[Sleep and chronic lung diseases: diffuse interstitial lung diseases, bronchial asthma, and COPD]. / Sono e doenças pulmonares crônicas: pneumopatias intersticiais difusas, asma brônquica e DPOC.

Chronic lung diseases can be aggravated by various factors and comorbidities, including sleep-disordered breathing. Although changes in the quality of life of patients with chronic lung disease are usually related to daytime variables, the physiological changes in sleep impair the quality of sleep and interfere with the natural history of the disease. Alterations in sleep architecture appear to be a common mechanism in these diseases. During sleep, the upper and lower airways are more interconnected: changes in upper airway resistance during sleep are added to the severe resistive alterations in the lower airways due to asthma and COPD. In addition, there are complex mechanical and ventilatory interactions. The recognition of these interactions allows better assessment of the exacerbations and the progression of chronic lung diseases.

Sono e doenças pulmonares crônicas: pneumopatias intersticiais difusas, asma brônquica e DPOC / Sleep and chronic lung diseases: diffuse interstitial lung diseases, bronchial asthma, and COPD

As doenças pulmonares crônicas podem ser agravadas por inúmeros fatores e comorbidades, inclusive pelos distúrbios respiratórios do sono. Embora alterações na qualidade de vida de pacientes com doenças pulmonares crônicas sejam normalmente determinadas a partir de variáveis diurnas, as alterações fisiopatológicas no sono pioram a qualidade de sono e interferem na história natural dessas doenças. Alterações da arquitetura do sono parecem ser um mecanismo comum entre essas doenças. Durante o sono, as vias respiratórias inferiores estão mais interligadas às vias respiratórias superiores, quando as alterações de resistências das vias aéreas superiores durante o sono somam-se às graves alterações resistivas de vias aéreas inferiores devido a asma e DPOC. Além disso, surgem complexas interações mecânicas e ventilatórias. O reconhecimento dessas interações possibilita uma melhor avaliação das exacerbações e da evolução dessas doenças.

Chronic lung diseases can be aggravated by various factors and comorbidities, including sleep-disordered breathing. Although changes in the quality of life of patients with chronic lung disease are usually related to daytime variables, the physiological changes in sleep impair the quality of sleep and interfere with the natural history of the disease. Alterations in sleep architecture appear to be a common mechanism in these diseases. During sleep, the upper and lower airways are more interconnected: changes in upper airway resistance during sleep are added to the severe resistive alterations in the lower airways due to asthma and COPD. In addition, there are complex mechanical and ventilatory interactions. The recognition of these interactions allows better assessment of the exacerbations and the progression of chronic lung diseases.

Systemic effects of nocturnal hypoxemia in patients with chronic obstructive pulmonary disease without obstructive sleep apnea syndrome.

OBJECTIVE: To study the effects of nocturnal hypoxemia in patients with chronic obstructive pulmonary disease without obstructive sleep apnea syndrome. METHODS: We studied 21 patients-10 desaturators and 11 nondesaturators-submitted to arterial blood gas analysis, polysomnography, spirometry, cardiopulmonary exercise testing (cycle ergometer), and hand-grip dynamometry, as well as measurements of maximal inspiratory pressure, maximal expiratory pressure, and C-reactive protein (CRP) levels. Patients with arterial oxygen tension > 60 mmHg were included; those with an apnea-hypopnea index > 5 events/hour of sleep were excluded. Maximal oxygen uptake, maximal power, systolic blood pressure, diastolic blood pressure (DBP), and maximal heart rate were measured during exercise in order to detect hemodynamic alterations. Patients presenting CRP levels above 3 mg/L were considered CRP-positive. RESULTS: Minimal peripheral oxygen saturation during sleep was significantly higher among nondesaturators (p = 0.03). More desaturators presented CRP > 3 mg/L (p < 0.05). No differences were observed in terms of any variables, However, mean peripheral oxygen saturation during sleep correlated with DBP and maximal inspiratory pressure (p < 0.001 and p = 0.001, respectively). CONCLUSIONS: Although nocturnal hypoxemia does not reduce exercise capacity or hand-grip strength in patients with mild/moderate COPD, its effect on maximal exercise DBP seems to depend on the degree of hypoxemia. In addition, there is a positive relationship between maximal inspiratory pressure and mean peripheral oxygen saturation during sleep, as well as evidence of pronounced inflammatory activation in patients with nocturnal hypoxemia.

Efeitos sistêmicos da hipoxemia noturna em pacientes com doença pulmonar obstrutiva crônica sem síndrome da apnéia obstrutiva do sono / Systemic effects of nocturnal hypoxemia in patients with chronic obstructive pulmonary disease without obstructive sleep apnea syndrome

OBJETIVO: Estudar os efeitos da hipoxemia noturna em pacientes com doença pulmonar obstrutiva crônica sem síndrome da apnéia obstrutiva do sono. MÉTODOS: Estudamos 21 pacientes-10 dessaturadores e 11 não-dessaturadores-submetidos a gasometria arterial, polissonografia, espirometria, teste de exercício cardiopulmonar (cicloergômetro), dinamometria manual e medidas de pressão inspiratória máxima, pressão expiratória máxima e proteína C reativa (PCR). Incluíram-se os pacientes com pressão parcial arterial de oxigênio > 60 mmHg; excluíram-se os com índice de apnéia-hipopnéia > 5 eventos/hora de sono. Foram medidos consumo máximo de oxigênio, potência máxima, pressão arterial sistólica, pressão arterial diastólica (PAD) e frequência cardíaca máxima durante exercício, visando detectar alterações hemodinâmicas. A PCR foi considerada positiva quando acima de 3 mg/L. RESULTADOS: A saturação periférica de oxigênio mínima durante o sono foi significativamente maior nos não-dessaturadores (p = 0,03). Mais dessaturadores apresentaram PCR > 3 mg/L (p < 0,05). Não houve diferença quanto a capacidade de exercício e demais variáveis. No entanto, PAD (p < 0,001) e pressão inspiratória máxima (p = 0,001) correlacionaram-se com saturação periférica de oxigênio média durante o sono. CONCLUSÕES: A hipoxemia noturna não reduz a capacidade de exercício e a força de preensao manual em pacientes com DPOC leve/moderada, mas o ajuste da PAD durante o exercício máximo parece depender do grau de hipoxemia. Além disso, há uma relação positiva entre pressão inspiratória máxima e saturação periférica de oxigênio média durante o sono, bem como indícios de ativação inflamatória diferenciada em pacientes com hipoxemia noturna.

OBJECTIVE: To study the effects of nocturnal hypoxemia in patients with chronic obstructive pulmonary disease without obstructive sleep apnea syndrome. METHODS: We studied 21 patients-10 desaturators and 11 nondesaturators-submitted to arterial blood gas analysis, polysomnography, spirometry, cardiopulmonary exercise testing (cycle ergometer), and hand-grip dynamometry, as well as measurements of maximal inspiratory pressure, maximal expiratory pressure, and C-reactive protein (CRP) levels. Patients with arterial oxygen tension > 60 mmHg were included; those with an apnea-hypopnea index > 5 events/hour of sleep were excluded. Maximal oxygen uptake, maximal power, systolic blood pressure, diastolic blood pressure (DBP), and maximal heart rate were measured during exercise in order to detect hemodynamic alterations. Patients presenting CRP levels above 3 mg/L were considered CRP-positive. RESULTS: Minimal peripheral oxygen saturation during sleep was significantly higher among nondesaturators (p = 0.03). More desaturators presented CRP > 3 mg/L (p < 0.05). No differences were observed in terms of any variables, However, mean peripheral oxygen saturation during sleep correlated with DBP and maximal inspiratory pressure (p < 0.001 and p = 0.001, respectively). CONCLUSIONS: Although nocturnal hypoxemia does not reduce exercise capacity or hand-grip strength in patients with mild/moderate COPD, its effect on maximal exercise DBP seems to depend on the degree of hypoxemia. In addition, there is a positive relationship between maximal inspiratory pressure and mean peripheral oxygen saturation during sleep, as well as evidence of pronounced inflammatory activation in patients with nocturnal hypoxemia.