Atrial Fibrillation in the ICU

Abstract

Atrial fibrillation (AF) is the most common arrhythmia encountered in the ICU. Preexisting AF is highly prevalent among older patients with chronic conditions who are at risk for critical illness, whereas new-onset AF can be triggered by accelerated atrial remodeling and arrhythmogenic triggers encountered during critical illness. The acute loss of atrial systole and onset of rapid ventricular rates that characterize new-onset AF often lead to decreased cardiac output and hemodynamic compromise. Thus, new-onset AF is both a marker of disease severity as well as a likely contributor to poor outcomes, similar to other manifestations of organ dysfunction during critical illness. Evaluating immediate hemodynamic effects of new-onset AF during critical illness is an important component of rapid clinical assessment aimed at identifying patients in need of urgent direct current cardioversion, treatment of reversible inciting factors, and identification of patients who may benefit from pharmacologic rate or rhythm control. In addition to acute hemodynamic effects, new-onset AF during critical illness is associated with both short- and long-term increases in the risk of stroke, heart failure, and death, with AF recurrence rates of approximately 50% within 1 year following hospital discharge. In the absence of a strong evidence base, there is substantial practice variation in the choice of strategies for management of new-onset AF during critical illness. We describe acute and long-term evaluation and management strategies based on current evidence and propose future avenues of investigation to fill large knowledge gaps in the management of patients with AF during critical illness.

Keywords: atrial fibrillation; critical illness; sepsis.

Figure 1

Proposed mechanisms and risk factors for new-onset AF during critical illness. AF develops through a two-step process: creation of an arrhythmogenic substrate followed by a triggering event. During critical illness, both acute (dark blue boxes) and chronic risk factors (light blue boxes) have roles in the development of AF. Prior to critical illness, chronic risk factors for AF may alter the normal atrial myocardium into an arrhythmogenic substrate predisposing to AF during critical illness. During critical illness, patients with both normal and arrhythmogenic atria can develop new-onset AF in the setting of acute risk factors. Risk factors potentially lead to accelerated structural and electrical remodeling and may then trigger AF through multiple mechanisms, including adrenergic stimulation. Proposed pathways by which these risk factors lead to AF may be optimal targets for future preventative strategies. AF = atrial fibrillation; CHF = congestive heart failure; CKD = chronic kidney disease; ROS = reactive oxygen species; TGF = transforming growth factor.

Figure 2

Acute management priorities in new-onset AF during critical illness. Identification of new-onset AF during critical illness should prompt a four-step rapid clinical assessment: (1) assessment for hemodynamic compromise requiring urgent DCCV, (2) removal of potential offending agents, (3) reversal of inciting acute factors, and (4) treatment to reduce rate or convert to sinus if AF persists and is associated with adverse effects. DCCV = direct current cardioversion; HR = heart rate. See Figure 1 legend for expansion of other abbreviation.