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Acute Management of Atrial Fibrillation FREE TO VIEW

Mengalvio Sleeswijk, MD; Trudeke van Noord, MD; Jack J. M. Ligtenberg, MD; Jan G. Zijlstra, MD, PhD
Author and Funding Information

Affiliations: Flevo Hospital Almere, the Netherlands,  University Medical Center Groningen Groningen, the Netherlands

Jan G. Zijlstra, MD, PhD, Department of Critical Care, University Medical Center Groningen, PO 30.001, 9700 RB, Groningen, the Netherlands; e-mail: j.g.zijlstra@int.umcg.nl


The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;136(2):651-652. doi:10.1378/chest.09-0622
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To the Editor:

Khoo and Lip (March 2009)1 have reviewed the therapy of acute atrial fibrillation (AAF) extensively. Patients presenting with AAF are very heterogeneous; however, all may show spontaneous conversion to sinus rhythm. The heterogeneity of the disease and its underlying mechanisms makes studies, reviews, and guidelines very complicated and confusing. The review by Khoo and Lip1 suggests that AAF leading to critical illness is the same as critical illness leading to AAF, and that, therefore, the therapeutic approach can also be the same. In our view, this is not correct.

AAF is a multifactorial disease involving structural cardiac abnormalities, inflammation, electrolyte disturbances, hormonal and autonomous nervous system dysregulation, and fluid imbalance, among others, as underlying causes. A difference in balance between causes in the two types of patients is more than likely.2 For example, arrhythmias can only develop by the combination of a trigger and a substrate. In outpatient clinic patients with AAF, there might be a larger role for the substrate, while in critically ill patients with AAF the trigger is of utmost importance. In critically ill patients, the underlying trigger should be treated first. Treatment of the underlying disease, pain and anxiety relief, oxygenation, and correction of hemodynamics are mandatory, and this essential therapy leads to conversion to sinus rhythm in the majority of cases without further intervention. Direct current cardioversion, based on our experience and supported by the literature,3 has no sustainable result if the underlying triggers are not eliminated. Direct current cardioversion therefore, should only be used in really desperate situations, although, as mentioned before, the efficacy remains debatable.

The best pharmacotherapeutic approach is also a point of discussion. However, much experience with a few drugs is probably better than little experience with many drugs, and amiodarone might be the drug with the best range.2 Most antiarrhythmic drugs, and especially class I drugs, have never been tested in critically ill patients, and their potential adverse effects might be exaggerated just in these patients. Whether magnesium is really effective or just buys time to spontaneous conversion remains to be elucidated.4 Critically ill patients may have thrombophilia, but they certainly have a high risk of bleeding.. This means that studies and guidelines about prophylaxis for the prevention of thromboembolism for outpatients or other patients cannot be extrapolated. There is no evidence we can rely on for anticoagulant therapy in patients with AAF due to critical illness.

In conclusion, the paucity of data about AAF in critically ill patients should not lead to the extrapolation of guidelines from only partially related diseases but instead should lead to more and better studies in critically ill patients.

Khoo CW, Lip GY. Acute management of atrial fibrillation. Chest. 2009;135:849-859. [PubMed] [CrossRef]
 
Sleeswijk ME, van Noord T, Tulleken JE, et al. Clinical review: treatment of new-onset atrial fibrillation in medical intensive care patients; a clinical framework. Crit Care. 2007;11:233. [PubMed]
 
Mayr A, Ritsch N, Knotzer H, et al. Effectiveness of direct-current cardioversion for treatment of supraventricular tachyarrhythmias, in particular atrial fibrillation, in surgical intensive care patients. Crit Care Med. 2003;31:401-405. [PubMed]
 
Sleeswijk ME, Tulleken JE, van Noord T, et al. Efficacy of magnesium-amiodarone step-up scheme in critically ill patients with new-onset atrial fibrillation: a prospective observational study. J Intensive Care Med. 2008;23:61-66. [PubMed]
 

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References

Khoo CW, Lip GY. Acute management of atrial fibrillation. Chest. 2009;135:849-859. [PubMed] [CrossRef]
 
Sleeswijk ME, van Noord T, Tulleken JE, et al. Clinical review: treatment of new-onset atrial fibrillation in medical intensive care patients; a clinical framework. Crit Care. 2007;11:233. [PubMed]
 
Mayr A, Ritsch N, Knotzer H, et al. Effectiveness of direct-current cardioversion for treatment of supraventricular tachyarrhythmias, in particular atrial fibrillation, in surgical intensive care patients. Crit Care Med. 2003;31:401-405. [PubMed]
 
Sleeswijk ME, Tulleken JE, van Noord T, et al. Efficacy of magnesium-amiodarone step-up scheme in critically ill patients with new-onset atrial fibrillation: a prospective observational study. J Intensive Care Med. 2008;23:61-66. [PubMed]
 
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