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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adjusted admission rates for respiratory distress (COPD, asthma, bronchitis, and pneumonia) varied up to 3.09-fold between the highest and lowest hospital market areas in 1986 for the state of Ohio. Reasons for the variability can be determined through small area analysis techniques with the help of area physicians. Substantial improvements in the availability, delivery, and cost of respiratory care would reasonably be anticipated as a result of such analysis and feedback.
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PMID:Small area analysis shows differences in utilization. 182 50

We reported earlier in the 1st report the use of treadmill walk apparatus and transcutaneous blood gas measurement apparatus as a newly designed exercise test. In this report, test was carried out in 90 persons (4 healthy, 66 recovered from pulmonary tuberculosis, 3 recovered from silico-pulmonary tuberculosis, 12 of COPD, and 5 of pulmonary fibrosis et bronchiectasis). The changing curves of transcutaneously measured O2 partial pressure (tPo2) were, as previously reported, classified into 4 types: 1. unchange-6, 2. slightly decreased-38, 3. moderately decreased-24, 4. markedly decreased-21. And unexpected odd curves were seen in 4 patients, 3 of whom were retested the other day, and their changing curves of tPo2 in the second test were corrected and classified into slightly or moderately decreased type. The decreasing slopes of 4 types of tPo2 curves were subclassified, in each type, into 3 to 4 forms. In recovered pulmonary tuberculosis patients, in general, when the spread of pathologic changes in the lungs was wider, the more decreased types of tPo2 curves were seen. But in COPD patients, such was not the case. In the exercise test, total tolerance time (minutes) against the definite load was significantly shorter in the more decreased type; unchanged-13.5-14.5, slightly decreased -7-10, moderately decreased-6-9, and markedly decreased-3-5. The recovering time of tPo2, pulse rate, blood pressure etc. from the records in the end of the exercise to the pre-exercise records, was longer in the more decreased type. On the other hand, usually the lower Pao2 of the patients were, the more their changing curves of tPo2 decreased. Pao2 was previously measured in blood taken from brachial artery in supine position before the test. But exceptionally in some patients with high Pao2 value, the curves belonged to markedly decreased type. The changes of oxygen values of some patients during exercise test were individually different, showing that this exercise test reflected their comprehensive respiratory function. Prognosis was especially bad in patients with markedly decreased type, 8 of whom had died from respiratory failure within 2 years after the test. In conclusion, it can be said that this exercise test was effective in judging the pulmonary reserve function and the prognosis in recovered pulmonary tuberculosis patients, but more detailed investigations are necessary, especially in more COPD patients, for the understanding of the respiratory distress.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Blood gas changes during treadmill exercise in convalescents from pulmonary tuberculosis. 2. Clinical results]. 192 Oct 94

While medical treatment of COPD has advanced, the failure to adhere to regimens for medication poses a significant barrier to effective management. Furthermore, no data are available regarding adherence for patients within the United States. Data from this investigation indicate that 78 outpatients from a medical center in the southeastern region of the United States were prescribed an average of 6.26 medications with both various dosing schedules and different modes of administration. Adherence was poor, with 42 patients (54 percent) underutilizing medications, 39 patients (50 percent) overutilizing medications during periods of respiratory distress, and 24 patients (31 percent) employing ineffective inhaler dosing techniques. Prescription patterns and adherence were not associated with demographic variables; however, adherence was related to classes of medication and situational variables.
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PMID:Medication adherence patterns in chronic obstructive pulmonary disease. 200 84

Dysphagia due to cricopharyngeal dysfunction is well known; however, there have been no previous data indicating an association between cricopharyngeal dysfunction and COPD. After observing marked cricopharyngeal dysfunction with aspiration in three patients who had frequent and severe exacerbations of COPD, we performed pharyngoesophageal examinations with videotaping in another 22 nonrandomized patients. Cineradiography or videofluoroscopic recording with capabilities of slow-motion and freeze-frame playback is mandatory, since the transit time of the bolus through the pharynx is rapid. Severe cricopharyngeal dysfunction was observed in 17 elderly patients with COPD. Deglutition disorders were elicited by careful questioning in 15 of these. In eight subjects, cricopharyngeal myotomy resulted in improvement of swallowing and complete or partial relief of acute exacerbations of respiratory distress. In one subject, myotomy relieved only the swallowing problem. The mechanism of cricopharyngeal dysfunction in elderly patients with COPD is unknown at this time, but may be related to gastroesophageal reflux, therapeutic agents, and/or alterations in pharyngoesophageal anatomic structures. We conclude that investigations for swallowing disorders should be considered in patients with COPD who have frequent acute exacerbations of respiratory distress.
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PMID:Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. 229 59

Pulmonary infection due to the filariform larvae of Strongloides stercoralis may occur in immunocompromised patients residing in endemic areas of the United States. Such infection usually presents as dyspnea with a cough that sometimes results in bloody sputum. Although the chest roentgenogram often reveals a patchy bilateral alveolar infiltrate, acute respiratory distress is unusual. We report a patient who experienced severe exacerbation of his underlying obstructive lung disease that was associated with chest infiltrates and recovery of S stercoralis from his sputum. Although initial improvement was accomplished with Thiobendazole treatment, a re-exacerbation occurred when antiparasitic therapy was completed. The persistence of his infection is correlated to factors that are commonly employed in the treatment of COPD but may be overlooked as predisposing causes of hyperinfection with S stercoralis.
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PMID:Exacerbation of chronic obstructive pulmonary disease due to hyperinfection with Strongyloides stercoralis. 234 69

When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known. When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred. Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated. The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients. The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 70% oxygen is probably safe for 24 hours; and after this time, 45% should be the approximate upper limit to the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxygen therapy and oxygen toxicity. 641 43

The lung is particularly exposed to various inhaled toxic products whose toxicity can be at least partly mediated by the generation of free radicals. Oxidants burden can also result from lung metabolism of xenobiotics or from activation of phagocytes. Free radicals are mainly derived from an univalent sequential reduction of molecular oxygen. Mitochondria is the main location of intracellular production which may also result from auto-oxidation of small molecules or function of some enzymes. To prevent the deleterious effects of free radicals produced by normal metabolism, cells are equipped with an antioxidant system composed of enzymes (superoxide dismutase, catalase, glutathione peroxidase) and non enzymatic substances such as glutathione, iron chelators, vitamin E and C, ceruleoplsamin). Targets of free radicals toxicity are phospholipids by initiation of lipid peroxidation, proteins which may be activated or inactivated via oxidation of sulfhydryl residues. Another target is DNA with possible strand breaks or mutation. Transcription activities can be also altered and it has been recently reported that some transcription factors such as NF-kB can be activated by oxidants. Under these circumstances free radicals may be considered as second messengers. Lung oxygen toxicity has been largely studied. Oxygen-induced lung lesions are non specific. It is possible to induce a resistance to 100% O2 by the pre-exposure of animals to 85% O2. This tolerance phenomenon is associated with an increased lung content in antioxidant substances. The mechanisms of gene regulation of antioxidant enzymes are still poorly understood in eukaryotes. Overproduction of free radicals in the lung is also involved in various clinical settings such as ischemia-reperfusion, exposure to ozone or NO2, acute respiratory distress syndrome, drug induced lung toxicity, pathogenesis of COPD, asthma, cancer and ageing. The precise role of free radicals among other mechanisms of lung injury is still unclear. A better knowledge of free radicals mechanisms of toxicity and of antioxidant regulation is needed to develop antioxidant therapeutic strategies.
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PMID:[Free radicals and respiratory pathology]. 773 56

Breathing 100% O2 is a way of slowing breathing rate, decompressing hyperinflated, low VA/Q lung units, reducing the FRC and allowing the patient with COPD in acute respiratory failure to breath at a more comfortable lung volume and with a higher tidal volume. This should also improve the efficiency of breathing, increasing the fractional turnover of alveolar gas. Simultaneously O2 protects the brain, heart and other organs from hypoxic injury. Breathing 100% O2 provides the major therapeutic approach for rapidly reversing the pathophysiological cycle of impaired respiratory mechanics which threatens the life of the patient in acute respiratory failure. It is a therapeutic approach which might be employed in the tachypnoeic patient in acute respiratory distress, before initiating airway intubation and mechanical ventilation. This provides the physician with time to allow other mechanisms of bronchodilating the patient to be started, and for the need of a more aggressive approach to airway management to be evaluated.
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PMID:Uses of oxygen in the treatment of acute respiratory failure secondary to obstructive lung disease. 831 15

Noninvasive positive pressure ventilation (NPPV) has been proposed in COPD patients with acute on chronic respiratory failure (ACRF) in order to avoid endotracheal intubation and to improve immediate outcome, but long-term outcome of this therapeutic approach is still undefined. We evaluated short- and long-term (1 year) outcome of early administration of NPPV in 24 patients with ACRF due to exacerbated COPD (Group A) in comparison with 24 matched historical-control patients treated conventionally (Group B). Patients of Group A were initially treated with NPPV via nasal mask in the presence of pH < or = 7.32, and/or Pa,O2 < 7.98 kPa, and/or Pa,CO2 > 7.18 kPa, plus signs of respiratory distress. In-hospital survival rate was not significantly different in Group A vs Group B, but the patients treated with NPPV showed an earlier improvement in blood gases and a better pH and respiratory rate at discharge. Only 2 patients of Group A needed endotracheal intubation as compared with 9 of Group B. Hospital stay was significantly reduced in survivors of Group A vs Group B. Further severe relapses of ACRF in Group A were treated using NPPV. The number and length of further hospitalizations for pulmonary exacerbations were significantly higher in Group B compared with Group A. The survival rate at 12 months was significantly lower in Group B than in Group A (50% vs 71%). In conclusion, NPPV administration in patients with ACRF due to exacerbated COPD improves not only immediate but also long-term outcome.
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PMID:Noninvasive mechanical ventilation improves the immediate and long-term outcome of COPD patients with acute respiratory failure. 872 99

Respiratory mechanics, using flow interruption, was previously studied during the complete breath in healthy ventilated man, numerical techniques relieving constraints regarding flow pattern. The classical linear model of non-Newtonian behaviour was found to be valid. The present study was extended to subjects with critical lung disease. Subjects with acute lung injury (ALI; n = 2), acute respiratory distress syndrome (ARDS; n = 4), and chronic obstructive pulmonary disease (COPD; n = 3) were studied with and without positive end-expiratory pressure (PEEP). Functional residual capacity (FRC) was measured with sulphur hexafluoride (SF6) wash-out. The static pressure-volume (P-V) curve was linear at zero end-expiratory pressure (ZEEP), but nonlinear at PEEP. Its hysteresis was nonsignificant. In ALI/ARDS, PEEP increased lung volume by distension and recruitment, but only by distension in COPD. In ALI/ARDS, resistance was increased, at ZEEP. In COPD, resistance became extremely high during expiration at ZEEP. In ALI/ARDS at ZEEP, non-Newtonian behaviour, representing tissue stress relaxation and pendel-luft, complied with the classical linear model. At PEEP, the non-Newtonian compliance became volume-dependent to an extent correlated to the nonlinearity of the static P-V curve. In COPD, non-Newtonian behaviour was adequately explained only with a model with different inspiratory and expiratory behaviour. The classical model of the respiratory system is valid in ALI/ARDS at ZEEP. More advanced models are needed at PEEP and in COPD.
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PMID:Respiratory mechanics in patients ventilated for critical lung disease. 877 62


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