英文精品课件chronicobstructive pulmonary disease and

Chronic Obstructive Pulmonary Disease and Sleep AWAKE Meeting Anstella Robinson, MD FCCP FAASM Introduction n Respiratory changes during sleep exacerbate gas exchange abnormalities present in those with COPD. Subsequent hypoxemia may predispose to secondary pulmonary hypertension, heart arrhythmias and premature death. More than 40% of COPD patients complain of sleep disturbances including reduced sleep time and increased arousals. Introduction contd n COPD patients complain of more daytime sleepiness than those without respiratory disease although the effects of this on daytime function and quality of life have not been studied. Respiratory changes during sleep n During sleep the metabolic rate diminishes. Respiratory responses to chemical mechanical and cortical inputs are reduced. Increased partial pressure of carbon dioxide is a physiological response to sleep as is a reduced partial pressure of arterial blood oxygen. Reduced tidal volume and minute ventilation are also natural consequences of sleeping. How respiratory function during sleep differs in COPD n Normal sleep related respiratory changes can be deleterious for those with COPD as they may lead to reduced gas exchange and ultimately hypoventilation, hypoxemia and hypercapnia particularly in REM sleep where muscle atonia is the rule. Hypercapnia may lead to a further reduction of diaphragmatic contractility and ventilatory responsiveness. How Respiratory function during sleep differs in COPD Contd n Hypoxia may provoke an arousal response although this effect varies widely. Patients may continue to sleep with significantly impaired oxygen levels. Women have an increased responsiveness to hypoxemic effects. Impaired respiratory muscle activity in COPD patients also effects breathing during sleep. Increases in airway resistance may cause exaggerated broncoconstriction that may be clinically significant. How Respiratory function during sleep differs in COPD Contd n Reduced intercostal muscle activity also affects breathing during sleep in those with impaired diaphragmatic contraction secondary to hyperinflation who may be more dependent on accessory muscle function in order to maintain ventilation. Hypoxemia and hypercapnia during sleep are probably related to hypoventilation in patients with reduced respiratory function How Respiratory function during sleep differs in COPD Contd n Arterial oxygen desaturation during sleep is due in mainly to ventilation perfusion mismatch. Lung volume changes that occur in sleep include a reduction in functional residual capacity. This change may lead to ventilation perfusion mismatch and significant hypoxemia in patients with COPD. How Respiratory function during sleep differs in COPD Contd n Reduced FRC is due to: n Respiratory muscle hypotonia Diaphragmatic displacement when the patient is lying recumbent Decreased lung adherence during sleep Which COPD Patients Desaturate during sleep and why? n The degree of arterial oxygen desaturation correlates poorly with measures of pulmonary function such as FEV1. arterial oxygen saturation while awake is considered to be the best predictor of sleep desaturation in patients with COPD. Patients with chronic bronchitis (so called blue bloaters) have the best correlation between awake arterial oxygen saturation and minimum arterial oxygen saturation during sleep. Which COPD Patients Desaturate during sleep and why? n Patients who are hypoxemic while awake are typically treated with supplemental oxygen. However those whose arterial oxygen saturations are borderline while awake and who do not meet criteria for supplemental oxygen may develop clinically significant hypoxemia while asleep. Which COPD Patients Desaturate during sleep and why? n Fletcher and colleagues evaluated gas exchange and cardiopulmonary hemodynamics in a group of COPD patients with borderline oxygen desaturations PaO2 60mmHg who had significant nocturnal oxyhemoglobin desaturation (NOD) and compared them to patients with similar pulmonary hemodynamics but no NOD Which COPD Patients Desaturate during sleep and why? n These investigators found: n PaO2 was approximately 12mmHg lower in those with NOD compared to those without NOD. n Arterial/alveolar oxygen tension ratios were more abnormal in those with NOD compared to those without NOD Which COPD Patients Desaturate during sleep and why? n Greater arterial oxygen desaturation occurs during sleep than in maximal exercise with a different mechanism. Awake PaO2 at rest has been found to be a better predictor of sleep arterial oxygen desaturation than exercise arterial desaturation. However awake PaCO2 has not been shown as an independent predictor of NOD. Coexistent COPD and OSAS (overlap Syndrome) n Epidemiologic studies show that contrary to what one might expect, the prevalence of OSAS in COPD patients is similar to that in an age matched population without COPD. n Coexistent COPD and OSAS is associated with more severe hypoxemia during sleep. Coexistent COPD and OSAS (overlap Syndrome) n Mean SaO2 is lower in patients with COPD and OSAS and the time spent in desaturation is longer than those with OSAS alone. Most patients with OSAS tend to resaturatre to normal SaO2 levels between apneas while those with coexistent COPD may be more hypoxemic at the start of the apnea. Coexistent COPD and OSAS (overlap Syndrome) n Thus those with coexistent COPD and OSAS are particularly prone to complications of hypoxemia such as cor pulmonale. Although early research on sleep in COPD had a selection bias towards those individuals who sought attention for a sleep disorder the Sleep Heart Health Study sought to correct this bias by Coexistent COPD and OSAS (overlap Syndrome) n Examining the relationship between COPD and OSAS in a large community population of 1132 participants with predominantly mild COPD who did not seek treatment for a sleep disorder. The investigation concluded that comorbid COPD and OSAS occurred by chance and that a common pathophysiological link was unlikely although an FEV1/FVC ratio 60 mmHG were compared to patients with and without NOD. The NOD was further characterized as episodic ( desaturation occurring mainly in REM sleep) or nonepisodic SaO2 30% of time in bed. At median follow up of 3.4 years n Mortality rated were significantly higher among patients with NOD. Conclusions n COPD management must be individualized to each patient especially with respect to sleep quality and the degree to which COPD sufferers are affected by changes in respiratory physiology. It is important to perform a sleep history in COPD patients as a normal sleep pattern for them might actually suggest recurrent nocturnal awakenings due to hypercapnia or significant excessive daytime sleepiness. Conclusions Contd n Many patients believe that excessive daytime sleepiness is a normal part of aging when it may, in fact, be part of a treatable condition. Sleep studies monitor a number of respiratory and neurologic variables and can yield valuable information in patients with COPD. Despite