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BACKGROUND: Evidence has emerged showing potential benefit of Remdesivir and dexamethasone in severe coronavirus disease 2019 (COVID-19) but results from large randomized control trials are conflicting. While initial data for dexamethasone indicated a mortality benefit, the impact of Remdesivir was best demonstrated in decreased time to recovery. Despite extensive disease burden throughout the world efficacy data of individual interventions is lacking in part due to extensive concurrent use of confounding investigational therapeutics. MATERIALS AND METHODS: We performed a retrospective analysis of the impact of Remdesivir and dexamethasone on real-world outcomes in severe COVID-19. All patients admitted to our community hospital between March 2020 and December 31, 2020 were included, and all patients admitted before national guidelines endorsed Remdesivir and dexamethasone outside of clinical trials were treated with only supportive care and used as historical controls. No other investigational therapeutics were utilized. This study was reviewed and approved by the Fort Belvoir Community Hospital IRB. RESULTS: 58 hospitalized patients met criteria for severe COVID-19 as confirmed by RT-PCR, and 14 (25%) were used as historical controls. Baseline demographics and overall mortality rate (7.1%) did not significantly differ between the groups. The median length of stay was 7 days and 6 days in the historical control group and interventional group, respectively (P = 0.55). CONCLUSIONS: We did not observe an appreciable impact on the duration of hospitalization when Remdesivir and dexamethasone were added to supportive care in a community hospital. This study was not sufficiently powered to detect the previously described mortality benefit of dexamethasone.
RESUMO
Sinus node dysfunction, previously known as sick sinus syndrome, describes disorders related to abnormal conduction and propagation of electrical impulses at the sinoatrial node. An abnormal atrial rate may result in the inability to meet physiologic demands, especially during periods of stress or physical activity. Sinus node dysfunction may occur at any age, but is usually more common in older persons. The causes of sinus node dysfunction are intrinsic (e.g., degenerative idiopathic fibrosis, cardiac remodeling) or extrinsic (e.g., medications, metabolic abnormalities) to the sinoatrial node. Many extrinsic causes are reversible. Electrocardiography findings include sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, chronotropic incompetence, or alternating bradycardia and tachycardia (i.e., bradycardia-tachycardia syndrome). Clinical symptoms result from the hypoperfusion of end organs. About 50% of patients present with cerebral hypoperfusion (e.g., syncope, presyncope, lightheadedness, cerebrovascular accident). Other symptoms include palpitations, decreased physical activity tolerance, angina, muscular fatigue, or oliguria. A diagnosis is made by directly correlating symptoms with a bradyarrhythmia and eliminating potentially reversible extrinsic causes. Heart rate monitoring using electrocardiography or ambulatory cardiac event monitoring is performed based on the frequency of symptoms. An exercise stress test should be performed when symptoms are associated with exertion. The patient's inability to reach a heart rate of at least 80% of their predicted maximum (220 beats per minute - age) may indicate chronotropic incompetence, which is present in 50% of patients with sinus node dysfunction. First-line treatment for patients with confirmed sinus node dysfunction is permanent pacemaker placement with atrial-based pacing and limited ventricular pacing when necessary.