By Zach Adams, OSUEM Resident // Edited by Michael Barrie, OSUEM Assistant Professor
A 34 year-old female with a prior history of arrhythmia presents to the ED with palpitations. The patient reports the symptoms began suddenly this AM at about 8AM. The monitor shows atrial fibrillation at a rate of 157. You do not have a prior ECG for review. After discussing options with the patient, the decision is made to attempt cardioversion. What are the risks, and do we need to anticoagulate afterwards?
As we well know, patients with atrial fibrillation (AF) are at an increased risk of thromboembolic events, most commonly stroke. Overall risk for patients with non-valvular atrial fibrillation can be calculated using the CHADS2 score or the more recent CHA2DS2-VASc score and helps guide long-term anticoagulant therapy for prevention. The HAS-BLED score furthermore stratifies bleeding risk in subsets of individuals who will require long-term anticoagulation. The overall risk of stroke in AF increases from baseline after both spontaneous and chemical or electrical cardioversion, with most events occurring within 10 days for patients on either warfarin or non-vitamin-K antagonist antithrombotics (1-4). In any instance of new onset atrial fibrillation, the risk of thrombus increases with risk factors and length of duration of AF, with up to 13 percent of patients having evidence of left atrial thrombus on TEE (5-7).
Guidelines suggest for patients with unknown duration of atrial fibrillation or duration >48 hours, 3 weeks of anticoagulation or TEE to document lack of atrial thrombus be utilized prior to cardioversion, with long-term anticoagulation guided by risk stratification above. Such patients are a relatively easy disposition depending on presentation. For patients with new onset atrial fibrillation of <48 hours, however, things can get tricky, especially considering that the vast majority of individuals with atrial fibrillation (up to 90%) are asymptomatic (8). Should we reliably use symptom onset to make a decision to perform ED cardioversion?
Historically, many practitioners perform cardioversion in patients with acute (<48 hour) symptoms attributed to atrial fibrillation. Some have even vouched for a “wait and see” approach in the ED, in which patients with onset of symptoms <48 are discharged with 24 hour follow-up and cardioversion as needed or observational protocol, as the spontaneous cardioversion rate is high – upwards of 70% (9). However, while embolization after return of sinus rhythm was previously attributed to dislodgment of a left atrial thrombus at the time of conversion, evidence shows that LA thrombi can also form in the immediate post-cardioversion state, regardless of the method (i.e. electrical, chemical, spontaneous) (10-13). In such instances, “stunning” of the atria secondary to conversion to sinus rhythm leads to thrombus formation, with recent guidelines calling this practice into question. More precisely, the Finnish CardioVersion study measured this risk, and found a pretty conclusive 0.7% 30-day risk of embolic stroke depending on patient risk factors (risk factors: age >60, OR 1.05; female sex, OR 2.1; heart failure, OR 2.9; diabetes, OR 2.3) (14). The aforementioned CHADS2 and CHA2DS2-VASc scores were also highly predictive of thromboembolic events for those undergoing cardioversion of AF <48 hours in the study population. The authors concluded that consideration should be given to periprocedural and postpostprocedural anticoagulation and broader group of patients with AF <48 hours. So what should we do? Should we anticoagulant during the cardioversion in these patients? What about after?
These are some difficult questions to answer, and various recommendations have been made. Recent AHA/ACC 2014 AF guidelines strongly recommend for heparin or a newer anticoagulant (NOAC) as soon as possible before cardioversion followed by long-term oral anticoagulation in patients at high risk. They further recommend for cardioversion with or without periprocedural anticoagulation followed by no long-term anticoagulation in patients at low risk (15). Alternatively, the 2011 European Society of Cardiology AF guidelines make a weak recommendation for periprocedural heparin in ALL patients with AF <48 hours with long-term oral anticoagulation in high risk patients (16). Sort of confusing.
In patients with unknown duration of AF or duration >48 hours, initiation of anticoagulation for 3 weeks prior to elective cardioversion or a TEE based approach with post-cardioversion anticoagulation is warranted. Such patients presenting in the ED should be dispositioned depending on the decision of rate versus rhythm control as well as anticoagulation therapy in conjunction with cardiology and the patient.
In patients with new onset AF or duration <48 hours, the decision to cardiovert the patient (either chemically or electrically if they haven’t spontaneously converted) warrants careful assessment of risk factors and periprocedural and post-cardioversion anticoagulation depending on the overall risk. Consideration might be given to utilization of pre-cardioversion heparin or NOAC before cardioversion in moderate to high risk patients (CHAD2DS2-VASc ≧ 1) followed by long-term anticoagulation. For low risk patients (CHA2DS2-VASc = 0), recommendations are either for no anticoagulation or pre-procedural anticoagulation and 4 weeks of anticoagulation thereafter to further reduce the risk of stroke. Bleeding risk assessment can guide therapy using the HAS-BLED score.
- Berger M, Schweitzer P. Timing of thromboembolic events after electrical cardioversion of atrial fibrillation or flutter: a retrospective analysis. Am J Cardiol 1998; 82:1545.
- Nagarakanti R, Ezekowitz MD, Oldgren J, et al. Dabigatran versus warfarin in patients with atrial fibrillation: an analysis of patients undergoing cardioversion. Circulation 2011; 123:131.
- Flaker G, Lopes RD, Al-Khatib SM, et al. Efficacy and safety of apixaban in patients after cardioversion for atrial fibrillation: insights from the ARISTOTLE Trial (Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation). J Am Coll Cardiol 2014; 63:1082.
- Cappato R, Ezekowitz MD, Klein AL, et al. Rivaroxaban vs. vitamin K antagonists for cardioversion in atrial fibrillation. Eur Heart J 2014; 35:3346.
- Manning WJ, Silverman DI, Keighley CS, et al. Transesophageal echocardiographically facilitated early cardioversion from atrial fibrillation using short-term anticoagulation: final results of a prospective 4.5-year study. J Am Coll Cardiol 1995; 25:1354.
- Weigner MJ, Thomas LR, Patel U, et al. Early cardioversion of atrial fibrillation facilitated by transesophageal echocardiography: short-term safety and impact on maintenance of sinus rhythm at 1 year. Am J Med 2001; 110:694.
- Klein AL, Grimm RA, Murray RD, et al. Use of transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation. N Engl J Med 2001; 344:1411.
- Page RL, Wilkinson WE, Clair WK, McCarthy EA, Pritchett EL. Asymptomatic arrhythmias in patients with symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia. Circulation. 1994; 89(1)224-7.
- Doyle B, Reeves M. “Wait and See” Approach to the Emergency Department Cardioversion of Acute Atrial Fibrillation. Emergency Medicine International. 2011, Article ID 545023.
- Stoddard MF, Dawkins PR, Prince CR, Longaker RA. Transesophageal echocardiographic guidance of cardioversion in patients with atrial fibrillation. Am Heart J 1995; 129:1204.
- Black IW, Hopkins AP, Lee LC, Walsh WF. Evaluation of transesophageal echocardiography before cardioversion of atrial fibrillation and flutter in nonanticoagulated patients. Am Heart J 1993; 126:375.
- Black IW, Fatkin D, Sagar KB, et al. Exclusion of atrial thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atrial fibrillation. A multicenter study. Circulation 1994; 89:2509.
- Moreyra E, Finkelhor RS, Cebul RD. Limitations of transesophageal echocardiography in the risk assessment of patients before nonanticoagulated cardioversion from atrial fibrillation and flutter: an analysis of pooled trials. Am Heart J 1995; 129:71.
- Juhani Airaksinen KE, Gronberg Toni, Nuotio I, Nikkinen M, Antti Y, Biancari F, Hartikainen J. Thromboembolic complications after cardioversion of acute atrial fibrillation. J Am Coll Cardiol. 2013 Sep 24;62(13):1187-92.
- January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW, ACC/AHA Task Force Members. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the Heart Rhythm Society. Circulation. 2014;130(23):e199
- European Heart Rhythm Association, European Association for Cardio-Thoracic Surgery, Camm AJ, Kirchhof P, Lip GY, Schotten U, Savelieva I, Ernst S, Van Gelder IC, Al-Attar N, Hindricks G, Prendergast B, Heidbuchel H, Alfieri O, Angelini A, Atar D, Colonna P, De Caterina R, De Sutter J, Goette A, Gorenek B, Heldal M, Hohloser SH, Kolh P, Le Heuzey JY, Ponikowski P, Rutten FH. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2010;31(19):2369.
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Patient's Resting ECG
Whilst under investigation in the Emergency Department the patient was placed on cardiac telemetry and during clinical assessment a brief rhythm change was noted, captured below.
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- No P waves present
- Accelerated Idioventricular Rhythm (AIVR)
- QRS - Prolonged (160ms)
- Discordant ST segment changes
- Excessive depression in lead V5 and excessive elevation V3 (just on -0.25 ST elevation / QRS depth)
- LBBB Morphology
- Deep S in V1-3
- Broad R wave in lateral leads
- T waves massively disproportionate and peaked
- Note in leads V5-6 terminal portion of T wave becomes positive
The key abnormalities on this ECG are:
- LBBB with abnormal ST changes
- Massive peaked T waves
Broad differentials would include
- Drug toxicity
- Acid-base disturbance
- Electrolyte abnormality
At first glance I'd favour hyperkalaemia as the culprit and an urgent VBG was taken - K 8.8 mmol/L !
I unfortunately don't have a follow-up ECG and I expect following treatment sinus rhythm was restored and the T wave changes normalised. I would be interested to know if the LBBB was longstanding or secondary to the hyperkalaemia,
References / Further Reading
Life in the Fast Lane
- Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
As part of the last two EDE 3 events, Dr. Tom Jelic held an online journal club. Tom did a great job summarizing some of the latest articles from the POCUS literature, with comments from several EDE 3 instructors and participants who chimed in with their take and experience. Several JCs were held this fall to accommodate everyone’s schedule. We got our act together and recorded the last one. Over the next few weeks, we will be posting the discussion of each article on the blog. Feel free to chime in with your own comments and experience.
Here’s the first article by Tessaro et al. looking at filling the ET tube cuff with saline. It was published in Resuscitation earlier this year. Click on the video to hear and see TJ’s presentation.