[Pickwickian syndrome reconsidered. Relations between sleep apnea syndrome and obesity-hypoventilation syndrome].
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Humans↗
Biomedical subjects
E Weitzenblum
Publications and source records attributed to E Weitzenblum.
[Long-term oxygen therapy in chronic respiratory insufficiency. Usefulness, indications, modes of administration].
Long-term oxygen therapy improves the life expectancy of hypoxaemic patients with chronic obstructive pulmonary disease (COPD), provided the hypoxaemia is sufficiently pronounced under stable conditions (PaO2 less than 55 mmHg) and oxygen is given for more than 16 out of 24 hours. By extension, the same indications are applicable to hypoxaemia due to other causes (diffuse fibrosis, pneumoconiosis, cystic fibrosis, etc.). Long-term oxygen therapy improves the patients' quality of life and also has favourable effects on oxygen transport, neuropsychological status, polycythaemia and pulmonary hypertension. It is usually delivered by means of O2 extractors, to which may be added small flasks of O2 gas for walking and moving about. Liquid O2 is a good solution for subjects who are motivated and are obliged to do a great deal of walking. The O2 flow rate administered must be such that it rises the PaO2 level above 60 mmHg. Oxygen therapy is only a symptomatic treatment and cannot replace other types of therapy, such as bronchodilators, physiotherapy, etc. It gives satisfactory results but it has not transformed the prognosis of severe hypoxaemic COPD.
Blood Gas Analysis↗
[Dyspnea. Diagnostic orientation].
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Acute Disease↗
Benefit from long-term O2 therapy in chronic obstructive pulmonary disease patients.
The Nocturnal Oxygen Therapy Trial (NOTT) and Medical Research Council (MRC) trial have clearly indicated that long-term oxygen therapy (LTO) improved survival in patients with hypoxemic chronic obstructive pulmonary disease (COPD), but the mechanisms accounting for this improved survival could not be established. In particular, there was no link between survival and changes in pulmonary hemodynamics. More recent studies have shown even better results of survival in patients under LTO after at least 5 years. LTO improves the quality of life in these patients by improving their neuropsychological condition, by increasing their walking distance, and by reducing the time spent in hospital. Whether LTO improves pulmonary hemodynamics and right ventricular function is still debated. No significant changes in mean pulmonary artery pressure (PAP) were observed in the MRC study in patients receiving O2 during greater than 15 h/day, whereas a modest but significant fall in PAP was noticed after 6 months in the NOTT patients receiving O2 during greater than 18 h/day. In our own study, confirmed by more recent data from our laboratory, a reversal in the progression of pulmonary hypertension was observed in patients receiving O2 during greater than 16 h/day, but it is not possible to say whether a rather small decrease in PAP and pulmonary vascular resistance will have favorable effects on life expectancy. Presently, we do not know whether LTO can reverse, at least partially, the structural changes in the pulmonary vessels possibly induced by chronic alveolar hypoxia, and we need to perform further studies in this field.
Clinical Trials as Topic↗
Frequency and correlates of the saw-tooth pattern of flow-volume curves in an epidemiological survey.
The object of this report was to assess the possibility of identifying saw-tooth patterns on flow-volume curves in men aged 28 to 58 years. We studied the frequency of these patterns and their relationships with two indirect signs of UAO increase in FEV1/PEF and FEF50%/FIF50% ratios--as well as with clinical and functional data. Twenty-six of the 360 subjects surveyed, ie, 7.2 percent, had flow oscillations in the inspiratory and/or expiratory part of flow-volume curves, corresponding to the definition of the saw-tooth pattern. We observed significant relationships between the saw-tooth pattern and the mean FEV1/PEF ratio. In 97 subjects, the proportion of those with saw-tooth patterns was 13.4 percent, and the mean FEF50%/FIF50% ratio was 1.53 in those with the pattern vs 1.07 in those without it. These results show that the saw-tooth pattern was not rare in these men.
Adult↗
Chronic obstructive pulmonary disease and sleep apnea syndrome.
The term "overlap syndrome" was introduced by Flenley to describe the association of sleep apnea syndrome (SAS) with chronic obstructive pulmonary disease (COPD). Epidemiologic data on the prevalence of the overlap syndrome are not available, but the frequency of an associated COPD in SAS patients has been emphasized in almost all the studies analyzing the development of respiratory insufficiency in SAS patients. In a large series (n = 264) of unselected SAS patients who had undergone detailed pulmonary function tests, we observed an obstructive ventilatory defect (FEV1/VC < 60%) in 30 of 264 patients (11%). These patients had lower daytime PaO2 and higher PaCO2 than the other patients and they had higher resting and exercising pulmonary artery mean pressure (right heart catheterization was performed in 215 of 264 patients). We conclude that the risk of developing respiratory insufficiency and cor pulmonale is higher in overlap patients.
Adult↗
[Sequential administration of a reduced dose of almitrine to patients with chronic obstructive bronchopneumopathies. A controlled multicenter study].
Recent multi-centre studies have shown that high doses of Almitrine (100-200 mg per day), lead to a significant improvement in the hypoxaemia of patients presenting with chronic airflow obstruction, but that a high blood level (greater than 500 ng/ml) is often seen after 1 year, sometimes associated with signs of peripheral neuropathy. In order to maintain Almitrine blood levels in the range 200-300 ng/ml we have used an intermittent regime (with a "window" of 1 month every 3 months) and a dose limited to 100 mg per day. 102 hypoxic patients with chronic airflow obstruction, who were in a stable state were included. 65 patients were in the Almitrine group (A) and 37 patients in the placebo group (P). The treatment lasted for 1 year. In addition there was a 3 monthly follow up with arterial blood gases and spirometry, a clinical neurological examination and also electrophysiology, initially and after 6 and 12 months. 43% of patients in group A and 32% of patients in group P, left the study, most often due to poor cooperation, but sometimes as a result of side effects. After 12 months the PaO2 rose significantly in group A from 59.1 +/- 0.7 to 65.8 +/- 1.6 mmHg (p less than 0.001) whilst it was not changed in group P. The PaCO2 did not change in either group. On the other hand there was a significant fall in the subgroup of patients with hypercapnia in group A (p less than 0.001). The outcome of the neurological and electrophysiological assessments did not show any significant difference between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Sleep-related oxygen desaturation and daytime pulmonary haemodynamics in COPD patients.
It has been hypothesized that in chronic obstructive pulmonary disease (COPD), sleep-related hypoxaemia could lead to pulmonary hypertension (PH) and cor pulmonale, even in patients with only mild daytime hypoxaemia. We investigated the relationships between sleep variables and daytime pulmonary haemodynamics in 40 COPD patients with daytime arterial oxygen tension (PaO2) between 60-70 mmHg (8-9.3 kPa). Patients were considered as desaturators if they spent at least 30% of the sleep recording time with a transcutaneous O2 saturation (StcO2) less than 90%. Daytime arterial blood gases and pulmonary volumes could not discriminate desaturators "D" (n = 18) from non-desaturators "ND" (n = 22), but awake baseline StcO2, measured just prior to the onset of sleep, was lower in group D. Pulmonary artery mean pressure was significantly higher in group D (19.1 +/- 4.7 vs 16.8 +/- 1.9 mmHg, p less than 0.05) and all patients with PH (6 out of 40) belonged to group D. PH was observed in 6 of the 15 patients whose mean nocturnal StcO2 was less than 90% but in none of the 25 with a mean nocturnal StcO2 greater than 90%. The PH patients (n = 6), all desaturators, differed from the desaturators with no PH (n = 12), and from ND (n = 22) in having higher numbers of desaturation dips, longer durations of dips, and lower mean nocturnal arterial oxygen saturation (SaO2). We conclude that a causal relation between nocturnal desaturation and permanent PH is very likely. Further studies are needed to see whether oxygen therapy can prevent PH in these patients.
Blood Gas Monitoring, Transcutaneous↗
[Pulmonary artery hypertension in chronic respiratory diseases].
Pulmonary hypertension (PH) is one of the evolutive complications in respiratory diseases leading to chronic respiratory insufficiency (CRI). In most cases PH is mild, but acute worsening can happen and especially during exercise, during sleep (particularly during rapid-eye-movement sleep) and during acute respiratory failure. Usually, pulmonary artery pressure finds again the level observed prior to the worsening. Although PH is usually mild, it is of prognostic value in CRI and particularly in patients with chronic obstructive pulmonary disease (CODP): the survival rate is significantly lower in patients with PH compared with those without PH and the higher PAP is the lower the survival rate. In general, long-term changes in PAP in COPD patients are mild. Long-term oxygen therapy can reverse the progression of PH and increase the survival rate. PH can lead with more or less delay to cor pulmonale and right heart failure (RHF). Oedema can be due to RHF but in some cases they can also be explained by the stimulation of the renin-angiotensin system with increasing of the aldosterone level, due to the fall in renal blood flow. These renal hemodynamic changes are related to arterial blood gas changes (hypercapnic acidosis, hypoxemia).
Chronic Disease↗
[Pulmonary artery hypertension and hypoxemia in sleep].
Sleep apnea syndrome is responsible for repeated and sometimes deep arterial oxygen desaturations occurring during apneas, followed by episodes of transient pulmonary hypertension (PH). In chronic obstructive pulmonary disease (COPD) patients with respiratory insufficiency, a worsening of hypoxemia occurs during sleep, due to alveolar hypoventilation and/or ventilation-perfusion mismatching. This hypoxemia is also responsible for pulmonary hypertensive dips due to pulmonary hypoxic vasoconstrictiveness. But there is presently no evidence that sleep-related and transient PH may lead to daytime and permanent PH, in either sleep apnea syndrome or COPD. In fact permanent PH seems to be related, in most cases, to the presence of daytime (permanent) hypoxemia.
Humans↗
Evolution of physiological variables in patients with chronic obstructive pulmonary disease before and during long-term oxygen therapy.
In 24 patients with severe chronic obstructive pulmonary disease (COPD), we investigated the evolution of pulmonary volumes, arterial blood gases (ABG) and mean pulmonary artery pressure (PAP), before (T0-T1) and during (T1-T2) long-term oxygen therapy (LTO). LTO was initiated at T1 on usual criteria (PaO2 persistently less than or equal to 55 mm Hg) and was given during greater than or equal to 16 h/day. The T0-T1 period ranged from 12 to 186 months (mean 53 +/- 41 months) and the T1-T2 period from 12 to 120 months (mean 44 +/- 30 months). There was a significant worsening of the obstructive pattern (FEV1 decreasing from 1,084 +/- 326 to 879 +/- 318 ml, p less than 0.005) and of ABG (PaO2 decreasing from 58.2 +/- 9.2 to 51.6 +/- 6.5 mm Hg, p less than 0.01) before the onset of LTO, whereas there was a rather good stability of ABG during LTO and the changes in pulmonary volumes were modest and statistically nonsignificant (FEV1 decreased from 879 +/- 318 to 809 +/- 247 ml). PAP tended to increase from T0 to T1 and to decrease from T1 to T2, but these changes only reached the level of statistical significance when they were expressed as changes per year (+1.0 +/- 2.7 vs. -1.3 +/- 4.5 mm Hg, p less than 0.05). The evolution of physiological variables was nearly identical in subgroups of patients who had died (n = 13) or were still alive (n = 11) at the time of data collection (T3) and this held particularly true for PAP.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood Pressure↗
Pulmonary hemodynamics in chronic obstructive pulmonary disease of the emphysematous type.
Pulmonary hemodynamics have been extensively investigated in patients with chronic bronchitis or in 'mixed' patients (chronic bronchitis + emphysema) but rarely in patients with markedly predominant emphysema. We have investigated a large series (n = 151) of such patients, emphysema having been assessed on radiological, clinical and functional grounds. The mean age was 58 +/- 10 years; vital capacity (VC, % of predicted) = 81 +/- 19; forced expiratory volume in 1 s (FEV1) = 1,198 +/- 589 ml; FEV1/VC = 38 +/- 12%; PaO2 = 72 +/- 11 mm Hg; PaCO2 = 37.5 mm Hg. Pulmonary hypertension (PH), defined by a resting pulmonary artery pressure (PAP) of greater than or equal to 20 mm Hg, was present in only 31 of 151 patients. During steady-state exercise (40 W or less) an abnormally high PAP (greater than or equal to 30 mm Hg) was observed in 99 of 151 patients. Resting and exercising PAP were poorly correlated with resting PaO2 and PaCO2, but were better correlated with the amplitude of the respiratory pressure swings, FEV1, the transfer factor and exercising PaO2. Patients with PH (n = 31) showed significantly more obstruction and pulmonary distension than the remainder, but they did not differ from the non-PH patients with regard to resting PaO2. It is concluded that: (1) resting PH is not the rule in diffuse emphysema but exercising hypertension is frequent (2 of 3 patients), and (2) hypoxemia is not a determining factor of hemodynamic abnormalities in emphysema.
Adult↗
One year treatment with almitrine improves hypoxaemia but does not increase pulmonary artery pressure in COPD patients.
Almitrine bismesylate, a chemoreceptor agonist, improves hypoxaemia in a high percentage of chronic obstructive pulmonary disease (COPD) patients and its long-term use may thus be of interest in these patients. The course of pulmonary haemodynamics during a one year treatment was investigated in severe COPD patients (forced expiratory volume in one second FEV1 = 1,040 +/- 80 SEM ml) with persistent hypoxaemia (initial arterial oxygen tension (PaO2) in the range 6.6-8.6 kPa (50-65 mmHg]. Patients were given either almitrine (A, n = 27), 100 mg.day-1, during two consecutive months per quarter followed by a one month wash-out period (intermittent "schedule"), or placebo (P, n = 18) with the same schedule. Eleven patients in group A and 8 in group P could not complete the one year study because of lack of compliance, worsening of respiratory insufficiency, or for other reasons. In the remaining patients, PaO2 significantly increased in group A (n = 16) from 7.6 +/- 0.1 to 8.3 +/- 0.2 kPa (56.9 +/- 1.0 to 62.7 +/- 1.7 mmHg) (p less than 0.001) but not in group P (n = 10) from 7.5 +/- 0.3 to 7.9 +/- 0.3 kPa (56.1 +/- 2.3 to 59.1 +/- 2.1 mmHg). PaCO2 did not significantly change in either group. Pulmonary artery mean pressure (PAP) was stable in both groups: from 26.8 +/- 2.1 to 25.4 +/- 1.9 mmHg in group A, and from 20.6 +/- 1.1 to 20.9 +/- 1.5 mmHg in group P.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[The results of a survey on the attitude of pneumonologists toward sleep apnea syndrome].
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Attitude of Health Personnel↗
Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome.
In order to study the frequency and the mechanisms of daytime pulmonary hypertension (PH) in obstructive sleep apnoea syndrome (OSAS) lung function tests, blood gas analysis and right-heart catheterization were performed in 46 consecutive patients. OSAS was assessed by polysomnography. 9 patients only (20%) had PH (mean pulmonary artery pressure (Ppa) greater than or equal to 20 mmHg). Patients with PH had lower daytime PaO2 (60.8 +/- 7.6 vs. 76.2 +/- 9.4 mmHg; p less than 0.001), higher daytime PaCO2 (44.8 +/- 4.2 vs. 38.0 +/- 4.0 mmHg; p less than 0.001), lower forced vital capacity (FVC) and forced expiratory volume (FEV1) (p less than 0.001), but the severity of OSAS was not different whether PH was present or not (apnoea index: 62 +/- 34 hour in the PH group vs. 65 +/- 40 hour, apnoea + hypopnoea index 102 +/- 33 hour in the PH group vs. 86 +/- 36 hour, lowest sleep SaO2: 59 +/- 21% in the PH group vs. 66 +/- 18%). There were significant correlations between Ppa and: daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), FEV1 (r = -0.52; p less than 0.001) but not between Ppa and apnoea index, apnoea + hypopnoea index, lowest sleep SaO2. PH and daytime hypoxaemia were associated either with chronic airway obstruction or with severe obesity.
Adult↗
AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli.
The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.
Blood Pressure↗
[Pulmonary artery hypertension and nocturnal hypoxemia in chronic obstructive bronchopneumopathy].
Permanent and marked hypoxemia (PaO2 less than or equal to 60 mmHg) is a major cause of pulmonary hypertension (PH) in patients with chronic obstructive lung disease (COLD). In these patients PH, although mild to moderate (with a mean pulmonary artery pressure generally comprised between 20 and 35 mmHg), is by itself an indicator of poor prognosis. During sleep, hypoventilation and exaggerated ventilation/perfusion ratio inequalities can induce severe desaturation dips responsible for sudden peaks of PH. However, in hypoxemic COLD patients, the prognostic value of sleep-related desaturation (and resulting PH) has not been demonstrated. In COLD patients without marked daytime hypoxemia (PaO2 greater than or equal to 60 mmHg) permanent PH in rather rare. Ventilatory changes during sleep may account for nocturnal desaturation and transient PH. Do these repeated transient pulmonary hypertensive peaks finally lead to permanent PH? This attractive hypothesis supposes that significant sleep desaturation can develop in patients without pronounced daytime hypoxemia, which has not been demonstrated yet. In fact very few studies have been devoted to the occurrence of nocturnal desaturation (and PH) in such patients and the above mentioned hypothesis could not be confirmed. Long-term oxygen therapy (greater than or equal to 16-18 h/day) is generally prescribed in COLD patients with marked and persistent daytime hypoxemia. Oxygen therapy including sleep time and several studies have shown that usual O2 flows (1, 5-3 l/mn) are efficient and increase O2 saturation during sleep over 90%, with a resulting improvement of nocturnal PH. It has been demonstrated that daytime PH is stabilized (or improved) in patients receiving long-term O2 therapy. In COLD patients with less severe daytime (and nighttime) hypoxemia, almitrine could be of interest. The benefit of isolated nocturnal oxygen therapy has not been yet clearly established.
Darkness↗
Should patients have right heart catheterization prior to long-term oxygen treatment?
The presence of pulmonary hypertension (PH) is not an obligatory prerequisite for prescribing long-term oxygen therapy (LTO) in patients with chronic obstructive pulmonary disease (COPD), at least when PaO2 is repeatedly less than 55 mmHg in a stable state of the disease. It is generally accepted that LTO is indicated in patients whose PaO2 is in the range 55-59 mmHg, but exhibiting polycythaemia, "cor pulmonale", and (or) PH. The clinical signs of "cor pulmonale" occur late and the noninvasive diagnosis of PH is not yet satisfactory; it ensues that right heart catheterization is useful in these patients, before prescribing LTO. Pulmonary hypertension is probably the most important consequence of long-standing hypoxaemia and, in our opinion, the presence and the degree of PH should be assessed in every patient before starting such a heavy therapy as LTO.
Cardiac Catheterization↗