The beneficial effects of nocturnal oxygen therapy (NOT) in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate daytime hypoxaemia (arterial oxygen tension (Pa,O 2 ) in the range 7.4±9.2 kPa (56±69 mmHg)) and exhibiting sleep-related oxygen desaturation remains controversial. The effectiveness of NOT in that category of COPD patients was studied. The end points included pulmonary haemodynamic effects after 2 yrs of follow-up, survival and requirement for long-term oxygen therapy (LTOT).Seventy-six patients could be randomized, 41 were allocated to NOT and 35 to no NOT (control). The goal of NOT was to achieve an arterial oxygen saturation of >90% throughout the night. All these patients underwent polysomnography to exclude an associated obstructive sleep apnoea syndrome. The two groups exhibited an identical meanSD daytime Pa,O 2 of 8.40.4 kPa (633 mmHg) at baseline.Twenty-two patients (12 in the NOT group and 10 in the control group, p=0.98) required LTOT during the whole follow-up (3514 months). Sixteen patients died, nine in the NOT group and seven in the control group (p=0.84). Forty-six patients were able to undergo pulmonary haemodynamic re-evaluation after 2 yrs, 24 in the NOT and 22 in the control group. In the control group, mean resting pulmonary artery pressure increased from 19.85.6 to 20.56.5 mmHg, which was not different from the change in mean pulmonary artery pressure in the NOT group, from 18.34.7 to 19.55.3 mmHg (p= 0.79).Nocturnal oxygen therapy did not modify the evolution of pulmonary haemodynamics and did not allow delay in the prescription of long-term oxygen therapy. No effect of NOT on survival was observed, but the small number of deaths precluded any firm conclusion. These results suggest that the prescription of nocturnal oxygen therapy in isolation is probably not justified in chronic obstructive pulmonary disease patients. Eur Respir J 1999; 14: 1002±1008. The beneficial effects of long-term oxygen therapy (LTOT) have been demonstrated in chronic obstructive pulmonary disease (COPD) patients with marked daytime hypoxaemia, i.e. in patients with an arterial oxygen tension (Pa,O 2 ) measured in the stable state of the disease, of <7.3 kPa (<55 mmHg) or in the range 7.4±7.8 kPa (56±59 mmHg), and exhibiting "cor pulmonale" or polycythaemia [1, 2]. These beneficial effects include improved survival [1, 2], but also an amelioration of pulmonary haemodynamics [3,4]. The beneficial effects of LTOT on survival have not been observed in COPD patients with moderate hypoxaemia (Pa,O 2 in the range 7.4±8.6 kPa (56±65 mmHg)), as indicated by a very recent Polish study [5].The worsening of hypoxaemia during sleep, and particularly during rapid eye movement sleep, has been well established in patients with advanced COPD [6±10]. It must be underlined, however, that most of these studies have included patients with severe COPD, exhibiting marked daytime hypoxaemia. Conventional LTOT, given for >15±18 h . day -1 , compulsorily includes sleep time and, accordingly, sle...

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, sleeprelated desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conventional O 2 therapy (daytime arterial oxygen tension (Pa,O 2 ) in the range 7.4-9.2 kPa (56-69 mmHg)). Nocturnal desaturation was defined by spending ≥30% of the recording time with a transcutaneous O 2 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,O 2 (8.4±0.6 vs 8.4±0.4 kPa (63±4 vs 63±3 mmHg)) but arterial carbon dioxide tension (Pa,CO 2 ) was higher in Group 1 (6.0±0.7 vs 5.3±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. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia. Is sleep-related hypoxaemia present in patients with less severe COPD with mild or absent daytime hypoxaemia? Several studies of the literature [11][12][13] have shown that a relatively high percentage of these COPD patients exhibit significant nocturnal hypoxaemia, which naturally raises the question: Does this hypoxaemia, limited to sleep, deserve treatment with nocturnal oxygen? Such a treatment could be justified if nocturnal hypoxaemia had deleterious effects on life expectancy, which is rather controversial [14,15], and on pulmonary haemodynamics. It has been hypothesized [16,17] that isolated nocturnal hypoxaemia, occurring in patients without significant daytime hypoxaemia, could lead to permanent (daytime) pulmonary hypertension, but this hypothesis has not, so...

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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 ¢30% of the nocturnal recording time with arterial oxygen saturation v90%.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,CO 2 ) (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 followup, 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,CO 2 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. Eur Respir J 2001; 17: 848-855.

RESUMOIntrodução: Avaliar a privação do sono e seus efeitos sobre os jovens médicos relativamente à capacidade de concentração e desempenho psicomotor. Material e Métodos: Dezoito médicos, com idades entre 26 -33 anos, divididos em dois grupos: grupo sem privação de sono (sem trabalho nocturno) e grupo com privação de sono (no mínimo 12 horas de trabalho nocturno / semana). Aplicámos o Índice de Qualidade de Sono de Pittsburgh para rastrear a presença de patologia do sono e a Escala de Sonolência Epworth para avaliar subjectivamente a sonolência diurna; usamos actigrafia e o diário de sono para avaliar a higiene do sono e os ciclos de sono-vigília. Para demonstrar os efeitos da privação do sono, foi aplicado o teste de Toulouse-Piéron (teste de concentração) e uma bateria de três testes de tempo de reação após o período de trabalho nocturno. Resultados: O grupo com privação de sono apresentou maior sonolência diurna na Escala de Sonolência Epworth (p < 0,05) e durante a semana a privação de sono foi maior (p < 0,010). A duração média do sono durante o período de trabalho nocturno foi de 184,2 minutos para o grupo com privação de sono e 397,7 minutos para grupo sem privação de sono (p < 0,001). No teste Toulouse-Piéron o grupo com privação de sono apresentou maior número de omissões (p < 0,05) com um pior resultado no índice de concentração (p < 0,05). Os testes psicomotores que avaliaram a resposta a estímulos simples revelaram maior latência na resposta (p < 0,05) e mais erros (p < 0,05) no grupo com privação de sono; no teste de reacção a instrução o e grupo com privação de sono apresentou pior índice de perfeição (p < 0,05); no teste de movimentos finos não houve diferença estatisticamente significativa entre os grupos. Discussão: A privação de sono aguda resultante do trabalho nocturno em profissões médicas está associada a uma diminuição da atenção e concentração e no atraso de resposta a estímulos. Isto pode comprometer o atendimento ao paciente, bem como a saúde e a qualidade de vida do próprio médico. Conclusão: É essencial estudar os efeitos da privação aguda de sono sobre a capacidade cognitiva e de desempenho dos profissionais de saúde. Palavras-chave: Médicos; Privação de Sono; Tolerância ao Trabalho Programado; Ritmo Circadiano; Transtornos do Sono. ABSTRACT Introduction:To evaluate sleep deprivation and its effects on young physicians in relation to concentration capacity and psychomotor performance. Material and Methods:Eighteen physicians aged 26 -33 years were divided into 2 groups: non-sleep deprived group (with no night work) and sleep deprived group (minimum 12 hour of night work/week). We applied Pittsburgh Sleep Quality Index to screen the presence of sleep pathology and Epworth Sleepiness Scale to evaluate subjective daytime sleepiness; we used actigraphy and sleep diary to assess sleep hygiene and standard sleep-wake cycles. To demonstrate the effects of sleep deprivation, we applied ToulousePiéron's test (concentration test) and a battery of three reaction time tasks after the night duty...

Keywords:Insomnia Hyperarousal Default-mode network Cognitive-behavioral therapy for insomnia a b s t r a c t Psychophysiological insomnia (PI) is a common sleep disorder in which numerous variables interact. The mechanisms responsible for the etiology and maintenance of PI, though far from completely understood, point to the existence of hyperarousal of several systems. The frequent occurrence of ruminations and worries with a self-referential component (related or not with sleep complaints) during the pre-sleep period, and daytime wakefulness, seems to relate to the functions which have been associated with default-mode network (DMN) activity. This neural network seems to be involved in introspective thinking as well as emotional and episodic memory processing, among others. In this paper, we propose that PI may be conceptualized as a disorder associated with overactivity of some brain areas of DMN. Accordingly, it is also suggested that cognitive-behavioral therapy for insomnia (CBT-I), a kind of non-pharmacological treatment, may alter the function of this network, improving symptoms of patients, and overall quality of life.

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Primary insomnia (PI) is one of the most prevalent sleep disorders. For this reason, over the last decades, several comprehensive and etiological theories have been proposed. In this paper we review some of the main theoretical models of insomnia and discuss the two most studied processes for comprehension of insomnia: the hyperarousal and the failure to inhibit wakefulness or psychobiological inhibition hypotheses. Some clinical implications of the models are described. In the end, we propose that the two processes are complementary and both are relevant to the understanding of clinical insomnia.