"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%.The second (and major) part of the study deals with the causes and mechanisms of PH in OSA. Pulmonary hypertension is rarely observed in the absence of daytime hypoxaemia, and the severity of nocturnal events (apnoea index (AI), apnoea+ hypopnoea index (AHI)) does not appear to be the determining factor of PH. Diurnal arterial blood gas disturbances and PH are most often explained by the presence of severe obesity (obesity-hypoventilation syndrome) and, principally, by association of OSA with chronic obstructive pulmonary disease (the so called "overlap syndrome"). Bronchial obstruction is generally of mild-to-moderate degree and may be asymptomatic.The final part of the review analyses the therapeutic consequences of the presence of PH in OSA patients. Pulmonary hypertension, which is generally mild-tomoderate, does not need a specific treatment. When nasal continuous positive airway pressure (CPAP) fails to correct sleep-related hypoxaemia, supplementary oxygen must be administered. In patients with marked daytime hypoxaemia (arterial oxygen tension (Pa,O 2 ), ≤7.3 kPa (55 mmHg) conventional O 2 therapy (nocturnal + diurnal) is required. Eur Respir J., 1996, 9, 787-794

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. Among the patients without resting PH, 14 had exercising PH (defined by a Ppa greater than 30 mm Hg during 40-watt, steady-state exercise). Patients with resting PH differed from the others by a lower daytime PaO2 (60.8 +/- 7.6 versus 76.2 +/- 9.4 mm Hg; p less than 0.001), a higher daytime PaCO2 (44.6 +/- 4.2 versus 38.0 +/- 4.0 mm Hg; p less than 0.001), and lower VC and FEV1 (p less than 0.001). There was no difference between the 2 groups with regard to apnea index (62 +/- 34 versus 65 +/- 40) or the lowest sleep SaO2 (59 +/- 21 versus 66 +/- 18%) or the time spent in apnea. For the group as a whole, there was a good correlation between Ppa and daytime PaO2 (r = -0.61; p less than 0.001), PaCO2 (r = 0.55; p less than 0.001), and FEV1 (r = -0.52; p less than 0.001), but there was no significant correlation between Ppa and the apnea index, the lowest sleep SaO2, or the time spent in apnea.(ABSTRACT TRUNCATED AT 250 WORDS)

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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 ≥20 mm Hg, was present in only 31 of 151 patients. During steady-state exercise (40 W or less) an abnormally high PAP (≥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

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