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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-six asthmatic patients who were hospitalised following an acute asthmatic attack and who had a peak expiratory flow of less than 50% predicted, without hypercapnia, received 5 mg. of salbutamol delivered by a micronebulizer LSA on admission (HO). At H1, 10 mg of additional salbutamol were nebulised in cases where there had been an increase of less than 20% of the PEF. At H2, all the subjects received steroid therapy. Group 1 in which success was defined by an increase of 20% of peak flow judged at H1 and H2, and group II where the increase in peak flow was less than 20%. Group II benefited at H2 by treatment with theophylline or salbutamol intravenously given in a randomised fashion. At H8 the 2 treatments were associated in group II in cases of failures. 15 men, and 11 women aged 40 +/- 17 suffering from severe asthma (65% of Charpin Stage IV) were included. The mean peak flow at HO was 32 +/- 9% of the predicted PEF. 21 subjects, or 81% improved their peak flow by more than 20% at H2. The toleration for salbutamol was very good from the cardiovascular point of view. At HO there was no clinical criteria nor peak flow assessment which would enable one to predict the failures from nebulized salbutamol for a given subject. Nevertheless a level of dyspnoea of greater than 5 on Borg's scale and a peak flow of less than 150 l/min made failure likely.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Mal Respir 1990
PMID:[Effect of nebulized salbutamol in 26 patients hospitalized for asthma attack]. 232 Jul 83

The syndrome of obstructive sleep apnoea is associated with an increased morbidity (the consequence of diurnal hypersomnolence and cardiovascular complications). The contraction of the dilator muscles of the upper airways (nose and pharynx) allows their patency at the time of inspiration. The obstruction of the airways resulted in a disequilibrium between the forces which tend to their collapse (negative inspiratory transpharyngeal pressure gradient) and those which contribute to their opening (muscle contraction). The mechanisms which underlie the triggering of obstructive apnoea are multiple including a reduction in the calibre of the superior airways, an increase in their compliance, and a reduction in the activity of the muscle dilators. This latter is intimately linked to the respiratory muscles and these muscles respond in a similar manner to a stimulation or a depression of the respiratory centre. The ventilatory fluctuations observed during sleep (alternately hyper and hypo ventilation of periodic respiration) thus favours an instability of the superior airways and the occurrence of oropharyngeal obstruction. The depth of post-apnoeic desaturation depends on the value of the arterial oxygen saturation at the beginning of apnoea, the duration of the period of apnoea and the pulmonary volume as the period of apnoea passes off. The cardiovascular consequences of apnoea include disorders of rhythm (bradycardia, auriculoventricular block, ventricular extrasystoles) and haemodynamic (pulmonary and systemic hypertension). This results in a stimulatory metabolic and mechanical effect on the autonomic nervous system. The electroencephalographic awakening which precedes the easing of obstruction of the upper airways is responsible for the fragmentation of sleep. The factors implicated in the cessation of the apnoea include hypoxia and hypercapnia but one also invokes a role for the negative pressure generated during the course of the apnoea.
Rev Mal Respir 1989
PMID:[Physiopathology of obstructive sleep apneas]. 269 Feb 8

Sarcoidosis very rarely progresses towards severe subacute respiratory failure. We report three observations of recent atypical cases of pulmonary sarcoidosis which were proven by open lung biopsy and developed severe diffuse pulmonary granulomatosis in a few weeks with an associated interstitial fibrosis. In these patients there were diffuse crepitant rales, a dramatic reduction in lung function of 30-60% of lung volumes and diffusion capacity accompanied by major hypoxemia (m +/- DS: 63.3 +/- 4.0 mmHg) without hypercapnia. Bronchoalveolar lavage showed an alveolar neutrophil leucocytosis (7.3 +/- 5.5%) without a lymphocytosis (4.3 +/- 11.5%). In the three cases under study, the clinical picture, the radiological and lung function studies, as well as the data from the bronchoalveolar lavage, were more suggestive of an acute diffuse interstitial fibrosis than of sarcoidosis.
Rev Mal Respir 1989
PMID:[Pulmonary sarcoidosis simulating primary acute interstitial fibrosis at presentation. Clinical, radiologic, functional and bronchoalveolar cytologic study in 3 cases]. 274 May 89

A double blind randomised multicentre clinical trial against placebo was performed in Italy on 128 patients with chronic airflow obstruction and hypoxaemia. On entry to the study all the patients were hypoxaemic (PaO2 less than or equal to 70 mmHg), 22 were normocapnic (PaCO2 less than or equal to 41 mmHg), 106 hypercapnic (PaCO2 greater than or equal to 43 mmHg). The patients (107 males and 21 females) with a mean age of 64 received oral Almitrine bismesylate for two months in a dose of 100 mg per day or placebo taken in two doses with the main meals. After inclusion in the study (TO), patients were reviewed after 30 and 60 days of treatment to evaluate pulmonary function and blood gases. The results were as follows: Almitrine bismesylate did not produce any significant variations in lung volumes, tests of airflow obstruction (for large or small airways) or the distribution of intra-pulmonary inspired air. The blood gas values at the end of treatment showed statistically significant changes (p less than 0.001: PaCO2 + 7.6 mmHg in patients overall and PaCO2 - 4.1 mmHg in those patients with hypercapnia.) The changes in arterial blood, already apparent after 30 days, were even more marked at the end of the study. These favourable blood gas changes might be the result (for the greater part) of the intra-pulmonary haemodynamic effect induced by Almitrine bismesylate (improved VA/QC ratios described in the literature) and (for a smaller part) a better ventilatory pattern with a reduction in the (A-a) DO2 and the functional dead space.(ABSTRACT TRUNCATED AT 250 WORDS)
Rev Mal Respir 1985
PMID:[The first Italian clinical experience with almitrine bismesylate]. 287 May 48

In the human species, foetal breathing movements are detectable from the fifteenth week of gestation and their incidence increases until the start of the third trimester. Over the last 10 weeks, breathing movements are present for 30% of the time. These are contemporaneous with body and ocular movements, suggesting an association between breathing movements and paradoxical sleep, as has been seen in the foetal lamb. These phases of activity alternate with phases of foetal immobility during which breathing movements are often absent. The incidence of foetal movements rises in the late post-prandial period, under the effect of maternal hyperglycaemia. After the establishment of regular uterine contractions, foetal breathing movements disappear, perhaps under the effect of prostaglandins E2 and/or a reduction in placental blood flow. Maternal hypercapnia leads to a rise in foetal breathing movements, which corresponds in the animal to the paradoxical sleep state. In the foetal lamb, hypoxaemia is accompanied by a cessation of breathing movements coinciding with a passage to quiet sleep. It is probable that the human foetus produces a similar reaction to hypoxaemia. During quiet sleep an inhibition of the respiratory centres would exist, disappearing during paradoxical sleep. Alcohol and certain anaesthetic agents lead to an inhibition of foetal breathing movements. The effect of tobacco remains controversial. The role of foetal breathing movements in pulmonary maturation is discussed in the human species.
Rev Mal Respir 1988
PMID:[Fetal respiratory movements]. 313 63

Hypercapnia is common in chronic respiratory failure (IRCO), and may be further increased in a significant way by oxygen therapy, used for severe hypoxaemia in acute exacerbations. The determinants of PaCO2 are metabolic (hence importance of alkalosis) and ventilatory. In chronic airflow obstruction, CO2 production and ventilation are normal; thus the factor responsible for hypercapnia is essentially the fraction of total ventilation lost in the anatomical and alveolar (VD/VT ratio) dead space, whose effect on PaCO2 is all the more marked on account of the high starting point. From the time of administering pure oxygen hypercapnia is only weakly linked to changes in total ventilation (which, after a few minutes returns to its initial level) and only slightly to the correction of hypoxaemia and desaturation (Haldane effect). On the other hand, the ventilation-perfusion ratios are altered, as evidenced by increased VD/VT ratios. The exact mechanisms are ill understood, but one could consider the worsening venous admixture effect by the reduction of hypoxic vasoconstriction and micro-atelectasis in the poorly ventilated zones, as well as the rise in the anatomical dead space (broncho-dilatation) and alveolar dead space (redistribution of ventilation to poorly perfused zones). In comparison with standard ideas, the genesis of hypercapnia from oxygen therapy depends more on an AIR/BLOOD mis-match, than on the suppression of the hypoxic ventilatory stimulus.
Rev Mal Respir 1988
PMID:[Relationship between hypercapnia and hypoxemia in chronic obstructive respiratory insufficiency]. 314 Mar 17

Graft versus host reaction (GVH) is a major complication of allogenic marrow transplants. The GVH present is a pluri-visceral syndrome in which certain pulmonary disorders are recognised. Amongst these respiratory failure by bronchiolitis is not an exceptional presentation. The case reported here is of an 18 year old man who developed, immediately following a marrow graft for acute lymphoblastic leukaemia, a lethal obstructive respiratory failure after progression for 2 1/2 years. The respiratory function data (TVO with elevated residual volume (VR) and VR/Total lung capacity (CT) hypoxia which corrected on exercise with normocapnia then hypoxic hypercapnia; compliance normal at low frequency but fell at high frequency and inspiratory and expiratory resistance was raised: DLCO/VA was normal) allowed the confirmation of obstructive respiratory failure by disease of the small airways. The pathogenesis of CVH is equivocal. Recurring infections seem to play a role, favoured by iatrogenic factors such as chemotherapy and total body irradiation. In the case reported here the first pulmonary signs followed an episode of influenza with sero-conversion.
Rev Mal Respir 1987
PMID:[Bronchiolitis caused by graft versus host reaction after bone marrow allograft]. 332 32

Hypoxaemia secondary to chronic bronchopulmonary disease may lead to total invalidity and be complicated by right heart failure. Consistent and meticulous medical care may produce a notable improvement by not smoking, using bronchodilators, mucolytics and physiotherapy. If, despite these measures, frank hypoxaemia persists, then domiciliary oxygen should be considered. The need for prolonged oxygen therapy of more than 15 hours is often countered by the scepticism and lack of discipline of the patient and family. In cases of hypoxaemia which are partially refractory or are associated with hypercapnia prolonged mechanical ventilation with a tracheotomy will ensure considerable salvage in those with severe restrictive defects and right heart failure. The supervision of oxygen therapy requires not only adequate control of blood gases, but also collaboration between the family doctor, the respiratory physician and home visitors such as the nurse or technician.
Rev Fr Mal Respir 1983
PMID:[General problems posed by the domiciliary treatment of chronic respiratory insufficiency]. 641 Apr 69

The authors review the recent literature on hypercapnia at rest and on exertion in patients suffering from chronic airflow obstruction. At rest, the data in the literature has shown that for varying degrees of airflow obstruction, chronic hypercapnic patients show similar occlusion pressures to normocapnic patients. (The occlusion pressure is an index of the amplitude of neuro-muscular signals coming from the respiratory centre). However, their respiratory profile is characterised by a smaller tidal volume due to a reduction of the inspiratory time and often of a more rapid respiratory rate at a lower minute ventilation (VE). This pattern alone could explain CO2 retention by alveolar hypoventilation. On effort, various authors have shown that hypercapnic patients, or those becoming so during exercise, differ from normals by adopting a ventilatory pattern characterised by a reduction in ventilation linked to their airflow obstruction and a smaller tidal volume. The limited increase in tidal volume on effort is dependent on the duration of inspiration and the reduction of vital capacity and inspiratory capacity. As at rest, the two populations cannot be distinguished in terms of occlusion pressure.
Rev Mal Respir 1984
PMID:[Chronic hypercapnia at rest or exercise-induced and ventilatory patterns in patients suffering from chronic obstructive bronchopulmonary disease]. 646 57

Intravenous amiodarone (5 mg/kg) was administered to 10 patients with chronic obstructive airways disease, hypercapnia and hypoxia, and pulmonary hypertension. Respiratory function tests, arterial blood gases, ECG, blood pressure and subjective tolerance were monitored. Subjective tolerance was excellent. The parameters investigated showed no significant changes either biologically or statistically, excepting a slowing of the cardiac rhythm. The authors conclude that amiodarone has no undesirable cardiopulmonary side effects.
Arch Mal Coeur Vaiss 1980 Feb
PMID:[Use of injectable amiodarone in patients with chronic respiratory insufficiency]. 676 11


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