The repurposing of medications to combat an ever-growing COVID-19 pandemic has reached fever pitch, with a variety of drug classes being used, with the vast majority showing unclear benefit. The use of beta-blockers has become ubiquitous in the treatment of patients with cardiac disease however, there remains considerable variation on the optimal timing of the initiation, withholding, and restarting of beta-blocker therapy in critically ill patients. There remains a considerable gap in knowledge in the understanding of the complex balance between beneficial sympathetic stimulation and the multitude of derangements caused by persistent sympathetic overactivity in critically ill individuals. However, conflicting evidence exists in other critically ill populations ( 16), with individuals who received beta-blockers 30 days before elective cardiac surgery showing increased risk of death and stroke associated with an increased incidence of hypotension, bradycardia, and bleeding ( 17). The use of continuous infusion of esmolol, an intravenous short-acting beta-blocker, showed a decreased need for fluids and vasopressors as well as improved 28-day mortality in patients with sepsis ( 11). Furthermore, discontinuation of these drugs during their hospital stay was associated with higher mortality rates independent of the cause of respiratory failure. Several observational studies have shown a reduced mortality in patients in the intensive care unit who were on preadmission beta-blockers ( 14, 15) and specifically those with acute respiratory failure ( 10). There is a growing body of literature regarding the role of beta-blockers in a wide variety of critically ill patients with sepsis and before major surgery, acute respiratory distress syndrome, and traumatic brain injury ( 8-13). There has been an ever-increasing interest in the role of beta-blockers in critically ill patients in blunting this adrenergic response ( 3). The 2013 American College of Cardiology/American Heart Association Heart Failure guidelines recommend β-blockade in patients with a history of myocardial infarction or acute coronary syndrome and reduced ejection fraction to reduce mortality ( 4) and use of beta-blockers in all patients with reduced ejection fraction to prevent symptomatic heart failure and hospitalization.ĭuring critical illness, the initial adrenergic stimulation may be beneficial however, sympathetic overactivity, if persistent, may become deleterious, leading to further oxygen consumption, catabolism, hyperglycemia, hypercoagulability, cardiac dysfunction, modulation of systemic inflammatory cytokines, and ensuing multiorgan failure ( 2, 5-7). Beta-blockers along with their beneficial cardiac profile also exhibit important metabolic and immunomodulatory effects ( 2, 3) that are often overlooked.īeta-blockers have become ubiquitous in the treatment of patients with heart failure and ischemic heart disease. This results in both a negative chronotropic and inotropic effect on the heart that leads to decreased blood pressure, heart rate, and myocardial work ( 1). Beta-blockers inhibit the sympathomimetic stimulation of β-1 adrenergic receptors primarily found on cardiomyocytes as well as the sinoatrial and atrioventricular nodes. Beta-blockers are a commonly prescribed medication for patients with cardiovascular comorbidities, such as ischemia, heart failure, hypertension, and arrhythmias.
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