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IMPORTANCE While current reports suggest that a disproportionate share of US coronavirus disease 2019 (COVID-19) cases and deaths are among Black residents, little information is available regarding how race is associated with in-hospital mortality. OBJECTIVE To evaluate the association of race, adjusting for sociodemographic and clinical factors, on all-cause, in-hospital mortality for patients with COVID-19. DESIGN, SETTING, AND PARTICIPANTS This cohort study included 11 210 adult patients (age Ն18 years) hospitalized with confirmed severe acute respiratory coronavirus 2 (SARS-CoV-2) between February 19, 2020, and May 31, 2020, in 92 hospitals in 12 states: Alabama (6 hospitals), Maryland (1 hospital), Florida (5 hospitals), Illinois (8 hospitals), Indiana (14 hospitals), Kansas (4 hospitals), Michigan (13 hospitals), New York (2 hospitals), Oklahoma (6 hospitals), Tennessee (4 hospitals), Texas (11 hospitals), and Wisconsin (18 hospitals). EXPOSURES Confirmed SARS-CoV-2 infection by positive result on polymerase chain reaction testing of a nasopharyngeal sample. MAIN OUTCOMES AND MEASURES Death during hospitalization was examined overall and by race. Race was self-reported and categorized as Black, White, and other or missing. Cox proportional hazards regression with mixed effects was used to evaluate associations between all-cause in-hospital mortality and patient characteristics while accounting for the random effects of hospital on the outcome. RESULTS Of 11 210 patients with confirmed COVID-19 presenting to hospitals, 4180 (37.3%) were Black patients and 5583 (49.8%) were men. The median (interquartile range) age was 61 (46 to 74) years. Compared with White patients, Black patients were younger (median [interquartile range] age, 66 [50 to 80] years vs 61 [46 to 72] years), were more likely to be women (2259 [49.0%] vs 2293 [54.9%]), were more likely to have Medicaid insurance (611 [13.3%] vs 1031 [24.7%]), and had higher median (interquartile range) scores on the Neighborhood Deprivation Index (−0.11 [−0.70 to 0.56] vs 0.82 [0.08 to 1.76]) and the Elixhauser Comorbidity Index (21 [0 to 44] vs 22 [0 to 46]). All-cause in-hospital mortality among hospitalized White and Black patients was 23.1% (724 of 3218) and 19.2% (540 of 2812), respectively. After adjustment for age, sex, insurance, comorbidities, neighborhood deprivation, and site of care, there was no statistically significant difference in risk of mortality between Black and White patients (hazard ratio, 0.93; 95% CI, 0.80 to 1.09). CONCLUSIONS AND RELEVANCE Although current reports suggest that Black patients represent a disproportionate share of COVID-19 infections and death in the United States, in this study, mortality (continued) Key Points Question Is race associated with mortality among patients hospitalized with coronavirus disease 2019 (COVID-19) in the United States? Findings In this cohort study of 11 210 individuals with COVID-19 presenting for care at 92 hospitals across 12 states, there was no difference in all-cause, in-hospital mortali...

Background: The coronavirus disease 2019 (COVID-19) pandemic has had a considerable impact on US hospitalizations, affecting processes and patient population. Methods: We evaluated the impact of COVID-19 pandemic in 78 US hospitals on central line associated bloodstream infections (CLABSI) and catheter associated urinary tract infections (CAUTI) events 12 months pre-COVID-19 and 6 months during COVID-19 pandemic. Results: There were 795,022 central line-days and 817,267 urinary catheter-days over the two study periods. Compared to pre-COVID-19 period, CLABSI rates increased during the pandemic period from 0.56 to 0.85 (51.0%) per 1,000 line-days (p<0.001) and from 1.00 to 1.64 (62.9%) per 10,000 patient-days (p<0.001). Hospitals with monthly COVID-19 patients representing >10% of admissions had a NHSN device standardized infection ratio for CLABSI that was 2.38 times higher compared to those with <5% prevalence during the pandemic period (p=0.004). Coagulase-negative staphylococcus CLABSI increased by 130% from 0.07 to 0.17 events per 1,000 line-days (p<0.001), and Candida sp. by 56.9% from 0.14 to 0.21 per 1,000 line-days (p=0.01). In contrast, no significant changes were identified for CAUTI (0.86 vs. 0.77 per 1,000 catheter-days; p=0.19). Conclusions: The COVID-19 pandemic was associated with substantial increases in CLABSI but not CAUTI events. Our findings underscore the importance of hardwiring processes for optimal line care, and regular feedback on performance to maintain a safe environment.

The response to PACs during tachycardia can distinguish JT and AVNRT with 100% specificity in adult patients.

Ventricular arrhythmia (VA) in structurally normal hearts can be broadly considered under non-life-threatening monomorphic and life-threatening polymorphic rhythms. Monomorphic VA is classified on the basis of site of origin in the heart, and the most common areas are the ventricular outflow tracts and left ventricular fascicles. The morphology of the QRS complexes on electrocardiogram is an excellent tool to identify the site of origin of the rhythm. Although these arrhythmias are common and generally carry an excellent prognosis, rare sudden death events have been reported. Very frequent ventricular ectopy may also result in a cardiomyopathy in a minority of patients. Suppression of VA may be achieved using calcium-channel blockers, beta-adrenergic blockers, and class I or III antiarrhythmic drugs. Radiofrequency ablation has emerged as an excellent option to eliminate these arrhythmias, although certain foci including aortic cusps and epicardium may be technically challenging. Polymorphic ventricular tachycardia (VT) is rare and generally occurs in patients with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, and short QT syndrome. Unlike monomorphic VT, these arrhythmic syndromes are associated with sudden death. While the cardiac gross morphology is normal, suggesting a structurally normal heart, abnormalities exist at the molecular level and predispose them to arrhythmias. Another fascinating area, idiopathic ventricular fibrillation and early repolarization syndrome, are undergoing research for a genetic basis.