Faculty Bibliography

BACKGROUND:Cigarette smoking remains the leading cause of preventable death in the United States, with high prevalence among hospitalized patients. Hospitalization presents an opportunity to initiate and engage patients in tobacco treatment, yet guidance for tobacco treatment in this setting has been limited. This clinical practice guideline provides evidence-based recommendations for tobacco treatment in the inpatient setting. STUDY DESIGN AND METHODS/METHODS:A multidisciplinary panel followed CHEST's standardized clinical practice guideline methodology, including systematic literature searches in MEDLINE, Embase, and the Cochrane Database. Key clinical questions were framed using the PICO format. Eligible studies included randomized controlled trials and cohort studies. Evidence was appraised using GRADE, and recommendations were formulated through a modified Delphi process to achieve consensus. RESULTS:We identified 9330 abstracts, assessed 252 full texts, and included 142 studies. The literature review and analysis, based on 6 PICO questions, yielded 8 recommendations. No recommendations were supported by high-certainty evidence specific to inpatient tobacco treatment settings. Of the eight recommendations, four were supported by moderate-certainty evidence, two by low-certainty evidence, and two by very low-certainty evidence, supplemented by expert consensus. INTERPRETATION/CONCLUSIONS:Hospitalization offers a critical window to initiate tobacco treatment. This guideline synthesizes the existing literature to inform key components of inpatient tobacco treatment, including an opt-out population-based approach that proactively provides counseling and pharmacotherapy to all patients who smoke unless they explicitly decline; the initiation and selection of pharmacotherapies during hospitalization; counseling approaches delivered during the inpatient stay; and post-discharge counseling approaches following hospital discharge. Implementing these approaches is likely to improve smoking-cessation outcomes and reduce hospital readmissions and costs. The guideline also evaluates the strength and limitations of the current evidence base and identifies priority areas for future research, including identifying optimal implementation strategies, equity considerations, and the evaluation of cost-effectiveness across diverse hospital settings and patient populations.

Background: Patients hospitalized for severe COVID-19 infection are at risk for in-hospital cardiac arrest (IHCA). It is unknown whether certain characteristics of cardiac arrest care and outcomes of IHCAs during the COVID-19 pandemic differed compared to a pre-COVID-19 period. Methods: All patients who experienced an IHCA at our hospital from March 1st through May 15th 2020, during the peak of the COVID-19 pandemic, and those who had an IHCA from January 1st 2019 to December 31st 2019 were identified. All patient data was extracted from our hospital's Get With The Guidelines-Resuscitation (GWTG-R) registry, a prospective hospital-based archive of IHCA data. Baseline characteristics of patients, interventions and overall outcomes of IHCAs during the COVID-19 pandemic were compared to IHCAs in 2019, prior to the COVID-19 pandemic. Results: There were 125 IHCAs during a 2.5-month period at our hospital during the peak of the COVID-19 pandemic compared to 117 IHCAs in all of 2019. IHCAs during the COVID-19 pandemic occurred more often on general medicine wards than in intensive care units (46% vs 33%; 19% vs 60% in 2019, p<0.001), were overall shorter in duration (median time of 11 min (8.5-26.5) vs 15 min (7.0-20.0), p=0.001), led to fewer endotracheal intubations (52% vs 85%, p<0.001) and had overall worse survival rates (3% vs 13%, p=0.007) compared to IHCAs prior to the COVID-19 pandemic. Conclusions: Patients who experienced an IHCA during the COVID-19 pandemic had overall worse survival compared to those who had an IHCA prior to the COVID-19 pandemic. Our findings highlight important differences between these two time periods. Further study is needed on cardiac arrest care in patients with COVID-19.

Diagnosis of asthma in obese individuals frequently relies on clinical history, as airflow by spirometry may remain normal. This study hypothesised that obese subjects with self-reported asthma and normal spirometry will demonstrate distinct clinical characteristics, metabolic comorbidities and enhanced small airway dysfunction as compared with healthy obese subjects. Spirometry, plethysmography and oscillometry data pre/post-bronchodilator were obtained in 357 obese subjects in three groups as follows: no asthma group (n=180), self-reported asthma normal spirometry group (n=126), and asthma obstructed spirometry group (n=51). To assess the effects of obesity related to reduced lung volume, oscillometry measurements were repeated during a voluntary inflation to predicted functional residual capacity (FRC). Dyspnoea was equally prevalent in all groups. In contrast, cough, wheeze and metabolic comorbidities were more frequent in the asthma normal spirometry and asthma obstructed spirometry groups versus the no asthma group (p<0.05). Despite similar body size, oscillometry measurements demonstrated elevated R_5-20 (difference between resistance at 5 and 20 Hz) in the no asthma and asthma normal spirometry groups (0.19±0.12; 0.23±0.13 kPa/(L·s^-1), p<0.05) but to a lesser degree than the asthma obstructed spirometry group (0.34±0.20 kPa/(L·s^-1), p<0.05). Differences between groups persisted post-bronchodilator (p<0.05). Following voluntary inflation to predicted FRC, R_5-20 in the no asthma and asthma normal spirometry groups fell to similar values, indicating a reversible process (0.11±0.07; 0.12±0.08 kPa/(L·s^-1), p=NS). Persistently elevated R_5-20 was seen in the asthma obstructed spirometry group, suggesting chronic inflammation and/or remodelling (0.17±0.11 kPa/(L·s^-1), p<0.05). Thus, small airway abnormalities of greater magnitude than observations in healthy obese people may be an early marker of asthma in obese subjects with self-reported disease despite normal airflow. Increased metabolic comorbidities in these subjects may have provided a milieu that impacted airway function.