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

Of 16 patients with hyperventilation syndrome (HVS), 11 experienced hypoxemic episodes (defined as PaO2 < or = 60 Torr or SaO2 < or = 90%). To investigate the relationship between hypoxemia in HVS patients and their hypoxic ventilatory response (HVR), we examined 9 of 11 HVS patients who experienced hypoxemic episodes after acute hyperventilation attacks. In order to investigate the genesis of hypoxemia after hyperventilation, we also examined minute ventilation and visual analog scale (VAS) scores representing the sensation of dyspnea at the start and at 70% arterial O2 saturation (SaO2) during HVR in 9 normal subjects under isocapnia and hypocapnia following voluntary hyperventilation (VHV). The HVR of 9 HVS patients who experienced hypoxemic episodes was normal. In 9 normal subjects, minute ventilation and VAS scores representing the sensation of dyspnea at 70% SaO2 during HVR were higher under isocapnia than under hypocapnia following VHV (p < 0.01). VAS scores taken during the HVR immediately following VHV and at 70% SaO2 were not significantly different. HVR and VAS scores representing the sensation of dyspnea were decreased under hypocapnia following VHV. These reductions were thought to be the main factors responsible for the genesis of hypoxemia following acute hyperventilation attacks in HVS patients. We conclude that hypoxemia is an important clinical sign in HVS patients, and it is important to investigate the breathing and chemical drive under hypocapnia, in order to understand the chemical regulation of breathing in HVS patients.
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PMID:[Hyperventilation syndrome]. 130 18

The symptoms of the hyperventilation syndrome (HVS) are sometimes diffuse, and HVS may resemble other clinical conditions. A diagnosis of HVS was made in 25 patients referred for neurological assessment because of atypical, shortlasting, episodic complaints. The referral diagnoses varied within a wide range. A need for more indepth knowledge about this group of patients thus arose. During a provocation test with forced respiration, all patients reported symptoms similar to those during attacks. Eight patients described numbness or paraesthesias with unilateral predominance. End-tidal pCO2 levels were monitored prior to and during a forced hyperventilation test. Compared with controls, the patients had significantly decreased end-tidal pCO2 even during symptom free periods. After hyperventilation, hypocapnia followed a protracted course in the patient group. Sensory symptoms may be asymmetric and mimic focal cerebral disease. Strained respiration may be denied during spontaneous attacks. Personality characteristics were evaluated with the Minnesota Multiphasic Personality Inventory (MMPI). A mean group profile very similar to profiles reported on "pseudoepileptic" patients was found. The profile indicates a neurotic pattern where patients tend to respond to psychological stress with somatic symptoms.
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PMID:Hyperventilation syndrome: clinical, ventilatory, and personality characteristics as observed in neurological practice. 236 Mar 97

A 52-year-old woman developed subjective right hemiparesthesias over a two-day period. Because of a paucity of physical findings, apparent anxiety with tachypnea, and a respiratory alkalosis with hypocapnia, a diagnosis of hyperventilation syndrome was considered. However, because of the unilateral symptoms, a computed tomography scan was performed, demonstrating a left posterior thalamic infarct. Most reports of thalamic infarct indicate altered mental status, vertical gaze palsies, or sensorimotor hemiparesis with sensory involvement predominant. The case of a patient with thalamic hemorrhage who presented with only hemiparesthesia is reported to heighten clinicians' awareness of this diagnosis.
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PMID:Thalamic hemorrhage imitating hyperventilation. 238 66

A hyperventilation provocation test (HVPT) was performed on a group (n = 63) of consecutive patients, below the age of 40 years, attending an emergency care unit complaining of chest pain without obvious organic cause. The results were compared with those for a control group (n = 32). There was no tendency to hyperventilate in the patient group, either after discontinuing hyperventilation or during the ensuing relaxation period. PETCO2 measurements during this time thus showed no significant differences between the patient group and the control group. During the HVPT, 44% of patients reported three or more listed symptoms familiar to them from earlier occasions and regarded as typical of hyperventilation, compared to 23% of the controls (P less than 0.05). In a previously reported study, 38% of the patients were found to have similar symptoms during standardized mental stress, despite lack of hypocapnia. It is concluded that, on the basis of PETCO2 measurements, there were no signs of abnormal hyperventilation in the patient group. Moreover, the HVPT did not appear to be specific for diagnosis of hyperventilation syndrome, since mental stress itself was able to reproduce symptoms without concomitant hypocapnia, and since the provocation test was 'positive' in many control subjects.
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PMID:Acute chest pain without obvious organic cause before the age of 40 years: response to forced hyperventilation. 205 66

There is uncertainty about the diagnosis and definition of the hyperventilation syndrome. We prefer to regard hyperventilation (or hypocapnia with which it is synonymous) as a physiological response to abnormally increased respiratory "drive", which can be caused by a wide range of organic, psychiatric and physiological disorders, or a combination of these. This review outlines a clinical scheme for the diagnosis and assessment of hyperventilation and its causes.
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PMID:Hyperventilation clinical practice. 277 33

A review of literature comprises the main data on etiological factors, pathogenetic mechanisms, clinical peculiarities and methods of diagnosis of the hyperventilation syndrome. Physicians' insufficient knowledge of this disease is emphasized. Various clinical manifestations are based on the same pathogenetic mechanisms of acute or chronic respiratory disregulation resulting in hypocapnia, a rise of vascular tone, and electrolytic disorders. Of great practical importance is the use of a unified clinical classification, of which a variant is proposed by the authors. The main therapeutic modalities are: 1) psychotherapy, 2) pharmacotherapy, 3) exercise therapy.
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PMID:[The hyperventilation syndrome]. 306 57

A 42 year old woman with long standing Raynaud's disease, unresponsive to medical and surgical treatment, was noted to have a typical history of the hyperventilation syndrome. Rewarming of the hands following cold challenge was markedly prolonged in the presence of hypocapnia. It is suggested that hyperventilation may have an aetiological role in maintaining digital artery spasm in Raynaud's disease, which would benefit from recognition and treatment.
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PMID:Hyperventilation and Raynaud's disease. 367 Dec 72

The heart rate and electrocardiographic responses were documented in 40 subjects undergoing hyperventilation provocation tests. Forced overbreathing produced a similar mean heart rate increase in all subjects, regardless of whether the result of the provocation tests suggested the hyperventilation syndrome. In contrast subjects diagnosed as hyperventilators by virtue of prolonged hypocapnia in response to psychological provocation showed significant increased heart rate responses compared to the remaining subjects (p less than 0.001). Significant electrocardiographic abnormalities were also produced. The view is presented that the hypocapnia may allow persistence of the cardiovascular responses in the presence of emotional challenge.
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PMID:Heart rate response, emotional disturbance and hyperventilation. 376 Dec 28

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

The hyperventilation syndrome (HVS) is a functional disorder with repeated involuntary hyperventilation attacks together with symptoms of respiratory alkalosis. We have studied the EEG and end-tibial pCO2 in the resting state and during hyperventilation activation in 12 HVS patients in order to find out whether there is a greater susceptibility to cerebral vasoconstriction in HVS patients than in controls, as indicated by slowing of the EEG. A surprisingly high proportion (58%) of abnormal resting EEGs was found in HVS patients, although the patients were neurologically normal. More theta and beta background activity was usually revealed in a quantitative computer analysis, especially frontally. Although the hyperventilation activation caused the same degree of hypocapnia in HVS patients and in controls, peripheral symptoms like tingling and numbness of fingers, as well as carpopedal spasms, occurred much more often in HVS patients. However, the EEG changes due to hyperventilation were similar in both HVS patients and normal controls, and it thus seems that the reason for cerebral symptoms in HVS patients is not a greater susceptibility to cerebral vasoconstriction.
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PMID:EEG and end-tidal carbon dioxide concentration in the hyperventilation syndrome. 616 Sep 92


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