Impact of the COVID-19 pandemic on children's sleep habits: an ECHO study.

BACKGROUND: Sleep in childhood is affected by behavioral, environmental, and parental factors. We propose that these factors were altered during the COVID-19 pandemic. This study investigates sleep habit changes during the pandemic in 528 children 4-12 years old in the US, leveraging data from the Environmental Influences on Child Health Outcomes (ECHO) Program. METHODS: Data collection occurred in July 2019-March 2020 (pre-pandemic) and two pandemic periods: December 2020-April 2021 and May-August 2021. Qualitative interviews were performed in 38 participants. RESULTS: We found no changes in sleep duration, but a shift to later sleep midpoint during the pandemic periods. There was an increase in latency at the first pandemic collection period but no increase in the frequency of bedtime resistance, and a reduced frequency of naps during the pandemic. Qualitative interviews revealed that parents prioritized routines to maintain sleep duration but were more flexible regarding timing. Children from racial/ethnic minoritized communities slept less at night, had later sleep midpoint, and napped more frequently across all collection periods, warranting in-depth investigation to examine and address root causes. CONCLUSIONS: The COVID-19 pandemic significantly impacted children sleep, but parental knowledge of the importance of sleep might have played a significant protective role. IMPACT: During the COVID-19 pandemic, US children changed their sleep habits, going to bed and waking up later, but their sleep duration did not change. Sleep latency was longer. Parental knowledge of sleep importance might have played a protective role. Regardless of data collection periods, children from racial/ethnic minoritized communities slept less and went to bed later. This is one of the first study on this topic in the US, including prospective pre-pandemic qualitative and quantitative data on sleep habits. Our findings highlight the pandemic long-term impact on childhood sleep. Results warrants further investigations on implications for overall childhood health.

Racial/ethnic disparities in subjective sleep duration, sleep quality, and sleep disturbances during pregnancy: an ECHO study.

In the United States, racial/ethnic minoritized groups experience worse sleep than non-Hispanic Whites (nHW), but less is known about pregnant people. This is a key consideration since poor sleep during pregnancy is common and associated with increased risk of adverse perinatal outcomes. This study reports the prevalence of subjective sleep measures in a multi-racial/ethnic pregnant population from the Environmental influences on Child Health Outcomes (ECHO) program. Participants' self-reported race and ethnicity were grouped into: nHW, non-Hispanic Black/African American (nHB/AA), Hispanic, non-Hispanic Asian (nHA). Analyses examined trimester-specific (first (T1), second (T2), third (T3)) nocturnal sleep duration, quality, and disturbances (Pittsburgh Sleep Quality Index and ECHO maternal sleep health questionnaire). Linear or multinomial regressions estimated the associations between race/ethnicity and each sleep domain by trimester, controlling for body mass index and age, with nHW as reference group. We repeated analyses within maternal education strata. nHB/AA participants reported shorter sleep duration (T2: ß = -0.55 [-0.80,-0.31]; T3: ß = -0.65 [-0.99,-0.31]) and more sleep disturbances (T2: ß = 1.92 [1.09,2.75]; T3: ß = 1.41 [0.09,2.74]). Hispanic participants reported longer sleep duration (T1: ß = 0.22 [0.00004,0.44]; T2: ß = 0.61 [0.47,0.76]; T3: ß = 0.46 [0.22,0.70]), better sleep quality (Reference group: Very good. Fairly good T1: OR = 0.48 [0.32,0.73], T2: OR = 0.36 [0.26,0.48], T3: OR = 0.31 [0.18,0.52]. Fairly bad T1: OR = 0.27 [0.16,0.44], T2: OR = 0.46 [0.31, 0.67], T3: OR = 0.31 [0.17,0.55]), and fewer sleep disturbances (T2: ß = -0.5 [-1.0,-0.12]; T3: ß = -1.21 [-2.07,-0.35]). Differences persisted within the high-SES subsample. Given the stark racial/ethnic disparities in perinatal outcomes and their associations with sleep health, further research is warranted to investigate the determinants of these disparities.

Pediatric Obstructive Sleep Apnea: Update for the Primary Care Provider.

Pediatric obstructive sleep apnea (OSA) is a common entity that can cause both daytime and nighttime issues. Children with symptoms should be screened for OSA. If possible, polysomnography should be performed to evaluate symptomatic children. Depending on the severity, first-line options for treatment of pediatric OSA may include observation, weight loss, medication, or surgery. Even after adenotonsillectomy, about 20% of children will have persistent OSA. Sleep endoscopy and cine MRI are tools that may be used to identify sites of obstruction, which in turn can help in the selection of site-specific treatment.

The effect of ventilation on spectral analysis of heart rate and blood pressure variability during exercise.

Heart rate variability (HRV) and systolic blood pressure variability (BPV) during incremental exercise at 50, 75, and 100% of previously determined ventilatory threshold (VT) were compared to that of resting controlled breathing (CB) in 12 healthy subjects. CB was matched with exercise-associated respiratory rate, tidal volume, and end-tidal CO(2) for all stages of exercise. Power in the low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, >0.15-0.4 Hz) for HRV and BPV were calculated, using time-frequency domain analysis, from beat-to-beat ECG and non-invasive radial artery blood pressure, respectively. During CB absolute and normalized power in the LF and HF of HRV and BPV were not significantly changed from baseline to maximal breathing. Conversely, during exercise HRV, LF and HF power significantly decreased from baseline to 100% VT while BPV, LF and HF power significantly increased for the same period. These findings suggest that the increases in ventilation associated with incremental exercise do not significantly affect spectral analysis of cardiovascular autonomic modulation in healthy subjects.

Supplemental oxygen increases arterial stiffness in chronic obstructive pulmonary disease.

STUDY OBJECTIVES: Recently, we demonstrated significantly improved baroreflex sensitivity (BRS) and autonomic balance after 31% supplemental oxygen (SuppO2) in resting patients with chronic obstructive pulmonary disease (COPD). In order to investigate whether peripheral arterial stiffness changes may play a role, we evaluated changes in peripheral arterial stiffness and BRS after SuppO2. DESIGN: Single blinded crossover design. SETTING: Pulmonary exercise testing laboratory. PARTICIPANTS: Seventy subjects with moderate to severe COPD. INTERVENTIONS: We measured arterial vascular stiffness using the augmentation index via contour analysis of the radial pulse obtained from applanation tonometry. BRS was derived using the sequence method before and after treatments with compressed air (CA) and 30% SuppO2 in 70 individuals with COPD via a counterbalanced crossover design. RESULTS: Paired t-tests indicated significant differences in oxygen saturation (SaO2) following SuppO2 when compared to CA (mean 96.0+/-2.0% SuppO2 versus mean 92.6+/-3.6% CA, P<0.001). BRS was significantly greater following SuppO2 compared to CA (mean 3.5+/-2.3 ms/mmHg SuppO2 versus mean 3.1+/-2.1 CA ms/mmHg, P<0.03). Vascular stiffness was significantly increased with SuppO2 when compared with CA (mean 13.3+/-6.1% SuppO2 versus mean 10.8+/-4.9% CA, P<0.001). CONCLUSIONS: Our findings indicate that oxygen supplementation ameliorates BRS by changes in vasomotor activity. The amelioration of the BRS into a more normal range is a move towards the restoration of more normal physiology.

Lower airway obstruction, bronchial hyperresponsiveness, and primary pulmonary hypertension in children.

We investigated the prevalence and reversibility of lower airway obstruction (LAO) and its correlation with pulmonary artery pressure in children with primary pulmonary hypertension (PPH). The analysis was performed retrospectively in a cohort of children with PPH between 5-18 years of age. PPH was defined as mean pulmonary artery pressure (PAPm) >25 mmHg at rest, or >30 mmHg during exercise, with normal pulmonary capillary wedge pressure in the absence of other causes. Lower airway function was assessed by spirometry and maximal expiratory flow-volume curves. Lung volumes were measured by body plethysmography. Patients were assigned according to their pattern of lung function into "normal," "obstructive," and "restrictive" groups. The reversibility of LAO was defined as an increase of > or = 15% from baseline in forced expiratory volume at 1 sec (FEV1) and/or > or =20% in forced expiratory flow at 25-75% of forced vital capacity (FEF25-75%) in response to nebulized albuterol. An "obstructive" pattern was found in 23 children (59%), a "restrictive" pattern in 2 children (5%), and a "normal" pattern in 14 children (36%). Response to bronchodilator was documented in 78% of children with an "obstructive" pattern and in 22% of those with a "normal" pattern. The PAPm showed a significant positive correlation with the TLC, RV, and RV/TLC, but a negative one with the ratio FEV1/FVC. Our findings suggest that reversible LAO is the most common lung function abnormality among pediatric patients with PPH. Whether airway reactivity is a cause of or the result of PPH remains to be determined.

High-frequency modulation of heart rate variability during exercise in patients with COPD.

STUDY OBJECTIVES: To evaluate cardiac autonomic modulation in patients with COPD during peak exercise. METHODS: Fifty-three patients with COPD (mean FEV(1), 35% predicted [SD, 11% predicted]; mean PaO(2), 68 mm Hg [SD, 11 mm Hg]; mean PaCO(2), 40 mm Hg [SD, 7 mm Hg]; mean age, 61 years [SD, 10 years]; 26 women and 27 men) and 14 healthy control subjects aged 60 years (SD, 8 years) [seven women and seven men] were studied at rest and during ramped bicycle ergometry to their volitional peak. Patients were not receiving autonomic medications other than inhaled beta-agonist agents and/or anticholinergic agents. Control subjects were not receiving any medications. Cardiac autonomic modulation was assessed via time-frequency analysis (Wigner-Ville) of ECG-derived heart rate variability as the power in the low-frequency (LF) band (ie, 0.04 to 0.15 Hz) and the high-frequency (HF) band (ie, > 0.15 to 0.4 Hz) averaged from > 3 min at rest and minutes 2 through 5 of their exercise period. RESULTS: Patients with COPD had a significantly increased mean, ln-transformed HF band from rest to peak exercise (9.9 ms(2) [SD, 1.4 ms(2)] vs 10.7 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01), while the HF band was unchanged for the control group (10.7 ms(2) [SD, 1.5 ms(2)] vs 10.4 ms(2) [1.3 ms(2)], respectively; difference not significant). The mean ln-transformed LF band was significantly increased from rest to peak exercise in patients with COPD (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.4 ms(2)], respectively; p < 0.01) and in control subjects (10.9 ms(2) [SD, 1.5 ms(2)] vs 11.5 ms(2) [SD, 1.3 ms(2)], respectively; p < 0.01). The mean LF/HF ratio was significantly decreased from rest to peak exercise in patients with COPD (3.1 [SD, 1.5] vs 2.5 [SD, 1.0], respectively; p < 0.01) and was increased in control subjects (1.9 [SD, 0.8] vs 2.4 [1.0], respectively; p < 0.01). When expressed in normalized units ([absolute power of the components]/[total power - very low frequency power] x 100), the HF band was again significantly greater during peak exercise than at rest in the patients with COPD and was unchanged during peak exercise for the control group. Autonomic changes were not significantly correlated with age, gender, body mass index, spirometry, lung volumes, resting gas exchange, or oxygen saturation during exercise. CONCLUSION: These data suggest that, in contrast to control subjects, the balance of sympathetic to parasympathetic cardiac modulation decreases in patients with COPD during maximal volitional exercise.

Arterial stiffness increases during obstructive sleep apneas.

STUDY OBJECTIVES: Obstructive sleep apnea (OSA) appears to be an independent risk factor for diurnal systemic hypertension, but the specific biologic markers for this association have not been well established. Increased arterial stiffness is an important measure of increased left ventricular load and a predictor of cardiovascular morbidity and may precede the onset of systemic hypertension in humans. However, arterial stiffness has not been measured in association with obstructive apneas in patients with OSA, nor related to systemic blood pressure (BP) activity in this setting. Our objective was to test the hypothesis that arterial stiffness may be utilized as a sensitive measure of arterial vasomotor perturbation during obstructive events in patients with OSA, by demonstrating that (1) arterial stiffness increases acutely in association with obstructive apnea and hypopnea, and that (2) such increased stiffness may occur in the absence of acute BP increase. DESIGN: Prospective, cross-sectional. SETTING: A tertiary-care university-based sleep and ventilatory disorders center. PATIENTS: Forty-four normo- and hypertensive adult patients (11 women, 33 men) with polysomnographically diagnosed moderate to severe OSA. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Beat-to-beat BP was recorded from the radial artery by applanation tonometry during nocturnal polysomnography. Arterial augmentation index (AAI), a measure of arterial stiffness, was calculated as the ratio of augmented systolic BP (SBP) to pulse pressure and expressed as a percentage for the following conditions: awake, the first 10 ("early apnea") and last 10 ("late apnea") cardiac cycles of obstructive events, and the first 15 cardiac cycles following apnea termination ("post apnea"). Mean AAI (+/-SD) for the group was significantly increased during NREM sleep from early apnea to late apnea (12.02 +/- 2.70% vs 13.35 +/- 3.54%, p<0.05, ANOVA). During REM (analyzed in 20 patients), MI again significantly increased from early apnea to late apnea (11.75 +/- 2.81% vs 13.43 +/- 4.97%). Conversely, neither mean SBP nor mean arterial BP was significantly changed from early apnea to late apnea in NREM (SBP 130 +/- 14 mmHg vs 129 +/- 14 mmHg) or REM (SBP 128 +/- 22 mmHg vs 127 +/- 21 mmHg). CONCLUSIONS: Arterial stiffness increases acutely during obstructive apneas in both NREM and REM sleep, in the absence of measurable BP change. These data suggest that arterial stiffness may be a sensitive measure of acute arterial vasomotor perturbation in this setting and may have implications concerning cardiovascular sequelae in patients with OSA.