Daytime hypoventilation in obstructive sleep apnoea syndrome.

Chronic alveolar hypoventilation is a classic feature of the "pickwickian syndrome" (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients.

[Short-duration nocturnal hypoxemia and persistent pulmonary hypertension].

Can daily short-duration hypoxemia (4-8 hours) induce pulmonary hypertension and right ventricular hypertrophy? A clinical model of this type of hypoxemia does exist: isolated nocturnal hypoxemia in patients with obstructive sleep apnea syndrome (OSAS) or chronic obstructive pulmonary disease (COPD). By investigating the pulmonary hemodynamics of these patients, it should be possible to determine whether nocturnal hypoxemia alone can induce pulmonary hypertension. Although nocturnal hypoxemia (in OSAS as well as in COPD) can induce acute episodes of pulmonary hypertension, it would not appear that nocturnal hypoxemia alone would be sufficient to provoke permanent diurnal pulmonary hypertension.

Pulmonary hypertension in the obstructive sleep apnoea syndrome: prevalence, causes and therapeutic consequences.

"Cor pulmonale" is a classic feature of the "Pickwickian syndrome". Earlier studies have reported a high prevalence of pulmonary hypertension (PH) in obstructive sleep apnoea (OSA) patients, but this has not been confirmed by recent studies with a more adequate methodology, including larger groups of patients. The first part of this review is devoted to the prevalence of PH in OSA; most recent studies agree on prevalence of 15-20%.

Pulmonary hemodynamics in patients with chronic obstructive pulmonary disease before and during an episode of peripheral edema.

We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory insufficiency, exhibiting marked peripheral edema. All the patients had previously undergone, within the last 6 months (T1), a right heart catheterization, in a stable state of their disease, when they were free of edema. Patients were subdivided into two groups according to the level of right ventricular end-diastolic pressure (RVEDP) during the episode of edema (T2): patients with a markedly elevated RVEDP (> 12 mm Hg) indicating the presence of right ventricular failure (RVF) = group 1, n = 9; patients with a normal or slightly elevated RVEDP (< 12 mm Hg) = group 2 (no RVF), n = 7.

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.

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.

[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.

[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.

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).

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.

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).

Long-term effects of treatment with nasal continuous positive airway pressure on daytime lung function and pulmonary hemodynamics in patients with obstructive sleep apnea.

Fifty-four patients with obstructive sleep apnea (OSA) syndrome received long-term treatment with nasal continuous positive airway pressure (CPAP). The effects on daytime lung function and pulmonary hemodynamics were prospectively evaluated by repeating pulmonary function tests, including right heart catheterization after a follow-up period of at least 1 yr (554 +/- 28 days, mean +/- SEM). PaO2 increased in the patient group as a whole from 69.

Alpha-1-antitrypsin deficiency in a large sibship.

We studied alpha 1-antitrypsin deficiency in a large family of 10 siblings: 3 subjects had PiZZ phenotype, but only 1 had emphysema; 2 subjects had no respiratory complaint. The patient with emphysema was a heavy smoker. According to the literature, this case suggests that, in PiZZ phenotype, emphysema appears earlier and is more severe if the patients smoke.

[Endobronchial aspergillosis associated with a carcinoid tumor].

We report a case of a 62 year old man who presented with effort dyspnoea accompanied by a cough and haemoptysis. The chest radiograph of the thorax showed atelectasis of the right upper lobe. Bronchoscopy showed evidence of a tumour like mass obstructing the right bronchus and this revealed itself to be a mass of organised fibrinous deposit in granulation tissue containing numerous colonies of Aspergillus.

Drug therapy of sleep-related hypoxaemia.

In patients with chronic obstructive pulmonary disease (COPD) exhibiting daytime hypoxaemia, a worsening of the latter occurs during sleep, particularly during REM sleep. The most efficient therapy of this sleep-related hypoxaemia is the nocturnal administration of O2 at a flow rate of 1.5-3 l/min.

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.

[Development of pulmonary arterial hypertension in chronic obstructive bronchopneumopathies].

In chronic obstructive bronchopneumopathies (COBP), pulmonary artery hypertension (PAH) is usually mild but may markedly intensify during episodes of acute respiratory failure, muscular exercise, and sleep, PAH may, even if of low level, lead to right heart failure. The prognostic value of PAH and its degree in COBP patients has been well established by a number of recent studies. Chronologic changes in pulmonary artery pressure (PAP) tend to be minimal in the majority of COBP patients (of the order of +0.

Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients.

To define the parameters of respiratory insufficiency in OSA, 114 consecutive patients (108 men, six women) were prospectively studied. In addition to standard polysomnography, they underwent pulmonary function tests, right heart catheterization, and ventilatory response tests to hypercapnia. Nineteen patients (19 percent) had a resting PAP greater than or equal to 20 mm Hg.

Evolution of pulmonary haemodynamics in COLD patients under long-term oxygen therapy.

The North-American Trial (NOTT) and the British MRC study clearly indicated that long-term oxygen therapy (LTO) increases the survival rate of patients with severe chronic obstructive long disease (COLD), but O2 must be given for more than 15 h/24 h. At present OT is largely prescribed in COLD patients whose (stable) PaO2 less than or equal to 55 mmHg. The pulmonary haemodynamic effects of OT are still a matter of debate.

Daytime pulmonary hypertension in patients with obstructive sleep apnea syndrome.

The frequency of daytime pulmonary hypertension (PH) in patients with obstructive sleep apnea syndrome (OSAS) has not been well established and its mechanisms are still under debate. We have thus performed right heart catheterization, in addition to standard spirography and arterial blood gas measurements, in a series of 46 consecutive patients in whom OSAS was firmly diagnosed by whole-night polysomnography. Only 9 of the 46 patients (20%) had PH defined by a mean resting pulmonary arterial pressure (Ppa) greater than or equal to 20 mm Hg.

[Hypoxia and pulmonary circulation. The importance of hypoxia in pulmonary arterial hypertension of chronic obstructive bronchopneumopathies].

In chronic airflow obstruction (CAO), there are grounds for distinguishing between the effects of acute alveolar hypoxia and those of chronic hypoxia. Acute hypoxia leads, in healthy subjects, to pulmonary vasoconstriction. In patients with CAO, there is however a great variability in the pulmonary vascular response to hypoxia.