Wang Sleep Med 2011 (original) (raw)
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Slow wave sleep in patients with respiratory failure
Sleep medicine, 2011
Slow wave sleep (SWS) has been theorized as reflecting a homeostatic sleep process and is considered a state of recuperation. SWS is reduced in obstructive sleep apnea (OSA) patients, but SWS has not been specifically studied in respiratory failure patients. The aim of this study is to investigate SWS in predominantly hypercapnic respiratory failure patients. We analyzed sleep and arterial blood gas records of all 97 respiratory failure patients who underwent polysomnography and bilevel non-invasive ventilation (NIV) treatment in our laboratory from 2008 to July 2009. We also analyzed 32 initial diagnostic study data from these 97 patients. The 97 patients had an average age of 58±15 (SD) years. Total sleep time was 320.3±82.8 (SD) min of which 32.9%±15.4 (%) was spent in SWS. This high percentage SWS correlated positively with awake arterial CO(2) pressure (PCO(2)) in both the 97 treatment studies (r=0.35, p=0.001) and the 32 initial diagnostic studies (r=0.40, p=0.025). The relati...
Characteristics and Consequences of Non-apneic Respiratory Events During Sleep
Rationale: Current scoring criteria of non-apneic events (ie, hypopnea) require the presence of oxyhemoglobin desaturation and/or arousal. However, other sleep study parameters may help to identify abnormal respiratory events (REs) and assist in making more accurate diagnosis. Objectives: To investigate whether non-apneic REs without desaturation or cortical arousal are associated with respiratory and cardiac consequences. Methods: Thirteen participants with sleep disturbances (snoring and/or excessive day time sleepiness), were screened using attended in laboratory pol-ysomnography (PSG) while monitoring pressure and airflow via a nasal mask with an attached pneumotach. To separate the contribution of the upper airway resistance (R UA) and total pulmonary resistance (R L), supraglottic and esophageal pressures were measured using Millar pressure catheters. R L and R UA were calculated during baseline and hypopneas. R L was defined as the resistive pressure divided by the maximal flow during inspiration and expiration. Hypopnea was defined 30% decrease in flow with 3% desaturation and/or cortical arousal. REs was defined as 30% decrease in the flow without desaturation and/or cortical arousal. In eight subjects continuous positive airway pressure (CPAP) was titrated to optimal pressure. R-R interval (RRI) was defined as consecutive beat-to-beat intervals on single lead electrocardiograph (ECG) during baseline, RE/hypopnea and on optimal CPAP. Results: REs associated with increased expiratory R UA (14.6 ± 11.3 vs. 7.5 ± 4.5 cmH 2 O L −1 s −1 ; p < .05), and increased expiratory R L relative to baseline (29.2 ± 14.6 vs. 20.9 ± 11.0 and 23.7 ± 12.1 vs. 14.3 ± 5.6 cmH 2 O L −1 s −1 during inspiration and expiration, respectively; p < .05). RRI decreased significantly following RE and hypopnea relative to baseline (804.8 ± 33.1 vs. 806.4 ± 36.3 vs. 934.3 ± 45.8 ms; p < .05). Optimal CPAP decreased expiratory R UA (4.0 ± 2.5 vs. 7.5 ± 4.5 cmH 2 O L −1 s −1 ; p < .05), decreased inspiratory R L (12.6 ± 14.1 vs. 7.5 ± 4.5 cmH 2 O L −1 s −1 ; p < .05), and allowed RRI to return to baseline (p < .05). RRI dips index was an independent predictor of sleep-disordered breathing (SDB) when non-apneic REs were accounted for in symptomatic patients (p < .05). Conclusions: Non-apneic REs without cortical arousal or desaturation are associated with significant respiratory and heart rate changes. Optimal CPAP and the reduction of resistive load are associated with the normalization of heart rate indicating potential clinical benefit.
Critical Care Medicine, 2010
oninvasive ventilation (NIV) is the treatment of choice for hypercapnic exacerbations in patients with chronic respiratory failure. Nevertheless, the failure rate remains relatively high, with 5% to 40% of patients requiring endotracheal intubation (1-3). Most NIV failures occur within 24 hrs to 48 hrs after admission to the intensive care unit (ICU) (1). Several studies have evaluated early NIV failure and a number of predictors of early NIV failure have been identified: a very low pH, marked mental status alterations at NIV initiation, and a high severity score (4). However, approximately 15% to 25% of patients experience late NIV failure (after Ն48 hrs), in some cases despite an initial improvement (5, 6). Despite the poor prognosis for these patients (5, 6), few studies have investigated the poorly understood causes of late NIV failure. Chronic comorbidities (5) and a greater number of complications at hospital admission (6) may predict late NIV failure but lack specificity. Patients receiving endotracheal mechanical ventilation exhibit severe sleep disturbances, even after sedation is withdrawn during weaning (7, 8). Although the consequences of sleep disturbances in ICU patients are unknown, studies in ambulatory patients have shown multiple cardiovascular, respiratory, metabolic, and cognitive alterations (9). Sleep disturbance may promote delirium, an independent risk factor for death in ICU patients receiving mechanical ventilation (10). Additionally, poor sleep quality has been reported during NIV (11). The main objective of our study was to determine whether sleep disturbances that occur shortly after initiation of NIV in the ICU were associated with late NIV failure in patients with hypercapnic respiratory failure requiring Ͼ48 hrs of NIV. MATERIALS AND METHODS The study was approved by the Ethics Committee of the Société de Réanimation de Langue Française. All patients gave their informed consent. Patients Consecutive patients admitted to our medical ICU between November 2006 and August 2007 and requiring NIV were screened for eligibility. All patients with hypercapnic acuteon-chronic respiratory failure treated by NIV for Ͼ24 hrs were eligible. Hypercapnic respiratory failure was defined as a respiratory rate Ͼ22 breath/min, pH Ͻ7.35, and PaCO 2 Ͼ45 torr (Ͼ6 kPa). We focused on patients with chronic obstructive pulmonary disease and on elderly patients with cardiogenic pulmonary edema. In this last group, we included only patients aged Ͼ65 yrs, assuming that most *See also p. 705.
Obesity Hypoventilation Syndrome as a Spectrum of Respiratory Disturbances During Sleep
Chest, 2001
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).
Predictor factors of sleep-disordered breathing in heart failure
Egyptian Journal of Bronchology, 2017
Background Heart failure (HF) is characterized by its high mortality, frequent hospitalizations, and reduced quality of life. Sleep-disordered breathing (SDB), one of the common comorbidities, accelerates the progression of HF. Objectives The objectives of the study were (a) to investigate the prevalence and type of SDB in HF patients and (b) to determine the predictors of SDB. Materials and methods In a cross-sectional analytic study, all eligible patients of Assiut Chest and Cardiology Department admitted (100 patients) during the period from August 2015 to March 2016 were included in this study. Clinical assessment, full-night attended polysomnography, and echocardiography were recorded and compared between patients with (SDB) (85 patients) and those without SDB (15 patients). Results SDB was found in 85% of patients [53% had obstructive sleep apnea (OSA) and 32% had central sleep apnea (CSA)]. OSA patients are characterized by higher BMI and neck and waist circumference. There was a higher prevalence of hypertension, as well as mean blood pressure, systolic blood pressure, diastolic blood pressure, in OSA patients. Loud snoring was the only clinical symptom associated with OSA as compared with CSA. CSA patients had a significant reduction in PaCO 2. OSA patients showed a significant increase in desaturation index and time spent with oxygen saturation less than 90%. Maximum heart rate and brady/tachy index were significantly increased in OSA. Cycle length was significantly increased in CSA. Conclusion The prevalence of sleep apnea was high in patients with stable HF (85%). OSA was the predominant type (53%). The predictors of SDB were BMI (≥30), systemic hypertension, neck circumference more than 40 cm, waist circumference more than 110 cm, and ejection fraction (left ventricular ejection fraction) (≤45%).
Sleep and Breathing, 2012
Introduction Obstructive sleep apnea (OSA) is influenced by sleep architecture with rapid eye movement (REM) sleep having the most adverse influence, especially in women. There is little data defining the influence of slow-wave sleep (SWS) on OSA. We wished to study the influence of SWS on OSA and identify differences attributable to gender and/ or age, if any. Methods Retrospective study of polysomnography (PSG) records of adult patients referred for diagnostic PSG. Records were excluded if they underwent split night or positive airway pressure titration studies, had <180 min of total sleep time (TST) and/or <40% sleep efficiency, or had SWS <5 min and/or <1% of TST. The apnea-hypopnea index (AHI) recorded during SWS was compared with that measured during other non-rapid eye movement (NREM) sleep and during REM sleep. The REM-SWS difference in AHI was measured, and compared between genders. Results Records from 239 patients were included. The mean AHI in all subjects was 17.7±22.6. The SWS AHI was 6.8±18.9, compared to the REM AHI of 24.9±25.8, and NREM AHI of 15.8±22.8. Females had significantly higher SWS by percentage, and lower NREM AHI (P<0.0001) and SWS AHI (P00.03). Among patients with OSA (AHI ≥5), the difference between REM AHI and SWS AHI was greater in women than in men (34.2±27.4 vs. 21.6±26.0, P00.006). Conclusions The upper airway appears to be less susceptible to OSA during SWS than during REM and other NREM sleep. This may be related to phase-specific influences on both dynamic upper airway control as well as loop gain. Gender and age appear to modify this effect.
Posthypoxic ventilatory decline during NREM sleep: influence of sleep apnea
Journal of Applied Physiology
We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/ hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O 2 saturation , and end-tidal PCO2. To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 Ϯ 0.5 l/min (83.8 Ϯ 5.7% of room air control) vs. 6.7 Ϯ 0.9 l/min, 69.1 Ϯ 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects (P Ͻ 0.05). Nadir tidal volume was 0.55 Ϯ 0.05 liter (80.0 Ϯ 6.6% of room air control) in OSA patients vs. 0.42 Ϯ 0.03 liter, 86.5 Ϯ 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (TE) occurred in the recovery period. There was a significant difference in TE prolongation between normal subjects (2.61 Ϯ 0.3 s, 120 Ϯ 11.2% of C) and OSA patients (5.6 Ϯ 1.5 s, 292 Ϯ 127.6% of C) (P Ͻ 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of TE; and 2) posthypoxic ventilatory prolongation of TE was more pronounced in patients with sleep apnea relative to normal subjects.