Hall M J, Xie A, Rutherford R, Ando S, Floras J S, Bradley T D
Queen Elizabeth Hospital Sleep Research Laboratory, University of Toronto Ontario, Canada.
Am J Respir Crit Care Med. 1996 Aug;154(2 Pt 1):376-81. doi: 10.1164/ajrccm.154.2.8756809.
Because apnea length during periodic breathing varies according to the preceding increase in ventilation and reduction in PaCO 2, differences in the cycle length of periodic breathing among patients with normal and impaired cardiac function might be explained by the influence of lung-to-carotid body circulatory delay, as reflected by lung-to-ear circulation time (LECT), on hyperpnea length rather than on apnea length. It was therefore hypothesized that circulatory delay is an important determinant of periodic-breathing hyperpnea length but not apnea length. To test this hypothesis, LECT, periodic-breathing cycle length, apnea length, and hyperpnea length were compared in 10 patients with idiopathic central sleep apnea (ICSA), whose cardiac function was normal, as opposed to 10 with Cheyne-Stokes respiration and central sleep apnea (CSR-CSA) in association with congestive heart failure (CHF). As compared with ICSA patients, cycle length was significantly longer in patients with CSR-CSA (37.3 +/- 3.0 s versus 59.0 +/- 4.9 s, p < 0.005). This difference was due to significantly longer hyperpnea length in the CSR-CSA patients (16.7 +/- 2.8 s versus 36.7 +/- 3.4 s, p < 0.001), since apnea length was similar in the two groups. In addition, LECT was longer in the CSR-CSA patients (24.3 +/- 2.0 s versus 10.3 +/- 1.0 s, p < 0.001), and correlated strongly with cycle length (r = 0.88, p < 0.001) and hyperpnea length (r = 0.90, p < 0.001) but not with apnea length. LECT correlated inversely with cardiac output (r = -0.72, p < 0.006), indicating that LECT is a valid measure of circulatory delay. Thus, circulatory delay is an important determinant of hyperpnea length but not of apnea length in patients with ICSA and CSR-CSA.
由于周期性呼吸期间的呼吸暂停时长会根据先前通气量的增加和动脉血二氧化碳分压（PaCO₂）的降低而变化，心脏功能正常和受损的患者之间周期性呼吸的周期时长差异，可能是由肺到颈动脉体循环延迟（如肺到耳循环时间（LECT）所反映）对通气过度时长而非呼吸暂停时长的影响来解释。因此，有人提出假设，循环延迟是周期性呼吸通气过度时长而非呼吸暂停时长的重要决定因素。为了验证这一假设，对10名心脏功能正常的特发性中枢性睡眠呼吸暂停（ICSA）患者与10名伴有充血性心力衰竭（CHF）的陈 - 施呼吸和中枢性睡眠呼吸暂停（CSR - CSA）患者的LECT、周期性呼吸周期时长、呼吸暂停时长和通气过度时长进行了比较。与ICSA患者相比，CSR - CSA患者的周期时长显著更长（37.3±3.0秒对59.0±4.9秒，p<0.005）。这种差异是由于CSR - CSA患者的通气过度时长显著更长（16.7±2.8秒对36.7±3.4秒，p<0.001），因为两组的呼吸暂停时长相似。此外，CSR - CSA患者的LECT更长（24.3±2.0秒对10.3±1.0秒，p<0.001），并且与周期时长（r = 0.88，p<0.001）和通气过度时长（r = 0.90，p<0.001）密切相关，但与呼吸暂停时长无关。LECT与心输出量呈负相关（r = -0.72，p<0.006），表明LECT是循环延迟的有效指标。因此，循环延迟是ICSA和CSR - CSA患者通气过度时长而非呼吸暂停时长的重要决定因素。
