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

The time course of the decrease in ventilation immediately after 1 min of voluntary isocapnic hyperventilation was studied in eight healthy subjects. The hyperventilation tests were done at three different levels of alveolar CO2 tension (PACO2), and at each PACO2 level with a fixed respiratory frequency and with a freely chosen (increased) frequency. The time constant of the decrease in ventilation after free-frequency hyperventilation was inversely related to the PACO2, with a regression equation of tau 1 (s) = 78.6 - 1.2 PACO2. After the fixed-frequency hyperventilation, the time constant of the decrease in ventilation was virtually zero and independent of PACO2. These results do not agree with earlier findings in anesthetized animals. The fact that hypocapnia increases the excitability of neurons might explain the findings. The extreme respiratory afterdischarge phenomenon in hypocapnic patients suffering from the hyperventilation syndrome is consistent with the outcome of this study.
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PMID:Time course of posthyperventilation breathing in humans depends on alveolar CO2 tension. 640 75

The effect of beta-adrenergic blockade on ventilatory parameters and on subjective complaints was studied in 73 patients suffering from hyperventilation syndrome. The beta-blockade made the PA,CO2 increase as much as tranquillizer therapy. No effect of any kind of therapy was found on the subjective complaints. A remarkable dissociation was found between the measured ventilatory parameters and the quantified subjective complaints. It is concluded that beta-blockade is an effective therapy for the basic problem of hypocapnia in the hyperventilation syndrome; in this respect it is to be preferred over other therapies such as tranquillizers.
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PMID:Beta-blockade in the hyperventilation syndrome. A retrospective assessment of symptoms and complaints. 682 3

Hyperventilation syndrome is a frequent, but poorly understood clinical entity. The clinical expression is a rich combination of respiratory, cardiac and neurological signs which can simulate various organic diseases. Hypocapnia remains the primum movens for most authors although the relationship with psychiatric situations, in particular in anxious patients, is increasingly emphasized. The diagnosis is currently based on the elimination of diseases associated with hyperventilation, then on Nijmegen's questionnaire and is confirmed by the reproduction of the same clinical picture in a voluntary hyperventilation test. Respiratory function tests offer little information. Treatment is based on combining rehabilitation therapy focused on the diaphragm and on relaxation. Specialized care may be needed in psychiatric patients.
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PMID:[Chronic hyperventilation syndrome]. 756 61

Hyperventilation syndrome is considered an established diagnosis if it is confirmed that the patient's complaints correlate with arterial hypocapnia. In the diagnostic criteria set up by a group in Nijmegen, paCO2 is determined indirectly by measuring the end tidal CO2. Values below 4 kPa measured at rest and 10 or more minutes after deliberate hyperventilation are classified positive diagnostic criteria for hyperventilation syndrome. However, it has not been proven that end tidal pCO2 agrees well with paCO2 during the entire manoeuvre. We performed simultaneous measurements of both parameters in 10 healthy non-smokers, before, during and after 3 minutes of deliberate hyperventilation. A comparison of the values employed for diagnosing a hyperventilation syndrome (during normal respiration before and 10 and more minutes after hyperventilation) yields a mean difference of 0.39 kPa according to the statistical computation described by Bland and Altman (limits of the range of agreement between 0.98 and -0.18). The end tidal CO2 values measured during the normal respiratory phase as well as 10 and more minutes after hyperventilation, agree well with the arterial values (the arterial values being slightly higher). During and shortly after hyperventilation the values obtained by both methods differ from one another, so that the exact degree of hypocapnia during a hyperventilation period cannot be assessed by measuring the end tidal CO2.
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PMID:[Simultaneous measurement of arterial and end-expiratory carbon dioxide before, during and after voluntary hyperventilation]. 853 42

The Hyperventilation Provocation Test (HVPT) has become a routine procedure in the diagnosis of hyperventilation syndrome (HVS). During an HVPT the patient voluntarily overbreathes for several minutes to produce hypocapnia. The test is considered positive if the induced symptoms are recognized by the patient as similar to those experienced in daily life. The present study tests the assumption that hypocapnia is the primary trigger for symptoms during an HVPT. In a randomized double-blind crossover design. 115 patients suspected of HVS and 40 healthy controls performed an HVPT and a placebo test (PT, isocapnic overbreathing). The HVPT induced more symptoms than the PT, especially more neuromuscular symptoms, cerebral symptoms, paresthesias, and temperature sensations. However, the absolute difference between the number of symptoms induced by the HVPT and PT was small. In patients, the PT induced 66% of symptoms induced by the HVPT. In the control group this percentage was 60%. The low specificity of the HVPT implies that symptom recognition during the HVPT is invalid as a diagnostic criterion for HVS.
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PMID:The low specificity of the Hyperventilation Provocation Test. 903 8

A 92-year-old woman was admitted to our hospital due to hypertension, nausea, pain in the anterior part of the chest, epigastralgia, and tachypnea. During the initial examination of the patient in the emergency ward, she was very excited, howled, and both her hands were numb. Arterial blood gas analysis revealed a marked alkalemia (pH greater than 7.55) and hypocapnia (Pco2 24.1 mmHg). After paper bag re-breathing, the pH and Pco2 were within normal limits. Because there was no lesion in the lungs or the brain that would account for hyperventilation and convulsions, the attack was considered to be a manifestation of hyperventilation syndrome should be carefully considered in the differential diagnosis of disturbance of consciousness even in elderly patients.
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PMID:[Hyperventilation syndrome in a very old woman]. 915 99

Hyperventilation is defined as breathing in excess of the metabolic needs of the body, eliminating more carbon dioxide than is produced, and, consequently, resulting in respiratory alkalosis and an elevated blood pH. The traditional definition of hyperventilation syndrome describes "a syndrome, characterized by a variety of somatic symptoms induced by physiologically inappropriate hyperventilation and usually reproduced by voluntary hyperventilation". The spectrum of symptoms ascribed to hyperventilation syndrome is extremely broad, aspecific and varying. They stem from virtually every tract, and can be caused by physiological mechanisms such as low Pa,CO2, or the increased sympathetic adrenergic tone. Psychological mechanisms also contribute to the symptomatology, or even generate some of the symptoms. Taking the traditional definition of hyperventilation syndrome as a starting point, there should be three elements to the diagnostic criterion: 1) the patient should hyperventilate and have low Pa,CO2, 2) somatic diseases causing hyperventilation should have been excluded, and 3) the patient should have a number of complaints which are, or have been, related to the hypocapnia. Recent studies have questioned the tight relationship between hypocapnia and complaints. However, the latter can be maintained and/or elicited when situations in the absence of hypocapnia in which the first hyperventilation and hypocapnia was present recur. Thus, the main approach to diagnosis is the detection of signs of (possible) dysregulation of breathing leading to hypocapnia. The therapeutic approach to hyperventilation syndrome has several stages and/or degrees of intervention: psychological counselling, physiotherapy and relaxation, and finally drug therapy. Depending on the severity of the problem, one or more therapeutic strategies can be chosen.
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PMID:The pathophysiology of hyperventilation syndrome. 1054 83

The role of carbon dioxide (CO2) is underestimated in the pathomechanism of neuropsychiatric disorders, though it is an important link between psyche and corpus. The actual spiritual status also influences respiration (we start breathing rarely, frequently, irregularly, etc.) causing pH alteration in the organism; on the other hand the actual cytosolic pH of neurons is one of the main modifiers of Ca2+-conductance, hence breathing directly, quickly, and effectively influences the second messenger system through Ca2+-currents. (Decreasing pCO2 turns pH into alkalic direction, augments psychic arousal, while increasing pCO2 turns pH acidic, diminishes arousal.) One of the most important homeostatic function is to maintain or restore the permanence of H+-concentration, hence the alteration of CO2 level starts cascades of contraregulation. However it can be proved that there is no perfect compensation, therefore compensational mechanisms may generate psychosomatic disorders causing secondary alterations in the "milieu interieur". Authors discuss the special physico-chemical features of CO2, the laws of interweaving alterations of pCO2 and catecholamine levels (their feedback mechanism), the role of acute and chronic hypocapnia in several hyperarousal disorders (delirium, panic disorder, hyperventilation syndrome, generalized anxiety disorder, bipolar disorder), the role of "locus minoris resistentiae" in the pathomechanism of psychosomatic disorders. It is supposed that the diseases of civilization are caused not by the stress itself but the lack of human instinctive reaction to it, and this would cause long-lasting CO2 alteration. Increased brain-pCO2, acidic cytosol pH and/or increased basal cytosolic Ca2+ level diminish inward Ca2+-current into cytosol, decrease arousal--they may cause dysthymia or depression. This state usually co-exists with ATP-deficiency and decreased cytosolic Mg2+ content. This energetical- and ion-constellation is also typical of ageing-associated and chronic organic disorders. It is the most important link between depression and organic disorders (e.g. coronary heart disease). The above-mentioned model is supported by the fact that H+ and/or Ca2+ metabolism is affected by several drugs (catecholemines, serotonin, lithium, triaecetyluridine, thyroxine) and sleep deprivation, they act for the logically right direction.
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PMID:The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders. Are the diseases of civilization caused by learnt behaviour, not the stress itself? 2012 95

Dysfunctional breathing is a term describing breathing disorders where chronic changes in breathing pattern result in dyspnoea and other symptoms in the absence or in excess of the magnitude of physiological respiratory or cardiac disease. We reviewed the literature and propose a classification system for the common dysfunctional breathing patterns described. The literature was searched using the terms: dysfunctional breathing, hyperventilation, Nijmegen questionnaire and thoraco-abdominal asynchrony. We have summarised the presentation, assessment and treatment of dysfunctional breathing, and propose that the following system be used for classification. 1) Hyperventilation syndrome: associated with symptoms both related to respiratory alkalosis and independent of hypocapnia. 2) Periodic deep sighing: frequent sighing with an irregular breathing pattern. 3) Thoracic dominant breathing: can often manifest in somatic disease, if occurring without disease it may be considered dysfunctional and results in dyspnoea. 4) Forced abdominal expiration: these patients utilise inappropriate and excessive abdominal muscle contraction to aid expiration. 5) Thoraco-abdominal asynchrony: where there is delay between rib cage and abdominal contraction resulting in ineffective breathing mechanics.This review highlights the common abnormalities, current diagnostic methods and therapeutic implications in dysfunctional breathing. Future work should aim to further investigate the prevalence, clinical associations and treatment of these presentations.
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PMID:Dysfunctional breathing: a review of the literature and proposal for classification. 2758 28


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