Pulmonary hypertension in patients affected by sleep-related breathing disorders: up to date from the literature.

Sleep-related breathing disorders (SBD) are conditions of abnormal and difficult respiration during sleep, including chronic snoring, obstructive sleep apnea (OSA), central sleep apnea (CSA), sleep-related hypoventilation disorders and sleep-related hypoxemia. Some of them have a limited impact on health, but others (e.g., OSA) can have serious consequences, because of their dangerous effects on sleep and the hematic balance of oxygen and carbon dioxide. According to several population-based studies, prevalence of OSA is relatively high, approximately 3-7% for adult males and 2-5% for adult females in the general population. However, methodological differences and difficulties in characterizing this syndrome yielded to variability in estimates. Moreover, it is estimated that only about 40% of patients with OSA are diagnosed, which can lead to underestimation of disease prevalence. OSA is directly correlated with age and male sex and to risk factors such as obesity. Several studies found that OSA is associated with an increased risk of diabetes, some cancer types, cardiovascular and cerebrovascular diseases, such as hypertension, coronary artery disease and stroke. Pulmonary hypertension (PH), a noted cardiovascular disease, is significantly associated with sleep-related breathing disorders and lot of scientific studies published in the literature demonstrated a strong link between these conditions and the development of pulmonary hypertension PH. PH is relatively less common than sleep-related breathing disorders. The purpose of this systematic review is to analyze both the current knowledge around the consequences that SBD may have on pulmonary hemodynamics and the effects resulting from pharmacological and non-pharmacological treatments of SDB on PH.

The Importance of the Diaphragm in Neuromotor Function in the Patient with Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a constant and chronic narrowing of the respiratory airways, with numerous associated symptoms, not always related to the pathological adaptation of the lungs. Statistical projections show that COPD could become the third leading cause of death globally by 2030, with a significant increase in deaths by 2060. Skeletal muscle dysfunction, including the diaphragm, is one of the causes linked to the increase in mortality and hospitalization. Little emphasis is given by the scientific literature to the importance of the diaphragm towards functional neuromotor pathological expressions. The article reviews the adaptation of the skeletal muscles, with greater attention to the adaptations of the diaphragm, thereby highlighting the non-physiological variations that the main respiratory muscle undergoes and the neuromotor impairment found in COPD. The text could be an important reflection from a clinical and rehabilitation point of view, to direct greater attention to the function and adaptation of the diaphragm muscle.

Obstructive Sleep Apnea and Role of the Diaphragm.

Obstructive sleep apnea (OSA) causes multiple local and systemic pathophysiological consequences, which lead to an increase in morbidity and mortality in patients suffering from this disorder. OSA presents with various nocturnal events of apnoeas or hypopneas and with sub-clinical airflow limitations during wakefulness. OSA involves a large percentage of the population, particularly men, but the estimate of OSA patients could be much broader than data from the literature. Most of the research carried out in the muscle field is to understand the causes of the presence of chronic nocturnal desaturation and focus on the genioglossus muscle and other muscles related to dilating the upper airways. Sparse research has been published regarding the diaphragm muscle, which is the main muscle structure to insufflate air into the airways. The article reviews the functional anatomy of the muscles used to open the upper respiratory tract and the non-physiological adaptation that follows in the presence of OSA, as well as the functional anatomy and pathological adaptive aspects of the diaphragm muscle. The intent of the text is to highlight the disparity of clinical interest between the dilator muscles and the diaphragm, trying to stimulate a broader approach to patient evaluation.