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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracorporeal membrane oxygenation (ECMO) is a new and, in the hands of an experienced team, safe method for treating severe acute respiratory insufficiency. It protects the patient against the risk of hypoxia and respiratory acidosis and, provided there is a chance of survival, allows the repair of the damaged lung tissue. The chances of success depend on whether the lung damage is reversible since, so far as is known, ECMO has not, or only very rarely, any effect on the actual lesion. Reliable prognostic criteria are therefore needed in the choice of suitable cases. Persons with acute non-infectious lung disease who receive this treatment within a few hours or days after the onset of the disease have the best chances of survival.
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PMID:[Indications for and results of extracorporeal membrane oxygenation (author's transl)]. 91 70

Circumstances under which the use of oxygen-therapy in lung disease can be effective and harmless, depend upon a careful evaluation of its indications: they are suggested by the clinical need of correction of hypoxaemia as well as by the awareness of factors determining respiratory failure and of problems concerning O(2) transport and supply to tissues in health and disease. Blood gases monitoring enables to control the effects of treatment on arterial O2 and CO2 tensions thus giving all the useful data for oxygen administering particularly as far as components of hyperoxygenated mixtures, flow rate, duration, use of very effective low-risk devices (Venturi masks) are concerned. Correction of hypoxaemia involves the reduction of hypertension of the pulmonary circulation and hyperglobulia, improvement of tolerance of exertion, and attention to the metabolic compensation of respiratory acidosis. These results are influenced by the nature of the pathogenetic factors behind broncho-obstructive disease, which may lead to either a primarily "bronchitis" or a primarily "emphysematous" syndrome. An interesting feature relates to prognosis in the case of patients making home use of hyperoxygenated mixtures as part of a rehabilitation program, or to improve their quality of life. The cost and benifits of such treatment should be carefully weighed. Lastly, in the event of protracted treatment, attention must be paid to the possibility of toxicity and the means to be adopted for its prevention.
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PMID:[Oxygen therapy in pneumology]. 101 8

A new automatic ionized calcium analyser ICA 2 (Radiometer, Copenhagen, Denmark) was used for studies of ionized calcium (cCa2+) in the arterial blood of patients with a compensated respiratory acidosis due to chronic lung disease. The data for 16 patients showed an unexpectedly high level of variation in cCa2+ (range, 1.01-1.25 mmol l-1) despite the fact that there was only a small degree of variability in pH (range, 7.38-7.51). cCa2+ was not correlated with pH as has been observed in acute respiratory disturbances. A highly significant negative correlation was found between cCa2+ and base excess (BE) (r = -0.81, P less than 0.0001), and between cCa2+ and carbon dioxide tension (PCO2) (r = 0.71, P less than 0.002). These correlations differed from those reported previously in acute respiratory disturbances. CCa2+ showed a significant positive correlation with oxygen tension (PO2) (r = 0.71, P less than 0.002). It is concluded that cCa2+ in arterial blood from patients with chronic lung disease is correlated with acid-base and gas quantities in an entirely different manner to that observed in acute acid-base disturbances in normal adults.
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PMID:Ionized calcium in blood: studies on patients with pulmonary disease. 191 74

Cor pulmonale is right ventricular enlargement secondary to pulmonary hypertension. Although most often caused by parenchymal lung disease, derangements of the ventilatory drive, the respiratory pumping mechanism, or the pulmonary vascular bed may also result in right ventricular hypertrophy and dilatation. Arterial hypoxemia (and resultant polycythemia), hypercapnia, and respiratory acidosis all contribute to the increased afterload on the right ventricle. Diagnosis is often difficult, since pulmonary vascular disease, pulmonary hypertension, and cor pulmonale have few specific manifestations, especially early in their evolution. Treatment is primarily directed at the underlying pulmonary or ventilatory disorder, rather than at the right ventricular failure per se. Supplemental oxygen is essential to avoid hypoxia; corticosteroids, anticoagulants, vasodilators, and other specific therapies are used as indicated to treat the underlying pulmonary disorders. When medical therapies fail, lung or heart-lung transplantation has become a possibility for selected patients.
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PMID:Chronic cor pulmonale. Etiology and management. 239 36

The inability to increase alveolar ventilation can lead to CO2 retention and acute respiratory acidosis in patients with ventilatory limitation. In this case, a young woman receiving maximum ventilatory support was unable to excrete excess CO2, associated with increasing dianeal concentrations of peritoneal dialysis. Since the patient's lung disease had necessitated a large amount of ventilatory support, the patient was unable to increase VE appropriately to handle excess CO2. Peritoneal dialysate was an additional source of carbohydrates. Peritoneal dialysate is an additional carbohydrate source that may result in hypercapnia and respiratory acidosis in patients with respiratory compromise. To our knowledge, this is the first case report in an adult which demonstrates that peritoneal dialysis with high glucose loads produced an acute respiratory acidosis that was reversed by decreasing the glucose concentrations in the dialysate. Excess CO2 production should be considered with respiratory disorders associated with dialysis.
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PMID:Dialysis-induced respiratory acidosis. 222 84

This paper describes 19 consecutive episodes (18 patients) of status asthmaticus managed in a medical intensive care. Eleven patients required mechanical ventilatory support [MV] and 2 (11%) died. Most patients had acute respiratory acidosis although arterial blood gases alone could not predict the need for MV. The peak inspiratory airway pressure measured during MV was a useful index of the severity of underlying lung disease. The most serious complication of MV was barotrauma. On follow up studies, two distinctive patterns of chronic asthma could be identified. One group of patients had highly labile pulmonary function with unpredictable and wide changes in peak flow rates while another group had poorly reversible obstruction.
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PMID:Status asthmaticus in a medical intensive care. 281 33

It is common practice to use endotracheal continuous positive airway pressure for various time periods up to 24 hours before attempting extubation in infants who are mechanically ventilated. A few studies in newborns have indicated that airway resistance is increased through small endotracheal tubes. This increases the work of breathing and the likelihood of subsequent ventilatory failure. In this study, 27 very low birth weight infants who were 1/2 to 28 days old at the time of extubation were randomly divided into two groups. One group of 13 study infants were extubated directly from intermittent mandatory ventilation rates of six to ten per minute, and the other 14 control infants were placed on continuous positive airway pressure through endotracheal tubes for six hours prior to an attempt to extubate. There was no difference between the two groups in gestational age, postnatal age, weight, or severity of lung disease at the time of extubation. All 13 study infants were successfully extubated without significant apnea or respiratory acidosis. Of the 14 control infants, only seven were successfully extubated; six infants had significant apnea and in one infant respiratory acidosis with pH 7.13 and PCO2 65 developed while receiving continuous positive airway pressure (13/13 v 7/14, P less than .005). The seven infants who failed the preextubation trial of continuous positive airway pressure were later extubated from low intermittent mandatory ventilation rates without significant apnea or respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Successful direct extubation of very low birth weight infants from low intermittent mandatory ventilation rate. 311 10

To test the hypothesis that furosemide would cause metabolic alkalosis and thus alveolar hypoventilation, normal rabbit pups were given either furosemide (4 mg/kg/day) or saline solution for the first 8 to 10 days of life. Pups given furosemide developed primary metabolic alkalosis and reduced ventilation, which resulted in secondary respiratory acidosis. Lung compliance was improved by furosemide, and the ventilatory response to CO2 was unaffected. KCl injection in alkalotic pups increased ventilation and decreased pH. The data show that conventional doses of furosemide can (1) cause metabolic alkalosis and reduce ventilation; (2) increase the PaCO2, which reflects changes in acid-base status and not changes in lung function; and (3) increase lung compliance, perhaps by decreasing lung water. When these effects occur in infants with chronic lung disease, the beneficial effect of furosemide may be obscured.
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PMID:Furosemide decreases ventilation in young rabbits. 391 2

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

The pulmonary course and respiratory management of 65 asphyxiated infants with at least one arterial pH less than or equal to 7.00 within the first 2 hours of life was determined. Asphyxia in the preterm and term infants in the absence of respiratory distress syndrome or meconium aspiration syndrome was associated with a transient respiratory insufficiency requiring assisted ventilation which markedly improved in the first 24 hours of life. In contrast, infants with asphyxia complicated by respiratory distress syndrome or meconium aspiration syndrome developed profound lung disease including pulmonary hemorrhage and persistence of the fetal circulation. The course of their illness was significantly worse than control infants without asphyxia. Ineffective neonatal resuscitation allowing for the development of meconium aspiration syndrome and persistent respiratory acidosis contributed to the severity of illness in more than 50% of the infants. Central nervous system pathologic conditions were present in asphyxiated infants with and without severe pulmonary disease. We conclude that severe asphyxia in the absence of underlying lung disease results in a predictable postasphyxial transient respiratory insufficiency, with marked improvement in the first 24 hours of life.
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PMID:Postasphyxial lung disease in newborn infants with severe perinatal acidosis. 648 2


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