Bradley T D
University of Toronto Faculty of Medicine, Ontario, Canada.
Clin Chest Med. 1992 Sep;13(3):459-79.
Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
阻塞性睡眠呼吸暂停可能主要通过继发于缺氧的肺血管收缩，导致肺动脉高压和右心室衰竭的发生。然而，最近的几项研究表明，间歇性呼吸暂停相关的缺氧不足以导致持续性肺动脉高压。这些研究一致表明，肺动脉高压和右心室衰竭几乎总是在存在日间缺氧的情况下出现。因此，持续性肺动脉高压似乎与持续性缺氧有关，慢性阻塞性肺疾病（COPD）的情况也是如此。患有阻塞性睡眠呼吸暂停且清醒时存在缺氧的患者通常肥胖，并有轻度至中度弥漫性阻塞性气道疾病。因此，与阻塞性睡眠呼吸暂停相关的大多数肺动脉高压病例是由阻塞性睡眠呼吸暂停、肥胖和弥漫性阻塞性气道疾病共同作用导致的，即所谓的重叠综合征。然而，从治疗角度来看，显然在这种情况下，通过无创持续气道正压通气（NCPAP）或气管切开术治疗阻塞性睡眠呼吸暂停通常足以逆转肺动脉高压和右心室衰竭。最近的研究提供了强有力的证据，表明阻塞性睡眠呼吸暂停在病因不明的慢性心力衰竭（CHF）患者左心室心力衰竭的发病机制中可能起作用。这可能是由于阻塞性呼吸暂停期间过度的负压波动、间歇性缺氧以及长期升高的交感肾上腺活动导致左心室后负荷增加共同作用的结果。在这些患者中，通过NCPAP逆转阻塞性睡眠呼吸暂停可能会缓解左心室心力衰竭。这些发现为我们理解阻塞性睡眠呼吸暂停对心血管系统的病理生理影响增添了新的维度，表明左心室是一个可能因阻塞性睡眠呼吸暂停施加的压力而遭受功能损害的结构。最后，现在已经很明显，慢性心力衰竭患者的中枢性睡眠呼吸暂停（CSR）与间歇性缺氧和睡眠中觉醒相关时，可导致睡眠呼吸暂停综合征的症状。通过NCPAP逆转睡眠期间的中枢性睡眠呼吸暂停可减轻这些症状，并可能减轻心脏性呼吸困难和改善左心室收缩功能。综上所述，这表明在心血管疾病的调查中，可能有必要更广泛地使用多导睡眠图。原因很有说服力：睡眠呼吸暂停障碍很常见且是可有效治疗的疾病，其逆转可导致右心和左心功能改善，并使心肌功能受损患者的症状得到改善。
