Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND. Mortality in pulmonary thromboembolism (PTE) decreases considerable when it is diagnosed early. The suspicion based on clinical and complementary data is essential for an early diagnosis. METHODS. Retrospective review of the clinical features in patients diagnosed of PTE in an Internal Medicine department from January 1993 to December 1999. RESULTS. A total of 117 patients with PTE were identified. The median age was 68.8 years. Sixty-six patients (56.4%) had one or more risk factors for PTE. The most common risk factor was immobilization (37.6%). Dyspnea was the most common symptom (74.4%) and tachypnea the most common sign (66.7%). Fever/low grade fever and leukocytosis were present in 16.2% and 31.6% of patients, respectively. Respiratory failure, alkalosis and hypocapnia were present in 44.4%, 38.5% and 47% of patients, respectively. An alveolar-arterial oxygen gradient > 20 mmHg was demonstrated in 96.6% of patients. Chest radiographs and electrocardiograms were normal in 52.1% and 23.9% of patients, respectively. A vein echo-duplex of the lower limbs demonstrated deep vein thrombosis (DVT) in 52.1% of patients. The hospital mortality rate was 6.8%. CONCLUSIONS. PTE still affects older patients mainly and frequently known risk factors are not detected. The presence of fever/low grade fever and/or leukocytosis does not rule out PTE. Both chest radiographs and electrocardiograms may be normal. Not demonstrating DVT in the lower limbs by the vein echo-duplex does not rule out PTE. The hospital mortality rate has not decreased considerably in the last few years.
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PMID:[The current clinical spectrum of pulmonary thromboembolism]. 1199 39

Air hunger (uncomfortable urge to breathe) is a component of dyspnea (shortness of breath). Three human H(2)(15)O positron emission tomography (PET) studies have identified activation of phylogenetically ancient structures in limbic and paralimbic regions during dyspnea. Other studies have shown activation of these structures during other sensations that alert the organism to urgent homeostatic imbalance: pain, thirst, and hunger for food. We employed blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) to examine activation during air hunger. fMRI conferred several advantages over PET: enhanced signal-to-noise, greater spatial resolution, and lack of ionizing radiation, enabling a greater number of trials in each subject. Six healthy men and women were mechanically ventilated at 12-14 breaths/min. The primary experiment was conducted at mean end-tidal PCO(2) of 41 Torr. Moderate to severe air hunger was evoked during 42-s epochs of lower tidal volume (mean = 0.75 L). Subjects described the sensation as "like breath-hold," "urge to breathe," and "starved for air." In the baseline condition, air hunger was consistently relieved by epochs of higher tidal volume (mean = 1.47 L). A control experiment in the same subjects under a background of mild hypocapnia (mean end-tidal PCO(2) = 33 Torr) employed similar tidal volumes but did not evoke air hunger, controlling for stimulus variables not related to dyspnea. During each experiment, we maintained constant end-tidal PCO(2) and PO(2) to avoid systematic changes in global cerebral blood flow. Whole-brain images were acquired every 5 s (T2*, 56 slices, voxel resolution 3 x 3 x 3 mm). Activations associated with air hunger were determined using voxel-based interaction analysis of covariance that compared data between primary and control experiments (SPM99). We detected activations not seen in the earlier PET study using a similar air hunger stimulus (Banzett et al. 2000). Limbic and paralimbic loci activated in the present study were within anterior insula (seen in all 3 published studies of dyspnea), anterior cingulate, operculum, cerebellum, amygdala, thalamus, and basal ganglia. Elements of frontoparietal attentional networks were also identified. The consistency of anterior insular activation across subjects in this study and across published studies suggests that the insula is essential to dyspnea perception, although present data suggest that the insula acts in concert with a larger neural network.
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PMID:BOLD fMRI identifies limbic, paralimbic, and cerebellar activation during air hunger. 1220 70

People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to altitude and anxiety are apparent in all three leading models of panic, namely, hyperventilation (hypoxia leads to hypocapnia), suffocation false alarms (hypoxia counteracted to some extent by hypocapnia), and cognitive misinterpretations (symptoms from hypoxia and hypocapnia interpreted as dangerous). Furthermore, exposure to high altitudes produces respiratory disturbances during sleep in normals similar to those in panic disorder at low altitudes. In spite of these connections and their clinical importance, evidence for precipitation of panic attacks or more gradual increases in anxiety during altitude exposure is meager. We suggest some improvements that could be made in the design of future studies, possible tests of some of the theoretical causal links, and possible treatment applications, such as systematic exposure of panic patients to high altitude.
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PMID:High altitudes, anxiety, and panic attacks: is there a relationship? 1221 35

Anecdotal observations suggest that hypoxia does not elicit dyspnea. An opposing view is that any stimulus to medullary respiratory centers generates dyspnea via "corollary discharge" to higher centers; absence of dyspnea during low inspired Po(2) may result from increased ventilation and hypocapnia. We hypothesized that, with fixed ventilation, hypoxia and hypercapnia generate equal dyspnea when matched by ventilatory drive. Steady-state levels of hypoxic normocapnia (end-tidal Po(2) = 60-40 Torr) and hypercapnic hyperoxia (end-tidal Pco(2) = 40-50 Torr) were induced in naive subjects when they were free breathing and during fixed mechanical ventilation. In a separate experiment, normocapnic hypoxia and normoxic hypercapnia, "matched" by ventilation in free-breathing trials, were presented to experienced subjects breathing with constrained rate and tidal volume. "Air hunger" was rated every 30 s on a visual analog scale. Air hunger-Pet(O(2)) curves rose sharply at Pet(O(2)) <50 Torr. Air hunger was not different between matched stimuli (P > 0.05). Hypercapnia had unpleasant nonrespiratory effects but was otherwise perceptually indistinguishable from hypoxia. We conclude that hypoxia and hypercapnia have equal potency for air hunger when matched by ventilatory drive. Air hunger may, therefore, arise via brain stem respiratory drive.
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PMID:Hypoxic and hypercapnic drives to breathe generate equivalent levels of air hunger in humans. 1239 Oct 41

At least 31 cases of familial fibrocystic pulmonary dysplasia, within 10 families, have been described in the world literature. The mode of genetic transmission of this disease, however, has been uncertain until now. The author observed three unequivocal and five probable cases of familial fibrocystic pulmonary dysplasia among 56 members of one family. Diagnostic criteria included progressive dyspnea and cyanosis, digital clubbing, pulmonary hypertension, negative sweat tests, polycythemia, arterial hypoxia and hypocapnia, chest radiographs showing diffuse bilateral pulmonary fibrosis, and diffuse fibrocystic pulmonary dysplasia at postmortem examination (two cases). Among the three unequivocal cases one father-to-son transmission was observed. Non-sex-linked dominant transmission of familial fibrocystic pulmonary dysplasia is thereby proved for the first time. One patient also developed a bronchial carcinoma in addition to fibrocystic pulmonary dysplasia; this is considered to be a cause-and-effect relationship and not a coincidental complication.
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PMID:FAMILIAL FIBROCYSTIC PULMONARY DYSPLASIA: OBSERVATIONS IN ONE FAMILY. 1427 97

Idiopathic hyperventilation (IH) is a poorly understood condition of sustained hypocapnia and controversial etiology. Although behavioral/emotional factors may contribute, it is uncertain whether chemosensitivity is altered, hyperventilation is maintained during exercise, and the associated breathlessness reflects the hyperventilation. In 39 patients with IH and 23 control subjects, we described ventilatory responses to isocapnic-hypoxia, hyperoxic-hypercapnia, and exercise; breath-hold tolerance; breathlessness; and psychologic status. Patients demonstrated hyperventilation at rest, with hypocapnia (28 +/- 3.8 mm Hg), a normal (slightly alkaline) arterial pH and [H(+)]a, and a significant base excess (-4.5 +/- 2.7 mEq/L), consistent with compensated respiratory alkalosis. Hyperventilation was sustained during exercise, despite hyperoxic-hypercapnic ventilatory responsiveness being normal and isocapnic-hypoxic ventilatory responsiveness being low relative to control (but exceeding control [2.4 +/- 1.0 vs. 1.6 +/- 0.5 L/min/%, p < 0.05] with acute restoration to normocapnia). Hyperventilation was maintained during exercise, at the resting CO(2) "setpoint." Relative to control, the breath-hold tolerance was attenuated, and dyspnea during exercise was significantly greater and not simply ascribable to the high ventilation. These observations suggest that patients with IH have a sustained hyperventilatory and dyspneic drive that, although not attributable to central chemosensitivity, may possibly have peripheral chemoreflex contributions. The nature and etiology of this chronic hyperventilatory drive remain unclear.
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PMID:Ventilatory responses to inhaled carbon dioxide, hypoxia, and exercise in idiopathic hyperventilation. 1524 48

An 82 year old woman was admitted with worsening dyspnoea. Arterial blood gases were taken on air and revealed a pH of 7.39, with a partial pressure of CO2 (pCO2) of 1.2 kPa, pO2 of 19.3 kPa, HCO3 of 13.8 mmol/litre, and base excess of -16.3 mmol/litre: a compensated metabolic acidosis with hyperventilation induced hypocapnia, which is known to be a feature of lactic acidosis. There was also an increased anion gap ((Na140 + K4.0) - (Cl 106 + HCO3 13.8) = 24.2 mEq/litre (reference range, 7-16)), consistent with unmeasured cation. Lactate was measured and found to be raised at 3.33 mmol/litre (reference range, 0.9-1.7). After exclusion of common causes of lactic acidosis Atorvastatin was stopped and her acid-base balance returned to normal. Subsequently, thiamine was also shown to be deficient. The acidosis was thought to have been the result of a mitochondrial defect caused by a deficiency of two cofactors, namely: ubiquinone (as a result of inhibition by statin) and thiamine (as a result of dietary deficiency).
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PMID:Statin precipitated lactic acidosis? 1533 64

Tracheomalacia is a process characterized by softness of the supporting tracheal cartilages, by the extension of the posterior membranous wall and by reduction of the tracheal antero-posterior diameter. Exceptionally, tracheomalacia can be associated with tracheobronchomegaly or Mounier-Kuhn syndrome. Fibro-bronchoscopy represents the ''gold standard'' for diagnosis. The case of a 79-year-old male observed after hospitalization in a medical ward for chronic pulmonary obstructive disease (COPD) decompensation, and with basal left bronchopulmonary focus, is described. During this period, a progressive worsening of clinical conditions occurred, despite cortisone and antibiotic therapy, and the patient was transferred to the ICU for dyspnea, hypoxia, hypocapnia and with a diagnosis of pulmonary fibrosis. Bronchoscopy, performed during spontaneous breathing, revealed tracheomalacia which was responsible for tracheal dynamic complete stenosis during expiration and dynamic subtotal stenosis of the left primary bronchus in the first tract, together with sputum retention. Moreover, this investigation confirmed the diagnosis of tracheobronchomegaly already seen on CT. It was suggested to place a Freitag stent, since the insertion of another model would not have had enough chance of stability, due to the enormous extension of the tracheal lumen and could not have guaranteed good clearance of the secretions. Seven days after this intervention, performed in an outpatients' setting, the patient was dismissed from the ICU, without the help of O2, with good ventilation, saturation in line with his age and good expectoration.
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PMID:Tracheomalacia associated with Mounier-Kuhn syndrome in the Intensive Care Unit: treatment with Freitag stent. A case report. 1546 97

Idiopathic hyperventilation (IH) is a condition of uncertain aetiology characterized by sustained arterial and alveolar hypocapnia and a plethora of symptoms, the most commonly reported being shortness of breath, and breathlessness. We previously reported that anxiety increases respiratory frequency and minute ventilation with no change in metabolism in normal subjects. In this study, we compared the breathing frequency response to 5% and 7% of CO(2) gas mixtures in normal subjects (n = 13) and in subjects with IH (n = 9), taking into account anxiety and breathlessness in order to determine how breathing patterns may vary with changes in the degree of involvement of higher brain centers because of anxiety and the perception of breathlessness. CO(2) produced a significantly higher value in respiratory frequency (f) in subjects with IH. Subjects with IH also showed lower P(ET)CO(2) than normal subjects. During the inhalation of room air, a significant correlation between f and trait anxiety scores was observed in normal subjects (r = 0.49) and IH subjects (r = 0.69). However, the IH group showed no significantly higher trait anxiety in comparison with normal subjects. There was a significant correlation between the level of perceived breathlessness and f during the inhalation of 5% and 7% CO(2), even during the inhalation of room air in IH subjects. This study suggests that an excessive increase in f in subjects with IH may be due to the interaction of two factors, trait anxiety and breathlessness.
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PMID:Breathing patterns associated with trait anxiety and breathlessness in humans. 1566 70

Physiological activation is a cardinal symptom of anxiety, although physiological measurement is still not used for psychiatric diagnosis. An ambulatory study of phobics who were afraid of highway driving showed a concordance between self-reported anxiety during driving, autonomic activation, hypocapnia, and sighing respiration. Patients with panic attacks do not exhibit autonomic activation when they are quietly sitting and not having panic attacks, but do have the same respiratory abnormalities as driving phobics, suggesting that these abnormalities could be a marker for panic disorder. Such abnormalities are compatible with both the false suffocation alarm (D. Klein) and hyperventilation (R. Ley) theories of panic. Hypocapnia, however, is often absent during full-blown panic attacks. Since activation functions as preparation for physical activity, it may not occur when a patient has learned that avoidance of fear by flight or fight is futile. We developed a capnometry feedback assisted breathing training therapy for panic disorder designed to reduce hyperventilation and making breathing regular. Without feedback, conventional therapeutic breathing instructions may actually increase hyperventilation by increasing dyspnea. Five weekly therapy sessions accompanied by daily home practice with a capnometer produced marked clinical improvement compared to changes in an untreated group. Improvement was sustained over a 12-month follow-up period. The therapist avoided any statements or procedures designed to alter cognitions. Improvement occurred regardless of whether patients initially reported mostly respiratory or non-respiratory symptoms during their attacks. There is evidence that modifying any of the three systems comprising a fear network can be therapeutic, as exemplified by cognitive therapy modifying thoughts, exposure therapy modifying avoidance, and breathing training procedures modifying pCO(2).
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PMID:Physiological markers for anxiety: panic disorder and phobias. 1613 80


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