Kirkness Jason P, Schwartz Alan R, Patil Susheel P, Pichard Luis E, Marx Jason J, Smith Philip L, Schneider Harmut
John Hopkins Sleep Disorders Center, Baltimore, MD 21224, USA.
J Appl Physiol (1985). 2006 Nov;101(5):1489-94. doi: 10.1152/japplphysiol.00173.2006. Epub 2006 Jul 6.
To examine the dynamic modulation of upper airway (UA) function during sleep, we devised a novel approach to measuring the critical pressure (Pcrit) within a single breath in tracheostomized sleep apnea patients. We hypothesized that the UA continuously modulates airflow dynamics during transtracheal insufflation. In this study, we examine tidal pressure-flow relationships throughout the respiratory cycle to compare phasic differences in UA collapsibility between closure and reopening. Five apneic subjects (with tracheostomy) were recruited (2 men, 3 women; 18-50 yr; 20-35 kg/m2; apnea-hypopnea index >20) for this polysomnographic study. Outgoing airflow through the UA (face mask pneumotachograph) and tracheal pressure were recorded during brief transtracheal administration of insufflated airflow via a catheter. Pressure-flow relationships were generated from deflation (approaching Pcrit) and inflation (after Pcrit) of the UA during non-rapid eye movement sleep. During each breath, UA function was described by a pressure-flow relationship that defined the collapsibility (Pcrit) and upstream resistance (Rus). UA characteristics were examined in the presence and absence of complete UA occlusion. We demonstrated that Pcrit and Rus changed dynamically throughout the respiratory cycle. The UA closing pressure (4.4 +/- 2.0 cm H2O) was significantly lower than the opening pressure (10.8 +/- 2.4 cm H2O). Rus was higher for deflation (18.1 +/- 2.4 cm H2O x l(-1) x s) than during inflation (7.5 +/- 1.9 cm H2O x l(-1) x s) of the UA. Preventing occlusion decreases UA pressure-flow loop hysteresis by approximately 4 cm H2O. These findings indicate that UA collapsibility varies dynamically throughout the respiratory cycle and that both local mechanical and neuromuscular factors may be responsible for this dynamic modulation of UA function during sleep.
为研究睡眠期间上气道(UA)功能的动态调节,我们设计了一种新颖的方法来测量气管切开的睡眠呼吸暂停患者单次呼吸内的临界压力(Pcrit)。我们假设UA在经气管吹气期间持续调节气流动力学。在本研究中,我们检查整个呼吸周期的潮式压力-流量关系,以比较UA在关闭和重新开放之间可塌陷性的相位差异。招募了五名呼吸暂停受试者(行气管切开术)(2名男性,3名女性;年龄18 - 50岁;体重指数20 - 35 kg/m2;呼吸暂停低通气指数>20)进行这项多导睡眠图研究。在通过导管进行短暂经气管吹气期间记录通过UA(面罩呼吸流速仪)的呼出气流和气管压力。压力-流量关系由非快速眼动睡眠期间UA的放气(接近Pcrit)和充气(超过Pcrit)产生。在每次呼吸期间,UA功能由定义可塌陷性(Pcrit)和上游阻力(Rus)的压力-流量关系描述。在存在和不存在完全UA阻塞的情况下检查UA特征。我们证明Pcrit和Rus在整个呼吸周期中动态变化。UA关闭压力(4.4±2.0 cm H2O)显著低于开放压力(10.8±2.4 cm H2O)。UA放气时的Rus(18.1±2.4 cm H2O·l⁻¹·s)高于充气时(7.5±1.9 cm H2O·l⁻¹·s)。防止阻塞可使UA压力-流量环滞后减少约4 cm H2O。这些发现表明UA可塌陷性在整个呼吸周期中动态变化,并且局部机械和神经肌肉因素可能共同导致睡眠期间UA功能的这种动态调节。