阻塞性睡眠呼吸暂停低通气综合征患者睡眠过程中呼吸力学的变化

目的 研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者在睡眠过程中的呼吸力学变化特点.方法 60例疑似OSAHS患者及21例无OSAHS临床表现的志愿者入选本研究,其中男70例,女11例,平均年龄(44±13)岁.所有受试者均接受整夜多导睡眠图监测,并同时采用面罩旁气流技术动态描记整个睡眠过程中的呼吸力学指标和潮气量流速容量环(TBFVL).根据呼吸暂停低通气指数(AHI)将入选者分为OSAHS组(AHI≥15次/h)54例和对照组(AHI＜15次/h)27例.采用重复测量方差分析比较OSAHS组各期潮气吸气容积(VTI)/潮气呼气容积(VTE)及对照组各期呼吸力学指标变化;自身比较采用配对t检验;组间比较采用x2检验.结果 清醒状态下呼吸周期的VTI/VTE为0.99±0.04,说明吸气和呼气潮气量大致相等.OSAHS组发生睡眠呼吸暂停后第1个呼吸周期VTI/VTE(1.37±0.18)明显升高,在睡眠呼吸暂停前5次内和最后一次呼吸周期VTI/VTE均值(0.86±0.08和0.72±0.19)明显降低,说明呼吸暂停前一段时间内呼气量明显多于吸气量,而呼吸暂停后吸气量多于呼气量.OSAHS组无呼吸事件浅睡眠期VTI[(463±122)ml]、VTE[(466±127)ml]和分钟通气量[(6.4±1.6)L/min]比睡前[(554±134)ml、(565±147)ml和(8.3±1.9)L/min]明显减少.TBFVL结果显示,OSAHS组吸气阻力升高者占100%(54/54),呼气阻力升高者和两种阻力同时升高者均占96.3%(52/54).结论 在发生睡眠呼吸暂停前OSAHS患者呼气量明显多于吸气量,直至呼吸停止,这使患者发生睡眠呼吸暂停前的功能残气量明显减少,从而上气道更加狭窄,此病理生理过程在OSAHS整个发病过程中占有重要地位.OSAHS患者浅睡眠期的潮气量和通气量较睡前降低,睡眠过程中以上气道吸气相阻力升高为主的同时普遍存在呼气相阻力升高.     

Lung volume and continuous positive airway pressure requirements in obstructive sleep apnea

Previous studies have demonstrated that lung volume during wakefulness influences upper airway size and resistance, particularly in patients with sleep apnea. We sought to determine the influence of lung volume on the level of continuous positive airway pressure (CPAP) required to prevent flow limitation during non-REM sleep in subjects with sleep apnea. Seventeen subjects (apnea-hypopnea index, 42.6 +/- 6.2 [SEM]) were studied during stable non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. An epiglottic pressure catheter plus a mask/pneumotachometer were used to assess flow limitation. When lung volume was increased by 1,035 +/- 22 ml, the CPAP level could be decreased from 11.9 +/- 0.7 to 4.8 +/- 0.7 cm H(2)O (p < 0.001) without flow limitation. The decreased CPAP at the same negative extrathoracic pressure yielded a final lung volume increase of 421 +/- 36 ml above the initial value. Conversely, when lung volume was reduced by 732 +/- 74 ml (n = 8), the CPAP level had to be increased from 11.9 +/- 0.7 to 17.1 +/- 1.0 cm H(2)O (p < 0.001) to prevent flow limitation, with a final lung volume decrease of 567 +/- 78 ml. These results demonstrate that relatively small changes in lung volume have an important effect on the upper airway in subjects with sleep apnea during non-REM sleep.     

Palate and hypopharynx--sites of inspiratory narrowing of the upper airway during sleep

In order to determine the specific site of inspiratory narrowing within the upper airway during sleep, we measured supralaryngeal, oropharyngeal, and nasopharyngeal pressures and inspiratory flow in 11 healthy nonsnoring male subjects awake and in NREM sleep. Resistance was calculated at 0.01 L/s, a point along the linear portion of the pressure-flow relationship, and at peak inspiratory pressure, a point within the curvilinear section of the pressure-flow relationship. During sleep, nasal resistance increased minimally. At peak inspiratory pressure, both transpalatal and hypopharyngeal resistances increased more than 700% in NREM sleep. At 0.01 L/s inspiratory flow, transpalatal and hypopharyngeal resistances increased 200 and 400%, respectively. Six subjects had a greater increase in transpalatal than hypopharyngeal resistance, and five subjects had a greater increase in hypopharyngeal than transpalatal resistance. Three subjects in each of these two subgroups had an increase in resistance exclusively across the palate or the hypopharynx. The site of increased resistance during sleep was not predictable from awake resistance measurements. From these data, we conclude that the site of inspiratory narrowing within the upper airway during sleep occurs primarily at either the level of the palate or hypopharynx and is variable among subjects. The pattern of palatal or hypopharyngeal narrowing is the same as that observed in obstructive sleep apnea patients, but quantitatively different.     

Acute effects of automated continuous positive airway pressure on blood pressure in patients with sleep apnea and hypertension

BACKGROUND: The obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as myocardial infarction, arrhythmias, and systemic and pulmonary hypertension. Objectives: We investigated the acute effects of automatic continuous positive airway pressure (automated CPAP) on blood pressure in patients with OSAHS and hypertension. METHODS: Polysomnography was used and ambulatory blood pressure measurements were done in 12 patients with OSAHS. Blood pressure and heart rate were measured at night (10 p.m. to 6 a.m.) and during the day (6 a.m. to 10 p.m.). During these periods systolic, diastolic and mean blood pressure and heart rate of the patients on the diagnostic day were compared with those on the treatment day. RESULTS: Patients had moderate or severe OSAHS; their mean age was 52.8+/-4.2 years. Systolic, diastolic and mean blood pressure and heart rate between the diagnostic and treatment day were not significantly different. Standard deviations of all these parameters during the night of the treatment day (9.1+/-4.5, 7.5+/-3.3, 8.0+/-3.0 mm Hg, and 4.8+/-1.5 beats/min, respectively) were significantly lower than during the night of the diagnostic day (12.6+/-4.9 mm Hg, p=0.023, 10.8+/-3.5 mm Hg, p=0.004, 11.6+/-4.4 mm Hg, p=0.006 and 6.9+/-1.6 beats/min, p=0.003, respectively). We did not find similar results during daytime periods. CONCLUSIONS: Automated CPAP therapy in patients with sleep apnea and hypertension did not decrease systolic and diastolic blood pressures and heart rates acutely. However, it might reduce the variability of these parameters during sleep in patients, but not during the day. It might be suggested that automated CPAP reduces cardiovascular morbidity of OSAHS via stabilizing heart rate and blood pressure during sleep.     

Changes in inspiratory muscle electrical activity and upper airway resistance during periodic breathing induced by hypoxia during sleep

We hypothesized that: the balance of electrical activities between the upper airway and chest wall inspiratory muscles affects upper airway inspiratory caliber, and at low levels of central respiratory neural efferent activity, an imbalance between the electrical activities of these 2 inspiratory muscle groups exists that results in a decreased upper airway caliber. These hypotheses were tested during periodic breathing induced by mild hypoxemia in NREM sleep in 9 healthy male subjects. In 6 subjects during periodic breathing as central respiratory neural activity decreased, the tonic and phasic EMG activity of the upper airway inspiratory muscles decreased at a rate greater than that of the chest wall EMG activity. When the ratio of upper airway to chest wall EMG activity decreased below a critical level, which was reproducible across subjects, upper airway inspiratory resistance increased hyperbolically. Resistance at peak inspiratory flow increased from 4.10 +/- 0.97 (mean +/- SEM) to 48.70 +/- 21.00 cmH2O/L/s as tidal volume decreased from 0.79 +/- 0.12 to 0.20 +/- 0.02 L during periodic breathing in these subjects. In the 3 remaining subjects, the ratio of the upper airway to chest wall EMG activity did not decrease below the critical level as the activity of both muscle groups decreased during periodic breathing, and upper airway resistance did not increase. We conclude that within the confines of this study the nonlinear activation of upper airway and chest wall inspiratory muscles contributed to fluctuations in upper airway resistance observed during periodic breathing in sleep.(ABSTRACT TRUNCATED AT 250 WORDS)     

The determinants of therapeutic levels of continuous positive airway pressure in elderly sleep apnea patients

We have examined the role of age on the continuous positive airway pressure (CPAP) levels required to treat two groups of elderly (n=70) and young (n=70) sleep apneic patients, matched for disease severity (apnea/hypopnea index), body mass index and neck circumference. Elderly patients required lower CPAP levels compared to young [mean (sd): 6.9(1.9)cm H(2)O and 9.4(3.5)cm H(2)O, respectively; P<0.0001]. To investigate this finding, we studied the effects of CPAP and its components (inspiratory and expiratory positive airway pressure) on lung volume and upper airway resistance in two groups of elderly [n=9, age 71.7(3.3) years] and young [n=9, age 36.7(4.4)] patients with sleep apnea during wakefulness. CPAP produced a greater decrease in airway resistance (P=0.009) and a greater increase in lung volume (P=0.008) in the elderly compared to young patients. We conclude that both the greater lung inflation and the greater direct splinting of the upper airway contributed to the lower CPAP level required by the elderly. Ageing may be an important determinant of therapeutic CPAP levels in clinical practice, especially in older sleep apneic patients.     

Effect of nasal obstruction on upper airway muscle activation in normal subjects

It is not known whether nasal occlusion produces obstructive sleep apnea (OSA) by decreasing upper airway muscle activation via nasal reflexes or by increasing upper airway resistance and hence lowering the pressure in the pharnyx. The purpose of this study was to determine the effect of nasal occlusion on upper airway muscle activation. We studied seven men and measured alae nasi (AN) and genioglossal (GG) electromyograms (EMGs) during two nights of sleep, one with their nose open and the other with their nose occluded. Nasal occlusion produced OSA in all subjects and also increased the percentage of time during sleep in which phasic AN and GG EMG activity was present. Apneas tended to occur at the nadirs of EMG activity. This suggests that nasal occlusion generally increases respiratory drive to upper airway muscles during sleep and that it does not cause OSA by merely decreasing respiratory drive to these muscles.     

The influence of aging on pharyngeal collapsibility during sleep

BACKGROUND: Aging increases vulnerability to obstructive sleep apnea (OSA), but the underlying mechanisms remain unclear. Recent data in awake healthy volunteers show a decrease in the genioglossus negative pressure reflex and anatomic compromise with increasing age, suggesting an age-related predisposition to pharyngeal collapse. However, aging effects on pharyngeal collapsibility have not been studied extensively during sleep. We tested the hypotheses that upper airway closing pressure (PCLOSE) and the increase in pharyngeal resistance during sleep (primary outcomes) as well as measures of arousal threshold (secondary outcomes) increase with age. METHODS: We studied 21 healthy individuals (8 women [mean (+/- SD) age, 36 +/- 18 years] and 13 men [mean age, 41 +/- 23 years]) who were between 18 and 75 years of age. During overnight polysomnography, we measured nasal pressure (PMASK) and epiglottic pressure (Pepi) during stage 2 sleep before and after airway occlusion (external valve) until arousal. PCLOSE was defined as the pressure at which PMASK plateaued despite further decreases in PEPI. RESULTS: Increasing age was correlated with both pharyngeal collapsibility ([PCLOSE] r = 0.69; p < 0.01) and an increase in pharyngeal resistance during sleep (r = 0.56; p < 0.01) independent of body mass index (BMI) and gender. There was no evidence for an effect of age on arousal threshold after airway occlusion during stage 2 sleep. CONCLUSIONS: Older age is associated with increased pharyngeal airway collapsibility during sleep independent of gender and BMI. These data may at least partially explain the mechanisms underlying the predisposition for pharyngeal collapse in the elderly.     

Alveolar pressure and airway resistance during maximal and submaximal respiratory efforts

A digital computing technique was used to extract continuous calculations of average alveolar pressure and airway resistance from body plethysmographic measurements during forced inspiratory and expiratory vital capacity maneuvers and tidal breathing in human subjects. Derived alveolar pressures were similar to those obtained using an interrupter technique (linear regression slope, 0.99 +/- 0.02; r = 0.98) and by comparison with esophageal pressure measurements. Studies in normal subjects revealed a characteristic pattern of increasing airway resistance throughout the expiratory phases of maximal and submaximal respiratory maneuvers, with maximal resistance of 33 to 110 cm H2O/L/s at low lung volumes during forced vital capacities. In contrast, inspiratory resistance remained low and constant throughout maximal and submaximal inspiratory maneuvers. Patients with COPD showed substantially higher inspiratory and expiratory resistances. In three patients with flow-volume loops suggestive of variable extrathoracic upper airway obstruction, measurements of alveolar pressure and airway resistance made it clear that two of the patients had upper airway obstruction, whereas the other was exerting an inadequate effort. We conclude that this noninvasive technique provides valid estimates of alveolar pressure and airway resistance continuously throughout both phases of the respiratory cycle over a wide range of volumes and flow rates. It may prove to be useful in the assessment of effort and airway obstruction in patients with a variety of pulmonary conditions.     

Upper airway mechanics and post-hypoxic ventilatory decline during NREM sleep

Termination of hypoxia results in a transient ventilatory decline referred to as post-hypoxic ventilatory decline (PHVD). We wished to determine whether PHVD is due to changes in ventilatory motor output or upper airway mechanics. We studied 19 healthy normal subjects (15 men, 4 women) during stable non-REM (NREM) sleep. Subjects were exposed to multiple episodes of brief (3 min) hypoxia that terminated with one breath of 100% FI_O2. Minute ventilation (V _I), tidal volume (V _T), timing, and upper airway resistance (R _ua) were measured during the control, hypoxia, and for the first six breaths immediately after cessation of hypoxia. In addition, we measured diaphragmatic electromyograms (EMGdia) via surface electrodes in four subjects. V _I and V _T decreased during the recovery period to a nadir of 81and 83% of room air control, respectively. However, there was no significant change in respiratory frequency or upper airway resistance during the post-hypoxic recovery period. Decreased V _I was associated with a comparable decrease in EMGdia. We conclude that: (1) PHVD occurs in normal humans during NREM sleep, (2) there is no evidence of post-hypoxic frequency decline in humans during NREM sleep, and (3) PHVD is centrally mediated and not driven by upper airway mechanics.     

Effect of sleep stages on measurements of passive respiratory mechanics in infants with bronchiolitis

The measurement of passive respiratory mechanics by the single-breath occlusion technique is one of the more frequently used tests of infant lung function. Measurements are routinely done under chloral hydrate sedation, and a possible influence of sleep stages on these measurements has not been evaluated so far. We combined the assessment of passive respiratory mechanics with sleep stage monitoring in 44 infants and toddlers with mild to moderately severe bronchiolitis. In 31 infants, only nonrapid eye movement (NREM) sleep was recorded. In 13 patients who showed both NREM and rapid eye movement (REM) sleep, compliance of the respiratory system was significantly lower during REM than NREM sleep (73.2 +/- 19.7 vs. 81.2 +/- 21.3 mL/kPa, P = 0.0007), while resistance remained essentially unchanged. This finding was explained by an unchanged airway opening pressure in combination with a significantly decreased extrapolated volume. As tidal volume did not change from NREM to REM, this indicates reduced dynamic elevation of lung volume during REM sleep and thus supports previous observations of decreased lung volume in this sleep stage. From a practical perspective, these findings argue for the monitoring of sleep stage during measurements of passive respiratory mechanics, thereby increasing the complexity of these measurements significantly.     

Effect of hypercapnia on total pulmonary resistance during wakefulness and during NREM sleep.

We investigated the effect of different levels of hypercapnia on total pulmonary resistance (RL) in 13 subjects ranging from nonsnorers with low RL to snorers with high RL and dynamic narrowing of the upper airway during inspiration. Added CO2 was adjusted to achieve a steady-state increase in PETCO2 of +2, +4, or +6 mm Hg. RL was measured at peak inspiratory flow (RLpf), at maximal resistance within breath (RLmax), and at 10 equally spaced points within inspiration in several trials. During wakefulness, hypercapnia was associated with decreased RLmax. During steady state +6 mm Hg hypercapnia, RLmax decreased by 30% (p less than 0.01). During NREM sleep, low levels of hypercapnia did not affect RL. However, +6 mm Hg hypercapnia was associated with decreased RLmax in six of eight subjects (p = 0.07), especially in subjects with high RLmax during room air breathing. The effects of hypercapnia on RLpf paralleled its effect on RLmax. We concluded that (1) the decrease in RL during awake hypercapnia suggests an increase in upper airway dimensions and stiffness, (2) the absence of increased RL during low level NREM hypercapnia (despite the increase in inspiratory flows and collapsing pressures) also suggests an increase in upper airway dimensions and stiffness, and (3) upper airway dilating muscles appear to be recruited in a coordinated fashion with inspiratory muscles in normal humans during NREM sleep. The implications of these findings in patients with obstructive sleep apnea are not clear at this point.     

Obesity hypoventilation syndrome as a spectrum of respiratory disturbances during sleep

OBJECTIVE: To identify the spectrum of respiratory disturbances during sleep in patients with obesity hypoventilation syndrome (OHS) and to examine the response of hypercapnia to treatment of the specific ventilatory sleep disturbances. DESIGNS AND METHODS: Twenty-three patients with chronic awake hypercapnia (mean [+/- SD] PaCO(2), 55 +/- 6 mm Hg) and a respiratory sleep disorder were retrospectively identified. Nocturnal polysomnography testing was performed, and flow limitation (FL) was identified from the inspiratory flow-time contour. Obstructive hypoventilation was inferred from sustained FL coupled with O(2) desaturation that was corrected with treatment of the upper airway obstruction. Central hypoventilation was inferred from sustained O(2) desaturation that persisted after the correction of the upper airway obstruction. Treatment was initiated, and follow-up awake PaCO(2) measurements were obtained (follow-up range, 4 days to 7 years). RESULTS: A variable number of obstructive sleep apneas/hypopneas (ie, obstructive sleep apnea-hypopnea syndrome [OSAHS]) were noted (range, 9 to 167 events per hour of sleep). Of 23 patients, 11 demonstrated upper airway obstruction alone (apnea-hypopnea/FL) and 12 demonstrated central sleep hypoventilation syndrome (SHVS) in addition to a variable number of OSAHS. Treatment aimed at correcting the specific ventilatory abnormalities resulted in correction of the chronic hypercapnia in all compliant patients (compliant patients: pretreatment, 57 +/- 6 mm Hg vs post-treatment, 41 +/- 4 mm Hg [p < 0.001]; noncompliant patients: pretreatment, 52 +/- 6 mm Hg vs post-treatment, 51 +/- 3 mm Hg; [difference not significant]). CONCLUSIONS: This study demonstrates that OHS encompasses a variety of distinct pathophysiologic disturbances that cannot be distinguished clinically at presentation. Sustained obstructive hypoventilation due to partial upper airway obstruction was demonstrated as an additional mechanism for OHS that is not easily classified as SHVS or OSAHS.     

Nocturnal asthma: snoring, small pharynx and nasal CPAP

We studied two populations of patients who snored and had frequent nocturnal asthma attacks: ten overweight men presenting with typical obstructive sleep apnoea syndrome, and a group of five adolescents with regular snoring and an increase in negative inspiratory oesophageal pressure during stage II non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. All subjects presented cranio-mandibular abnormalities at cephalometric evaluation, with a narrow space behind the base of the tongue. Both populations were treated with nasal continuous positive airway pressure (CPAP) during sleep. Snoring and partial or complete airway obstruction were eliminated, as were the nocturnal asthma attacks. Two adolescents treated with upper airway surgery after nasal CPAP showed no nocturnal asthma at short-term follow-up. Nasal CPAP had no effect on daytime asthma. One hypothesis is that a subgroup of asthmatic patients with small pharynxes may have enhanced vagal stimulation during sleep compared with other asthmatic patients. This enhancement would be related to the repetitive Müller manoeuvres noted with airway obstruction during sleep. Combined with the local effects of snoring, this extra vagal stimulation would be a precipitating factor in nocturnal asthma attacks.     

Upper-airway collapsibility: measurements and sleep effects.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) is characterized by repetitive pharyngeal collapse during sleep. Several techniques have been proposed to assess the collapsibility of the upper airway in awake humans, but sleep-wake comparisons have rarely been attempted and there are few studies comparing OSA patients to control subjects. We sought to compare two collapsibility measurement techniques between normal and apneic subjects, and between wakefulness and sleep. DESIGN: We conducted three studies. First, we examined whether collapsibility assessed by negative pressure pulses (NPPs) during wakefulness reflected values during sleep in 21 normal subjects. Second, we determined in these normal subjects whether collapsibility during sleep assessed by NPPs was predictive of collapsibility measured by inspiratory resistive loading (IRL). Finally, we compared upper-airway collapsibility between apnea patients (n = 22) and normal volunteers (n = 38) during wakefulness by NPPs. SETTING: Clinical and research laboratories at the Brigham and Women's Hospital. PARTICIPANTS: Two populations of normal subjects (n = 21 and n = 38) and OSA patients (n = 22). Measurements and results: Collapsibility during wakefulness, as measured by NPPs, correlated significantly with collapsibility during sleep (r = 0.62; p = 0.003). There was also a significant correlation between the two measures of collapsibility (IRL and NPP) during sleep (r = 0.53; p = 0.04). Both measures revealed a significant increase in pharyngeal collapsibility during sleep as compared to wakefulness. Finally, apnea patients had significantly greater pharyngeal collapsibility than control subjects during wakefulness (p = 0.017). CONCLUSIONS: These data suggest that upper-airway collapsibility measured during wakefulness does provide useful physiologic information about pharyngeal mechanics during sleep and demonstrates clear differences between individuals with and without sleep apnea.     

The effects of obstructive sleep apnea hypopnea syndrome on cardiovascular system]

Obstructive sleep apnea hypopnea syndrome (OSAHS) is characterized by repetitive upper airway obstruction during sleep and it is commonly seen in the adult population, 4% in the men, 2% in the women. The most common nocturnal symptom is snoring while the most common daytime symptom is excessive daytime sleepiness. The gold standard in the diagnosis is polysomnography. Nasal continuous positive airway pressure is the most efficient therapy in the treatment and prevention of the disease. The OSAHS may cause cardiovascular complications in long-term, including systemic hypertension, pulmonary hypertension, congestive heart failure, arrhythmias, stroke and myocardial infarction. All these complications increase the morbidity and mortality of OSAHS. In this paper, effects of OSAHS on cardiovascular system were reviewed.     

Obstructive sleep apnoea-hypoapnoea syndrome reversibly depresses cardiac response to exercise.

AIMS: To evaluate cardiac response to exercise in middle-aged normotensive obstructive sleep apnoea-hypoapnoea syndrome (OSAHS) adults with normal resting left ventricular systolic function and to test the hypothesis that nasal continuous positive airway pressure (CPAP) therapy might improve cardiac performance during exercise. METHODS AND RESULTS: We performed a prospective, randomized, double-blind, placebo-controlled, cross-over clinical trial including 31 consecutive newly diagnosed OSAHS patients and 15 healthy subjects. Cardiopulmonary exercise testing with cardiac output measurement, blood pressure (BP) recordings, and urinary excretion of catecholamine levels were obtained at baseline and after 3 months on both effective and sham CPAP. OSAHS subjects had higher systolic and mean nocturnal BP and higher nocturnal levels of catecholamines. In contrast, they had lower increments in cardiac output (Qt) and in stroke volume (SV) in response to exercise than control subjects. CPAP therapy was associated with highly significant improvements in all the indices of left ventricular systolic performance response during exercise, whereas with sham CPAP, all of them remained unchanged. CONCLUSION: OSAHS patients with normal resting left ventricular systolic function and no hypertension had a worse cardiac response to exercise than healthy subjects. In these patients, 3 months of CPAP improved both Qt and SV responses to exercise.     

The respiratory neuromuscular response to hypoxia, hypercapnia, and obstruction to airflow in asthma.

In chronic obstructive pulmonary disease (COPD), the neuromuscular response to an acute increase in airflow produced by external flow resistive loads (FRL) is impaired. The present study compared the response to FRL of 15 subjects with airway obstruction due to asthma and that of 15 normal subjects. FRL were applied during progressive hypercapnia and isocapnic hypoxia produced by rebreathing techniques to permit the response to be assessed at the same degree of CO2 or O2 drive. The neuromuscular response to FRL was assessed from the airway occlusion pressure developed 100 msec after the onset of inspiration (P100), as well as ventilation. During control rebreathing, ventilatory responses to hypercapnia (ratio of change in minute ventilation to change in PCO2, delta VE/delta PCO2) and hypoxia (ratio of change in VE to the change in percentage of O2 saturation, delta VE/deltaSO2) were the same in asthmatic and normal subjects despite differences in the mechanics of breathing. The P100 response to hypercapnia delta P100/delta PCO2) and hypoxia (delta P100/delta SO2) as well as absolute P100 at any given degree of O2 and CO2 drive was greater during control rebreathing in asthmatics than in normal subjects (P less than 0.05). FRL values of 9 and 18 cm H2O per L per sec applied during either hypercapnia or hypoxia increased the occlusion pressure to a greater extent in asthmatics than in normal subjects. Methacholine-induced bronchoconstriction was used to test the effect of acute airway obstruction on the response to FRL. Bronchoconstriction was associated with an increase in the P100 response to hypercapnia and to FRL, despite increases in lung volume and decreases in inspiratory muscle force. We conclude that: (1) asthmatics with airway dysfunction have an increased nonchemical drive to breathe mediated at least in part by sensory receptors in the airways; (2) asthmatics with airway obstruction respond supernormally to acute changes in resistance to airflow, unlike subjects with COPD. The failure of COPD subjects with prolonged airway obstruction to respond to FRL may be due to adaptation of the sensory mechanisms that respond to changes in airway resistance.     

OSAHS使用CPAP呼吸机治疗前后血中CO变化的研究

目的测定阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆中一氧化碳(CO)水平了解其价值。方法随机选择20例中～重度OSAHS患者使用CPAP呼吸机治疗30天。以OSAHS患者血浆的CO水平为因变量,其体块指数(BMI)、呼吸暂停低通气指数(AHI)、舒张压(DBP)、收缩压(SBP)、小于90%血氧饱和度的睡眠时间与总睡眠时间的比例(R)和年龄为自变量,作多元线性回归分析。结果OSAHS患者血浆中CO显著高于正常人,重度者的亦显著高于轻、中度者,OSAHS合并高血压者血浆CO也显著高于无伴高血压者,患者的血压变化与其CO的相同。20例OSAHS患者血浆的CO于使用CPAP呼吸机治疗第一天与治疗前比较无显著差异,但治疗一个月后则显著降低。另外,患者的血压应用CPAP呼吸机治疗一个月后逐渐降至正常范围。多元线性回归分析提示OSAHS患者血浆CO与R、AHI和DBP均呈正相关。结论重度OSAHS患者和OSAHS合并高血压者存在不同的病理生理改变,患者CO的显著增高由低氧所致,CO参与了OSAHS的病理生理指标,OSAHS患者血浆中CO水平可考虑作为考察是否有合并症的指标。