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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many physicians believe that the hyperventilation syndrome is invariably associated with anxiety or undiagnosed organic disease such as asthma and pulmonary embolus, or both. Twenty one patients referred by specialist physicians with unexplained somatic symptoms and unequivocal chronic hypocapnia (resting end tidal Pco2 less than or equal to 4 kPa (30 mm Hg) on repeated occasions during prolonged measurement) were investigated. All but one complained of inability to take a satisfying breath. Standard lung function test results and chest radiographs were normal in all patients, but histamine challenge showed bronchial hyper-reactivity in two of 20 patients tested, and skin tests to common allergens were positive in three of 18. Ventilation-perfusion scanning was abnormal in a further three of 15 patients studied, with unmatched perfusion defects in two and isolated ventilation defects in one. None of the 21 had thyrotoxicosis, severe coronary heart disease, or other relevant cardiovascular abnormalities. Ten of the 21 patients were neurotic and suffered from chronic psychiatric disturbance characterised by anxiety, panic, and phobic symptoms. The remainder had no detectable psychiatric disorders but reported proportionately more somatic than anxiety symptoms. Severe hyperventilation can occur in the absence of formal psychiatric or detectable respiratory or other organic abnormalities. Asthma and pulmonary embolus must be specifically excluded.
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PMID:Respiratory and psychiatric abnormalities in chronic symptomatic hyperventilation. 392 4

Ventilation (liters of air per minute) increases during an acute attack of asthma. Hypocapnia is the rule, although eucapnia may occur. This suggests both that respiratory center output is increased and that acidemia is not the major stimulus to augmented respiration. Mechanical receptors responding to change in end-expiratory respiratory system volume or airway dimensions, cortical stimulation to the medullary respiratory centers, and possibly hypoxemia function in concert to regulate ventilation in asthma. Newer laboratory techniques permit independent assessment of chemical and cortical components of ventilatory drive. These techniques have provided fresh insights into the effects of various therapeutic interventions upon respiration in asthma.
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PMID:Ventilatory control in asthma. 615 37

Hyperpnoea of canine peripheral airways with dry air results in airway obstruction, mucosal damage, and inflammation. The purpose of this study was to evaluate the effect of repeated dry air challenge (DAC) on airway obstruction, reactivity and the development of airway inflammation in dogs. Canine peripheral airways received DAC (delivered under general anaesthesia through a bronchoscope) every 48 h for two weeks. Peripheral airway resistance and reactivity were measured prior to each DAC. After the final DAC, bronchoalveolar lavage fluid (BALF) cells and soluble mediators from challenged and control airways were measured. Repeated bronchoscopy had no effect on airway mechanics. Repeated DAC produced cumulative increases in peripheral airway resistance and peak obstructive response to DAC. The response to hypocapnia was also increased in airways receiving repeated DAC. However, when the response to agonists was expressed as a change from baseline, consistent significant increases were not observed. Repeated bronchoscopy produced insignificant changes in BALF cells and eicosanoid mediators. Repeated DAC produced marked eosinophilic inflammation and increased prostaglandins D2, E2, and F2alpha, as well as leukotrienes C4-E4. In conclusion, repeated dry air challenge in dogs in vivo causes persistent airway obstruction and inflammation not unlike that found in human asthma.
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PMID:Repetitive hyperpnoea causes peripheral airway obstruction and eosinophilia. 1048 29

Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element.
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PMID:Carbon dioxide and the critically ill--too little of a good thing? 1052 Jun 49

Winter athletes have an increased incidence of asthma, suggesting that repetitive hyperventilation with cold air may predispose individuals to airways disease. We used a canine model of exercise-induced hyperpnea to examine the effects of repeated hyperventilation with cool, dry air (i.e., dry air challenge [DAC]) on peripheral airway resistance (Rp), reactivity, and inflammation. Specific bronchi were exposed to a single DAC on five consecutive days. Rp and Delta Rp to aerosolized histamine, intravenous histamine, or hypocapnia were measured daily. Bronchoalveolar lavage fluid (BALF) was obtained on the fifth day. Rp increased from 0.70 +/- 0.08 to 1.13 +/- 0.22 cm H(2)O/ml/s (n = 25) 24 h after the first DAC, rose to 1.49 +/- 0.24 cm H(2)O/ml/s by Day 3, and remained elevated throughout the remainder of the protocol. Repeated DAC increased reactivity to hypocapnia and intravenous histamine. Intravenous salbutamol failed to reduce Rp as effectively in challenged airways (111% of Day 1 baseline) as in naive airways (54% of baseline). Repeated DAC caused increased BALF neutrophils, eosinophils, and sulfidopeptide leukotrienes. We conclude that repeated DAC causes peripheral airways inflammation, obstruction, hyperreactivity, and impaired beta-agonist-induced relaxation. This suggests that other mechanisms in addition to increased smooth muscle tone may contribute to the development of repetitive hyperventilation-induced bronchial obstruction and hyperreactivity.
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PMID:Repeated hyperventilation causes peripheral airways inflammation, hyperreactivity, and impaired bronchodilation in dogs. 1154 33

A canine model of exercise-induced asthma was used to test the hypothesis that the development of a late phase response to hyperventilation depends on the acute production of pro-inflammatory mediators. Peripheral airway resistance, reactivity to hypocapnia and aerosol histamine, and bronchoalveolar lavage fluid (BALF) cell and eicosanoid content were measured in dogs approximately 5 h after dry air challenge (DAC). DAC resulted in late phase obstruction, hyperreactivity to histamine, and neutrophilic inflammation. Both cyclooxygenase and lipoxygenase inhibitors administered in separate experiments attenuated the late phase airway obstruction and hyperreactivity to histamine. Neither drug affected the late phase inflammation nor the concentrations of eicosanoids in the BALF obtained 5 h after DAC. This study confirms that hyperventilation of peripheral airways with unconditioned air causes late phase neutrophilia, airway obstruction, and hyperreactivity. The late phase changes in airway mechanics are related to the hyperventilation-induced release of both prostaglandins and leukotrienes, and appear to be independent of the late phase infiltration of inflammatory cells.
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PMID:Eicosanoids modulate hyperpnea-induced late phase airway obstruction and hyperreactivity in dogs. 1178 38

Examining the parameters of the blood oxygen-transport system and oxygen tissue balance in 71 patients with bronchial asthma (BA) and in 60 patients with BA concurrent with varying carbohydrate metabolic disturbances (CMDs) revealed differences in oxygen transport. In asthmatic patients without CMDs, the pattern of changes in oxygen balance permitted identification of arteriohypoxemic hypoxia. The high frequency of factors (alkalosis, hypocapnia) that enhance hemoglobin affinity for oxygen, which are compensated for by the increase in 2,3-DPH, as well as hypoxia of peripheral shunting are the specific features of impaired oxygen balance in asthmatic patients with concomitant CMDs that predispose to the development and progression of pulmonary hypertension and cor pulmonale which cause early disability. The determination of the leading link in impaired oxygen transport individualizes treatment approaches and provides evidence for a need for earlier use of metabolic and antihypoxic agents in asthmatic patients with CMDs.
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PMID:[The blood oxygen-transport system and oxygen tissue balance in patients with bronchial asthma (BA) concurrent with carbohydrate metabolic disturbances]. 1588 65

There is some evidence that breathing retraining may be beneficial for patients with asthma, but the mechanism behind this benefit is still unknown. One hypothesis is that individuals can be trained to raise carbon dioxide levels and thereby reverse the bronchoconstrictive effects of hypocapnia and utilize the bronchodilatory effects of hypercapnia. This theory presupposes that individuals with asthma have lower carbon dioxide levels than the healthy population. This article reviews the available evidence supporting the hypothesis and concludes that although attractive, there is currently insufficient evidence to attribute the benefits of breathing retraining to this mechanism.
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PMID:Hypocapnia and asthma: a mechanism for breathing retraining? 1588 63

Hypoxia and hypocapnia can cause broncho-constriction in human subjects, and this could have a bearing on performance at high altitude. The object of this study was to examine how pulmonary ventilatory functions during high-altitude trekking. This study is a cohort study on spirometric parameters at different altitudes. Fifty six healthy male volunteers from a university student population were enrolled in the study (ages 22.9+/-5.3 years). Pulmonary function was assessed with a Spirolab II in all participants before ascending at baseline (1150 meter), after ascending at different altitudes (2850, 4150 meter), and after descending at sea level during a 3-day trek in Sialan Mount. This study indicates that in an actual trek, ascending results in significant decrease in forced vital capacity (FVC). FVC significantly decreased with increasing altitude from baseline level and at the sea level it was significantly less than baseline level. Peak flow increased with increasing altitude from baseline (1150 m) to 2850 m and decreased with decreasing altitude (p<0.01). Maximal midexpiratory flow rate (FEF 25-75%) and forced expiratory volume in 1 second to forced expiratory volume ratio (FEV1.0%) significantly increased with increasing and decreasing altitude from baseline level (p<0.001). There was no significant change in FEV1. It could be concluded that changes in some pulmonary ventilatory parameters were proportional to the magnitude of change in altitude during a high-altitude trek. These changes are significant at the beginning of ascending.
Iran J Allergy Asthma Immunol 2008 Jun
PMID:Pulmonary function parameters changes at different altitudes in healthy athletes. 1855 9

In the absence of other explanations, exercise-induced dyspnea is often labeled as a manifestation of asthma. The aim of this study was to use exercise provocation in cold air among patients with exercise-induced dyspnea, but without any bronchoconstriction, in order to study induced symptoms and different physiological parameters and to measure the possible influence of exercise in cold air on capsaicin cough sensitivity. Eleven patients with exercise-induced dyspnea but no asthma, along with 11 healthy controls, performed a capsaicin inhalation provocation on two occasions. One of these provocations was preceded by an exercise provocation in a cold chamber. Number of coughs, airway symptoms, spirometry, respiratory rate, pulse rate, end-tidal CO(2), and PSaO(2) were registered. During exercise, the patients coughed more than the controls and also had more airway symptoms. After exercise provocation, spirometry values remained unchanged, but capsaicin cough sensitivity was increased and end-tidal CO(2) decreased among the patients, both in comparison to the controls and in comparison to the patients themselves prior to exercise. Exercise-induced dyspnea may be associated with hypocapnia from hyperventilation and increased capsaicin cough sensitivity. The diagnosis of exercise-induced asthma should be questioned when the patient has no signs of bronchoconstriction.
J Asthma 2008 Oct
PMID:Dyspnea from exercise in cold air is not always asthma. 1895 Dec 64


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