Perfunctory or faithful: The impact of self-professional identity on labor productivity of front-line employees in hotels.

Based on the theories of professional identity and emotional labor, this study investigates the mediating role of emotional labor in the relationship between self-professional identity and labor productivity among front-line employees in hotels. Drawing upon a validated scale, a survey was conducted with 238 front-line employees working in high-star hotels to examine the impact mechanism of self-professional identity on labor productivity. The findings reveal that self-professional identity significantly and positively influences labor productivity among hotel front-line employees. Self-professional identity is identified as the antecedent variable of emotional labor, whereby it enhances the deep acting of front-line staff while reducing surface acting and improving natural acting. Emotional labor acts as an intermediary between self-professional identity and labor productivity. However, different dimensions of emotional labor exhibit notable variations in their mediating effects and influence on outcomes. Effective hotel human resource management should prioritize the cultivation of front-line employees' self-professional identity, harness the positive role of emotional labor, and enhance labor productivity. This approach can lead to reduced operating costs, improved service quality, staff stability, and increased hotel revenue.

Sleep apnea: a review of diagnostic sensors, algorithms, and therapies.

While public awareness of sleep related disorders is growing, sleep apnea syndrome (SAS) remains a public health and economic challenge. Over the last two decades, extensive controlled epidemiologic research has clarified the incidence, risk factors including the obesity epidemic, and global prevalence of obstructive sleep apnea (OSA), as well as establishing a growing body of literature linking OSA with cardiovascular morbidity, mortality, metabolic dysregulation, and neurocognitive impairment. The US Institute of Medicine Committee on Sleep Medicine estimates that 50-70 million US adults have sleep or wakefulness disorders. Furthermore, the American Academy of Sleep Medicine (AASM) estimates that more than 29 million US adults suffer from moderate to severe OSA, with an estimated 80% of those individuals living unaware and undiagnosed, contributing to more than $149.6 billion in healthcare and other costs in 2015. Although various devices have been used to measure physiological signals, detect apneic events, and help treat sleep apnea, significant opportunities remain to improve the quality, efficiency, and affordability of sleep apnea care. As our understanding of respiratory and neurophysiological signals and sleep apnea physiological mechanisms continues to grow, and our ability to detect and process biomedical signals improves, novel diagnostic and treatment modalities emerge. OBJECTIVE: This article reviews the current engineering approaches for the detection and treatment of sleep apnea. APPROACH: It discusses signal acquisition and processing, highlights the current nonsurgical and nonpharmacological treatments, and discusses potential new therapeutic approaches. MAIN RESULTS: This work has led to an array of validated signal and sensor modalities for acquiring, storing and viewing sleep data; a broad class of computational and signal processing approaches to detect and classify SAS disease patterns; and a set of distinctive therapeutic technologies whose use cases span the continuum of disease severity. SIGNIFICANCE: This review provides a current perspective of the classes of tools at hand, along with a sense of their relative strengths and areas for further improvement.

Effects of inhaled fluticasone on upper airway during sleep and wakefulness in asthma: a pilot study.

STUDY OBJECTIVE: Obstructive sleep apnea is prevalent among people with asthma, but underlying mechanisms remain unknown. Inhaled corticosteroids may contribute. We tested the effects of orally inhaled fluticasone propionate (FP) on upper airway (UAW) during sleep and wakefulness. STUDY DESIGN: 16-week single-arm study. PARTICIPANTS: 18 (14 females, mean [ ± SD] age 26 ± 6 years) corticosteroid-naïve subjects with mild asthma (FEV1 89 ± 8% predicted). INTERVENTIONS: High dose (1,760 mcg/day) inhaled FP. MEASUREMENTS: (1) UAW collapsibility (passive critical closing pressure [Pcrit]); (2) tongue strength (maximum isometric pressure-Pmax, in KPa) and endurance-time (in seconds) able to maintain 50% Pmax across 3 trials (Ttot)-at anterior and posterior locations; (3) fat fraction and volume around UAW, measured by magnetic resonance imaging in three subjects. RESULTS: Pcrit overall improved (became more negative) (mean ± SE) (-8.2 ± 1.1 vs. -12.2 ± 2.2 cm H2O, p = 0.04); the response was dependent upon baseline characteristics, with older, male gender, and worse asthma control predicting Pcrit deterioration (less negative). Overall, Pmax increased (anterior p = 0.02; posterior p = 0.002), but Ttot generally subsided (anterior p = 0.0007; posterior p = 0.06), unrelated to Pcrit response. In subjects studied with MRI, fat fraction and volume increased by 20.6% and 15.4%, respectively, without Pcrit changes, while asthma control appeared improved. CONCLUSIONS: In this study of young, predominantly female, otherwise healthy subjects with well-controlled asthma and stiff upper airways, 16-week high dose FP treatment elicited Pcrit changes which may be dependent upon baseline characteristics, and determined by synchronous and reciprocally counteracting local and lower airway effects. The long-term implications of these changes on sleep disordered breathing severity remain to be determined.

Physiology in medicine: obstructive sleep apnea pathogenesis and treatment--considerations beyond airway anatomy.

We review evidence in support of significant contributions to the pathogenesis of obstructive sleep apnea (OSA) from pathophysiological factors beyond the well-accepted importance of airway anatomy. Emphasis is placed on contributions from neurochemical control of central respiratory motor output through its effects on output stability, upper airway dilator muscle activation, and arousability. In turn, we consider the evidence demonstrating effective treatment of OSA via approaches that address each of these pathophysiologic risk factors. Finally, a case is made for combining treatments aimed at both anatomical and ventilatory control system deficiencies and for individualizing treatment to address a patient's own specific risk factors.

Effects of stabilizing or increasing respiratory motor outputs on obstructive sleep apnea.

To determine how the obstructive sleep apnea (OSA) patient's pathophysiological traits predict the success of the treatment aimed at stabilization or increase in respiratory motor outputs, we studied 26 newly diagnosed OSA patients [apnea-hypopnea index (AHI) 42 ± 5 events/h with 92% of apneas obstructive] who were treated with O2 supplementation, an isocapnic rebreathing system in which CO2 was added only during hyperpnea to prevent transient hypocapnia, and a continuous rebreathing system. We also measured each patient's controller gain below eupnea [change in minute volume/change in end-tidal Pco2 (ΔVe/ΔPetCO2)], CO2 reserve (eupnea-apnea threshold PetCO2), and plant gain (ΔPetCO2/ΔVe), as well as passive upper airway closing pressure (Pcrit). With isocapnic rebreathing, 14/26 reduced their AHI to 31 ± 6% of control (P < 0.01) (responder); 12/26 did not show significant change (nonresponder). The responders vs. nonresponders had a greater controller gain (6.5 ± 1.7 vs. 2.1 ± 0.2 l·min(-1)·mmHg(-1), P < 0.01) and a smaller CO2 reserve (1.9 ± 0.3 vs. 4.3 ± 0.4 mmHg, P < 0.01) with no differences in Pcrit (-0.1 ± 1.2 vs. 0.2 ± 0.9 cmH2O, P > 0.05). Hypercapnic rebreathing (+4.2 ± 1 mmHg PetCO2) reduced AHI to 15 ± 4% of control (P < 0.001) in 17/21 subjects with a wide range of CO2 reserve. Hyperoxia (SaO2 ∼95-98%) reduced AHI to 36 ± 11% of control in 7/19 OSA patients tested. We concluded that stabilizing central respiratory motor output via prevention of transient hypocapnia prevents most OSA in selected patients with a high chemosensitivity and a collapsible upper airway, whereas increasing respiratory motor output via moderate hypercapnia eliminates OSA in most patients with a wider range of chemosensitivity and CO2 reserve. Reducing chemosensitivity via hyperoxia had a limited and unpredictable effect on OSA.

Role of central/peripheral chemoreceptors and their interdependence in the pathophysiology of sleep apnea.

Unstable periodic breathing with intermittent ventilatory overshoots and undershoots commonly occurs in chronic heart failure, in hypoxia, with chronic opioid use and in certain types of obstructive sleep apnea. Sleep promotes breathing instability because it unmasks a highly sensitive dependence of the respiratory control system on chemoreceptor input, because transient cortical arousals promote ventilatory overshoots and also because upper airway dilator muscle tonicity is reduced and airway collapsibility enhanced. We will present data in support of the premise that carotid chemoreceptors are essential in the pathogenesis of apnea and periodicity; however it is the hyperadditive influence of peripheral chemoreceptor sensory input on central chemosensitivity that accounts for apnea and periodic breathing. This chemoreceptor interdependence also provides a significant portion of the normal drive to breathe in normoxia (i.e. eupnea) and in acute hypoxia. Finally, we discuss the effects of preventing transient hypocapnia (via selective increases in FICO(2)) on centrally mediated types of periodic breathing and even some varieties of cyclical obstructive sleep apnea.

The heterogeneity of obstructive sleep apnea (predominant obstructive vs pure obstructive apnea).

STUDY OBJECTIVES: To compare the breathing instability and upper airway collapsibility between patients with pure OSA (i.e. 100% of apneas are obstructive) and patients with predominant OSA (i.e., coexisting obstructive and central apneas). DESIGN: A cross-sectional study with data scored by a fellow being blinded to the subjects' classification. The results were compared between the 2 groups with unpaired student t-test. SETTING AND INTERVENTIONS: Standard polysomnography technique was used to document sleep-wake state. Ventilator in pressure support mode was used to introduce hypocapnic apnea during CO(2) reserve measurement. CPAP with both positive and negative pressures was used to produce obstructive apnea during upper airway collapsibility measurement. PARTICIPANTS: 21 patients with OSA: 12 with coexisting central/mixed apneas and hypopneas (28% ± 6% of total), and 9 had pure OSA. MEASUREMENTS: The upper airway collapsibility was measured by assessing the critical closing pressure (Pcrit). Breathing stability was assessed by measuring CO(2) reserve (i.e., ΔPCO(2) [eupnea-apnea threshold]) during NREM sleep. RESULTS: There was no difference in Pcrit between the 2 groups (pure OSA vs. predominant OSA: 2.0 ± 0.4 vs. 2.7 ± 0.4 cm H(2)O, P = 0.27); but the CO(2) reserve was significantly smaller in predominant OSA group (1.6 ± 0.7 mm Hg) than the pure OSA group (3.8 ± 0.6 mm Hg) (P = 0.02). CONCLUSIONS: The present data indicate that breathing stability rather than upper airway collapsibility distinguishes OSA patients with a combination of obstructive and central events from those with pure OSA.

Association of obstructive sleep apnea risk with asthma control in adults.

BACKGROUND: Unrecognized obstructive sleep apnea (OSA) may lead to poor asthma control despite optimal therapy. Our objective was to evaluate the relationship between OSA risk and asthma control in adults. METHODS: Patients with asthma seen routinely at tertiary-care clinic visits completed the validated Sleep Apnea Scale of the Sleep Disorders Questionnaire (SA-SDQ) and Asthma Control Questionnaire (ACQ). An ACQ score of >or= 1.5 defined not-well-controlled asthma, and an SA-SDQ score of >or= 36 for men and >or= 32 for women defined high OSA risk. Logistic regression was used to model associations of high OSA risk with not-well-controlled asthma (ACQ full version and short versions). RESULTS: Among 472 subjects with asthma, the mean +/- SD ACQ (full version) score was 0.87 +/- 0.90, and 80 (17%) subjects were not well controlled. Mean SA-SDQ score was 27 +/- 7, and 109 (23%) subjects met the definition of high OSA risk. High OSA risk was associated, on average, with 2.87-times higher odds for not-well-controlled asthma (ACQ full version) (95% CI, 1.54-5.32; P = .0009) after adjusting for obesity and other factors known to worsen asthma control. Similar independent associations were seen when using the short ACQ versions. CONCLUSIONS: High OSA risk is significantly associated with not-well-controlled asthma independent of known asthma aggravators and regardless of the ACQ version used. Patients who have difficulty achieving adequate asthma control should be screened for OSA.

Influence of cerebral blood flow on breathing stability.

Our previous work showed a diminished cerebral blood flow (CBF) response to changes in Pa(CO(2)) in congestive heart failure patients with central sleep apnea compared with those without apnea. Since the regulation of CBF serves to minimize oscillations in H(+) and Pco(2) at the site of the central chemoreceptors, it may play an important role in maintaining breathing stability. We hypothesized that an attenuated cerebrovascular reactivity to changes in Pa(CO(2)) would narrow the difference between the eupneic Pa(CO(2)) and the apneic threshold Pa(CO(2)) (DeltaPa(CO(2))), known as the CO(2) reserve, thereby making the subjects more susceptible to apnea. Accordingly, in seven normal subjects, we used indomethacin (Indo; 100 mg by mouth) sufficient to reduce the CBF response to CO(2) by approximately 25% below control. The CO(2) reserve was estimated during non-rapid eye movement (NREM) sleep. The apnea threshold was determined, both with and without Indo, in NREM sleep, in a random order using a ventilator in pressure support mode to gradually reduce Pa(CO(2)) until apnea occurred. results: Indo significantly reduced the CO(2) reserve required to produce apnea from 6.3 +/- 0.5 to 4.4 +/- 0.7 mmHg (P = 0.01) and increased the slope of the ventilation decrease in response to hypocapnic inhibition below eupnea (control vs. Indo: 1.06 +/- 0.10 vs. 1.61 +/- 0.27 l x min(-1) x mmHg(-1), P < 0.05). We conclude that reductions in the normal cerebral vascular response to hypocapnia will increase the susceptibility to apneas and breathing instability during sleep.

Cerebrovascular response to arousal from NREM and REM sleep.

STUDY OBJECTIVE: To determine the effect of arousal from sleep on cerebral blood flow velocity (CBFV) in relation to associated ventilatory and systemic hemodynamic changes. PARTICIPANTS: Eleven healthy individuals (6 men, 5 women). MEASUREMENTS: Pulsed Doppler ultrasonography was used to measure CBFV in the middle cerebral artery with simultaneous measurements of sleep state (EEG, EOG, and EMG), ventilation (inductance plethysmography), heart rate (ECG), and arterial pressure (finger plethysmography). Arousals were induced by auditory tones (range: 40-80 dB; duration: 0.5 sec). Cardiovascular responses were examined beat-by-beat for 30 sec before and 30 sec after auditory tones. RESULTS: During NREM sleep, CBFV declined following arousals (-15% +/- 2%; group mean +/- SEM) with a nadir at 9 sec after the auditory tone, followed by a gradual return to baseline. Mean arterial pressure (MAP; +20% +/- 1%) and heart rate (HR; +17% +/- 2%) increased with peaks at 5 and 3 sec after the auditory tone, respectively. Minute ventilation (VE) was increased (+35% +/- 10%) for 2 breaths after the auditory tone. In contrast, during REM sleep, CBFV increased following arousals (+15% +/- 3%) with a peak at 3 sec. MAP (+17% +/- 2%) and HR (+15% +/- 2%) increased during arousals from REM sleep with peaks at 5 and 3 sec post tone. VE increased (+16% +/- 7%) in a smaller, more sustained manner during arousals from REM sleep. CONCLUSIONS: Arousals from NREM sleep transiently reduce CBFV, whereas arousals from REM sleep transiently increase CBFV, despite qualitatively and quantitatively similar increases in MAP, HR, and VE in the two sleep states.

Influence of cerebrovascular function on the hypercapnic ventilatory response in healthy humans.

An important determinant of [H(+)] in the environment of the central chemoreceptors is cerebral blood flow. Accordingly we hypothesized that a reduction of brain perfusion or a reduced cerebrovascular reactivity to CO(2) would lead to hyperventilation and an increased ventilatory responsiveness to CO(2). We used oral indomethacin to reduce the cerebrovascular reactivity to CO(2) and tested the steady-state hypercapnic ventilatory response to CO(2) in nine normal awake human subjects under normoxia and hyperoxia (50% O(2)). Ninety minutes after indomethacin ingestion, cerebral blood flow velocity (CBFV) in the middle cerebral artery decreased to 77 +/- 5% of the initial value and the average slope of CBFV response to hypercapnia was reduced to 31% of control in normoxia (1.92 versus 0.59 cm(-1) s(-1) mmHg(-1), P < 0.05) and 37% of control in hyperoxia (1.58 versus 0.59 cm(-1) s(-1) mmHg(-1), P < 0.05). Concomitantly, indomethacin administration also caused 40-60% increases in the slope of the mean ventilatory response to CO(2) in both normoxia (1.27 +/- 0.31 versus 1.76 +/- 0.37 l min(-1) mmHg(-1), P < 0.05) and hyperoxia (1.08 +/- 0.22 versus 1.79 +/- 0.37 l min(-1) mmHg(-1), P < 0.05). These correlative findings are consistent with the conclusion that cerebrovascular responsiveness to CO(2) is an important determinant of eupnoeic ventilation and of hypercapnic ventilatory responsiveness in humans, primarily via its effects at the level of the central chemoreceptors.

Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep.

To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired P(O2). We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78-80%), and hyperoxia (inspired O2 fraction = 50-52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sigh-like breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 +/- 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 +/- 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 +/- 13.8 s; P < 0.01). The apneic threshold end-tidal P(CO2) (Pet(CO2)) was defined as the Pet(CO2)) at the onset of apnea. During hypoxia, the apneic threshold Pet(CO2) was higher (38.9 +/- 1.7 Torr; P < 0.01) compared with normoxia (35.8 +/- 1.1; Torr); during hyperoxia, it was lower (33.0 +/- 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic Pet(CO2) and apneic threshold Pet(CO2) was smaller during hypoxia (3.0 +/- 1.0 Torr P < 001) and greater during hyperoxia (10.6 +/- 0.8 Torr; P < 0.05) compared with normoxia (8.0 +/- 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic Pet(CO2) was increased by hypoxia (3.44 +/- 0.63 l.min(-1).Torr(-1); P < 0.05) and decreased by hyperoxia (0.63 +/- 0.04 l.min(-1).Torr(-1); P < 0.05) compared with normoxia (0.79 +/- 0.05 l.min(-1).Torr(-1)). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.

Cerebrovascular response to carbon dioxide in patients with congestive heart failure.

RATIONALE: Cerebrovascular reactivity to CO(2) provides an important counterregulatory mechanism that serves to minimize the change in H(+) at the central chemoreceptor, thereby stabilizing the breathing pattern in the face of perturbations in Pa(CO(2)). However, there are no studies relating cerebral circulation abnormality to the presence or absence of central sleep apnea in patients with heart failure. OBJECTIVES: To determine whether patients with congestive heart failure and central sleep apnea have an attenuated cerebrovascular responsibility to CO(2). METHODS: Cerebral blood flow velocity in the middle cerebral artery was measured in patients with stable congestive heart failure with (n = 9) and without (n = 8) central sleep apnea using transcranial ultrasound during eucapnia (room air), hypercapnia (inspired CO(2), 3 and 5%), and hypocapnia (voluntary hyperventilation). In addition, eight subjects with apnea and nine without apnea performed a 20-second breath-hold to investigate the dynamic cerebrovascular response to apnea. MEASUREMENTS AND MAIN RESULTS: The overall cerebrovascular reactivity to CO(2) (hyper- and hypocapnia) was lower in patients with apnea than in the control group (1.8 +/- 0.2 vs. 2.5 +/- 0.2%/mm Hg, p < 0.05), mainly due to the prominent reduction of cerebrovascular reactivity to hypocapnia (1.2 +/- 0.3 vs. 2.2 +/- 0.1%/mm Hg, p < 0.05). Similarly, brain blood flow demonstrated a smaller surge after a 20-second breath-hold (peak velocity, 119 +/- 4 vs. 141 +/- 8% of baseline, p < 0.05). CONCLUSION: Patients with central sleep apnea have a diminished cerebrovascular response to PET(CO(2)), especially to hypocapnia. The compromised cerebrovascular reactivity to CO(2) might affect stability of the breathing pattern by causing ventilatory overshooting during hypercapnia and undershooting during hypocapnia.

The ventilatory responsiveness to CO(2) below eupnoea as a determinant of ventilatory stability in sleep.

Sleep unmasks a highly sensitive hypocapnia-induced apnoeic threshold, whereby apnoea is initiated by small transient reductions in arterial CO(2) pressure (P(aCO(2))) below eupnoea and respiratory rhythm is not restored until P(aCO(2)) has risen significantly above eupnoeic levels. We propose that the 'CO(2) reserve' (i.e. the difference in P(aCO(2)) between eupnoea and the apnoeic threshold (AT)), when combined with 'plant gain' (or the ventilatory increase required for a given reduction in P(aCO(2))) and 'controller gain' (ventilatory responsiveness to CO(2) above eupnoea) are the key determinants of breathing instability in sleep. The CO(2) reserve varies inversely with both plant gain and the slope of the ventilatory response to reduced CO(2) below eupnoea; it is highly labile in non-random eye movement (NREM) sleep. With many types of increases or decreases in background ventilatory drive and P(aCO(2)), the slope of the ventilatory response to reduced P(aCO(2)) below eupnoea remains unchanged from control. Thus, the CO(2) reserve varies inversely with plant gain, i.e. it is widened with hyperventilation and narrowed with hypoventilation, regardless of the stimulus and whether it acts primarily at the peripheral or central chemoreceptors. However, there are notable exceptions, such as hypoxia, heart failure, or increased pulmonary vascular pressures, which all increase the slope of the CO(2) response below eupnoea and narrow the CO(2) reserve despite an accompanying hyperventilation and reduced plant gain. Finally, we review growing evidence that chemoreceptor-induced instability in respiratory motor output during sleep contributes significantly to the major clinical problem of cyclical obstructive sleep apnoea.

Cardiorespiratory effects of added dead space in patients with heart failure and central sleep apnea.

BACKGROUND: Inhaled CO(2) has been shown to stabilize the breathing pattern of patients with central sleep apnea (CSA) with and without congestive heart failure (CHF). Added dead space (DS) as a form of supplemental CO(2) was effective in eliminating idiopathic CSA. The efficacy and safety of DS has not yet been evaluated in patients with CHF and CSA. METHODS: We examined the respiratory and cardiovascular effects of added DS in eight patients with CHF and CSA. The DS consisted of a facemask attached to a cylinder of adjustable volume. During wakefulness, the cardiorespiratory response to 200 to 600 mL of DS was tested. Cardiac output and stroke volume were measured using echocardiography with and without DS. During the nocturnal study, patients slept with and without DS, alternating at approximately 1-h intervals. RESULTS: Values are expressed as the mean +/- SE. The wakefulness study revealed a plateau in the partial pressure of end-tidal CO(2) (PETCO(2)) and the partial pressure of end-tidal O(2) between DS amounts of 400 and 600 mL. The mean stroke volume index (33 +/- 7 vs 34 +/- 7 mL/m(2), respectively) and the mean cardiac index (1.9 +/- 0.3 vs 1.9 +/- 0.4 L/min/m(2), respectively) were not affected by DS. Neither heart rate nor BP showed a significant change in response to DS of < or = 600 mL. During sleep, DS increased the PETCO(2) (40.7 +/- 2.7 vs 38.9 +/- 2.6 mm Hg, respectively; p < 0.05), reduced apnea (1 +/- 1 vs 29 +/- 7 episodes per hour, respectively; p < 0.01) and arousal (21 +/- 8 vs 30 +/- 8 arousals per hour, respectively; p < 0.05), increased the mean arterial oxygen saturation (SaO(2)) [94.4 +/- 1.0% vs 93.5 +/- 1.1%, respectively; p < 0.01), and reduced SaO(2) oscillations (DeltaSaO(2) from maximum to minimum, 1.8 +/- 0.4% vs 5.5 +/- 0.9%, respectively; p < 0.01). CONCLUSION: DS stabilized CSA and improved sleep quality in patients with CHF without significant acute adverse effects on the cardiovascular function.

Apnea-hypopnea threshold for CO2 in patients with congestive heart failure.

To understand the pathogenesis of central sleep apnea (CSA) in patients with congestive heart failure (CHF), we measured the end-tidal carbon dioxide pressure (PET(CO2)) during spontaneous breathing, the apnea-hypopnea threshold for CO2, and then calculated the difference between these two measurements in 19 stable patients with CHF with (12 patients) or without (7 patients) CSA during non-rapid eye movement sleep. Pressure support ventilation was used to reduce the PET(CO2) and thereby determine the thresholds. In patients with CSA, 1.5-3% CO2 was supplied temporarily to stabilize breathing before determining the thresholds. Unlike patients without CSA whose eupneic PET(CO2) increased during sleep (37.7 +/- 1.4 mm Hg versus 40.2 +/- 1.5 mm Hg, p < 0.01), patients with CSA showed no rise in PET(CO2) from wakefulness to sleep (37.5 +/- 0.9 mm Hg versus 38.2 +/- 1.0 mm Hg, p = 0.2). Patients with CHF and CSA had their eupneic PET(CO2) closer to the threshold PET(CO2) than patients without CSA (DeltaPET(CO2) [eupneic PET(CO2) - threshold PET(CO2)] was 2.8 +/- 0.3 mm Hg versus 5.1 +/- 0.7 mm Hg for apnea, p < 0.01; 1.7 +/- 0.7 versus 4.1 +/- 0.5 mm Hg for hypopnea, p < 0.05). In summary, patients with CHF and CSA neither increase their eupneic PET(CO2) during sleep nor proportionally decrease their apnea-hypopnea threshold. The resultant narrowed DeltaPET(CO2) predisposes the patient to the development of apnea and subsequent breathing instability.