The physiological stakes are high. Shortened diastolic filling time, loss of the atrial contribution to cardiac output, irregular ventricular activation, increased myocardial oxygen demand, reduced coronary perfusion, and impaired ventricular function can all combine to produce a rapid decline in cardiac output, particularly in patients with pre-existing ventricular dysfunction or limited cardiovascular reserve. The resulting hypotension and congestion trigger sympathetic activation and myocardial ischemia, which in turn make further arrhythmias more likely. This creates a self-perpetuating cycle in which the arrhythmia aggravates hemodynamic compromise while hemodynamic and metabolic deterioration increases arrhythmogenicity.

Central to the editorial’s message is the identification and simultaneous correction of potentially reversible precipitants. These include acute myocardial ischemia, electrolyte abnormalities, acidosis, hypoxemia, elevated filling pressures, infection, drug toxicity, and proarrhythmic medications. The authors emphasize that establishing causality requires meticulous clinical assessment, and they highlight a case reported by Li and colleagues in which left subclavian artery stenosis was identified as the cause of aVR ST-elevation in a patient after coronary artery bypass grafting, by limiting blood flow through the left internal mammary artery graft. The example illustrates how extra-coronary vascular lesions can drive recurrent ischemia even when the grafts themselves are patent.

Bedside echocardiography emerges as the cornerstone of assessment in this setting. According to the editorial, ultrasound imaging at the bedside plays a key role in evaluating ventricular systolic function, filling pressures, atrial size and function, predicting the likelihood of successful rhythm control, identifying valve disorders, and informing decisions about adequate anticoagulation. This complex assessment should enable more efficient pharmacological treatment while avoiding cardiac depressant medication in patients whose contractility is already compromised. At the same time, the authors caution against a universal reflex toward amiodarone: the drug shows less efficacy and worse outcome data in patients with a non-dilated left atrium, and its well-known multiorgan toxic side effects weigh against indiscriminate use.

Among the contributions gathered under the research topic, a state-of-the-art review by Tencer and colleagues offers a step-by-step approach that includes correction of triggers and individualized selection of a rate-control versus rhythm-control strategy based on echocardiographic findings. By blending physiological observations with existing randomized trial data, the review aims to refine therapeutic strategies in this high-risk population. Perhaps the most striking finding comes from an exploratory analysis by Balik and colleagues of a trial on supraventricular arrhythmias in mechanically ventilated patients with septic shock, registered as NCT03029169. In the presence of right ventricular dysfunction diagnosed by echocardiography, the class 1C antiarrhythmic propafenone was associated with four to five times fewer arrhythmia recurrences compared with amiodarone, despite similar short-term cardioversion rates.

The right ventricular dysfunction category included patients with decompensated cor pulmonale, a finding that challenges the vague definition of structural heart disease that is often presented as an alleged contraindication to class 1C antiarrhythmic drugs. Under certain conditions outlined by the authors, propafenone should be preferred to amiodarone for rhythm control in patients with right ventricular dysfunction, a conclusion with immediate practical implications for intensive care prescribing. Beyond pharmacology, the collection explores neuromodulation and interventional options. A narrative review by Zhang and An examined the potential role of stellate ganglion blockade in refractory arrhythmias, noting that the technique also influences stress responses, perception of pain, and multiple postoperative outcomes among surgical patients, and produces effects resembling vagus nerve stimulation that encompass insomnia, depression, and cognitive impairment.

For patients with severe hemodynamic instability, temporary mechanical circulatory support such as venoarterial extracorporeal membrane oxygenation or the Impella device may serve as a bridge to definitive treatment, including catheter ablation. The most established role for urgent ablation is in patients with incessant monomorphic ventricular tachycardia and electrical storm, though ablation may also be considered when recurrent polymorphic ventricular tachycardia or ventricular fibrillation is initiated by a reproducible premature ventricular complex, including Purkinje-related triggers. Both standard radiofrequency energy and novel pulsed field ablation have shown acceptable results in reducing ventricular tachycardia episodes. Catheter ablation is also feasible for incessant recurrent paroxysmal supraventricular tachycardia, atrial flutter, or pre-excited atrial arrhythmias, and when refractory atrial fibrillation with a high ventricular rate causes hypotension and circulatory compromise, atrioventricular node ablation combined with physiological pacing may be an option. Recent data support a combined pace-and-ablate concept with promising results for left ventricular function and QRS complex morphology.

The procedures themselves demand multiple imaging modalities, including fluoroscopy, three-dimensional electroanatomical mapping, and intracardiac echocardiography, although a zero-fluoroscopy approach is now the trend in many centers. In a notable demonstration, Stec and colleagues reported safe and effective ablation of maternal supraventricular tachycardia and idiopathic ventricular arrhythmias during pregnancy without fluoroscopy, with five-year follow-up, underscoring the importance of multidisciplinary pregnancy heart teams. Special populations receive particular attention as well. Patients with pulmonary hypertension can be highly sensitive to the loss of rhythm control; supraventricular arrhythmias in this group were associated with severe symptoms and increased mortality, and restoration of sinus rhythm improved clinical outcomes. However, an exploratory study by Dusik and colleagues of a randomized trial registered as NCT04053361 found that extensive catheter ablation for atrial fibrillation and atrial tachycardia in patients with pulmonary hypertension did not reduce arrhythmia recurrence over more than 40 months of follow-up. Nonetheless, cavo-tricuspid isthmus ablation appeared effective in preventing recurrence of typical atrial flutter, suggesting a more targeted role for intervention in this population.

On the biomarker front, Stekla and colleagues showed that growth differentiation factor 15 levels change after radiofrequency and pulsed field catheter ablation of atrial fibrillation. This protein from the transforming growth factor beta cytokine family is a potent marker of bleeding adverse events in anticoagulated patients with atrial fibrillation and a predictor of overall mortality, although data on biomarkers for predicting response to rhythm-control strategies remain inconclusive. The editorial rounds out its survey with several practical threads. A narrative review by Kim and colleagues suggested that proton pump inhibitor co-therapy in patients receiving non-vitamin K antagonist oral anticoagulants may represent a pragmatic strategy, reinforcing the point that a high-risk profile in atrial fibrillation does not itself contraindicate anticoagulation. A case series by Elahi and colleagues offered insight into the temporary use of theophylline in patients with sinus pauses, though the associated risk of atrial fibrillation warrants further research.

On the computational frontier, Wu and colleagues demonstrated that deep learning-based early prediction of life-threatening ventricular arrhythmias using long-term Holter electrocardiogram signals was efficient compared with traditional models and offers an extensible real-time solution with a high degree of accuracy. Taken together, the editors conclude that arrhythmia management in acute and intensive care rests on careful identification and correction of reversible triggers, bedside imaging, and tailored selection of antiarrhythmic, anticoagulation, and autonomic-modulating strategies, circulatory support, and catheter ablation, with advances in precise diagnostics, navigational ablation techniques, biomarker understanding, and artificial intelligence poised to expand the options available for this challenging population.

Subject of Research: Management of cardiac arrhythmias in acute and intensive care settings

Article Title: Editorial: Management of arrhythmias in acute and intensive care settings

Article References: Balik, M., & Havranek, S. (2026). Editorial: Management of arrhythmias in acute and intensive care settings. Frontiers in Cardiovascular Medicine, 13, 2020556. https://doi.org/10.3389/fcvm.2026.2020556

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.2020556

Keywords: cardiac arrhythmias, intensive care, atrial fibrillation, amiodarone, propafenone, catheter ablation, echocardiography, stellate ganglion blockade, pulmonary hypertension, anticoagulation, ventricular arrhythmias, artificial intelligence