Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality and may frequently be complicated by sleep disorders. Insomnia and obstructive sleep apnea are commonly encountered in patients with COPD. Nocturnal hypoxemia is also prevalent in COPD may occur despite adequate awake oxygenation and can be especially severe in rapid eye movement sleep. Additionally, several factors-some of them unique to COPD-can contribute to sleep-related hypoventilation. Recognition of hypoventilation can be vital as supplemental oxygen therapy itself can acutely worsen hypoventilation and lead to disastrous consequences. Finally, accruing data establish an association between restless leg syndrome and COPDan association that may be driven by hypoxemia and/or hypercapnia. Comorbid sleep disorders portend worse sleep quality, diminished quality of life, and multifarious other adverse consequences. The awareness and knowledge regarding sleep comorbidities in COPD has continued to evolve over past many years. There are still several lacunae, however, in our understanding of the etiologies, impact, and therapies of sleep disorders, specifi cally in patients with COPD. This review summarizes the latest concepts in prevalence, pathogenesis, diagnosis, and management of diverse sleep disorders in COPD. Keywords: COPD, insomnia, obstructive sleep apnea, restless legs syndrome, hypoventilation Citation: Budhiraja R, Siddiqi TA, Quan SF. Sleep disorders in chronic obstructive pulmonary disease: etiology, impact, and management. J Clin Sleep Med 2015;11(3):259-270.pii: jc-00080-14 http://dx.doi.org/10.5664/jcsm.4540 T hat sleep is adversely affected in chronic obstructive pulmonary disease (COPD) has been long recognized. 1 COPD affects 5% to 10% of the adult population in the United States and is a major contributor to global disease burden. 2 The prevalence of insomnia symptoms, insomnia disorder, restless leg syndrome, and hypoxemia is increased in COPD. [3][4][5] Furthermore, polysomnographic (PSG) evaluation generally reveals decreased sleep effi ciency and lower mean overnight oxygen saturation in COPD patients compared to controls. 6 In COPD, the pathogenesis of sleep disorders appears to be a complex and multifactorial process, likely consequent to one or more of the following: physiological changes associated with sleep, hypoxemia, hypercapnia, infl ammation, COPD medications, and/or nicotine use. Comorbid disorders as well as primary sleep disturbances may also contribute to disrupted sleep in COPD patients. For example, nocturnal gastroesophageal refl ux (GERD) is associated with both symptoms of sleep apnea and COPD, and may contribute to the pathogenesis, and concomitant occurrence of both disorders.7 GERD may also infl uence sleep quality which could potentially contribute to some of the sleep complaints reported by persons with COPD. 8 The following sections describe the diverse sleep disorders and sleep-related abnormalities encountered in patients with COPD. Sleep Disorders in Chronic Obstructiv...

Calcium channel blockers (CCBs) overdose can be life-threatening when manifest as catastrophic shock and non-cardiogenic pulmonary edema. We describe a case of massive overdose of multiple medications, including sustained-release verapamil, which was resistant to conventional support. Initial treatment for CCB overdose is primarily supportive, and includes fluid resuscitation. The mechanism of non-cardiogenic pulmonary edema is not well known, and reported cases have been successfully treated with mechanical ventilation. Circulatory shock may fail to respond to atropine, glucagon, and calcium in severely poisoned patients, and vasopressors are usually required. Attempting to overcome calcium-channel antagonism with the supra-therapeutic doses of calcium salts is clinically indicated to reverse hypotension and bradycardia. There is evidence that hyperinsulinemia-euglycemia therapy is superior to other therapies for CCB poisoning, and the mechanism is thought to be the insulin-mediated active transport of glucose into the cells, which counters the CCB-induced intra-cellular carbohydrate-deficient state. Conventional decontamination measures are ineffective in accelerating clearance of CCB. Experience with intravenous lipid emulsion for lipophilic drug overdose, such as verapamil, is limited, but has been proposed as a rescue therapy and might improve cardiac inotropy through intravascular sequestration of the lipophilic CCB.

Rationale: More than a million polysomnograms (PSGs) are performed annually in the United States to diagnose obstructive sleep apnea (OSA). Third-party payers now advocate a home sleep test (HST), rather than an in-laboratory PSG, as the diagnostic study for OSA regardless of clinical probability, but the economic benefit of this approach is not known. Objectives:We determined the diagnostic performance of OSA prediction tools including the newly developed OSUNet, based on an artificial neural network, and performed a cost-minimization analysis when the prediction tools are used to identify patients who should undergo HST. Methods:The OSUNet was trained to predict the presence of OSA in a derivation group of patients who underwent an in-laboratory PSG (n = 383). Validation group 1 consisted of in-laboratory PSG patients (n = 149). The network was trained further in 33 patients who underwent HST and then was validated in a separate group of 100 HST patients (validation group 2). Likelihood ratios (LRs) were compared with two previously published prediction tools. The total costs from the use of the three prediction tools and the third-party approach within a clinical algorithm were compared. Measurements and Main Results:The OSUNet had a higher 1LR in all groups compared with the STOP-BANG and the modified neck circumference (MNC) prediction tools. The 1LRs for STOP-BANG, MNC, and OSUNet in validation group 1 were 1.1 (1.0-1.2), 1.3 (1.1-1.5), and 2.1 (1.4-3.1); and in validation group 2 they were 1.4 (1.1-1.7), 1.7 (1.3-2.2), and 3.4 (1.8-6.1), respectively. With an OSA prevalence less than 52%, the use of all three clinical prediction tools resulted in cost savings compared with the third-party approach. Conclusions:The routine requirement of an HST to diagnose OSA regardless of clinical probability is more costly compared with the use of OSA clinical prediction tools that identify patients who should undergo this procedure when OSA is expected to be present in less than half of the population. With OSA prevalence less than 40%, the OSUNet offers the greatest savings, which are substantial when the number of sleep studies done annually is considered.

No abstract

No abstract