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过度通气在充血性心力衰竭患者中枢性睡眠呼吸暂停发病机制中的作用。

Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure.

作者信息

Naughton M, Benard D, Tam A, Rutherford R, Bradley T D

机构信息

Sleep Research Laboratory, Queen Elizabeth Hospital, Ontario, Canada.

出版信息

Am Rev Respir Dis. 1993 Aug;148(2):330-8. doi: 10.1164/ajrccm/148.2.330.

DOI:10.1164/ajrccm/148.2.330
PMID:8342895
Abstract

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.

摘要

睡眠期间伴有中枢性呼吸暂停的周期性呼吸通常由过度通气导致的低碳酸血症引发。因此,我们推测低碳酸血症是充血性心力衰竭(CHF)患者发生伴有中枢性睡眠呼吸暂停的陈-施呼吸(CSR-CSA)的一个重要决定因素。为验证这一假设,24例男性CHF患者接受了整夜多导睡眠监测,期间测量经皮二氧化碳分压(PtcCO2)。通过耳脉搏血氧仪得出肺到耳循环时间(LECT),以此作为循环延迟的一个估计值,并确定CSR-CSA周期长度。患者被分为CSR-CSA组(n = 12,每小时睡眠中平均±标准误为49.2±6.3次中枢性呼吸暂停和呼吸浅慢)和无CSR-CSA的对照组(n = 12,每小时睡眠中4.9±0.8次中枢性呼吸暂停和呼吸浅慢)。两组之间左心室射血分数、清醒时动脉血氧分压(PaO2)、夜间平均血氧饱和度(SaO2)或LECT均无显著差异。相比之下,CSR-CSA组的清醒时动脉血二氧化碳分压(PaCO2)和睡眠平均PtcCO2显著低于对照组(分别为33.0±1.2与37.5±1.0 mmHg,p < 0.01;以及33.2±1.2与42.5±1.2 mmHg,p < 0.0001)。两组均无显著的清醒时或与睡眠相关的低氧血症。此外,CSR-CSA周期长度与LECT相关(r = 0.939,p < 0.001)。我们得出结论:(1)低碳酸血症是CHF患者CSR-CSA的一个重要决定因素;(2)循环延迟在决定CSR-CSA周期长度方面起重要作用。

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