic disorder (PD) and somatic patients with (PA+) or without (PA-) a recent panic attack. On all symptom criteria, however, PD and PA+ patients obtained comparable scores, while both groups scored higher than PA- patients. On most measures for concomitant psychopathology, PD patients scored higher than PA+ patients, who on their part scored higher than PA- patients. CONCLUSION: Hyperventilation is of secondary importance in the pathogenesis of panic attacks and an early diagnosis of panic attacks or panic disorder may be conducive to more adequate treatment.

Adolescent↗
PubMed1993

Hyperventilation in patients with recurrent functional symptoms.

In view of the similarity between the reported effects of hyperventilation and recurrent functional symptom presented in primary care, a study was undertaken to establish whether such symptoms are attributable to hyperventilation. Twenty patients with two or more recurrent functional symptoms which their doctors found difficult to diagnose or treat, and 30 controls, were studied using symptom questionnaires and a series of hyperventilation provocation tests during which the partial pressure of carbon dioxide (PCO2) and symptoms were recorded. Sixteen cases (80%) had unexplained breathlessness compared with two of the controls (7%). All of the cases recognized familiar functional symptoms during provoked hyperventilation, and in 16 (80%), these included primary physical symptoms; only 23% of the controls recognized any previously experienced symptom. Considerable overlap of PCO2 values between groups meant that absolute values of PCO2 were not useful in differentiating between groups, but cases were more likely than controls to have a PCO2 of less than 4 kPa at rest, three minutes after hyperventilation, or during mental stress (75% of cases fulfilled one or more of these criteria versus 40% of controls). This is the first study in primary care to examine the effect of hyperventilation in a group of patients with multiple somatic symptoms. The findings have implications for the recognition and management of such patients.

Adult↗
PubMedDate not supplied

Hyperventilation-induced cerebral ischemia in patients with acute brain lesions: demonstration by xenon-enhanced CT.

PURPOSE: To examine the possibility that hyperventilation, commonly used to prevent or treat increased intracranial pressure in patients with acute brain lesions, may induce significant cerebral ischemia. METHODS: Local cerebral blood flow and vascular reactivity were measured before and after hyperventilation using xenon-enhanced CT in 12 patients with acute brain lesions. RESULTS: Five patients showed "paradoxical" reactivity (increased cerebral blood flow during hyperventilation) within the lesions. In five patients, hyperventilation induced ischemia in apparently normal regions of brain. In three patients, areas of luxury perfusion became ischemic during hyperventilation, while in three patients, lesions with moderate ischemia became more ischemic. Most patients showed more than one type of reactivity. CONCLUSIONS: These findings document hyperventilation-induced ischemia in acute brain lesions, and demonstrate that this phenomenon affects both injured and apparently intact areas of the brain. Further studies are required to determine the clinical significance of these pathophysiologic changes.

Acute Disease↗
PubMedDate not supplied

Refractoriness to bronchoconstriction following hyperventilation with cold dry air.

Fifteen subjects undertook repeated periods of hyperventilation of cold dry air and hyperventilation of warm humidified air followed by cold dry air. Hyperventilation of cold dry air induced a biphasic response with initial bronchodilatation followed by bronchoconstriction. However, exercise produced a greater rise in forced expiratory volume in 1 second (FEV1) than hyperventilation alone. Hyperventilation of cold dry air resulted in a period of refractoriness to a second stress of the same type. Refractoriness induced by exercise or hyperventilation of cold dry air may be the result of refractoriness of the trigger site in the large airways.

Adolescent↗
PubMed2002

Diagnosis of vasospastic angina by hyperventilation and cold-pressor stress echocardiography: comparison to I-MIBG myocardial scintigraphy.

OBJECTIVES: We assessed the usefulness of hyperventilation and cold-pressor stress echocardiography in the diagnosis of vasospastic angina compared with that of iodine-123 metaiodobenzylguanidine (123I-MIBG) myocardial scintigraphy. BACKGROUND: Various noninvasive methods have been used to detect vasospastic angina, but they are not very sensitive in the diagnosis of vasospastic angina. 123I-MIBG images and stress echocardiography have recently been proposed as a useful tool for detecting vasospastic angina. METHOD: Thirty patients (21 males and 9 females, mean age: 52 +/- 14 years) who complained of rest angina were enrolled for this study. The hyperventilation and cold-pressor stress echocardiography test consisted of hyperventilation for 6 minutes, followed by cold water pressor for 2 minutes under continuous electrocardiographic and echocardiographic monitoring. Left ventricular regional wall motion by echocardiogram was analyzed by using the 16-segment model, and wall motion ranging from normokinesis to dyskinesis was evaluated visually in each segment. Single-photon emission computed tomography images of 123I-MIBG myocardial scintigraphy were divided into 26 segments. Defect scores were established using the 4 grades. The echocardiographic criteria for coronary spasm was worsening wall motion and the scintigraphic criteria was defect score more than moderately reduced. Acetylcholine was selectively injected into the right coronary artery (20 microg and 50 microg) and left coronary artery (20 microg, 50 microg, and 100 microg). RESULTS: Of 30 patients, 20 patients had coronary spasm on coronary angiography with an intracoronary injection of acetylcholine, whereas 10 patients showed no spasm. Multivessel spasms were observed in 15 patients. Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy of hyperventilation and cold-pressor stress echocardiography for diagnosing in patients with vasospastic angina were 90%, 90%, 95%, 82%, and 90%, respectively. However, those of 123I-MIBG myocardial scintigraphy for diagnosing in patients with vasospastic angina were 90%, 40%, 75%, 67%, and 73%, respectively. The specificity of hyperventilation and cold-pressor stress echocardiography was significantly higher than that of 123I-MIBG myocardial scintigraphy (P <.05). CONCLUSION: The specificity of hyperventilation and cold-pressor stress echocardiography in diagnosing coronary spasm were higher than that shown by 201I-MIBG myocardial scintigraphy.

3-Iodobenzylguanidine↗
PubMed2001

Isocapnic hyperventilation increases carbon monoxide elimination and oxygen delivery.

Hyperventilation with mixtures of O2 and CO2 has long been known to enhance carbon monoxide (CO) elimination at low HbCO levels in animals and humans. The effect of this therapy on oxygen delivery (DO2) has not been studied. Isocapnic hyperventilation utilizing mechanical ventilation may decrease cardiac output and therefore decrease DO2 while increasing CO elimination. We studied the effects of isocapnic hyperventilation on five adult mechanically ventilated sheep exposed to multiple episodes of severe CO poisoning. Five ventilatory patterns were studied: baseline minute ventilation (RR. VT), twice (2. RR) and four times (4. RR) baseline respiratory rate, and twice (2. VT) and four times (4. VT) baseline tidal volume. The mean carboxyhemoglobin (HbCO) washout half-time (t1/2) was 14.3 +/- 1.6 min for RR. VT, decreasing to 9.5 +/- 0.9 min for 2. RR, 8.0 +/- 0.5 min for 2. VT, 6.2 +/- 0.5 min for 4. RR, and 5.2 +/- 0.5 min for 4. VT. DO2 was increased during hyperventilation compared with baseline ventilation for 2. VT, 4. RR, and 4. VT ventilatory patterns. Isocapnic hyperventilation, in our animal model, did not alter arterial or pulmonary blood pressures, arterial pH, or cardiac output. Isocapnic hyperventilation is a promising therapy for CO poisoning.

Animals↗
PubMed1987

How hyperventilation alters the electroencephalogram: a review of controversial viewpoints emphasizing neurophysiological mechanisms.

This paper reviews the literature on the EEG effects of hyperventilation, with particular emphasis on the literature concerning the mechanism of EEG slowing with hyperventilation. We suggest that there is no definite evidence to support the theory that the EEG slowing and "activation" are caused by hypoxia secondary to cerebral vasoconstriction induced by hypocapnia during voluntary hyperventilation. Since it is known that hypocapnia produces decreased activity in the mesencephalic reticular formation and that lesions of the thalamus abolish the hyperventilation response, we propose a strong, albeit speculative, analogy between awake-sleep transitory states and the mechanism of EEG "activation" by hyperventilation. Furthermore, it is proposed that both the EEG changes and the associated clinical symptomatology (as well as changes in level of anesthesia, which vary with arterial PCO2) may be explained by altered arousal, and that the vasoconstriction observed during hyperventilation is a central neurogenic response to hypocapnia at a brainstem level.

Electroencephalography↗
PubMedDate not supplied

Bronchial response to hyperventilation of dry air at room temperature in normals and asthmatics.

The bronchial effects of three levels (25, 40 and 60 1 X min-1) of voluntary isocapnic hyperventilation of dry air at room temperature (20-22 degrees C) have been studied in 18 normal, non-atopic subjects and in 25 nonperennial asthmatics who were asymptomatic and whose airway obstruction at the time of the study was mild, with a peak expiratory flow rate of 6.1 +/- 1.5 (SD) 1 X s-1 vs a predicted 8.4 +/- 1.3 1 X s-1. The bronchial response was assessed by use of maximal expiratory flow-volume curves obtained before and 1, 5, 10 and 15 min after the 5 min hyperventilation challenge. In normal subjects, there was a minimal though significant (p less than 0.001; two-way analysis of variance) fall in maximal expiratory flows which did not increase with the level of hyperventilation and was not accompanied by a fall in forced vital capacity. The bronchial response of asthmatics differed from that in normal: the fall in maximal expiratory flows was significantly greater, associated with a significant fall in forced vital capacity and increased with the level of hyperventilation. Results in 10 asthmatics studied on two different study days were highly reproducible. Sensitivity and specificity are excellent (approximately equal to 1) for the 40 1 X min-1 hyperventilation challenge. Our results suggest that isocapnic voluntary hyperventilation of dry air at room temperature (20-22 degrees C) is a highly satisfactory screening test to detect bronchial hyperreactivity.

Adolescent↗
PubMed1989

High incidence of primary cerebral lymphoma in tumor-induced central neurogenic hyperventilation.

An awake patient presented with central neurogenic hyperventilation induced by a cerebral tumor. Corticosteroid therapy and brain irradiation while the patient was anesthetized and respiration controlled under pancuronium-induced respiratory paralysis were followed by tumor regression and resolution of hyperventilation. Recurrence of tumor 6 weeks later was not accompanied by recurrence of hyperventilation. Cytologic study of cerebrospinal fluid revealed B-cell lymphoma. This patient brings to 10 the number of cases recorded with tumor-induced central neurogenic hyperventilation. Five of the eight patients with known tumor histology had a primary cerebral lymphoma, a rare neoplasm that comprises only 1% of all intracranial neoplasms. The disproportionately high frequency of central neurogenic hyperventilation in patients with cerebral lymphoma has therapeutic implications that are briefly reviewed.

Adrenal Cortex Hormones↗
PubMed1999

Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure.

Hyperventilation is frequently used to prevent or postpone the development of cerebral edema and intracranial hypertension in patients with fulminant hepatic failure (FHF). The influence of such therapy on regional cerebral blood flow (rCBF) remains, however, unknown. In this study the CBF-distribution pattern was determined within the first 12 hours after development of hepatic encephalopathy (HE) stage 4 before and during hyperventilation. Ten consecutive patients (median age 48 [range 33-57] years) with FHF and 9 healthy controls (median age 54 [24-58] years) had rCBF determined by single photon emission computed tomography (SPECT) using intravenous injection of 133Xenon. For determination of high resolution CBF pattern, the patients were also studied with 99mTc-hexa-methylpropyleneamine oxime (HMPAO) in the hyperventilation condition. There was no significant difference in the rCBF distribution pattern during normoventilation as compared with hyperventilation. The anterior to posterior (AP) ratio was significantly lower in patients as compared with healthy controls. After hepatic recovery and disappearance of HE, 3 patients had restored normal rCBF distribution pattern as compared with healthy controls. We conclude that in sedated patients with FHF, a relatively lower rCBF is found in the frontal regions and in the basal ganglia as compared with posterior regions. This rCBF-distribution pattern was not aggravated during hyperventilation. It is speculated that this change of rCBF in patients with FHF may render the frontal brain regions more susceptible to hypoxia. The relative frontal rCBF decrease was shown to be reversible with hepatic recovery and alleviation of HE.

Adult↗
PubMed1975

[Energy state of the cerebral cortex of the cat during hyperventilation (author's transl)].

Average Po2 and Pco2, local blood flow and pH values in the cerebral cortex of the cat were measured during passive hyperventilation (arterial Pco2 below 19 mm Hg). At defined intervals tissue samples were taken for metabolite analysis. The object of the study was to correlate the data obtained on the brain surface with metabolic responses. Immediately after the start of hyperventilation blood flow decreased, average cortical tissue pressures of O2 and CO2 fell, and there was a simultaneous rise in cortical pH. At a later stage in the experiment the local blood supply reverted to its resting level. Despite a fivefold rise in tissue lactate level during hyperventilation and a decrease in local O2 pressure on the brain surface to 5-10 mm Hg the degree of phosphorylation of energy rich phosphates was not less than under normal conditions of oxygenation. Our investigations showed no evidence of energy lack in cerebral cortex cells during hyperventilation. Cellular hypoxia and its characteristics are defined. The possible causes of raised tissue lactate levels during hyperventilation despite the lack of evidence of cellular hypoxia are discussed.

Adenosine Diphosphate↗
PubMed1998

Cerebral blood flow changes in the primary motor and premotor cortices during hyperventilation.

The aim of this study was to clarify the regional differences in cerebral blood flow (CBF) change during hyperventilation by using H2(15)O and positron emission tomography (PET). Eight healthy volunteers (age: 63.0 +/- 8.9 yr.) were studied. Regional CBF was measured by the H2(15)O autoradiographic method and PET. Statistical parametric maps (SPM) and conventional regions of interest (ROI) analysis were used for estimating regional CBF differences in the normocapnic state with normal breathing and the hypocapnic state induced by hyperventilation. Total CBF decreased during the hypocapnic state. The SPM revealed that primary motor and premotor cortices were significantly activated by hyperventilation. In these areas absolute CBF values were significantly higher than those in the temporal, occipital and parietal lobes in the hypocapnic state, but there were no significant regional differences in the normocapnic state. In the hypocapnic state induced by hyperventilation, the primary motor and premotor CBF shows combined changes with vasoreaction to hypocapnia and increase in activation due to hyperventilation.

Aged↗
PubMed2001

Intracranial pressure, brain PCO2, PO2, and pH during hypo- and hyperventilation at constant mean airway pressure in pigs.

OBJECTIVE: To evaluate in healthy, non-brain-traumatized animals the effects of hypo- and hyperventilation on intracranial pressure (ICP) and brain carbon dioxide, oxygen, and pH during the use of a ventilatory mode at constant mean airway pressure (MAwP). DESIGN AND SETTING: Prospective animal study in a university laboratory. SUBJECTS: Eight crossbred Landrace/Yorkshire pigs. INTERVENTIONS: The animals were ventilated in a pressure-controlled mode according to the open lung concept with an inspired oxygen fraction of 1.0. Starting at normoventilation, a stepwise hypo- and hyperventilation was performed to PaCO2 values of 90.4+/-10.4 and 26.9+/-4.1 mmHg, respectively. The ICP and brain parenchyma values [carbon dioxide (PbrCO2), oxygen (PbrO2), and pH (brpH)] measured by multiparameter sensors were recorded continuously during these maneuvres. RESULTS: During hypoventilation there was a significant increase in PbrCO2 tension, PbrO2 tension, and ICP. During hyperventilation there was a significant decrease in PbrCO2 tension and ICP while the change in PbrO2 was not significant. MAwP was kept stable during the stepwise hypo- and hyperventilation, and this resulted in a constant mean arterial pressure. CONCLUSIONS: Controlled hypo- and hyperventilation at constant MAwP in non-brain-traumatized pigs appears to induce changes in ICP and cerebral perfusion pressure which, however, do not necessarily lead to cerebral ischemia. To achieve adequate cerebral perfusion at an increased ICP level due to hypoventilation one must maintain sufficient arterial blood pressure. Hypercapnia resulted in a significant increase in brain oxygenation; however, this does not necessarily mean that permissive hypercapnia is neuroprotective.

Animals↗