Daytime Hypoxemia Research Articles

Pattern of Variables Describing Desaturator COPD Patients, as Revealed by Cluster Analysis

The aims of this study were to define, by cluster analysis, a pattern of clinical variables that differentiate desaturator (D) from nondesaturator (ND) patients affected by COPD, and to identify daytime variables that are predictive of nocturnal desaturation. Fifty-one random, consecutive COPD outpatients (20 women; mean [+/- SD] age, 69.6 +/- 4.0 years) with mild daytime hypoxemia (Pao(2), 60 to 70 mm Hg) were enrolled into the study. Obstructive sleep apnea syndrome patients were excluded. Lung volumes, arterial blood gas levels, and mean pulmonary artery pressure (MPAP) were measured, and nocturnal desaturation was evaluated with nighttime polygraphy. With least squares simple linear regression, the percentage of total recording time was highly correlated with a total nocturnal recording time of arterial oxygen saturation of < 90 mm Hg (T90) and MPAP (R = 0.84; R2= 71.20%); T90 was also highly correlated with daytime Paco2 (R = 0.70; R2= 48.96%). Multiple regression showed that T90 was highly correlated with both MPAP and Paco2 (R2= 97.75%). Hierarchical cluster analysis conducted with these three variables showed that D and ND patients differed in both nocturnal and daytime variables. The mean T90 was 30 +/- 3.5% in 19.2% and 8%, respectively, of the D and ND groups. Moreover, two D subgroups differing in MPAP and two ND subgroups differing in Paco2 were identified. D patients may be identified by a pattern of T90, MPAP, and Paco2 values, rather than by T90 alone, with the latter two variables being predictors of nocturnal desaturation severity.

James Preston Robb, MD (1914–2004)

<h3>OBJECTIVE:</h3> To review a series of patients with sleep apnea syndrome, to promote more awareness and alert local health professionals to early diagnosis and treatment. <h3>METHODS:</h3> We studied, prospectively, 48 consecutive patients who were managed at the university hospital from 1992 to 1996. <h3>RESULTS:</h3> The male:female ratio was 1.4:1. The mean interval between onset of symptoms and the diagnosis was 5.5 years (range 0.25 to 30). In over half of the patients the diagnosis was not suspected upon referral. The mean body mass index was 42.8kg/m2, (range 25 to 76). Daytime hypoxemia was present in 28 patients (58%), while 26 (54%) had Pa CO2 &gt; 45 mmHg, mainly as a result of obesity-hypoventilation syndrome. Significant proportions had systemic and pulmonary hypertension (60% and 23%), and 32% had ischemic heart disease. All patients, but one, tolerated continuous positive airway pressure, but cost of the equipment led some to prefer surgical treatment that is offered free. <h3>CONCLUSION:</h3> This series shows a bias towards female sex and frequent association with obesity-hypoventilation syndrome. In many cases the diagnosis was not suspected suggesting poor recognition and awareness of sleep apnea syndrome. Monitoring pulse oximetry during sleep was helpful in the diagnosis and titration of continuous positive airway pressure. Ways of providing continuous positive airway pressure under the health system need to be studied.

Sleep and chronic obstructive pulmonary disease.

Patients with COPD who are hypoxaemic during wakefulness become more hypoxaemic during sleep. The most severe episodes of nocturnal desaturation generally occur during REM sleep. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. The worsening of hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the predominant mechanism, at least during REM sleep. The consequences of sleep-related hypoxaemia include peaks of pulmonary hypertension due to hypoxic pulmonary vasoconstriction, generally observed in patients with marked daytime hypoxaemia. Cardiac arrhythmias have been described but their clinical relevance has not been established. The prevalence of obstructive sleep apnoea syndrome (OSAS) is not greater in chronic obstructive pulmonary disease (COPD) patients than in the general population, but this association (Overlap Syndrome) is not rare since COPD and OSAS are both frequent diseases. Overlap patients are at a higher risk of developing respiratory insufficiency than are pure OSAS patients. Polysomnography is only indicated in COPD patients who are suspected of having OSAS. The treatment of nocturnal hypoxaemia is conventional O2 therapy (> or = 16/24 h) in COPD patients with marked daytime hypoxaemia (PaO2 < 55-60 mmHg) and conventional O2 therapy plus nocturnal non-invasive ventilation in some patients with marked hypercapnia. At present data are not sufficient for justifying the use of isolated nocturnal oxygen therapy in COPD patients with nocturnal desaturation but with mild daytime hypoxaemia (PaO2 > 60 mmHg).

Daytime hypoxemia in patients with severe OSAHS is improved by nCPAP therapy

In this study, we examined whether the severity of apnea-hypopnea during sleep correlated with the daytime hypoxemia and whether daytime hypoxemia improved with long-term nasal continuous positive airway pressure (nCPAP) therapy. PaO2 significantly decreased from 89.8 ± 9.4 Torr (in the control group) to 78.2 ± 5.1 Torr (in the apnea-hypopnea index [AHI] > 90) with an increase in the AHI. Despite the aggravation of apnea-hypopnea 1 year after the nCPAP therapy, the daytime hypoxemia improved. In addition, it appears that daytime hypoxemia improves with long-term nCPAP therapy.

Sleep-Disordered Breathing and Cardio- and Cerebrovascular Diseases: 2003 Update of Clinical Significance and Future Perspectives. Schlafbezogene Atmungsstorungen und kardio- und zerebrovaskulare Erkrankungen: Update 2003 der klinischen Bedeutung und zukunftiger Entwicklungen

The purpose of this review is to summarize current knowledge about the link between sleep-disordered breathing (SDB) and cardiovascular and cerebrovascular diseases. Obstructive sleep apnoea (OSA) is a well-established risk factor for systemic arterial hypertension, and its treatment with continuous positive airway pressure leads to a decrease in daytime and night-time blood pressure profiles. Pulmonary arterial hypertension occurs in 20–30% of OSA patients and is usually mild. It is not yet clear if OSA per se leads to pulmonary hypertension or if the coexistence of chronic obstructive pulmonary disease with daytime and/or sleep-related hypoxaemia is required to provoke a persistent rise in pulmonary artery pressure. Furthermore, OSA is associated with nocturnal cardiac arrhythmias, especially cyclical fluctuations of the heart rate in response to recurrent apnoeas. Atrioventricular conduction blocks and ventricular premature beats are less often observed and seem to be confined to patients with severe OSA and those with accompanying ischaemic heart disease. The association between OSA and vaso-occlusive disease (i.e. atherosclerosis) is less clear. However, accumulating experimental and epidemiological data support such a link. Thus, OSA may lead to coronary artery disease (CAD) and stroke by promoting atherosclerosis. Correspondingly, patients with CAD or acute stroke show a high prevalence of SDB. Cheyne—Stokes respiration (CSR) is a specific pattern of central sleep apnoea occurring in patients with advanced congestive heart failure (CHF). If present, CSR clearly has a negative impact on the clinical course of CHF. Although the optimal treatment strategy for CSR is less well defined than that for OSA, the successful reversal of CSR might increase overll survival in affected patients.

Left Ventricular Hypertrophy Is a Common Echocardiographic Abnormality in Severe Obstructive Sleep Apnea and Reverses With Nasal Continuous Positive Airway Pressure

To determine cardiac structural abnormalities by echocardiography in subjects with severe obstructive sleep apnea (OSA), and to determine the long-term effects of nasal continuous positive airway pressure (CPAP) on such abnormalities. Polysomnography was conducted on oximetry-screened patients who showed a desaturation index > 40/h and > or = 20% cumulative time spent below 90%. From these, 25 patients with severe OSA but without daytime hypoxemia underwent echocardiography prior to, then 1 month and 6 months following initiation of CPAP treatment. Outpatient sleep disorders center. Of the 25 patients, 13 patients (52%) had hypertension by history or on physical examination. Baseline echocardiograms showed that severe OSA was associated with numerous cardiovascular abnormalities, including left ventricular hypertrophy (LVH) [88%], left atrial enlargement (LAE) [64%], right atrial enlargement (RAE) [48%], and right ventricular hypertrophy (16%). In all patients (intent to treat) as well as those patients compliant with CPAP therapy (84% > 3 h nightly), there was a significant reduction in LVH after 6 months of CPAP therapy as measured by interventricular septal distance (baseline diastolic mean, 13.0 mm; 6-month mean after CPAP, 12.3 mm; p < 0.02). RAE and LAE were unchanged after CPAP therapy. LVH was present in high frequency in subjects with severe OSA and regressed after 6 months of nasal CPAP therapy.

Sleep apnea in renal patients.

In Western societies, sleep apnea (SA) has emerged as a major medical problem with important social ([1][1]) and financial implications. The issue may be even more relevant in nephrology because some of the factors involved in the pathogenesis of renal disease are the same that cause, or are

A review of long-term oxygen therapy for chronic obstructive pulmonary disease

This study aimed to review the evidence for the use of long-term oxygen therapy for patients with chronic obstructive pulmonary disease (COPD).The design was a systematic Cochrane review of randomized controlled trials (RCTs) of long-term oxygen therapy for COPD and main outcome measure was survival on home oxygen therapy.Five RCTs were identified. Data from two trials of nocturnal oxygen therapy in mild to moderate hypoxaemia were aggregated. Data from the other three trials could not be aggregated because of differences in trial design and patient selection. Treatment with continuous versus nocturnal oxygen therapy produced a significant improvement in mortality after 24 months [Peto odds ratio 0·45, 95% confidence interval (95% CI) 0·25–0·81] for the continuous therapy group. Treatment with oxygen therapy versus no oxygen therapy showed a significant improvement in mortality after five years in the group receiving oxygen therapy (Peto odds ratio 0·42, 95% CI 0·18–0·98). There was no difference in mortality for patients with COPD and mild to moderate daytime hypoxaemia and nocturnal desaturation receiving nocturnal oxygen therapy versus no oxygen therapy or sham treatment. Long-term oxygen therapy versus no oxygen therapy in patients with COPD and moderate hypoxaemia had no effect on survival.In conclusion, long-term oxygen therapy improved survival in a selected group of COPD patients with severe hypoxaemia but few co-morbidities. Long-term oxygen therapy did not improve survival in patients with moderate hypoxaemia or in those with mild to moderate hypoxaemia and arterial desaturation at night.

Outcome of COPD patients with mild daytime hypoxaemia with or without sleep-related oxygen desaturation.

The aim of the present study was to compare the evolution of pulmonary haemodynamics and of arterial blood gases in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate hypoxaemia, with or without sleep-related oxygen desaturation. COPD patients with daytime arterial oxygen partial pressure in the range 56-69 mmHg were included prospectively. Sleep-related oxygen desaturation was defined as spending > or = 30% of the nocturnal recording time with arterial oxygen saturation <90%. From the 64 patients included, 35 were desaturators (group 1) and 29 were nondesaturators (group 2). At baseline (t0), patients with sleep-related desaturation had a significantly higher daytime (mean +/- SD) arterial carbon dioxide partial pressure (Pa,CO2) (44.9 +/- 4.9 mmHg versus 41.0 +/- 4.1 mmHg, p=0.001) whereas mean pulmonary artery pressure (mPAP) was similar in the two groups. After 2 yrs (t2) of follow-up, 22 desaturators and 14 nondesaturators could be re-evaluated, including pulmonary haemodynamic measurements. None of the nondesaturator patients became desaturators at t2. The difference between the two groups in terms of daytime Pa,CO2 was still present at t2. The mean changes in mPAP from t0 to t2 were similar between the two groups, as were the rates of death or requirement for long-term oxygen therapy (American Thoracic Society criteria) during follow-up of up to 6 yrs. The presence of sleep-related oxygen desaturation is not a transitional state before the worsening of daytime arterial blood gases, but is a characteristic of some chronic obstructive pulmonary disease patients who have a higher daytime arterial carbon dioxide partial pressure. Such isolated nocturnal hypoxaemia or sleep-related worsening of moderate daytime hypoxaemia does not appear to favour the development of pulmonary hypertension, nor to lead to worsening of daytime blood gases.

Left ventricular dysfunction, pulmonary hypertension, obesity, and sleep apnea.

The purpose of this study was to determine the frequency of central and obstructive sleep apnea in adult patients who have echocardiographic evidence of left ventricular dysfunction and pulmonary hypertension. Subjects with left ventricular dysfunction, pulmonary hypertension (pulmonary artery systolic pressure >30 mm Hg) and no lung disease were evaluated for risk factors associated with pulmonary hypertension. Of eight eligible adults, six completed the study. Subjects were from suburban and inner city family practices. Spirometric assessment, pulse oximetry on room air, rheumatologic evaluation, polysomnography, and additional history were taken. All six subjects had sleep apnea (apnea-plus-hypopnea index, or AHI, > or = 20): obstructive, central, or mixed. All were obese, and almost all the subjects had a restrictive pattern on spirometry, which is consistent with obesity. All had a pulmonary artery systolic blood pressure of 35 mm Hg or greater. None had daytime hypoxemia or collagen vascular disease, and none had ever used appetite suppressants. This study found a strong association between pulmonary hypertension and obstructive or central sleep apnea in obese patients with congestive heart failure (CHF). We propose that a pulmonary artery systolic pressure of 35 mm Hg or greater in ambulatory patients with CHF may signify an increased risk of sleep apnea.

Bilateral leg edema, obesity, pulmonary hypertension, and obstructive sleep apnea.

Pulmonary hypertension is usually due to an underlying cardiac or pulmonary condition. An association between unexplained pulmonary hypertension and bilateral leg edema in primary care patients was found previously. We undertook this study to identify the frequency of obstructive sleep apnea (OSA) in ambulatory, adult patients with pulmonary hypertension who initially presented with bilateral leg edema. Twenty ambulatory adults with bilateral leg edema, echocardiocardiographic evidence of pulmonary hypertension (estimated pulmonary artery systolic pressure >30 mm Hg) without left ventricular dysfunction, and no clinically apparent pulmonary disease [corrected] were enrolled from a suburban family practice and an inner-city family practice during a 3-year period. Spirometric assessment, pulse oximetry, rheumatologic evaluation, polysomnography, and questionnaire information regarding risk factors for pulmonary hypertension were obtained for each subject. Fifteen patients (75%) completed the study. Almost all of the subjects were obese. Nine (60%) of the 15 had OSA. None of the subjects demonstrated an obstructive pattern on spirometric evaluation results, but 9 (60%) had a restrictive spirometry pattern, consistent with their obesity. None of the subjects had daytime hypoxemia. Systemic hypertension was present in two-thirds of the subjects with OSA, and was absent in all of the subjects who lacked OSA. Bilateral leg edema in obese primary care patients is associated with both OSA and modest pulmonary hypertension. If these findings are generalizable, then bilateral leg edema may be an important clinical marker for underlying OSA.

Sleep quality, carbon dioxide responsiveness and hypoxaemic patterns in nocturnal hypoxaemia due to chronic obstructive pulmonary disease (COPD) without daytime hypoxaemia

In order to clarify whether nocturnal hypoxaemia (arterial oxygen saturation, SaO 2 <90% may exist in the long-term before daytime hypoxaemia ( PaO 2 <8·0 kPa) occurs in chronic obstructive pulmonary disease (COPD), 21 patients with stable severe COPD without daytime hypoxaemia ( PaO 2 ≥8·0 kPa) were studied prospectively. Subjects were monitored twice by polysomnography (PSG) 12 months apart. Spirometry was performed, and diffusion capacity ( D lCO) and hypercapnic respiratory drive response Δ P i 0·1 Δ PCO 2 −1) were measured during the daytime in conjunetion with polysomnography. At the start of the study our subjects had FEV 1%P (FEV 1 as a percentage of predicted value) of 26·1 ± 7·2%, a mean nocturnal nadir SaO 2 of 83 ± 5%, and a mean SaO 2 during nocturnal hypoxaemic episodes of 88·0 ± 0·7%. The patients' Δ P i 0·1 Δ PCO 2 −1 was 1·8 ± 1·4 cm H 2O kPa −1 (within the normal range). For the entire study group, no significant change in any lung function or blood gas parameter was noted during the year of observation, and nocturnal SaO 2 remained unaltered. Stage I sleep decreased ( P<0·05) after 12 months. Prolonged stage I sleep was associated with nocturnal hypoxaemia at the second PSG. Five subjects developed daytime hypoxaemia and they showed poorer lung function but similar nocturnal hypoxaemia and Δ P i 0·1 Δ PCO 2 −1 level compared to the rest of the patients. Patients with sudden SaO 2 dips had more pronounced nocturnal hypoxaemia and prolonged wakefulness than ‘non-dippers’. In conclusion, the mean level of nocturnal hypoxaemia may persist unaltered for at least 1 yr. COPD patients with exclusively nocturnal hypoxaemia have a hypercapnic drive response within the normal range. Prolonged nocturnal hypoxaemia and reduced whole night oxygenation are associated with increased superficial sleep. Sleep fragmentation and high carbon dioxide sensitivity may be important defence mechanisms against sleep-related hypoxaemia. The appearance of daytime hypoxaemia is preceded by a substantial deterioration in lung function, but by only a minor deterioration of nocturnal hypoxaemia.

Peripheral neuropathy in sleep apnea. A tissue marker of the severity of nocturnal desaturation.

Because chronic obstructive pulmonary disease (COPD) is well known to induce peripheral neuropathy and resistance to ischemic nerve conduction failure (RICF), we performed a case-control study examining peripheral nerve function during ischemia in 17 patients with severe obstructive sleep apnea (OSA) without daytime hypoxemia and 10 control subjects. Median nerve conduction was studied before, during, and after a 30-min period of ischemia. Preischemic sensory and mixed nerve potential amplitudes and sensory conduction velocity were lower in OSA patients than in control subjects despite higher supramaximal stimulation. During ischemia, seven OSA patients manifested RICF (OSA-RICF), whereas both the other 10 patients, who were nonresistant to ischemic conduction failure (OSA-NR), and control subjects did not. OSA-RICF patients had the lowest initial nerve-potential amplitude, whereas OSA-NR patients had a response intermediate between that of control subjects and OSA-RICF patients. OSA-RICF patients had a lower mean nocturnal SaO2 and a higher body mass index (BMI) and duration of SaO2 < 70% than did OSA-NR patients. Seven patients (four OSA-RICF and three OSA-NR) were reevaluated after at least 2 mo of treatment with nasal continuous positive airway pressure (nCPAP). RICF disappeared in all OSA-RICF patients, whereas preischemic nerve conduction parameters were unchanged in both OSA-RICF and OSA-NR patients. Thus OSA patients have peripheral nerve dysfunction whose severity is partly related to the level of nocturnal hypoxemia. Abnormal preischemic nerve conduction suggests axonal lesions, whereas RICF, which appears to be a sensitive but nonspecific tissue marker of the severity of hypoxemia, may result from adaptative mechanisms.

Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity.

Assessment of cardiorespiratory consequences of sleep apnoea syndrome (SAS) is difficult owing to confounding factors, especially obesity, that are strongly associated with SAS. This study was designed to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with massive obesity. In a retrospective chart-review study, we studied 60 patients with massive obesity defined by a body mass index (BMI) >40 kg.m(-2), presenting no chronic respiratory disease, who underwent an extensive assessment of cardiorespiratory consequences of obesity, including overnight polysomnography, lung function tests, arterial blood gas analysis, evaluation of vascular risk factors, myocardial scintigraphy with dipyridamole stress-test, isotopic ventriculography, Doppler echocardiography and Holter electrocardiogram recording. SAS defined by an apnoea + hypopnoea index (AHI) > or = 10 was diagnosed in 42% of patients (25 out of 60). Mean+/-SD AHI of SAS-positive (SAS+) patients was 38+/-24. Age, BMI, ventilatory function parameters, prevalence of smoking history and diabetes mellitus did not differ significantly in SAS+ versus SAS-negative (SAS-) groups. The following complications were observed more frequently in SAS+ than in SAS- patients: daytime hypoxaemia (35 vs 9%, p<0.02), pulmonary arterial hypertension (36 vs 7%, p<0.05) and increased interventricular septal thickness (50 vs 15%, p<0.03). No association was found between SAS on the one hand and systemic arterial hypertension, coronary artery disease, left ventricular dysfunction and nocturnal cardiac arrhythmias on the other. Nocturnal apnoeas in massive obesity may thus be associated with moderate daytime hypoxaemia, mild pulmonary arterial hypertension and moderate left ventricular hypertrophy, but not with severe cardiorespiratory complications.

HOME OXYGEN THERAPY

Home oxygen therapy has well-established benefits for patients with chronic obstructive pulmonary disease and resting hypoxemia. The indications for therapy have been clearly defined in the United States by the Health Care Financing Administration (HCFA), and these guidelines have been accepted by most third-party payers. Controversies regarding the use of oxygen during sleep and exercise when daytime hypoxemia is not present have important therapeutic and financial implications. HCFA has recently proposed a substantial reduction in reimbursement for home oxygen which could have a major adverse effect if done on a global, across-the-board, basis. Some of the new technological developments in oxygen delivery systems are presented in this article.

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia.

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COPD) patients without marked daytime hypoxaemia. We have investigated the relationships between pulmonary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O2 therapy (daytime arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending > or = 30% of the recording time with a transcutaneous O2 saturation < 90%. An obstructive sleep apnoea syndrome was excluded by polysomnography. Sixty six patients were desaturators (Group 1) and 28 were nondesaturators (Group 2). There was no significant difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4 vs 63+/-3 mmHg)) but arterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0.7 vs 53+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0.0001). Mean pulmonary artery pressure (Ppa) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual variable or combination of variables could predict the presence of pulmonary hypertension. It is concluded that in these patients with chronic obstructive pulmonary disease with modest daytime hypoxaemia, functional and gasometric variables (with the noticeable exception of arterial carbon dioxide tension) cannot predict the presence of nocturnal desaturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.

Sleep-related hypoxaemia in chronic obstructive pulmonary disease: causes, consequences and treatment.

Worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease has been extensively investigated in the past 20 years owing to the development of polysomnography and to the advent of reliable transcutaneous oximeters. Sleep-related hypoxaemia is characteristic of rapid-eye-movement (REM) sleep but may be present during other sleep stages. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. Sleep-related hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the preponderant mechanism during REM sleep. The deleterious effects of sleep-related hypoxaemia include cardiac arrhythmias, 'hypoxaemic stress' on the coronary circulation and especially, peaks of pulmonary hypertension. The treatment of nocturnal hypoxaemia is conventional O2 therapy (both nighttime and daytime) in patients who exhibit marked daytime hypoxaemia (PaO2 < 55-60 mm Hg). At present data are not sufficient for justifying the use of isolated nocturnal O2 therapy in patients with nocturnal desaturation who do not qualify for conventional O2 therapy.

Erythropoietin and base excess levels in patients with chronic pulmonary diseases

Factors which could influence serum erythropoietin (s-EPO) levels in patients with chronic pulmonary diseases were investigated, paying special attention to the role of changes in acid-base balance (PaCO2, HCO3− and base excess levels) in EPO production. Data from 30 patients with chronic pulmonary diseases (chronic pulmonary emphysema, chronic bronchitis and post-tuberculosis status) were obtained in the morning and were analyzed with a stepwise forward multiple regression analysis, evaluating the statistical significance of seven factors which may potentially influence s-EPO levels: arterial pH, PaCO2, PaO2, HCO3−, base excess (BE), SaO2 and hemoglobin (Hb). Significant simple correlations (P<0.01) of log(s-EPO) were obtained with PaO2 (r=−0.66), PaCO2 (r=0.59), HCO3− (r=0.67), BE (r=0.71) and SaO2 (r=−0.77). The stepwise forward multiple regression analysis revealed that significant correlate variables for the outcome variable of log(s-EPO) were SaO2 and BE, with r=0.823 (P<0.0001). In patients with chronic pulmonary diseases it was shown that SaO2 was a negative correlate and BE was a positive correlate of s-EPO levels. It was speculated that s-EPO levels in the morning reflected daytime hypoxemia (SaO2) and nocturnal desaturation evoked by hypopnea during sleep (indicated as BE) in these patients.

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%. 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 day-time 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-to-moderate, 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,O2), < or = 7.3 kPa (55 mmHg) conventional O2 therapy (nocturnal + diurnal) is required.

Visual attention in patients with chronic obstructive pulmonary disease

The selective visual attention of 39 patients with chronic obstructive pulmonary disease (COPD) was measured by the Bourdon-Vos test and compared with the attention performance of 38 healthy controls of the same age range. The correlation between the attenion of the COPD patients and day- and night-time parameters was determined. Furthermore, in 44 other COPD patients with daytime hypoxaemia, the effect of one night of oxygen supplementation and of a 7-day treatment with two respiratory stimulants (chlormadinone acetate) (CMA) or acetazolamide (ACET) on attention performance was studied. The results showed that the attention performance of COPD patients was lower than that of controls. Significant correlations were found between the mean line time (attention parameter) and the following parameters: age, inspiratory vital capacity (IVC), hypercapnic ventilatory response (HCVR), daytime arterial oxygen saturation (S aO 2) daytime arterial oxygen pressure (P aO 2) daytime arterial carbon dioxide pressure (P aCO 2), mean nocturnal S aO 2, lowest nocturnal S aO 2 and the standard deviation of the mean nocturnal S aO 2. Multiple linear regression analysis showed that, apart from age, only the nadir of the nocturnal S aO 2 contributed to the prediction of the attention. No clinically important short-term effect of oxygen or respiratory stimulating therapy on the attention performance was found.