Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome
ABSTRACT We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake ("blue and bloated", Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction ("pink and puffing", Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alternative explanation.
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- "In patients with severe COPD, oxygen saturation may fall during REM sleep by 20–30%   and PAP may rise by as much as 20 mm Hg . "
ABSTRACT: The development of pulmonary hypertension in COPD adversely affects survival and exercise capacity and is associated with an increased risk of severe acute exacerbations. Unfortunately not all patients with COPD who meet criteria for long term oxygen therapy benefit from it. Even in those who benefit from long term oxygen therapy, such therapy may reverse the elevated pulmonary artery pressure but cannot normalize it. Moreover, the recent discovery of the key roles of endothelial dysfunction and inflammation in the pathogenesis of PH provides the rationale for considering specific pulmonary vasodilators that also possess antiproliferative properties and statins.08/2012; 2012(2090-1836):203952. DOI:10.1155/2012/203952
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- "Although pulmonary hypertension in COPD is usually mild (mPAP 20–35 mm Hg), it may increase markedly during exercise (Horsfi eld et al 1968; Weitzenblum 2003), sleep (Coccagna et al 1978; Catterall et al 1983; Fletcher et al 1984), and exacerbations (Weitzenblum et al 1994). Frequent exacerbations can promote the development of right heart failure and this should be preventable by general management measures recommended for COPD. "
ABSTRACT: Hypoxia and endothelial dysfunction play a central role in the development of pulmonary hypertension. Cor pulmonale is a maladaptive response to pulmonary hypertension. The presence of peripheral edema in cor pulmonale is almost invariably associated with hypercapnia. Correction of abnormalities of gas exchange and ventilation can ameliorate pulmonary hypertension and improve survival. This review focuses on new information about the pathogenesis and treatment of pulmonary hypertension in COPD including information derived from lung volume reduction surgery, the role of brain natriuretic peptide, exhaled nitric oxide for diagnosis, and the treatment of cor pulmonale with recently available specific pulmonary vasodilators.International Journal of COPD 02/2007; 2(3):273-82. · 2.73 Impact Factor
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ABSTRACT: Nocturnal oxygen desaturation during the sleep is very frequent in patients affected by chronic obstructive pulmonary disease (COPD). Hypoventilation, rather than sleeping apnea, is commonly considered as the most relevant factor in the onset of nocturnal oxygen desaturation. On this topic, the Authors have carried on a study on the nocturnal hypoxemia in 70 hospitalized COPD patients with a mean FEV1% of 40 +/- 21 and a mean PaO2 of 67.7 +/- 6.1. Anthropometric features (sex, age, body mass index) and functional respiratory parameters (FEV1, FEV1/VC, PaO2, PaCO2, SaO2, pH) were considered. Moreover all the patients were monitorized with transcutaneous pulse oxymetry, while breathing environmental air, in nighttime. Mean oxyhemoglobinic nocturnal saturation (SaO2 noct.%), minimum registered value of nocturnal SaO2 (min SaO2 noct.%) and the minutes of nighttime SaO2 < or = 90% and < or = 85% (tSaO2 < or = 90% e < or = 85%) were considered. Fiftyfour patients (77.15%) were nocturnal desaturating (NOD), whereas 16 (22.85%) were not desaturating (nNOD). A statistically significant difference was found between the two groups as to the values of FEV1 (p < 0.05), PaCO2, pH, SaO2 noct.%, minimum SaO2 noct.% and tSaO2 < or = 90% and < or = 85% (p < 0.0001). A statistically significant correlation was found between tSaO2 < 90% and BMI (r = 0.44), PaCO2 (r = 0.48) and pH (r = -0.44), as well as between tSaO2 < 85% and PaCO2 (r = 0.57) and pH (r= -0.50), between SaO2 noct.% and BMI (r = -0.45), PaCO2 (r = -0,50), FEV1 (r = 0.44) and pH (r = 0.46) and finally between minimum SaO2 noct.% and PaCO2 (r = -0.47) was found. Eighty percent of the NOD patients had PaO2 < 75 mm Hg and PaCO2 > 44 mm Hg. All the patients with PaCO2 > 50 mm Hg were NOD. In conclusion, all COPD subjects with FEV1 < 49% and daytime PaO2 > 60 mm Hg, particularly when associated to elevated PaCO2 values and high BMI, should undergo a nocturnal pulse oxymetry in order to identify possible nocturnal desaturations. In these patients reduced FEV1, high BMI and/or elevated PaCO2 appear to be predictive indexes of nocturnal desaturation. A PaCO2 > 50 mm Hg is highly indicative for a nocturnal oxygen desaturation.European review for medical and pharmacological sciences 5(5-6):173-9. · 0.99 Impact Factor