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, SaO2 < 90%) may exist in the long-term before daytime hypoxaemia (PaO2 < 8.0 kPa) occurs in chronic obstructive pulmonary disease (COPD), 21 patients with stable severe COPD without daytime hypoxaemia (PaO2 > or = 8.0 kPa) were studied prospectively. Subjects were monitored twice by polysomnography (PSG) 12 months apart. Spirometry was performed, and diffusion capacity (DLCO) and hypercapnic respiratory drive response delta PI0.1 delta PCO2(-1)) were measured during the daytime in conjunction with polysomnography. At the start of the study our subjects had FEV1 %P (FEV1 as a percentage of predicted value) of 26.1 +/- 7.2%, a mean nocturnal nadir SaO2 of 83 +/- 5%, and a mean SaO2 during nocturnal hypoxaemic episodes of 88.0 +/- 0.7%. The patients' delta PI0.1 delta PCO2(-1) was 1.8 +/- 1.4 cm H2O 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 SaO2 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 delta PI0.1 delta PCO2(-1) level compared to the rest of the patients. Patients with sudden SaO2 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.     

Mechanisms underlying effects of nocturnal ventilation on daytime blood gases in neuromuscular diseases.

The hypothesis that, in neuromuscular and chest wall diseases, improvement in central respiratory drive explains the effects of night-time ventilation on diurnal gas exchanges was tested. The effects at 6 months, 1, 2 and 3 yrs of intermittent positive pressure ventilation (IPPV) on arterial blood gas tension, pulmonary function, muscle strength, sleep parameters, respiratory parameters during sleep and ventilatory response to CO2 were evaluated in 16 consecutive patients with neuromuscular or chest wall disorders. As compared with baseline, after IPPV daytime arterial oxygen tension (Pa,O2) increased (+2.3 kPa at peak effect) and arterial carbon dioxide tension (Pa,CO2) and total bicarbonate decreased (-1.8 kPa and -5 mmol x L(-1), respectively) significantly; vital capacity, total lung capacity, maximal inspiratory and expiratory pressures and alveolar-arterial oxygen gradient did not change; the apnoea-hypo-opnoea index and the time spent with an arterial oxygen saturation (Sa,O2) value <90% decreased (-24 and -101 min, respectively), sleep efficiency and mean Sa,O2 increased (+16% and +5%, respectively); and ventilatory response to CO2 increased (+4.56 L x min(-1) x kPa(-1)) significantly. The reduction in Pa,CO2 observed after IPPV correlated solely with the increase in the slope of ventilatory response to the CO2 curve (r=-0.68, p=0.008). In neuromuscular or chest wall diseases, improvement of daytime hypoventilation with nocturnal intermittent positive pressure ventilation may represent an adaptation of the central chemoreceptors to the reduction of profound hypercapnia during sleep or reflect change in the quality of sleep.     

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.     

Exercise hypercapnia in advanced chronic obstructive pulmonary disease: the role of lung hyperinflation

In severe chronic obstructive pulmonary disease (COPD), carbon dioxide retention during exercise is highly variable and is poorly predicted by resting pulmonary function and arterial blood gases or by tests of ventilatory control. We reasoned that in patients with compromised gas exchange capabilities, exercise hypercapnia could be explained, in part, by the restrictive consequences of dynamic lung hyperinflation. We studied 20 stable patients with COPD (FEV(1) = 34 +/- 3 percent predicted; mean +/- SEM) with varying gas exchange abnormalities (Pa(O(2)) range, 35 to 84 mm Hg; Pa(CO(2)) range, 31 to 64 mm Hg). During symptom-limited maximum cycle exercise breathing room air, Pa(CO(2)) increased 7 +/- 1 mm Hg (p < 0.05) from rest to peak exercise (range, -6 to 25 mm Hg). We measured the change in Pa(CO(2)) after hyperoxic breathing at rest as an indirect test of ventilation-perfusion abnormalities. The change in Pa(CO(2)) from rest to peak exercise correlated best with the acute change in Pa(CO(2)) during hyperoxia at rest (r(2) = 0.62, p < 0.0005) and with resting arterial oxygen saturation (r(2) = 0.30, p = 0.011). During exercise, the strongest correlates of serial changes in Pa(CO(2)) from rest included concurrent changes in end-expiratory lung volume expressed as a percentage of total lung capacity (partial correlation coefficient [r] = 0.562, p < 0.0005) and oxygen saturation (partial r = 0.816, p < 0.0005). In severe COPD, the propensity to develop carbon dioxide retention during exercise reflects marked ventilatory constraints as a result of lung hyperinflation as well as reduced gas exchange capabilities.     

Effects of different ventilator settings on sleep and inspiratory effort in patients with neuromuscular disease

Patients with neuromuscular disease (NMD) who require long-term ventilation normally have the ventilation set using empirical daytime parameters. We evaluated arterial blood gases (ABG), breathing pattern, respiratory muscle function, and sleep architecture during ventilation with two noninvasive Pressure Support Ventilation (nPSV) settings in nine patients with NMD. The two settings were randomly applied: the usual (US), with the nPSV setting titrated on simple clinical parameters, and the physiological (PHYS), tailored to the patient's respiratory effort. During wakefulness, nPSV significantly improved ABG and minute ventilation and reduced the diaphragmatic pressure-time product (PTPdi/breath), independently of the type of setting (PTPdi/breath spontaneous breathing 5.7 +/- 2.4, US 3.2 +/- 2, PHYS 3.6 +/- 1.6 cm H2O . seconds(-1), p < 0.001). However, during sleep, PHY nPSV resulted in a significant improvement of gas exchange, sleep efficiency (71.7% +/- 14 US vs. 80.6% +/- 8.3 PHYS, p < 0.01) and % of REM sleep (9.1% +/- 7 US vs. 17.3% +/- 5.4 PHYS, p < 0.01). This improvement was significantly correlated with the reduction in ineffective efforts. In NMD, nPSV is effective in improving daytime ABG and in unloading inspiratory muscles independently of whether it is set on the basis of the patient's comfort or the patient's respiratory mechanics. However, PHYS was associated with better sleep architecture and nighttime gas exchange.     

Effect of a nonrebreathing exhalation valve on long-term nasal ventilation using a bilevel device

STUDY OBJECTIVE: To determine whether an exhalation valve designed to minimize rebreathing improves daytime or nocturnal gas exchange or improves symptoms compared with a traditional valve during nocturnal nasal ventilation delivered using a bilevel pressure ventilation device. DESIGN: Prospective direct comparison trial with each patient sequentially using both valves, during a 2-week run-in period with a traditional valve, a 2-week trial with the nonrebreathing valve, and a 2-week washout period with the traditional valve. SETTING: Outpatient pulmonary function laboratory and home nocturnal monitoring. PATIENTS: Seven patients who received long-term (> 1 year) nocturnal nasal bilevel pressure ventilation with an expiratory pressure of 相似文献   

Daytime hypercapnia in obstructive sleep apnea syndrome

BACKGROUND: The pathogenesis of daytime hypercapnia (Paco2 >or= 45 mm Hg) may be directly linked to the existence of obstructive sleep apnea syndrome (OSAS) per se, although only some patients with OSAS exhibit daytime hypercapnia. OBJECTIVE: To investigate the prevalence of daytime hypercapnia in patients with OSAS; the association of daytime hypercapnia and obesity, obstructive airflow limitation, restrictive lung impairment, and severity of sleep apnea; and the response to continuous positive airway pressure (CPAP) therapy in a subset of subjects. METHODS: The study involved 1,227 patients with OSAS who visited a sleep clinic and were examined using polysomnography. As for the response to CPAP therapy, the patients were considered good responders if their daytime Paco2 decreased >or= 5 mm Hg and poor responders if it decreased < 5 mm Hg. RESULTS: Fourteen percent (168 of 1,227 patients) exhibited daytime hypercapnia. These patients had significantly higher body mass index (BMI) and apnea-hypopnea index (AHI) values compared with normocapnic patients, while percentage of predicted vital capacity (%VC) and FEV(1)/FVC ratio did not differ between the two groups. Logistic regression analysis showed that only AHI was a predictor of daytime hypercapnia (p < 0.0001), while BMI (p = 0.051) and %VC (p = 0.062) were borderline predictors of daytime hypercapnia. Daytime hypercapnia was corrected in some patients (51%, 19 of 37 patients) with severe OSAS after 3 months of CPAP therapy. CONCLUSION: The pathogenesis of daytime hypercapnia may be directly linked to sleep apnea in a subgroup of patients with OSAS.     

Apparent diffusion limitations for CO(2) excretion in rainbow trout are relieved by injections of carbonic anhydrase

Experiments were performed in vivo to elucidate the underlying mechanism(s) of apparent diffusion limitations for CO(2) excretion in rainbow trout (Oncorhynchus mykiss). Ligation of two gill arches and the associated expected reduction in gill surface area of 30% caused pronounced respiratory acidosis as indicated by elevated arterial blood P(CO(2)) (Pa(CO(2))) and reduced arterial blood pH. Under conditions of normoxia, arterial blood P(O(2)) (Pa(O(2))) was not significantly (statistically) reduced. However, during hypoxia (water P(O(2))=70-80 mmHg), the apparent trend for reduced Pa(O(2)) values became statistically significant in fish with 15% surface area reduction. To determine whether the elevated Pa(CO(2)) in fish with reduced surface area (30%) reflected true diffusion limitations or chemical equilibrium limitations imposed by the relatively slow rate of red blood cell Cl(-)/HCO(3)(-) exchange, fish were injected with carbonic anhydrase (CA) to permit catalysis of HCO(3)(-) dehydration within the plasma. Injection of CA caused a lowering of Pa(CO(2)) by 0.87+/-0.32 mmHg within 120 min and thus essentially eliminated the increase in Pa(CO(2)) (1.04+/-0.33 mmHg) that was caused by the reduction in surface area. These results clearly demonstrate that the elevation in Pa(CO(2)) evoked by gill surface area reduction is a consequence of chemical equilibrium limitations rather than true diffusion limitations, per se.     

Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea

The mechanisms responsible for the development of chronic hypercapnia in patients with obstructive sleep apnea (OSA) are not well defined. Therefore, we tested the hypothesis that diffuse airway obstruction may be involved by studying 50 patients with a well-documented OSA syndrome. Seven patients had daytime hypercapnia with a mean PaCO2 of 51 +/- 2 (SEM) mm Hg, compared to a PaCO2 of 35 +/- 1 in the other 43 patients. There were no differences between the 2 groups in the number or duration of nocturnal obstructive events. In contrast, the hypercapnic patients were significantly heavier than the normocapnic patients (body weight, 189 +/- 11 versus 148 +/- 6% of ideal; p less than 0.005) and had evidence of diffuse airway obstruction, as indicated by an increased residual volume and a reduction in all expiratory flow rates. When the hypercapnic patients were compared with a weight-matched group of 9 normocapnic patients (body weight, 196 +/- 8% of ideal), there were still no differences in nocturnal obstructive events, but the differences in tests of airway mechanics persisted. Multiple regression analysis of PaCO2 against several anthropometric, respiratory physiologic, and polysomnographic variables revealed that only 2 variables (expiratory reserve volume and FEV1/FVC), both of which are influenced by airway mechanics, were significantly correlated with PaCO2 (multiple r = 0.78; p = 0.0001). The findings suggest that OSA alone does not produce daytime hypercapnia even in obese patients, and that the presence of diffuse airway obstruction is an important predisposing factor to the development of chronic CO2 retention in such patients.     

Arterial hypoxaemia in endurance athletes is greater during running than cycling

The effect of both training discipline and exercise modality on exercise-induced hypoxaemia (EIH) was examined in seven runners and six cyclists during 5 min high intensity treadmill and cycle exercise. There were no significant interactions between training discipline, exercise modality and arterial P(O(2)) (Pa(O(2))) when subject groups were considered separately but when pooled there were significant differences between exercise modalities. After min 2 of exercise arterial hydrogen ion concentration, minute ventilation, alveolar P(O(2)) (PA(O(2))) and Pa(O(2)) were all lower with treadmill running with the largest differential for the latter occurring at min 5 (treadmill, 80.8+/-1.8; cycle, 90.2+/-2.5, mmHg, N=13, P< or = 0.05). At every min of exercise, the differences in Pa(O(2)) between the ergometers were strongly associated with similar differences in PA(O(2)) and alveolar to arterial P(O(2)) (PA(O(2))-Pa(O(2))). It is concluded that the greater EIH with treadmill running is a consequence of the combined effect of a reduced lactic acidosis-induced hyperventilation and greater ventilation-perfusion inequality with this exercise mode.     

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.     

Long-term non-invasive ventilation increases chemosensitivity and leptin in obesity-hypoventilation syndrome

BACKGROUND: Long-term nocturnal non-invasive mechanical ventilation (NIMV) is an effective treatment for obesity-hypoventilation syndrome (OHS), improving central carbon dioxide (CO(2)) sensitivity. Leptin might contribute to sustain adequate ventilation in obesity. The aim of the study was to investigate the role of leptin in the OHS pathogenesis looking at its relationship to CO(2) sensitivity before and after NIMV in OHS patients. METHODS: In six obese patients (3F/3M; aged 63+/-9 yr; BMI 47.0+/-4.5 kg/m(2)) with OHS and without obstructive sleep apnoea-hypopnoea (OSAH) diurnal arterial blood gases, fasting plasma leptin concentration and CO(2) chemosensitivity were determined before and after 10.3+/-5.6 (range 6-20) months of NIMV. RESULTS: After NIMV improvements were observed in gas exchange (PaO(2) from 51.3+/-6.7 to 75.0+/-10.3 mmHg, p<0.01; PaCO(2) from 55.5+/-4.8 to 43.7+/-1.2 mmHg, p<0.01; [HCO(3)(-)] from 33.3+/-3.8 to 29.8+/-1.7 mmol/l, p<0.05) and CO(2) chemosensitivity, measured as P(0.1)/PetCO(2) slope (from 0.09+/-0.07 to 0.18+/-0.07 cmH(2)O/mmHg, p<0.05) and V(E)/PetCO(2) slope (from 0.4+/-0.3 to 0.9+/-0.5l/min/mmHg, p=0.07). Plasma leptin increased from 34.5+/-21.1 ng/ml to 50.2+/-22.9 ng/ml (p<0.01) after NIMV and changes of the P(0.1)/PetCO(2) slope correlated with percent changes of plasma leptin (r(2)=0.79, p<0.05). CONCLUSIONS: These findings suggest a possible role of leptin in the recovery of neuromuscular response to hypercapnia obtained during long-term nocturnal NIMV in OHS patients without OSAH.     

Comparison of acetazolamide and medroxyprogesterone as respiratory stimulants in hypercapnic patients with COPD

BACKGROUND: Acetazolamide and medroxyprogesterone acetate (MPA) are two respiratory stimulants that can be used in patients with stable hypercapnic COPD. DESIGN AND METHODS: The effects of acetazolamide, 250 mg bid, and MPA, 30 mg bid, on daytime and nighttime blood gas values and the influences on the hypercapnic and hypoxic ventilatory and mouth occlusion pressure (P(0.1)) at 100 ms response were studied in a crossover design in 12 hypercapnic patients with stable COPD (FEV(1), 33 +/- 4% predicted [mean +/- SEM]). RESULTS: Daytime PaCO(2) decreased from 47.3 +/- 0.8 mm Hg (placebo) to 42.0 +/- 1.5 mm Hg during acetazolamide treatment (p < 0.05) and to 42.8 +/- 1.5 mm Hg during MPA treatment (p < 0.05). Daytime PaO(2) improved with acetazolamide from 65.2 +/- 2.3 to 75.0 +/- 3.0 mm Hg (p < 0.05), whereas no significant changes were seen with MPA. Mean nocturnal end-tidal carbon dioxide tension decreased with both treatments, from 42.0 +/- 2.3 to 35.3 +/- 2.3 mm Hg with acetazolamide (p < 0.05) and to 34.5 +/- 0.8 mm Hg with MPA (p < 0.05). The percentage of time that the nocturnal arterial oxygen saturation was < 90% was reduced significantly with acetazolamide, from 34.9 +/- 10.7% to 16.3 +/- 7.5% (p < 0.05). Mean nocturnal saturation did not change with MPA. Resting minute ventilation increased significantly only with MPA from 9.6 +/- 0.7 to 10.8 +/- 0.8 L/min (p < 0.05). The slope of the hypercapnic ventilatory response did not change during acetazolamide and MPA therapy. The hypoxic ventilatory response increased from - 0.2 +/- 0.05 to - 0.4 +/- 0.1 L/min/% during acetazolamide (p < 0.05) and to - 0.3 +/- 0.1 L/min/% during MPA (p < 0.05). The hypoxic P(0.1) response improved with acetazolamide treatment from - 0.05 +/- 0.008 to - 0.15 +/- 0.02 mm Hg/% (p < 0.05). CONCLUSIONS: This study shows that acetazolamide and MPA both have favorable effects on daytime and nighttime blood gas parameters in ventilatory-limited patients with stable COPD. However, the use of acetazolamide is preferred because of its extra effect on nocturnal saturation.     

Prognostic value of blood gas analyses in patients with idiopathic pulmonary arterial hypertension.

Blood gas abnormalities in patients with idiopathic pulmonary arterial hypertension (IPAH) may be related to disease severity and prognosis. The present authors performed a 12-yr retrospective analysis assessing arterialised capillary blood gases, haemodynamics, exercise variables and survival in 101 patients with IPAH. At baseline, arterial oxygen tension (P(a,O(2))) and carbon dioxide arterial tension (P(a,CO(2))) were 9.17+/-1.86 and 4.25+/-0.532 kPa, respectively. While P(a,O(2) )was not associated with survival, a low P(a,CO(2 ))was a strong and independent prognostic marker. When patients were divided according to a baseline P(a,CO(2 ))value above or below 4.25 kPa, a cut-off value determined by receiver operating characteristics analysis, survival rates were 98 and 86% at 1 yr, 82 and 69% at 2 years, 80 and 51% at 3 yrs, 77 and 41% at 5 yrs, and 65 and 12% at 8 yrs, respectively. P(a,CO(2 ))after 3 months of medical therapy was strongly associated with survival. Hypocapnia at rest and during exercise correlated with low cardiac output, low peak oxygen uptake and reduced ventilatory efficacy. Multiple regression analysis revealed that 6-min walking distance, right atrial pressure and P(a,CO(2 ))were independently associated with survival. In patients with idiopathic pulmonary arterial hypertension, hypocapnia (carbon dioxide arterial tension <4.25 kPa) is an independent marker of mortality.     

Decreased oxyhemoglobin affinity in patients with sleep apnea syndrome

Oxyhemogloblin affinity (P50 at pH 7.4, PaCO2 = 40 mm Hg, temperature = 37 degrees C) and 2,3-DPG concentration were assessed in 15 nonsmokers (14 men and one woman 46 to 63 yr of age) with sleep apnea syndrome (SAS) and in 10 normal subjects (eight men and two women 22 to 48 yr of age). In patients with SAS, mean nocturnal apnea index was 46 +/- 20/h, and mean nocturnal SO2 was 86 +/- 6% versus 94.6 +/- 1.8% during the daytime. Daytime mean P50 of the patients was 28.5 +/- 1.2 mm Hg versus 27.1 +/- 0.3 mm Hg in the normal subjects (p less than 0.05). Daytime mean 2.3-DPG was 1.23 +/- 0.25 moles DPG/mole hemoglobin versus 0.80 +/- 0.15 (p less than 0.05). Significant correlations were found in patients between P50 and mean nocturnal SO2 (r = -0.62, p less than 0.01) and between P50 and 2,3-DPG (r = 0.68, p less than 0.01). The measurements were repeated in five patients after surgical or positive-pressure treatment. P50 and 2,3-DPG both decreased and returned to normal values. In conclusion, the oxyhemoglobin dissociation curve is shifted to the right in patients with SAS and there is an increase in 2,3-DPG. These could be protective mechanisms against the development of polycythemia, pulmonary hypertension, and cor pulmonale.     

Lung function accurately predicts hypercapnia in patients with Duchenne muscular dystrophy

BACKGROUND: In patients with Duchenne muscular dystrophy (DMD), implementation of mechanical ventilation depends on sleep investigation and measurement of CO2 tension. The objective of this cross-sectional study was to determine which noninvasive lung function parameter best predicts nocturnal hypercapnia and diurnal hypercapnia in these patients. METHODS: According to transcutaneous CO2 (TcCO2) measurement, 114 DMD patients were classified into three groups: nocturnal hypercapnia (n = 38) [group N], diurnal hypercapnia (n = 39), despite nocturnal ventilation (group D), and 24-h normocapnia and spontaneous breathing (n = 37) [group S] as control. TcCO2 tension and lung function variables included vital capacity (VC) and maximal inspiratory pressure (MIP), and breathing pattern variables included tidal volume (Vt) and respiratory rate (RR), measured at the time of group inclusion. The rapid and shallow breathing index (RSBI [RR/Vt]) and Vt/VC ratio were calculated. Areas under the curve from the receiver operating characteristic (ROC) were calculated for those parameters. RESULTS: Compared to group S, lung function was significantly worse in group N and group D. VC, RR, and RSBI distinguished group S from group N by ROC comparison. Cut-off values of VC < or = 680 mL (ROC, 0.968), MIP < or = 22 cm H2O (ROC, 0.928), and Vt/VC > 0.33 (ROC, 0.923) accurately discriminated group D from group N, but RSBI, RR, and Vt did not. CONCLUSIONS: Lung function is useful to predict nocturnal hypercapnia in patients with DMD. Moreover, VC < 680 mL is very sensitive to predict daytime hypercapnia.     

阻塞性睡眠呼吸暂停低通气综合征与合并慢性阻塞性肺疾病患者的日间高碳酸血症的临床研究

目的 比较单纯阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)与合并慢性阻塞性肺疾病即重叠综合征(overlap syndrome,OS)患者肺功能变化,日间高碳酸血症与睡眠呼吸紊乱之间的关系.方法 42例OSAHS患者,23例为单纯OSAHS患者组,19例为OS患者组,两组均做多导睡眠仪监测、肺功能检测、血气分析检测.比较两组睡眠紊乱指标、肺功能及PaCO2情况并做相关性分析.结果 两组患者在睡眠呼吸暂停低通气指数相似的情况下,OS组的PaCO2明显高于OSAHS组;OS组的肺功能指标明显差于OSAHS组;两组患者的日间PaCO2与睡眠呼吸暂停严蘑程度之间无明显线性相关关系.结论 OS组患者的肺功能较OSAHS组差;OS组的日问高PaCO2与是否台并OSAHS无关.     

Tolerance and physiologic effects of nocturnal mask pressure support vs proportional assist ventilation in chronic ventilatory failure

STUDY OBJECTIVES: To compare the tolerance and physiologic effects of a 5-night treatment with either nasal proportional assist ventilation (PAV) or pressure support ventilation (PSV) in patients with chronic ventilatory failure. DESIGN: Cross-over, randomized, controlled study. SETTING: Rehabilitation units of pneumology department. PATIENTS OR PARTICIPANTS: Four patients with COPD and 10 patients with restrictive thoracic diseases with chronic hypercapnia (median baseline Paco(2), 55.1 mm Hg) were studied. INTERVENTIONS: In a cross-over study, nasal PAV and PSV set at the patient's comfort were randomly applied during 5 consecutive nights (with a 2-night washout period). MEASUREMENTS AND RESULTS: Continuous nocturnal pulse oximetric saturation (Spo(2)) and arterial blood gas results at wake-up were evaluated at baseline during spontaneous breathing and on the fifth day of ventilatory support. Dyspnea, sleep quality, adaptation, and comfort at inspiration and expiration by visual analog scale (VAS) were evaluated every day as well as a side effects score. On the fifth day, there were no significant differences in daytime Paco(2) (median PAV, 53.3 mm Hg; median PSV, 50.2; p = 0.168). Mean nocturnal Spo(2) improved significantly with both PAV and PSV without any significant differences between modes (baseline median, 92%; PAV median, 94.5%; PSV median, 95%). The percentage of the study night spent < 90% Spo(2) (T90) was slightly but significantly higher with PAV than with PSV (median PAV T90, 4%; median PSV T90, 2%; p = 0.049). The VAS symptom score was similar at day 5 between modes; however, nasal and oral dryness were lower (p = 0.05) and alarm noise was higher (p = 0.037) with PAV. CONCLUSIONS: After 5 days of treatment, both modes had similar tolerance, and were equally effective in reducing daytime hypercapnia and improving nocturnal saturation and symptoms. However, PAV induced less nasal and oral dryness but was associated with higher alarm noise.     

Sleep hypoventilation due to increased nocturnal oxygen flow in hypercapnic COPD patients

Background and objective: Several COPD treatment guidelines recommend increasing oxygen flow during sleep to avoid nocturnal desaturation. However, such an increase could have deleterious clinical and gas exchange effects. The objective of this study was to evaluate short‐term gas exchange alterations produced by increasing the nocturnal oxygen flow rate. Methods: Thirty‐eight COPD patients with chronic hypercapnic respiratory failure were evaluated. In a cross‐over study, patients were randomly assigned to receive the daytime oxygen flow rate on one night and an additional litre on the alternate night. Nocturnal pulse oximetry and arterial blood gases at awakening were measured, in each patient, on two consecutive days. Results: The administration of 1 L more oxygen during the night resulted in improved parameters of nocturnal oxygenation (oxygen pulse oximetry saturation—SpO₂; percentage of sleep time spent at SpO₂ < 90%—CT90; PaO₂ at awakening). Nevertheless, such an increase in oxygen flow during the night was also associated with greater hypercapnia and acidosis (p < 0.05) the next morning. Conclusions: The increase of oxygen flow in severe COPD patients with established daytime hypercapnia improved nocturnal oxygenation but it also led to greater hypercapnia and respiratory acidosis at awakening in a considerable proportion of these patients.     

Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal continuous positive airway pressure therapy

CONTEXT: Daytime hypercapnia in patients with obstructive sleep apnea syndrome (OSAS) has a highly variable prevalence in the published studies, and is usually thought to be the consequence of an associated disease, COPD, or severe obesity. STUDY OBJECTIVES: To assess the prevalence of daytime hypercapnia in a very large population of adult patients with OSAS, free of associated COPD, and with a wide range of body mass index (BMI), and to evaluate the relationship between daytime hypercapnia and the severity of obesity and obesity-related impairment in lung function. DESIGN: Retrospective analysis of prospectively collected data. METHODS: The database of the observatory of a national nonprofit network for home treatment of patients with chronic respiratory insufficiency (Association Nationale pour le Traitement a Domicile de l'Insuffisance Respiratoire Chronique) was used. Collected data at treatment initiation were age, apnea-hypopnea index, BMI, FEV(1), vital capacity (VC), and arterial blood gases. The study included 1,141 adult patients with OSAS treated in France with nocturnal nasal continuous positive airway pressure (CPAP), FEV(1) >/= 80% predicted, FEV(1)/VC >/= 70%, and absence of restrictive respiratory disease other than related to obesity. RESULTS: The prevalence of daytime hypercapnia (Paco(2) >/= 45 mm Hg) before initiating CPAP therapy was 11% in the whole study population. The prevalence of daytime hypercapnia was 7.2% (27 of 377 patients) with BMI < 30, 9.8% (58 of 590 patients) with BMI from 30 to 40, and 23.6% (41 of 174 patients) with BMI > 40. Patients with daytime hypercapnia had significantly higher BMI values and significantly lower VC, FEV(1), and Pao(2) values than the normocapnic patients. Stepwise multiple regression showed that Pao(2), BMI, and either VC or FEV(1) were the best predictors of hypercapnia, but these variables explained only 9% of the variance in Paco(2) levels. CONCLUSION: Daytime hypercapnia was observed in > 1 of 10 patients with OSAS needing CPAP therapy and free of COPD, and was related to the severity of obesity and obesity-related impairment in lung function. However, other mechanisms than obesity are probably involved in the pathogenesis of daytime hypercapnia in OSAS.