SEARCH · PubMed Health

Results for “Hyperventilation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed1997

Hyperventilation as a specific test for diagnosis of coronary artery spasm.

The hyperventilation test has been used as a clinical tool to induce coronary spasm. However, its diagnostic and prognostic values have not been fully elucidated. This study was designed to establish the sensitivity and specificity of the hyperventilation test and to clarify the characteristics of hyperventilation test-positive patients. We examined 206 patients in whom coronary spasm was documented by angiography (spasm group), and 183 patients without angina at rest in whom acetylcholine failed to induce spasm (nonspasm group). All patients performed vigorous hyperventilation for 6 minutes in the early morning. Of the spasm group patients, 127 showed positive responses to the test, including ST elevation (n = 111), ST depression (n = 15) and negative U wave (n = 1). None in the nonspasm group showed any ischemic electrocardiographic change. Thus, the sensitivity and specificity of this test for diagnosis of coronary spasm were 62% and 100%, respectively. In the spasm group, there were no significant differences between hyperventilation test-positive and test-negative patients in age, sex, the prevalence of hypertension, diabetes mellitus, obesity, smoking, and the number of diseased vessels. When clinical characteristics were compared, the proportions of the patients with high disease activity (> or =5 attacks a week), with severe arrhythmias (second- or third-degree atrioventricular block and/or ventricular tachycardia) during attacks, and with multivessel spasm were significantly higher in the hyperventilation test-positive patients than in the negative patients (69% vs 20%, p <0.0001; 31% vs 11%, p <0.005; and 58% vs 34%, p <0.01, respectively). These findings imply that hyperventilation is a highly specific test for the diagnosis of coronary artery spasm, and that hyperventilation test-positive patients are likely to have life-threatening arrhythmias during attacks and multivessel spasm.

Adult↗

PubMed1999

Ventilatory responses to hypercapnia and hypoxia after 6 h passive hyperventilation in humans.

1. Acute exposure to hypoxia stimulates ventilation and induces hypocapnia. Long-term exposure to hypoxia generates changes in respiratory control known as ventilatory acclimatization to hypoxia. The object of this study was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory acclimatization to hypoxia, in the absence of the primary hypoxic stimulus itself. 2. Three 6 h protocols were each performed on twelve healthy volunteers: (1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2) held 10 Torr below the eupnoeic value; (2) passive eucapnic hyperventilation, with PET,CO2 maintained eucapnic; (3) control. 3. Ventilatory responses to acute hypercapnia and hypoxia were assessed before and half an hour after each protocol. 4. The presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing PET,CO2 (P < 0.05, ANOVA), and a leftwards shift of the ventilatory response to hypercapnia (P < 0.05). The presence of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensitivity to CO2 (P < 0.05). No significant effects of any protocol were detected on the ventilatory sensitivity to hypoxia. 5. We conclude that following 6 h of passive hyperventilation: (i) the left shift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in slope of the VE-PET,CO2 relationship is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia is unaltered.

Acclimatization↗

PubMed1995

Proton magnetic resonance spectroscopy investigation of hyperventilation in subjects with panic disorder and comparison subjects.

OBJECTIVE: The purpose of this study was to investigate differential effects of hyperventilation on brain lactate in patients with panic disorder and comparison subjects as a possible mechanism for explaining previous observations of an excess rise in brain lactate among panic disorder subjects during lactate infusion. METHOD: Seven treatment-responsive patients with panic disorder and seven healthy comparison subjects were studied with proton magnetic resonance spectroscopy to measure brain lactate during controlled, voluntary hyperventilation over a period of 20 minutes. Hyperventilation was regulated with the use of capnometry to maintain end-tidal PCO2 at approximately 20 mm Hg during the period of hyperventilation. Blood lactate was measured prior to and at the end of hyperventilation. RESULTS: At baseline the two groups had similar brain lactate levels. Panic disorder subjects exhibited significantly greater rises in brain lactate than comparison subjects in response to the same level of hyperventilation. Blood lactate levels before and after 20 minutes of hyperventilation were not significantly different between groups. CONCLUSIONS: Controlled hyperventilation increases brain lactate and does so disproportionately in subjects with panic disorder. This increase in brain lactate may result from decreased cerebral blood flow due to hypocapnia, and individuals with panic disorder may have greater sensitivity to this regulatory mechanism.

Adult↗

PubMed2000

No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury.

OBJECT: Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). METHODS: Nine patients were studied a mean of 11.2+/-1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6+/-1.8 and their mean age 27+/-9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30+/-2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59+/-0.44 ml/100 g/minute [p < 0.01] and 0.31+/-0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5+/-8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8+/-0.56 ml/100 g (p < 0.001), OEF rose to 0.45+/-0.13 (p < 0.02), and CvO2 fell to 8.3+/-3 vol% (p < 0.02); CMRO2 remained unchanged. CONCLUSIONS: The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

Adult↗

PubMed1971

[Electrical picture of the brain under increased respiration in children. Studies on the structure of hyperventilation and its value as a provocation method in clinical electroencephalography in a model of multivariate analysis using electronic data processing].

In clinical electroencephalography, hyperventilation is the most used method of activation. However, knowledge of the conditions of hyperventilation with regard to their effects on the EEG is so far rather undifferentiated. For this reason the effects of hyperventilation in 1109 children are examined in this paper based on clinical and electroencephalographic parameters of a data configuration with a large number of criteria and the results obtained are calculated with the aid of electronic data processing. The statistical methods of examination were frequency and significance investigations by chi 2 tests, multifactorial analysis of variance, multiple regression analysis of influencing quantities, and determination of the reliability of the quantitative method of evaluation. New knowledge on group-statistical validity was obtained with this multivariant analysis and it was thus possible to extend the value of hyperventilation as a method of provocation in clinical electroencephalography. The increase in knowledge is based in particular on the facts that the hyperventilation effects are practically independent of sex, they do not require the consideration of certain age related development modalities of the EEG, they are diagnostically significant as regards unspecific changes of the bioelectrical activity, and they make a differentiated consideration with reference to their strength necessary, which results in 4 types of forms of changing the EEG spectrum. In addition to this, a recurrence of EEG changes was observed after the HV effect proper had faded, and the term "Reprise" is suggested for this and its clinico-encephalographic importance discussed. It was also found that occipital maxima dominate and that changes in frequency and amplitude require separate consideration. The influence of respiratory rate, tidal volume minute volume, alveolar CO2 tension, blood sugar and body weight on the strength of the effect of hyperventilation is not very significant. Mean controlled hyperventilation has proved useful to standardise arbitrary hyperventilation; an improvement could be achieved at the most by norming the respiratory rate. It was possible to prove that the applied method of non-mechanical quantitative EEG analyses had a high degree of accuracy and is consequently suitable for scientific investigations.

Adolescent↗

PubMedDate not supplied

[Pharmacotherapy of the hyperventilation syndrome].

Hyperventilation may be induced by several organic factors. The HVS-hyperventilation and symptoms such as hypertonia and pain-hypocapnia and disturbance of the acid-base balance--other symptoms--anxiousness--hyperventilation--etc. In the adaptation-hyperventilation and symptoms such as hypertonia and pain,-hupocapnia and disturbance of the acid-base balance-other symptoms--anxiousness--hyperventilation--etc. In the adaptation process one distinguishes the load, the strain and a tension or counterforce (stress). In the cause and effect relationship between the adaptation process and a specific pathology, it is obvious that the strain is the only element capable of eliciting the specific pathology or syndrome. Stress is a compensation for the strain and is therefore beneficial to the organism. The strain is associated with, amongst other things, anxiety and changes in the pyridoxine-L-tryptophan metabolism (nicotinic acid-ribonucleotide synthesis). Stress depends to a large extent on the intact serotonergic transmission in the cerebrum. But serotonin synthesis is critically dependent on the pyridoxine-L-tryptophan metabolism. Benzodiazepines improve the hyperventilation, anxiousness and strain, if these are of the free-floating anxiety type. Tricyclic preparations improve anxiousness in as much as it assumes the character of fear, phobia or an anxiety attack. They are active against strain when that reveals itself as an anxiety attack. Pyridoxine and L-tryptophan as serotonergic agonists, improve the hyperventilation, have a beneficial effect on symptoms such as hypertonia and pain, are effective against anxiousness and anxiety and potentiate the stress. In addition they directly correct the property of strain, i.e. the disturbance of the nicotinicacid-ribonucleotide synthesis. Clomipramine is the most potent serotonergic agonist available. That substance has a favourable effect on hyperventilation, hypertonia and pain, on anxiousness that expresses itself as fear, phobia or an anxiety attack. It favours stress. Further investigation is desirable, in particular of the new serotonergic agonists that have recently been made available or are still to come.

Adrenergic beta-Antagonists↗

PubMed1995

Pressor effect of hyperventilation in healthy subjects.

Hyperventilation is an important feature of panic disorder, and an association has been reported between panic disorder and hypertension. We have examined the effect of hyperventilation on the blood pressure (BP) of healthy subjects. Twenty six subjects were randomised in a balanced two-period cross-over study to compare the effects of hyperventilation with that of normal breathing on sitting BP, heart rate and the electrocardiogram. Each study phase lasted 40 min, with 15 min of baseline observation, 5 min of hyperventilation or normal breathing, and 20 min of continued observation. Hyperventilation significantly increased SBP by 8.9 mm Hg (95% CI 3.8-13.8, P < 0.01), diastolic blood pressure by 8.2 mm Hg (95% CI 1.7-14.7, P < 0.05), mean arterial pressure by 10.0 mm Hg (95% CI 3.3-16.7, P < 0.01) and heart rate by 36 beats/min (95% CI 31-44, P < 0.01). The changes in diastolic and mean arterial pressure correlated significantly with the total volume of air expired during hyperventilation (r = 0.57, p < 0.01 and r = 0.50 P < 0.01, respectively), but not with the change in expired carbon dioxide. In the electrocardiogram, T wave changes occurred in the inferior leads in 10 of 26 subjects, but there were no significant changes in other measurements. Hyperventilation significantly increased the BP of healthy subjects, and the role of hyperventilation in the link between panic disorder and hypertension deserves further study.

Adult↗

PubMed1996

Modification of the N-methyl-D-aspartate (NMDA) receptor in the brain of newborn piglets following hyperventilation induced ischemia.

The present study tests the hypothesis that cerebral ischemia induced by severe hypocapnia modifies the N-methyl-D-aspartate (NMDA) receptor/ion channel complex in the cerebral cortical cell membranes of newborn piglets. Studies were performed in six newborn piglets subjected to ischemic hypoxia induced by hyperventilation (PaCO2, 9-11 mmHg) for 1 h. Comparisons were made to a normoxic group on room air (n = 6). Following hyperventilation, phosphocreatine decreased 80%, but ATP remained unchanged. NMDA receptor activation was determined by measuring [3H]MK-801 binding at concentrations varying from 2.5 to 50 nM. Following hyperventilation, Bmax decreased 52% to 0.50 +/- 0.04 pmol/mg protein (P = 0.001); however, the Kd value was unchanged at 7.45 +/- 0.79 nM. Spermine and magnesium dependent activation of the NMDA receptor was determined in the hyperventilated and control groups. With spermine concentrations increasing from 2.5 to 50 microM the maximal spermine dependent activation in the normoxic group was 13.7 +/- 7.93% which occurred at a concentration of 3.75 +/- 1.37 microM. In the hyperventilated group maximal activation was 32.4 +/- 23.5% (P = 0.095) at 4.58 +/- 2.46 microM (P = ns). With magnesium concentrations increasing from 2.5 to 100 microM the maximal magnesium dependent activation in the normoxic group was 17.0 +/- 13.6% which occurred at a concentration of 22.5 +/- 6.12 microM. In the hyperventilated group maximal activation was 26.3 +/- 14.9% (P = ns) at 4.58 +/- 2.92 microM (P < 0.0001). These data show that with less severe tissue hypoxia, as evidenced by conservation of ATP, there is less modification of the NMDA receptors. Ischemia induced by hyperventilation leads to an increase in spermine activation of the NMDA receptor, and the NMDA receptor is much more sensitive to magnesium as evidenced by the maximal activation occurring at a significantly lower magnesium concentration. Ischemia induced by hyperventilation modifies the spermine, magnesium, and MK-801 binding sites of the NMDA receptor and may result in increased NMDA receptor mediated neurotoxicity in the newborn brain.

Animals↗

PubMed1982

Protective effect of CO2-induced hyperventilation on the hepatotoxicity elicited by carbon tetrachloride.

Following oral intake or inhalation, halogenated hydrocarbons are metabolized to hepatotoxic intermediates in the liver to only a small extent, the major part being eliminated via the lungs without biochemical transformation. Following intoxication, increased pulmonary elimination of hydrocarbons can be achieved in patients by treatment with CO2-induced hyperventilation. To investigate the efficacy of this new therapy under exact experimental conditions, female Wistar rats received 2.5 ml CCl4/kg BW by gastric intubation and were then treated with CO2-induced hyperventilation. In comparison to untreated animals, hyperventilated rats showed only a few signs of hepatic injury by histological evaluation, whereas massive centrolobular necroses and fatty infiltrations were observed in non-hyperventilated animals. By biochemical assessment, significant decreases of GOT, GPT and GDH activity were observed in the serum, when hyperventilated rats were compared to untreated animals. Moreover, the LD50 for CCl4 was almost trebled after hyperventilation compared to the non-hyperventilated animals. The increased LD50, and the biochemical and histological results therefore substantiate the usefulness of CO2-induced hyperventilation therapy in the treatment of intoxications by hydrocarbons under standardized experimental conditions.

Alanine Transaminase↗

PubMed1983

Comparison of airway reactivity induced by histamine, methacholine, and isocapnic hyperventilation in normal and asthmatic subjects.

In an investigation of a rapid screening test for airway reactivity using isocapnic hyperventilation with room air and cold air the results of this test were compared with the airway response to histamine and methacholine challenge. Twelve non-atopic, non-smoking normal subjects and 11 subjects with stable asthma who had an FEV1 above 74% of the predicted value were studied. In the normal subjects isocapnic hyperventilation with room air (75 l/min; 22 degrees C (SEM 0.2 degrees); 10 mg H2O/l air) and isocapnic hyperventilation with cold air (77 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) produced no significant change in FEV1. In the asthmatic subjects, hyperventilation with room air (71 l/min; 22 degrees C (0.8 degrees); 10 mg H2O/l air) caused a mean fall in FEV1 of 11.7%; cold air hyperventilation (70 l/min; -10 degrees C (0.9 degrees); 2.4 mg H2O/l air) caused a mean fall in FEV1 of 20.4%. Cold air hyperventilation produced greater separation between normal and asthmatic subjects than room air. The provocative concentration of histamine required to reduce the FEV1 by 20% (PC20) correlated closely with the PC20 for methacholine (r = 0.95; p less than 0.001). Both tests separated normal from asthmatic subjects. PC20 for both histamine and methacholine correlated with the fall in FEV1 after cold air hyperventilation (r = 0.93, p less than 0.001; r = 0.87, p less than 0.001 respectively). We conclude that the results of a rapid screening test based on hyperventilation with cold air correlate well with a standard pharmacological challenge.

Adult↗

PubMed1995

Hyperventilation therapy for severe traumatic brain injury.

The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. That hyperventilation therapy might exacerbate secondary brain injury seems likely based on abnormalities in cerebral blood flow (CBF) and metabolism which result from TBI, and the potential for hyperventilation to worsen those abnormalities. Both global and regional CBF are critically reduced, and metabolism increased, during the first several hours and days after injury. As a result, focal ischemia is common following severe TBI. Hyperventilation causes a further decrease in CBF, often without a concomitant reduction in ICP. In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.

Brain↗

PubMed1990

Relationship between the airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in asthmatic subjects.

To determine whether bronchoconstriction induced by sulfur dioxide can be predicted by the airway response to inhaled histamine, we exposed on two days 46 patients with asthma to air or 0.5 ppm SO2. The exposure protocol consisted of 10 min of tidal breathing followed by 10 min of isocapnic hyperventilation at a rate of 30 l/min. Airway response was measured before (baseline) and after hyperventilation in terms of specific airway resistance, SRaw. Exposure to air increased baseline mean (SD) SRaw from 6.27 (2.12) to mean (SD) maximum post-hyperventilation SRaw of 9.10 (4.38) cmH2O*s (P less than 0.0001). Exposure to SO2 increased mean (SD) baseline SRaw from 6.93 (3.29) to mean (SD) maximum post-hyperventilation SRaw of 18.21 (18.69) cmH2O*s (P less than 0.0001). Mean (SD) effect of SO2 defined as difference between maximum post-hyperventilation SRaw after SO2 versus air was 9.11 (16.14) cm H2O*s. When evaluated individually, 26 and 34 of the 46 patients showed an airway response to hyperventilation of air and SO2, respectively. Airway response to histamine was determined as the histamine concentration necessary to increase specific airway resistance by 100%, PC100SRaw. The airway response after SO2 and PC100SRaw showed a weak but significant correlation (R = -0.48), whereas the responses to hyperventilation and SO2 did not correlate. We suggest that the mechanisms by which histamine and SO2 exert their bronchomotor effects are different and that in asthmatic patients the risk of pollutant-induced asthmatic symptoms can be poorly predicted by histamine responsiveness.

Administration, Inhalation↗

PubMed1989

Does acute hyperventilation provoke cerebral oligaemia in comatose patients after acute head injury?

In 27 comatose patients with acute head injury, 45 paired studies of regional cerebral blood flow (rCBF) were performed before and after hyperventilation. In total 676 regions were studied, and rCBF was calculated as initial slope index using the intracarotid washout technique of 133 Xe. The tests were applied from one day to three weeks after the acute trauma. In total hyperventilation from PaCO2 averaging 4.8 to 3.5 kPa increased the frequency of regions with oligaemia defined CBF less than 20 ml/100 g/min from 5 to 16%. Before hyperventilation oligaemia was observed in 11 of 45 studies (9 of 27 patients); after hyperventilation the frequency increased to 21 studies (15 patients). The frequency of severe oligaemia (CBF less than 15 ml) increased from 0.1 to 3% of all regions, or from 2 to 8 of all studies (from 2 to 9 patients). The increased frequency of oligaemia after hyperventilation was correlated to a poor outcome (dementia, vegetative survival or death), where it was observed in 21% of all regions, in 16 of 26 studies and 11 of 15 patients, whereas the frequency in patients with a good recovery was found to be 7% of all regions and observed in 5 of 19 studies (4 of 12 patients). The high frequency of oligaemia after hyperventilation was associated to a low hemispheric CBF before hyperventilation, but not to the level of PaCO2, the level of intracranial pressure, cerebral perfusion pressure or CSF-pH or lactate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Comparison of the distribution of myocardial blood flow between exercise-induced and hyperventilation-induced attacks of coronary spasm: a study with thallium-201 myocardial scintigraphy.

Exercise and hyperventilation tests are often used as the provocative tests for coronary artery spasm. To examine the distribution of myocardial blood flow during exercise-induced and hyperventilation-induced attacks of coronary spasm, thallium-201 myocardial scintigraphy was performed in 47 patients with variant angina. The extent and severity scores and severity index (severity score/extent score) of scintigraphic perfusion defect were calculated. In 32 patients, anginal attack associated with ST elevation on the electrocardiogram was induced by exercise; in 23 patients, the attack was induced by hyperventilation. In patients with either anterior or inferior wall ischemia, both the extent and severity scores and severity index in the scintigram were significantly greater in exercise-induced anginal attack than those in hyperventilation-induced attack. In patients with simultaneous anterior and inferior wall ischemia, they tended to be greater in exercise-induced attack. In eight patients in whom anginal attack was induced by both exercise and hyperventilation, these scores and index were significantly greater in exercise-induced attack than those in hyperventilation-induced attack. These data suggest that myocardial ischemia during exercise-induced attack is enhanced as compared with that during hyperventilation-induced attack. Thallium-201 scintigraphy combined with exercise testing seems to be more sensitive for detecting myocardial ischemia induced by coronary spasm.

Aged↗

PubMed1993

Suppression of hyperventilation-induced attacks with infusion of atrial natriuretic peptide in patients with variant angina pectoris.

Atrial natriuretic peptide (ANP) is reported to dilate a major coronary artery in both experimental animals and humans. Spasm of a major coronary artery is the cause of variant angina pectoris and can be induced by hyperventilation. The effect of the ANP infusion on anginal attack induced by hyperventilation was studied in patients with variant angina pectoris. The study was performed in the early morning on 3 consecutive days in 11 patients with variant angina pectoris in whom the attacks were reproducibly induced by hyperventilation. On days 1 and 3 (saline solution infusion), and day 2 (ANP infusion), hyperventilation was started 14 minutes after beginning infusion of ANP (0.1 microgram/kg/min) or saline solution for 6 minutes. The attacks were induced in all 11 patients by hyperventilation on days 1 and 3. However, the attacks were not induced in any patient on day 2 of the ANP infusion. The plasma ANP level increased from 33 +/- 7 pg/ml to the peak level of 2,973 +/- 479 pg/ml (p < 0.01) at the end of the ANP infusion, and the plasma level of cyclic guanosine monophosphate (cGMP) increased from 5 +/- 1 pmol/ml to the peak level of 58 +/- 6 pmol/ml (p < 0.01) 5 minutes after the ANP infusion. The plasma levels of ANP and cGMP did not change after hyperventilation on days 1 and 3. It is concluded that the ANP infusion suppresses the attacks induced by hyperventilation in patients with variant angina pectoris, and cGMP is related to the mechanisms of suppression of the attacks.

Adult↗

PubMed1990

Affective responses to hyperventilation: a test of the cognitive model of panic.

A cognitive explanation of the association between acute hyperventilation and panic attacks has been proposed: the extent to which sensations produced by hyperventilation are interpreted in a negative and catastrophic way is said to be a major determinant of panic. Non-clinical subjects were provided with a negative or a positive interpretation of the sensations produced by equivalent amounts of voluntary hyperventilation. As predicted, there was a significant difference between positive and negative interpretation conditions on ratings of positive and negative affect. Subjects in the positive interpretation condition experienced hyperventilation as pleasant, and subjects in the negative interpretation condition experienced hyperventilation as unpleasant, even though both groups experienced similar bodily sensations and did not differ in their prior expectations of the affective consequences of hyperventilation. When the subjects were given a positive interpretation, the number of their sensations correlated with positive affect; when a negative interpretation was given, the number of bodily sensations correlated with negative affect. The results provide support for a cognitive model of panic and are inconsistent with the view that panic is simply a symptom of hyperventilation syndrome.

Adult↗

PubMed1994

Hyperventilation in the treatment of metabolic acidosis does not adversely affect pulmonary gas exchange.

BACKGROUND: Hyperventilation has been recommended to increase blood pH during metabolic acidosis. However, hypocapnia may adversely affect arterial blood oxygenation, especially in the presence of lung disease. We therefore studied the effects of metabolic acidosis, with and without normalization of pH by hyperventilation, on pulmonary gas exchange in dogs with permeability pulmonary edema. METHODS: Six pentobarbital-anesthetized dogs were administered 0.06 ml/kg of oleic acid at least 150 min before study. Ventilation was set with an inspired O2 fraction of 0.90 and a tidal volume of 18 ml/kg, and the respiratory rate was adjusted to alter the arterial CO2 tension (PaCO2) per the experimental protocol. The protocol in random order was (1) normal pH (7.36 +/- 0.01)/normal PaCO2 (39 +/- 1 mmHg); (2) low pH 7.20 +/- 0.01)/normal PaCO2 (40 +/- 1 mmHg); (3) low pH (7.18 +/- 0.01)/hyperventilation with inspired CO2 (PaCO2 = 40 +/- 1 mmHg); and (4) normal pH (7.35 +/- 0.01)/hyperventilation with low PaCO2 (24 +/- 1 mmHg). In phases 2-4, the pH was slowly reduced by intravenous infusion of 2 N hydrochloric acid. The pH was normalized in phase 1 where necessary by infusion of sodium bicarbonate. The pH in phase 4 was normalized by reducing the PaCO2 by increasing the respiratory rate. Gas exchange was assessed by the multiple inert-gas elimination technique. RESULTS: The hemodynamic measurements remained constant throughout the protocol. Arterial O2 tension increased from 244 +/- 55 to 293 +/- 49 mmHg in the presence of metabolic acidosis (P < 0.05). Hyperventilation to normalize the pH during metabolic acidosis (phase 4), increased arterial O2 tension (313 +/- 44 mmHg, P < 0.05), and reduced shunt (from 20 +/- 5% to 12 +/- 3%, P < 0.05) compared with normal acid-base conditions (phase 1). No change in shunt was observed with hyperventilation compared with metabolic acidosis alone (phase 2). The decrease in pulmonary shunt was not attributable to the direct effects of hyperventilation, because shunt was increased (20 +/- 5%) when PaCO2 was normalized during hyperventilation by inspiration of CO2 (phase 3). CONCLUSIONS: Hyperventilation to normalize blood pH during hydrochloric acid-induced metabolic acidosis did not adversely affect pulmonary gas exchange in dogs with permeability pulmonary edema.

Acidosis↗

PubMed1998

Quantitative topographical analysis of EEG during nonstandardized and standardized hyperventilation.

The aim of this study was to compare the topographical quantitative EEG (qEEG) changes induced by nonstandardized hyperventilation and those induced by standardized hyperventilation (with the end-tidal PCO2 being maintained at 2 kPa [15 mm Hg]). We examined 18 healthy volunteers during nonstandardized and 20 during standardized hyperventilation. During nonstandardized hyperventilation, the mean spectral power density in this group significantly increased 1.9 fold within the delta-, 2.2 fold within the theta-, 1.8 fold within the alpha-, and 1.9 fold within the beta-frequency band. There was no significant change of the power ratio and was no topographic difference between 4 frequency bands investigated. During standardized hyperventilation, the mean spectral power density in the group significantly increased to 12.9 fold within the delta-, to 7.6 fold within the theta-, to 1.4 fold within the alpha-, and to 2.4 fold within the beta frequency band. The power ratio decreased significantly. Such a pronounced EEG slowing with delta and theta augmentation was never found during nonstandardized hyperventilation. We conclude that a consistent slowing of the qEEG in all leads including a constant topographical maximum can only be induced by standardized, sufficiently pronounced hyperventilation.

Adult↗