New-Onset Atrial Fibrillation in the Critically Ill COVID-19 Patients Hospitalized in the Intensive Care Unit

Abstract

New-onset atrial fibrillation (NOAF) is the most frequently encountered cardiac arrhythmia observed in patients with COVID-19 infection, particularly in Intensive Care Unit (ICU) patients. The purpose of the present review is to delve into the occurrence of NOAF in COVID-19 and thoroughly review recent, pertinent data. However, the causality behind this connection has yet to be thoroughly explored. The proposed mechanisms that could contribute to the development of AF in these patients include myocardial damage resulting from direct virus-induced cardiac injury, potentially leading to perimyocarditis; a cytokine crisis and heightened inflammatory response; hypoxemia due to acute respiratory distress; disturbances in acid-base and electrolyte levels; as well as the frequent use of adrenergic drugs in critically ill patients. Additionally, secondary bacterial sepsis and septic shock have been suggested as primary causes of NOAF in ICU patients. This notion gains strength from the observation of a similar prevalence of NOAF in septic non-COVID ICU patients with ARDS. It is plausible that both myocardial involvement from SARS-CoV-2 and secondary sepsis play pivotal roles in the onset of arrhythmia in ICU patients. Nonetheless, there exists a significant variation in the prevalence of NOAF among studies focused on severe COVID-19 cases with ARDS. This discrepancy could be attributed to the inclusion of mixed populations with varying degrees of illness severity, encompassing not only patients in general wards but also those admitted to the ICU, whether intubated or not. Furthermore, the occurrence of NOAF is linked to increased morbidity and mortality. However, it remains to be determined whether NOAF independently influences outcomes in critically ill COVID-19 ICU patients or if it merely reflects the disease's severity. Lastly, the management of NOAF in these patients has not been extensively studied. Nevertheless, the current guidelines for NOAF in non-COVID ICU patients appear to be effective, while accounting for the specific drugs used in COVID-19 treatment that may prolong the QT interval (although drugs like lopinavir/ritonavir, hydrochlorothiazide, and azithromycin have been discontinued) or induce bradycardia (e.g., remdesivir).

Keywords: COVID-19; ICU; critical illness; new-onset atrial fibrillation; trigger factors.

Figure 1

Proposed pathophysiological mechanisms and risk factors for new-onset atrial fibrillation in ICU COVID-19 ARDS patients. During SARS-CoV-2 infection, chronic factors (age, pre-existing comorbidities), COVID-19-specific factors (inflammation, cytokine storm, direct viral invasion, treatments received)) and ICU risk factors (secondary sepsis, associated with adrenergic-endogenous/exogenous-overstimulation, right ventricular overload: ARDS/mechanical ventilation, hypoxemia, electrolyte imbalances, and acid-base disturbances) may contribute to NOAF emergence. The most significant factor in ICU patients, in the authors’ opinion, is secondary sepsis (orange box) which typically occurs relatively late in the course since SARS-CoV-2 infection. The arrow width indicates the degree of contribution of each factor in NOAF emergence. ACE2, angiotensin converting enzyme 2; ARDS, acute respiratory distress syndrome; COVID-19, Corona Virus Disease 2019; IL-1, interleucin-1; IL-6, interleukin-6; NLRP3, NOD-like receptor pyrin domain-containing 3; NOAF, new-onset atrial fibrillation; RNA, rivonucleic acid; RV, right ventricle.