Historia del síndrome de apnea-hipopnea obstructiva del sueño (SAHOS)

La historia de la apnea obstructiva del sueño es larga y complicada desde sus primeras descripciones en el siglo XIX con el relato de Pickwick en la primera novela de Charles Dickens. La definición de este término por parte de diferentes investigadores resalta la importancia de comprender las entidades asociadas al síndrome, como la hipoventilación alveolar y la somnolencia diurna excesiva. De esta forma, los estudios neurofisiológicos adelantados desde entonces, el desarrollo de la conferencia de la sociedad europea de neurología de 1964, la descripción del síndrome en pacientes pediátricos, la confirmación de la comorbilidad cardiovascular asociada a la enfermedad, la traqueostomía como tratamiento y la creación de implantes de estimuladores del nervio hipogloso —pasando por el descubrimiento de Sullivan de la presión positiva como tratamiento en casa— han sido esenciales para la comprensión de este síndrome.The history of obstructive sleep apnea is long and complicated, and some descriptions can be traced back to the early nineteenth century in The Posthumous Papers of the Pickwick Club, the first novel written by Charles Dickens. The definition of this term by different researchers highlights the importance of understanding the entities associated with the syndrome, such as alveolar hypoventilation and excessive daytime sleepiness.Thus, the neurophysiological studies carried out since then, as well as the European Society of Neurology conference held in 1964, the description of the syndrome in pediatric patients, the confirmation of cardiovascular co-morbidity associated with the disease, tracheostomy as treatment and the creation of hypoglossal nerve stimulus implants —including Sullivan’s discovery of positive pressure as a home treatment— have been essential for the understanding of this syndrom

Development of Central Sleep Apnea After Sleep Surgery

Central sleep apnea (CSA) is defined as an absence of breathing without respiratory drive during sleep. It can occur after treatment of obstructive sleep apnea (OSA), a phenomenon known as treatment-emergent central sleep apnea (TECSA). We present a case of a 23-year-old male who developed CSA after pharyngeal and nasal surgery for severe OSA. High loop gain and increased ventilations from frequent arousal are likely explanations for our patient’s central apnea, which resolved with positive airway pressure therapy that possibly alleviated residual airway obstruction and ventilatory instability. This case suggests that effectiveness of treatment for OSA should be based on careful long-term observation with multiple follow-up polysomnography tests, especially in patients at high risk of TECSA

Development of Central Sleep Apnea After Sleep Surgery

Central sleep apnea (CSA) is defined as an absence of breathing without respiratory drive during sleep. It can occur after treatment of obstructive sleep apnea (OSA), a phenomenon known as treatment-emergent central sleep apnea (TECSA). We present a case of a 23-year-old male who developed CSA after pharyngeal and nasal surgery for severe OSA. High loop gain and increased ventilations from frequent arousal are likely explanations for our patient’s central apnea, which resolved with positive airway pressure therapy that possibly alleviated residual airway obstruction and ventilatory instability. This case suggests that effectiveness of treatment for OSA should be based on careful long-term observation with multiple follow-up polysomnography tests, especially in patients at high risk of TECSA.ope

Ventilatory support during sleep in patients with chronic obstructive pulmonary disease

In conclusion, currently there is no conclusive evidence that NIV should be provided routinely to stable patients with COPD. Nevertheless, patients who are clearly hypercapnic, who receive confirmed effective ventilation by applying higher inspiratory pressures, and have a better compliance might show clinical benefits. The combination of rehabilitation and nocturnal ventilatory support seems to provide more benefits than rehabilitation alone, so this might be a situation in which chronic NIV is effective

Mechanisms of improvement of respiratory failure in patients with COPD treated with NIV

Annabel H Nickol1,2, Nicholas Hart1,3, Nicholas S Hopkinson1, Carl-Hugo Hamnegård4, John Moxham5, Anita Simonds1, Michael I Polkey11Respiratory Muscle Laboratory, Royal Brompton Hospital, London, UK; 2Oxford Centre for Respiratory Medicine, Churchill Hospital, Oxford, UK; 3The Lane Fox Unit, St Thomas’ Hospital, London, UK; 4Department of Pulmonary Medicine and Clinical Physiology, Sahlgrenska University, Gotenborg, Sweden; 5Respiratory Muscle Laboratory, King’s College London School of Medicine, King’s College Hospital, London, UKBackground: Noninvasive ventilation (NIV) improves gas-exchange and symptoms in selected chronic obstructive pulmonary disease (COPD) patients with hypercapnic respiratory failure. We hypothesized NIV reverses respiratory failure by one or all of increased ventilatory response to carbon-dioxide, reduced respiratory muscle fatigue, or improved pulmonary mechanics.Methods: Nineteen stable COPD patients (forced expiratory volume in one second 35% predicted) were studied at baseline (D0), 5–8 days (D5) and 3 months (3M) after starting NIV.Results: Ventilator use was 6.2 (3.7) hours per night at D5 and 3.4 (1.6) at 3M (p = 0.12). Mean (SD) daytime arterial carbon-dioxide tension (PaCO2) was reduced from 7.4 (1.2) kPa to 7.0 (1.1) kPa at D5 and 6.5 (1.1) kPa at 3M (p = 0.001). Total lung capacity decreased from 107 (28) % predicted to 103 (28) at D5 and 103 (27) % predicted at 3M (p = 0.035). At D5 there was an increase in the hypercapnic ventilatory response and some volitional measures of inspiratory and expiratory muscle strength, but not isolated diaphragmatic strength whether assessed by volitional or nonvolitional methods.Conclusion: These findings suggest decreased gas trapping and increased ventilatory sensitivity to CO2 are the principal mechanism underlying improvements in gas-exchange in patients with COPD following NIV. Changes in some volitional but not nonvolitional muscle strength measures may reflect improved patient effort.Keywords: COPD; hypercapnic respiratory failure; NIV; pulmonary mechanics; ventilatory driv

Age, gender, neck circumference, and Epworth sleepiness scale do not predict obstructive sleep apnea (OSA) in moderate to severe chronic obstructive pulmonary disease (COPD): The challenge to predict OSA in advanced COPD

The combination of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) is associated with substantial morbidity and mortality. We hypothesized that predictors of OSA among patients with COPD may be distinct from OSA in the general population. Therefore, we investigated associations between traditional OSA risk factors (e.g. age), and sleep questionnaires [e.g. Epworth Sleepiness Scale] in 44 patients with advanced COPD. As a second aim we proposed a pilot, simplified screening test for OSA in patients with COPD. In a prospective, observational study of patients enrolled in the UCSD Pulmonary Rehabilitation Program we collected baseline characteristics, cardiovascular events (e.g. atrial fibrillation), and sleep questionnaires [e.g. Pittsburgh Sleep Quality Index (PSQI)]. For the pilot questionnaire, a BMI =25 kg/m2 and the presence of cardiovascular disease were used to construct the pilot screening test. Male: 59%; OSA 66%. FEV1 (mean ± SD) = 41.0±18.2% pred., FEV1/FVC = 41.5±12.7%]. Male gender, older age, and large neck circumference were not associated with OSA. Also, Epworth Sleepiness Scale and the STOP-Bang questionnaire were not associated with OSA in univariate logistic regression. In contrast, BMI =25 kg/m2 (OR = 3.94, p = 0.04) and diagnosis of cardiovascular disease (OR = 5.06, p = 0.03) were significantly associated with OSA [area under curve (AUC) = 0.74]. The pilot COPD-OSA test (OR = 5.28, p = 0.05) and STOP-Bang questionnaire (OR = 5.13, p = 0.03) were both associated with OSA in Receiver Operating Characteristics (ROC) analysis. The COPD-OSA test had the best AUC (0.74), sensitivity (92%), and specificity (83%). A tenfold cross-validation validated our results. We found that traditional OSA predictors (e.g. gender, Epworth score) did not perform well in patients with more advanced COPD. Our pilot test may be an easy to implement instrument to screen for OSA. However, a larger validation study is necessary before further clinical implementation is warranted

Respiratory responses to CO2 stimulation in hypercapnic patients with obstructive sleep apnea syndrome

Obstructive sleep apnea can be associated with daytime chronic hypercapnia in some patients, but the prevalence of the phenomenon is highly variable in the published literature. The most often it is found in patients with coexisting COPD. There is also an evidence of persisting hypercapnia in OSA patients without other respiratory disease. In previous studies lung function impairment, obesity, gender, severity of OSAS have been considered to contribute to daytime hypercapnia. Several studies demonstrated that the defect in control of breathing can play a role in the development of chronic hypercapnia in patients with OSAS. The aim of the study was to estimate respiratory responses to hypercapnic stimulation in patients with OSAS and chronic daytime hypercapnia. Material consisted of 38 patients with OSAS and chronic hypercapnia (COPD was present in 24 - group B, "pure" OSA in 14 - group A) and 40 normocapnic OSA patients (group C). Lung function testing, blood gases and chemical control of breathing tests were performed in all of them before initiating therapy with nCPAP. Diagnosis of OSAS was stated with standard polisomnography and AHI was similar in mentioned groups. Results: Respiratory responses to hypercapnic stimulation were significantly lower in hypercapnic patients (A 10.6 &plusmn; 4.6; B 9.5 &plusmn; 5.6) in opposition to normocapnics (C 23.3 &plusmn; 14.0 l/min/kPa). In all studied patients PaCO2 level significantly correlated with respiratory responses to hypercapnic stimulation (r = &#8211;.61), lung function indices (VC r = &#8211;.69 and FEV1 r = &#8211;.71), mean SaO2 during sleep (r = &#8211;.68), and BMI (r = .49), but not with the factors like age, AHI or minimal SaO2 during sleep. Analysis with multiple regression revealed that hypercapnic drive, mean SaO2 during sleep, FEV1 and BMI were the best predictors of hypercapnia in studied group, being responsible for 72% of the total variance in PaCO2 in our OSA patients (R2 = 0.72; p < 0.0001). Conclusion: predisposition to daytime hypercapnia in our OSA patients was related to dimished chemosensitivity to CO2, mean desaturation during sleep, the severity of obesity and impairment of lung function mainly due to coexisting COPD

Uneaegsed hingamishäired ja hormoonid

Uneaegsed hingamishäired (UHH) kujutavad endast süsteemset seisundit, mis põhjustab organismis endokriinseid ja metaboolseid muutusi. Järjest enam saadakse tõendeid selle kohta, et UHHd tekitavad muutusi erinevate hormoonide sekretsioonis ja vere kontsentratsioonitasemes, samuti võivad erinevad endokriinsed muutused ja hormoonravi kutsuda esile, süvendada või kergendada UHHd. Enamik teabest hormoonide ja UHHde koostoime kohta pärineb uuringutest, kus on kasutatud nasaalset positiivse õhuvoolu surve (CPAP) ravi, mis on kerge kuni raske obstruktiivse uneapnoe sündroomi valikraviks. Hormoonide ja hingamise seoste parem tundmaõppimine aitab avada uusi suundi UHHde ning nende süsteemsete tagajärgede ärahoidmisel, leevendamisel ja ravistrateegiate väljatöötamisel. Eesti Arst 2005; 84 (7): 488–49