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Objective This systematic review and meta-analysis were conducted to study the prevalence and pattern of sleep disturbances in children and adolescents during the COVID-19 pandemic. Methods MEDLINE, EMBASE, and Web of Science were searched for original studies describing sleep abnormalities in children and adolescents with or without pre-existing neurobehavioral disorders during the COVID-19 pandemic. The pooled estimates for various sleep abnormalities were calculated using a random-effect model. Results Of 371 articles screened, 16 studies were included. Among these, five studies were in preschool children, two were in children with pre-existing neurobehavioral disorders and the remaining were in school going children and adolescents. The outcome measures used for sleep were markedly heterogeneous across the studies. The pooled prevalence of any sleep disturbance in children during the pandemic was 54%(95%CI:50–57%). Interestingly, the prevalence in pre-school children was lower than pre-pandemic times (RR = 0.87; 95% CI:0.58–1.30) but this was not statistically significant. The pooled prevalence of children not meeting sleep recommendation was 49% (95%CI: 39–58%). Conclusion The prevalence of sleep problems in children and adolescents during the COVID-19 pandemic is alarming. Pre-school children had a trend towards relatively fewer sleep disturbances due to home confinement measures in comparison with pre-pandemic times. Sleep duration recommendations were not met in nearly half of healthy children. However, these conclusions need to be seen in light of limited literature on the topic, few included studies done in heterogenous populations, and dubious quality of inferences drawn from these studies which were predominantly online surveys. Prospero registration id CRD42020213788.

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The development of intrapulmonary shunts with increased cardiac output during exercise in healthy humans has been reported in several recent studies, but mechanisms governing their recruitment remain unclear. Dobutamine and dopamine are inotropes commonly used to augment cardiac output; however, both can increase venous admixture/shunt fraction (Qs/Qt). It is possible that, as with exercise, intrapulmonary shunts are recruited with increased cardiac output during dobutamine and/or dopamine infusion that may contribute to the observed increase in Qs/Qt. The purpose of this study was to examine how dobutamine and dopamine affect intrapulmonary shunt and gas exchange. Nine resting healthy subjects received serial infusions of dobutamine and dopamine at incremental doses under normoxic and hyperoxic (inspired O2fraction = 1.0) conditions. At each step, alveolar-to-arterial Po2difference (A-aDo2) and Qs/Qt were calculated from arterial blood gas samples, intrapulmonary shunt was evaluated using contrast echocardiography, and cardiac output was calculated by Doppler echocardiography. Both dobutamine and dopamine increased cardiac output and Qs/Qt. Intrapulmonary shunt developed in most subjects with both drugs and paralleled the increase in Qs/Qt. A-aDo2was unchanged due to a concurrent rise in mixed venous oxygen content. Hyperoxia consistently eliminated intrapulmonary shunt. These findings contribute to our present understanding of the mechanisms governing recruitment of these intrapulmonary shunts as well as their impact on gas exchange. In addition, given the deleterious effect on Qs/Qt and the risk of neurological complications with intrapulmonary shunts, these findings could have important implications for use of dobutamine and dopamine in the clinical setting.

BACKGROUND: Pulmonary rehabilitation (PR) is a recommended intervention in the management of individuals with chronic lung disease. It is important to study the characteristics and capacity of programs in Canada to confirm best practices and identify future areas of program improvement and research.OBJECTIVE: To identify all Canadian PR programs, regardless of setting, and to comprehensively describe all aspects of PR program delivery. The present article reports the results of the survey related to type of program, capacity and program characteristics.METHODS: All hospitals in Canada were contacted to identify PR programs. A representative from each program completed a 175-item online survey encompassing 16 domains, 10 of which are reported in the present article.RESULTS: A total of 155 facilities in Canada offered PR, of which 129 returned surveys (83% response rate). PR programs were located in all provinces, but none in the three territories. Most (60%) programs were located in hospital settings, 24% were in public health units and 8% in recreation centres. The national capacity of programs was estimated to be 10,280 patients per year, resulting in 0.4% of all Canadians with chronic obstructive pulmonary disease (COPD) and 0.8% of Canadians with moderate to severe COPD having access to PR. COPD, interstitial lung disease, and asthma were the most common diagnoses of patients. The majority of programs had at least four health care professionals involved; 9% had only one health care professional involved.CONCLUSION: The present comprehensive survey of PR in Canada reports an increase in the number of programs and the total number of patients enrolled since the previous survey in 2005. However, PR capacity has not kept pace with demand, with only 0.4% of Canadians with COPD having access.

The cardiopulmonary exercise test (CPET) is an important physiological investigation that can aid clinicians in their evaluation of exercise intolerance and dyspnea. Maximal oxygen consumption (V˙O2max) is the gold-standard measure of aerobic fitness and is determined by the variables that define oxygen delivery in the Fick equation (V˙O2 = cardiac output × arterial-venous O2 content difference). In healthy subjects, of the variables involved in oxygen delivery, it is the limitations of the cardiovascular system that are most responsible for limiting exercise, as ventilation and gas exchange are sufficient to maintain arterial O2 content up to peak exercise. Patients with lung disease can develop a pulmonary limitation to exercise which can contribute to exercise intolerance and dyspnea. In these patients, ventilation may be insufficient for metabolic demand, as demonstrated by an inadequate breathing reserve, expiratory flow limitation, dynamic hyperinflation, and/or retention of arterial CO2. Lung disease patients can also develop gas exchange impairments with exercise as demonstrated by an increased alveolar-to-arterial O2 pressure difference. CPET testing data, when combined with other clinical/investigation studies, can provide the clinician with an objective method to evaluate cardiopulmonary physiology and determination of exercise intolerance.

Revue canadienne des soins respiratoires et critiques et de la médecine du sommeil

Chronic obstructive pulmonary disease (COPD) patients have increased central arterial stiffness and muscle sympathetic nervous activity (MSNA), both of which contribute to cardiovascular (CV) dysfunction and increased CV risk. Previous work suggests that COPD patients have elevated carotid chemoreceptor (CC) activity/sensitivity, which may contribute to the elevated MSNA and arterial stiffness. Accordingly, the effect of CC inhibition on central arterial stiffness, MSNA and CV function at rest in COPD patients was examined in a randomized placebo-controlled study. Thirteen mild-moderate COPD patients (forced expired volume in 1 s (FEV ) predicted ± SD: 83 ± 18%) and 13 age- and risk-matched controls completed resting CV function measurements with either i.v. saline or i.v. dopamine (2 μg kg min ) while breathing normoxic or hyperoxic air (100% O ). On a separate day, a subset of COPD patients and controls completed MSNA measurements while breathing normoxic or hyperoxic air. Arterial stiffness was determined by pulse-wave velocity (PWV) and MSNA was measured by microneurography. Brachial blood flow was determined using Doppler ultrasound, cardiac output was estimated by impedance cardiography, and vascular conductance was calculated as flow/mean arterial pressure (MAP). CC inhibition with dopamine decreased central and peripheral PWV, and MAP (P < 0.05) while increasing vascular conductance in COPD. No change in CV function was observed with dopamine in controls. CC inhibition with hyperoxia decreased peripheral PWV and MSNA (P < 0.05) in COPD, while no change was observed in controls. CC inhibition decreased PWV and MSNA, and improved vascular conductance in COPD, suggesting that tonic CC activity is elevated at rest and contributes to the elevated arterial stiffness in COPD.