Atrial fibrillation (AFib) is an irregular and often rapid heart rhythm that can increase the risk of stroke, heart failure, and other complications. In critical care, healthcare providers work to control the heart rate, restore normal rhythm when feasible, and administer treatments to prevent complications like blood clots. The treatment of AFib in this setting typically involves heart rate reducing agents that allow the patient to convert to sinus rhythm. Close monitoring and specialized interventions are integral to managing atrial fibrillation effectively.
Critical Care
Critical care is a specialized branch of medicine dedicated to managing and treating patients with severe, life threatening conditions.
Critical care teams work collaboratively to assess, diagnose, and treat patients in critical conditions, including hemodynamic stabilization, organ support when needed, and treating the underlying cause of the illness. Critical care patients require constant medical attention and monitoring due to life threatening conditions or severe injuries.
Atrial Fibrillation
New-Onset Atrial Fibrillation (NOAF) in Critical Illness
New-Onset Atrial Fibrillation (NOAF) in Critical Illness
Systemic Inflammatory Response Syndrome (SIRS)
- SIRS, a highly prevalent, nonspecific, inflammatory state, is primarily seen in acute care and critical care settings.
 - Non-infectious causes such as trauma, burns and major surgery predominate over infectious causes (sepsis) for both US and worldwide hospital and ICU admissions and for adult emergency department visits. [Horesczko 2014; Baddam 2025]
 - SIRS is a key indicator of patients at high risk for end-organ dysfunction and increased mortality.
 - Supraventricular tachyarrhytmias and atrial fibrillation are common and serious complications in critical care.
 
New-onset atrial fibrillation (NOAF) is a frequent arrhythmia in critically ill patients, particularly with infectious or non-infectious SIRS.
- The critical care setting is characterized by a state of "sympathetic overdrive," with high levels of circulating catecholamines, which serve as a compensatory mechanism to maintain organ perfusion but can lead to NOAF.
 - Persistent tachycardia and adrenergic overstimulation can lead to cardiac dysfunction and worsen outcomes.
 - Longer ICU stays, prolonged hospitalization, increased hospital mortality, and a higher risk of stroke or myocardial infarction are observed in patients who develop NOAF. [Klein Klowenberg 2018; Moss 2017]3,4
 
Overcoming Limitations of Current β-blockers to Improve Management of NOAF in Critical Care Patient
- Need Improvement in Speed of Onset of Action: Rapid onset of action would allow for rapid titration, immediate discontinuation if instability occurs, and effective control of ventricular rate in acute situations like new-onset atrial fibrillation.
 - Need Shorter Elimination Half-life: If the patient becomes hypotensive or bradycardic, the infusion can be stopped, and the drug's effects will dissipate very quickly if half-life is extremely short, allowing for a rapid return to baseline hemodynamics. This "on-demand" nature provides clinicians with a high degree of control and safety.
 - Precise Heart Rate (HR) Control with Minimal Blood Pressure Impact is Needed: Important in critically ill patients to achieve substantial HR reduction without causing a profound decrease in mean arterial pressure in individuals who are often prone to hypotension.
 - Higher Selectivity for β-1 Receptors Versus β -2 Receptors Is Needed: Receptor selectivity is important because β-1 receptors are predominantly located in the heart, and their blockade is responsible for the desired negative chronotropic (HR-lowering) effect. By minimizing its effect on β-2 receptors, which are found in the vasculature and bronchioles, the risk of peripheral vasodilation and bronchospasm, which are potential side effects of non-selective β -blockers are reduced.
 - Treatment that Reduces ICU Complications: Treatment that results in improved oxygen delivery and reduced inflammatory stress markers.
 
References:
- Horeczko T, Green JP, Panacek EA. Epidemiology of the Systemic Inflammatory Response Syndrome (SIRS) in the emergency department. West J Emerg Med. 2014 May;15(3):329-36. doi: 10.5811/westjem.2013.9.18064.
 - Baddam S, Burns B. Systemic Inflammatory Response Syndrome. [Updated 2025 Jun 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-.
 - CIDRAP 2020. WHO says sepsis causes 20% of global deaths.
 - Nasir N, Jamil B, Siddiqui S, Talat N, Khan FA, Hussain R. Mortality in Sepsis and its relationship with Gender. Pak J Med Sci. 2015 Sep-Oct;31(5):1201-6. doi: 10.12669/pjms.315.6925
 - Robertson CM,Coopersmith CM, The systemic inflammatory response syndrome, Microbes and Infection 2006;, 8(5),1382-1389.
 - Yoshida, T.;Fujii, T.; Uchino, S.; Takinami, M. Epidemiology, prevention, and treatment of new-onset atrial fibrillation in critically ill: A systematic review. J. Intensive Care 2015, 3, 19.
 - Kuipers, S.; Klouwenberg, P.M.K.; Cremer, O.L. Incidence, risk factors and outcomes of new-onset atrial fibrillation in patients with sepsis: A systematic review. Crit. Care 2014, 18, 688.
 - Bosch, N.A.; Cimini, J.;Walkey, A.J. Atrial Fibrillation in the ICU. Chest 2018, 154, 1424–1434.
 - O'Bryan LJ, Redfern OC, Bedford J, et al. Managing new-onset atrial fibrillation in critically ill patients: a systematic narrative review. BMJ Open 2020;10:e034774. doi:10.1136/