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)

The Asthma Symptom Checklist (ASC), describing the subjective symptoms reported to occur during asthmatic attacks, has been developed previously. In the present study, the ASC key cluster solution was replicated and refined within a sample of 374 asthmatic inpatients. All of the original symptom categories were reporduced, including two mood categories, Panic-Fear and Irritability, a Fatigue category, and two somatic categories. Hyperventilation-Hypocapnia and Airway Obstruction. Two refinements were notable: (1) The Airway Obstruction category was empirically divided into two conceptually clear components, Dyspnea anc Congestion, and (2) three secondary mood categories, Worry, Loneliness, and Anger, were identified, which describe a continuum of mood between the polar extremes of panic and irritability. Of the symptom categories, only Panic-Fear was related to the intensity of the discharge drug regimens recommended 2 to 6 mouths after ASC administration. Panic-Fear scores were independent of pulmonary function measurements. A combined index based on pulmonary functions and panic-fear yielded the best prediction of discharge steroid regiments. Finally, those physicians rated highest in "sensitivity" to their patients by their supervisors prescribed less steroids overall, but most frequently prescribed discharge steriod regimens in relation to their patients' Panic-Fear scores. In contrast, physicians rated lower on sensitivity prescribed higher steroid regimens overall, but based these drug recommendations more cleary on objective pulmonary functioning, and not in relation to their patients' Panic-Fear scores. The results strongly suggest that the ASC Panic-Fear scale is associated with coping behaviors that importantly affect the patient's overall clinical picture by increasing the apparent severity of the asthma, thereby leading to intensified treatment. The findings stress the need to evaluate independently the objective medical condition and subjective symptomatology with its related coping behavior, in order to direct appropriate modes of therapy to each.
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PMID:Obervations on subjective symptomatology, coping behavior, and medical decisions is asthma. 40 66

The purpose of this study was to compare psychologic and physiologic variables during intense dyspnea to those at times of no or low dyspnea in people with asthma. Thirty-six adults ranging from 19 to 76 years old were tested when they first came to the emergency department in acute dyspnea and again when they had no or low dyspnea just prior to discharge. Clinical signs found to be higher during high dyspnea than low dyspnea were respiratory rate, pulse, wheezing, and accessory muscle use. Peak expiratory flow rates and oxygen saturation were significantly lower, while anxiety, depression, somatization, and hostility were higher during times of high dyspnea. The panic/fear, fatigue, dyspnea, hyperventilation/hypocapnia, congestion, and rapid breathing subscales of the Asthma Symptom Checklist were also higher during high dyspnea compared to low dyspnea.
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PMID:Psychologic and physiologic aspects of acute dyspnea in asthmatics. 185 43

We studied the relationship between contractile function and intracellular pH (pHi) in the isolated rat diaphragm when superfusate PCO2 was changed during hyperoxia or hypoxia. Superfused diaphragm strips were field stimulated at 0.5 Herz, and twitch tension (TT) was recorded. The pHi was calculated from the volume distribution of a weak acid, dimethyl-oxazolidinedione. In hyperoxia, hypercapnic acidosis (pH 7.06-6.63) depressed diaphragm pHi and TT, whereas hypocapnic alkalosis (pH 7.82-8.15) increased pHi but did not significantly affect TT. TT was maximum at physiological pHi (7.06), but in hyperoxic hypercapnic muscles substantial force was still generated at pHi values as low as 6.44. Hypoxia (PO2 30-38 mm Hg) markedly reduced TT; this effect was slightly exacerbated by hypercapnia and attenuated by hypocapnia. Hypoxia lowered pHi by about 0.2 units, which was insufficient to account for the hypoxic contractile failure. Knowledge of the hyperoxic muscle TT/pHi relationship suggests that, in other contexts, caution should be exercised in attributing severe muscle fatigue or force loss to modest falls in pHi.
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PMID:The effect of pH and hypoxia on function and intracellular pH of the rat diaphragm. 210 18

We studied 10 open-chest dogs and measured the pressure across the diaphragm (Pdi) in each period of the protocol during stimulation at frequencies of 1, 20, 50, and 80 Hz. Three ranges of arterial PCO2 (PaCO2) were examined: less than or equal to 26, 36-50, and greater than or equal to 89 Torr. The diaphragm was fatigued with repetitive phrenic stimulation (30 Hz). During the fatiguing activity, five of the animals were subjected to hypercapnia and the other five to hypocapnia. A frequency-Pdi curve was generated for each period in the protocol. The data show that 1) fatiguing to 50% of the initial Pdi value during hypercapnia was significantly more rapid than during hypocapnia; 2) both the prefatigue and postfatigue mean Pdi values over all interactions of frequency, fatigue, and PaCO2 were unaffected by the fatiguing environment (hypercapnia vs. hypocapnia); 3) the percent reduction of Pdi by hypercapnia was the same at all four frequencies; 4) hypocapnia did not alter either the pre- or postfatigue frequency-Pdi curve; and 5) one-half relaxation time, unaffected by PaCO2, was prolonged by fatigue. We conclude that the hypercapnic diaphragm has less endurance than the hypocapnic diaphragm and that although both fatigue and hypercapnia decrease Pdi, they appear to be separate entities working through different mechanisms.
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PMID:Interaction of fatigue and hypercapnia in the canine diaphragm. 313 51

A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.
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PMID:Primary pulmonary hypertension. A national prospective study. 360

We studied the effects of acute changes in the partial pressure of arterial carbon dioxide on diaphragmatic contractility and performance in four normal men. To study contractility we measured the ability of the diaphragm to generate pressure at a given level of excitation by determining the relation between the electrical activity of the diaphragm and transdiaphragmatic pressure during a voluntary quasi-isometric inspiratory effort carried out at different levels of end-tidal carbon dioxide. Our results show that contractility was reduced with hypercapnia (when end-tidal carbon dioxide was 7.5 per cent or higher), although hypocapnia (end-tidal carbon dioxide, 3 per cent) had no effect on diaphragmatic contractility. We also studied the development of diaphragmatic fatigue before and during carbon dioxide breathing. Subjects were studied at the same diaphragmatic tension-time index, a value analogous to the more familiar myocardial tension-time index, while the same inspiratory flow was maintained. Electromyographic signs of fatigue appeared at a lower tension-time index during hypercapnia than during normocapnia, indicating that endurance is diminished during hypercapnia. These findings show that acute respiratory acidosis equivalent to an arterial carbon dioxide tension of about 54 mm Hg decreases the contractility and endurance time of the diaphragm in human beings.
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PMID:Effect of carbon dioxide on diaphragmatic function in human beings. 642 98

The syndrome of chronic heart failure is characterized by exercise intolerance. Exercise is limited by shortness of breath and fatigue, and either symptom occurs in the same patient depending on the type of exercise performed. Exercise capacity correlates poorly with indices of central hemodynamic function, but the increased ventilatory response in chronic heart failure correlates well with exercise capacity. Possible pulmonary causes have been explored, including increased dead space ventilation, abnormal airway function, and abnormal diffusion capacity. However, the finding of hypocapnia and hyperoxemia in arterial blood during exercise in patients with heart failure suggests that blood gas values reflect hyperventilation, and that any abnormality of pulmonary function is secondary to changes elsewhere. Skeletal muscle is abnormal in chronic heart failure, and shows changes in structure, bulk, exercise capacity, blood flow, and intrinsic metabolic activity. The relative importance of these abnormalities is not clearly determined, but the possible presence of an ergo- or metaboloreceptor connection between abnormal exercising muscle and the ventilatory response to exercise suggest a mechanism linking the two cardinal symptoms of chronic heart failure.
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PMID:Mechanisms of exercise intolerance in cardiac failure: abnormalities of skeletal muscle and pulmonary function. 804 88

During exercise: the Kety-Schmidt-determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by (133)Xe clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a approximately 25% increase is detected with a parallel increase in metabolism. During activation, an increase in cerebral O(2) supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units, and supplemental O(2) enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also, the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise, the perceived exertion is related to accumulation of ammonia in the brain, and data support the theory that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin-6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow-twitch muscle fiber populations.
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PMID:Cerebral blood flow and metabolism during exercise: implications for fatigue. 1796 75

In about 20% of patients admitted to an Intensive Care Unit (ICU) the indication of mechanical ventilation (MV) is a neurological disease. These patients have a prolonged MV stay and high mortality. The appropriate use of MV in patients with acute brain injury (ABI) is critical considering that MV by itself is able to induce or worsen an underlying lung injury. Patients with ABI have a higher risk to develop pulmonary complications. During endotracheal intubation the activation of airway reflexes should be prevented, because they may increase intracranial pressure. Tracheostomy is indicated to improve airway management and it is performed in about 33% of these patients. Indications for MV are loss of spontaneous respiratory effort, changes in lung compliance, gas exchange impairment and ventilatory failure due to muscle fatigue or neuromuscular junction dysfunction. During MV, hypoxemia should be avoided. The pC0(2) level has a critical role in cerebral blood flow regulation; therefore a normal pCO must be maintained in order to guarantee an optimal cerebral blood flow. Despite that, hypocapnia has been used in patients with increased intracranial pressure, at the present it is not recommended. Its use should be limited to the emergency management of intracranial hypertension, while the underlying cause is being treated. Non-conventional ventilatory modes as prone position ventilation, high-frequency oscillatory ventilation and extracorporeal C02 removal can be used in patients with ABI. All of them have specific risks and should be employed cautiously This paper reviews upper airway management and MV in patients with acute brain injury.
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PMID:[Mechanical ventilation in patients with acute brain injury]. 2187 73

Patients affected by pulmonary arterial hypertension (PAH) show a reduced exercise tolerance with early occurrence of dyspnoea and fatigue. The origin of functional capacity limitation is multifactorial and several mechanisms have been proposed, including right heart failure, which leads to a limited increase in cardiac output during exercise, and hyperventilation with a reduced perfusion of properly ventilated alveoli. In addition, abnormalities in arterial blood gases are observed, with the occurrence of hypoxemia and hypocapnia, related to an abnormal ventilation/perfusion match, gas diffusion abnormalities, low mixed venous oxygen saturation and to the development of intra- and extra-pulmonary right-to-left shunts. At present, the 6-minute walking test is the most used method to assess exercise tolerance in PAH; it is also useful to monitor the response to therapy and provides prognostic information. However, the assessment of functional capacity by cardiopulmonary exercise test (CPET) seems to be more complete, because CPET allows for discrimination between the metabolic, cardiovascular and pulmonary components of exercise limitation. Moreover, CPET estimates the severity of disease and assesses patients' prognosis and response to therapy. In PAH, a typical CPET-response is observed, characterized by a severe reduction in peak VO2, work rate, O2 pulse and anaerobic threshold and by a marked increase in VE/VCO2 slope and in the dead space to tidal volume ratio. However, the use of CPET should be limited to experienced centres. This review will focus on resting lung function and exercise tolerance tests, showing that CPET can provide the physiological explanation of functional limitation in PAH.
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PMID:Exercise testing in the clinical management of patients affected by pulmonary arterial hypertension. 2312


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