Electrical cardioversion in the ED: who crashes and how to improve

Authors: Rachel Lynn Graves, MD (EM Resident Physician, University of Pennsylvania) and Gillian Bach, MD (Medical Education Scholarship Fellow, Interim Assistant Residency Program Director, University of Pennsylvania) // Reviewed by: Edward Lew, MD (@elewMD); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case:

A 36-year-old male with a past medical history of migraines, GERD, anxiety, depression, and alcohol use disorder presents to the ED with palpitations. He experienced sudden onset of palpitations about 12 hours ago while lying in bed watching a movie. He’s never had similar symptoms in the past. He endorses associated lightheadedness and shortness of breath but denies chest pain. He drinks about three 16-ounce cups of coffee and 8 beers per day. He denies recent travel and illicit drug use. On exam, the patient is a comfortable-appearing, well-developed male, wearing a suit and reclining in a stretcher. He has a temperature of 97.9°F, blood pressure of 135/90, heart rate of 119, respiratory rate of 13, and SpO2 99% on room air. He has no jugular venous distention, abnormal lung sounds, abdominal tenderness or distention, or lower extremity edema or asymmetry. His extremities are warm and well-perfused with 2+ bilateral radial and dorsalis pedis pulses.

An EKG shows the following:

After discussion of different management options, the decision is made to pursue cardioversion in the ED.

Is this patient low-risk or high-risk for electrical cardioversion? Why? What would be your approach to cardioverting this patient?

Electrical cardioversion (henceforth referred to simply as “cardioversion”) is the application of a synchronized electrical impulse to convert a perfusing tachydysrhythmia back to normal sinus rhythm.^1,2 It is indicated for hemodynamically unstable patients who present in ventricular tachycardia (VT), supraventricular tachycardia (SVT), atrial flutter, and atrial fibrillation (AF). Cardioversion may also be considered, along with pharmacologic cardioversion, for stable patients with these dysrhythmias.¹

While cardioversion is generally well-tolerated, complications can occur. Most of these complications are self-limiting (e.g. EKG changes, hypotension related to sedation delivered to perform the procedure) or relatively benign (e.g.superficial skin burns). However, cardioversion does have the potential to cause life-threatening complications, including thromboembolic events, dangerous dysrhythmias, and hemodynamic decompensation.

Understanding which patients are at highest risk for immediate, life-threatening complications following cardioversion—as well as how to manage those risks—is of critical importance for the emergency medicine physician.

High risk patients: who crashes?

Patients with pre-existing cardiovascular diseases, older patients

Older age and certain chronic cardiovascular diseases have been implicated in the development of acute onset, life-threatening complications following cardioversion.^3-9

Multiple studies have shown that patients with pre-existing structural heart disease are at risk for developing acute pulmonary edema following electrical cardioversion.^3,4,10,11

A 2017 retrospective study by Leitman et al. found that, among the subset of patients who underwent electrical cardioversion for AF and subsequently developed complications, the strongest independent predictor of any complication and death during hospitalization was severe mitral or aortic regurgitation, followed by pulmonary hypertension. Other cardiovascular diseases—including diabetes, left ventricular hypertrophy (LVH), left ventricular dysfunction, and recurrent AF—were also predictive of severe complications and/or in-hospital mortality, though not independently.Among the subset of patients who died in the acute period following electrical cardioversion, fatal complications included: respiratory failure, pulmonary edema, arrythmias, and pulmonary embolism, among others.³

Case reports have described the development of stress cardiomyopathy following electrical cardioversion.^12-16 In all of these cases, the patients were older, had chronic cardiovascular disease, or both. In most of these patients, stress cardiomyopathy led to the development of pulmonary edema and/or cardiogenic shock requiring intensive supportive management. The exact mechanism by which electrical cardioversion led to stress cardiomyopathy in these patients is not known, though catecholamine-induced cardiac injury and direct electrical injury have both been proposed as mechanisms.¹⁷

The presence of cardiovascular disease and age also have a bearing upon risk of thromboembolism. It is well-known that thromboembolism is a risk for patients who undergo any type of cardioversion for AF (even spontaneous), especially in the absence of anticoagulation or if AF has been present for 12 hours or more.^5-8,18 In certain subgroups—including older patients, female patients, and patients with heart failure or diabetes—the risk is particularly high.^5,7 Thromboembolism can occur due to dislodgement of left atrial thrombi present at the time of cardioversion or when a new thrombus forms during the period of post-cardioversion left atrial mechanical dysfunction.^2,19

Multiple studies have shown that a non-negligible proportion of individuals, despite being on appropriate anticoagulation therapy, still have left atrial thrombus visible on TEE prior to planned cardioversion. Structural heart disease also appears to be a risk factor in these cases.^19-24

Patients who undergo inappropriate unsynchronized cardioversion

Arrhythmias and conduction abnormalities are frequently observed after cardioversion. These arrhythmias are usually benign, but clinically or hemodynamically significant arrhythmias such as ventricular fibrillation (VF) and sustained VT occur as well.^2,25-32

If cardioversion is performed inappropriately, particularly during the relative refractory period of the cardiac cycle, it may induce VF. Shocks that are not correctly synchronized to the QRS complex can occur due to operator error (i.e. the operator does not engage the “sync” function on the defibrillator) or machine error (i.e. the defibrillator does not correctly identify the QRS complexes).

Numerous case reports describe the phenomenon of inappropriate synchronization with T waves leading to VF immediately after cardioversion. ^25-32  In all of these cases, the presenting rhythm was AF with a pre-excitation syndrome such as Wolff-Parkinson-White (WPW) syndrome.

In patients with WPW, the simultaneous occurrence of AF can cause rapid ventricular activation via the accessory pathway and lead to an irregular wide-complex tachycardia.³³  In these cases, there is usually variable QRS morphology, depending on how much conduction is through the AV node and how much is through the accessory pathway. If the refractory period of the accessory pathway is short, antegrade conduction to the ventricles occurs mostly via the accessory pathway, and the QRS complexes are relatively wide and bizarre in appearance. The ventricular rate might be very rapid (>300 beats per minute) due to 1:1 conduction from the atrium to the ventricles.³⁴ QRS complexes in these cases may also have small amplitude relative to the T wave, making them difficult to distinguish from T waves. Thus, a defibrillator may mistake the T waves for QRS complexes and deliver an unsynchronized shock during the vulnerable repolarization phase of the cardiac cycle.

Patients with AF and pre-excitation syndromes such as WPW may have bizarre QRS complexes that are difficult to distinguish from T waves. In these cases, a mechanical defibrillator may inappropriately identify a T wave as a QRS complexes and deliver an asynchronous shock. Patients who receive asynchronous shocks are at high risk of developing VF.

How can we improve?

Assess risk of electrical cardioversion using historical data, a targeted physical exam, data obtained on the day of presentation, and risk stratification tools

Minimizing complications associated with electrical cardioversion begins with careful patient selection. Ideally (that is, if the patient is stable and time allows), the emergency medicine physician should do the following:

1. Search the medical record for relevant historical information, with particular attention to prior EKGs, echocardiograms, and evidence of pre-existing cardiac disease (g. cardiac catheterization reports, stress tests, and cardiology office visits). Patient often do not know or do not communicate these crucial historical data.
2. Perform a targeted physical exam. Does the patient appear well, obese, or chronically ill? Do they have evidence of volume overload (g. rales on pulmonary auscultation, lower extremity edema)? Do they have sequelae of uncontrolled diabetes such as decreased sensation in the distal extremities, diabetic ulcers, or amputation?
3. Collect pertinent data on the data of the visit, including a complete metabolic panel (CMP), a complete blood count (CBC), and PT/PTT/INR for patients who are prescribed anticoagulation. Obtain an EKG and compare to prior EKGs if available. Does the patient have LVH, evidence of conduction abnormalities, or other abnormalities suggestive of structural heart disease? Has the patient presented with a dysrhythmia before, or have they historically been in sinus rhythm? If able, obtain a bedside echocardiogram to assess for the presence of systolic dysfunction, LVH, and other structural abnormalities.
4. Use risk stratification tools (g. CHA₂DS₂-VASc score for stroke risk in patients with AF), patient demographics, and details of the history can help emergency medicine physicians weigh the risks and benefits of cardioversion.

All of this information will inform the physician’s overall assessment of a patient’s risk, even for patients who provide vague or limited history, or for whom prior data is not available. While exact quantification of risk is difficult, it is critical to consider carefully and, when able, have an informed discussion with the patient about their particular risk factors.

Some risk factors are binary; for example, a patient does or does not have diabetes, or heart failure, etc. Other risk factors, particularly age, exist along a spectrum. Various studies have found different age cut offs at which the risk of a particular complication or complications in general becomes statistically significant. Leitman et al. found that patients older than 72 were at risk for a number of complications.³ Davarashvili et al. found that patients who were 79 (+/- 9) years old were at greater risk of pulmonary congestion (p < 0.001).⁴ Airaksinen et al. found that thromboembolic complications were statistically more likely in patient aged 69.9 (+/- 9.3) (p < 0.0001).⁵ From a practical perspective, use of the age cut offs in the CHA₂DS₂-VASc score is a reasonable approach to risk stratification by age, wherein patients aged 65-74 are considered at increased risk, and patients 75 or older are at especially increased risk.

If the decision is made to proceed with anticoagulation, be aware of—and prepared to manage—potential procedural complications, particularly in high risk patients.

Treat potentially modifiable conditions.

Treatment of potentially modifiable conditions that may be contributing to the presenting dysrhythmia should be considered prior to cardioversion if possible in high risk patients—to avoid the risks of electrical cardioversion, optimize the patient should cardioversion become necessary, and to facilitate maintenance of sinus rhythm if successful cardioversion is achieved.^7,35  Optimization might include the management of hypertension, treatment of volume overload with diuresis, volume repletion, respiratory support with BiPAP or high flow oxygen via nasal cannula, provision of antibiotics if there is concern for infection, and symptom management, depending on the patient.

Strongly consider anticoagulation in appropriate patients.

Appropriate anticoagulation reduces the risk of thromboembolism following cardioversion, particularly in higher risk patients.^5-8 Current guidelines recommend systemic anticoagulation for at least 3 weeks with a novel oral anticoagulant (NOAC) or vitamin K antagonist (VKA) prior to cardioversion for AF among patients with an unknown duration of AF, definite duration of AF greater than 48 hours, or an identified thrombus on TEE.⁷ Anticoagulation should also be continued for at least 4 weeks after elective electrical cardioversion in all but patients at lowest risk for stroke (i.e.CHA₂DS₂-VASc 0 in men, 1 in women, for whom it may be optional).^[7]  

Of course, there are emergent cases in which it is not possible to adhere to these guidelines regarding optimal anticoagulation status prior to pursuing electrical cardioversion. Following cardioversion in these cases, the entire care team should be vigilant for changes in neurologic status that might suggest CVA. If the patient experiences changes in vital signs—particularly hypotension, tachycardia, and hypoxia—pulmonary embolism should be considered on the differential. Anticoagulation with either a NOAC, low-molecular-weight heparin, or heparin should be strongly considered in all but the lowest risk patients and/or those with absolute contraindications to anticoagulation therapy.⁷

Know how to distinguish AF with pre-excitation syndrome from other dysrhythmias on EKG.

It may not be known, by the physician or the patient, whether a patient has a pre-excitation syndrome like WPW. Individuals with accessory pathways only display features characteristic of pre-excitation when impulses are actually conducted over the accessory pathway, which is usually intermittent.³³ Emergency medicine physicians may mistake AF with pre-excitation for other dysrhythmias, including VT, or AF with left bundle branch block (LBBB), which can lead to inappropriate, even dangerous, management of the patient. Knowing what EKG features distinguish AF with pre-excitation may help prevent these complications.

The ECG features of AF with WPW include a rapid (200-300 bpm), irregular rhythm with wide QRS complexes showing variable shape and morphology.^[3]

Further Reading: How can the rhythm in the EKG above be distinguished from AF with LBBB?

(See answer at https://litfl.com/pre-excitation-syndromes-ecg-library/.)

Further Reading: How can this EKG be distinguished from torsades de pointes?

(See answer at https://litfl.com/pre-excitation-syndromes-ecg-library/.)

 Case Conclusion:

After discussion of risks and benefits, the emergency medicine team and the patient decided to proceed with electrical cardioversion, primarily because the patient preferred the earliest possible resolution of his symptoms. He was successfully cardioverted to sinus rhythm after a single shock was administered under light procedural sedation without complication. Because the patient’s CHA₂DS₂-VASc score was zero, he was considered low risk and did not wish to initiate anticoagulation. He was discharged home in improved condition with a referral for expedited cardiology follow up.

Take Home Points:

• Patients with pre-existing cardiovascular disease, particularly structural heart disease and older patients (defined as age 65 and older, to error on the side of inclusion) are at risk for life-threatening complications following cardioversion. Be prepared to manage complications when cardioverting these patients.
• Patients with pre-excitation syndromes may have bizarre QRS complexes that are difficult to distinguish from T waves, which can lead to asynchronous shock delivery and the development of VF.
• All but the lowest risk patients should be anticoagulated prior to and following cardioversion unless they have a direct contraindication.

References:

1. Ong MEH, Leong BSH, Ng YY. Defibrillation and electrical cardioversion. In Tintinalli JE, ed. Tintinalli’s Emergency Medicine: A Comprehensive Study-Guide. 9^th United States of America: McGraw-Hill Education; 2020: 149-153.
2. Knight BP. Cardioversion for Specific Arrhythmias. UpToDate. https://www.uptodate.com/contents/cardioversion-for-specific-arrhythmias?search=cardioversion%20complications&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H2560757. Published May 1, 2019. Accessed March 6, 2021.
3. Leitman M, Tyomkin V, Peleg E, et al. When cardioversion may be complicated. Isr Med Assoc J. 2017;19(5):282-288.
4. Davarashvili I, Acha MR, Glikson M, et al. Pulmonary congestion complicating atrial fibrillation cardioversion. Am J Cardiol. 2018;122(10):1701-1706.
5. Airaksinen KEJ, Gronberg T, Nuotio I, et al. Thromboembolic complications after cardioversion of acute atrial fibrillation: the FinCV (Finnish CardioVersion) study. J Am Coll Cardiol. 2013;62(13):1187-1192.
6. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC guidelines for the management of atrial fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2016;37:2893-2962.
7. Hindricks G, Potpara T, Dagres N, et al. 2020 ESC guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association of Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2020;42(5):373-498.
8. Hansen ML, Jepsen RM, Olesen JB, et al. thromboembolic risk in 16 274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy. 2015;17:18-23.
9. Khan MU, Khouzam RN, Khalid H, et al. Cardiogenic shock following electro-cardioversion of new onset atrial flutter. Heart Lung. 2013;42(6):462-464.
10. Gowda RM, Misra D, Khan IA, Schweitzer P. Acute pulmonary edema after cardioversion of cardiac arrhythmias. Int J Cardiol. 2003;92(2-3):271-274.
11. Wang RN, Khordipour E. Acute pulmonary edema: a rare cause of dyspnea after electrical cardioversion. J Emerg Med. 2020;58(3):497-499.
12. Pir MS, Saqib N, Oza F, Rao M. Iatrogenic heartbreak: stress cardiomyopathy after electrical cardioversion. J Am Coll Cardiol. 2019;73(9_Supplement_1): 2701
13. Landi A, De Servi S. Takotsubo syndrome and electrical storm following electrical cardioversion of atrial fibrillation: cause, consequence or both? J Cardiovasc Med (Hagerstown). 2021;22(2):139-142.
14. Zaghlol R, Hritani R, O’Donoghue S. Shock begets shock: a case of direct current cardioversion-induced takotsubo cardiomyopathy. HeartRhythm Case Rep. 2019;5(6):310-313.
15. McCutcheon K, Butler I, Vachiat A, Manga P. Takotsubo syndrome in an elderly woman due to electrical cardioversion. Int J Cardiol. 2016;224:69-71.
16. Siegfried JS, Bhusri S, Guttenplan N, Coplan NL. Takotsubo cardiomyopathy as a sequela of elective direct-current cardioversion for atrial fibrillation. Tex Heart Inst J. 2014;41(2):184-187.
17. Ghadri JR, Wittstein IS, Prasad A et al. International expert consensus document on takotsubo syndrome (part I): clinical characteristics, diagnostic criteria, and pathophysiology. Eur Heart J. 2018;39(2018):2032-2046.
18. Nuotio I, Hartikainen JE, Gronberg et al. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. 2014;312:647-649.
19. Bursi F, Santangelo G, Ferrante G, et al. Prevalence of left atrial thrombus by real time three-dimensional echocardiography in patients undergoing electrical cardioversion of atrial fibrillation: A contemporary cohort study. Echocardiography. 2021;0. https://doi.org/10.1111/echo.15015. Accessed March 7, 2021.
20. Durmaz E, Karpuz MH, Bilgehan K, et al. Left atrial thrombus in patients with atrial fibrillation and under oral anticoagulant therapy; 3-D transesophageal echocardiographic study. Int J Cardiovasc Imaging. 2020;36(6):1097-1103.
21. Hwang J, Park HS, Jun SW, et al. The incidence of left atrial appendage thrombi on transesophageal echocardiography after pretreatment with apixaban for cardioversion in the real-world practice. PLoS One.2018;13(12):e0208734.
22. Niku AD, Shiota T, Siegel RJ, Rader F. Prevalence and resolution of left atrial thrombus in patients with nonvalvular atrial fibrillation and flutter with oral anticoagulation. Am J Cardiol. 2019;123(1):63-68.
23. Zylla MM, Pohlmeier M, Hess A, et al. Prevalence of intracardiac thrombi under phenprocoumon, direct oral anticoagulants (dabigatran and rivaroxaban), and bridging therapy in patients with atrial fibrillation and flutter. Am J Cardiol. 2015;115(5):635-640.
24. Fukuda S, Watanabe H, Shimada K, et al. Left atrial thrombus and prognosis after anticoagulation therapy in patients with atrial fibrillation. J Cardiol. 2011;58(3):266-277.
25. Danon A, Militianu A, Schliamser JE. Cardioversion of pre-excited atrial fibrillation leading to ventricular fibrillation-case report and review of literature. Am J Emerg Med. 2019;37(8):1539-1543.
26. Kaufmann MR, McKillop MS, Burkart TA, et al. Iatrogenic ventricular fibrillation after direct-current cardioversion of preexcited atrial fibrillation caused by inadvertent t-wave synchronization. Tex Heart Inst J. 2018;45(1):39-41.
27. Ikeda S, An Y, Yanagisawa M, et al. Iatrogenic ventricular fibrillation caused by inappropriately synchronized cardioversion in a patient with pre-excited atrial fibrillation: A case report. J Cardiol Cases. 2020;23(1):31-34.
28. Ebrahimi R, Rubin SA. Electrical cardioversion resulting in death from synchronization failure. Am J Cardiol.1994;74(1):100-102.
29. Adlam D, Azeem T. Ventricular fibrillation during electrical cardioversion of pre-excited atrial fibrillation. Postgrad Med J. 2003;79(931):297-299.
30. Taylor N. Direct current cardioversion causing ventricular fibrillation in Wolff-Parkinson-White syndrome. Emerg Med Australas. 2013;25(5):612-614.
31. Xavier LC, Memon A. Synchronized cardioversion of unstable supraventricular tachycardia resulting in ventricular fibrillation. Ann Emerg Med. 2004;44:178-180.
32. O’Connell M, Bernard A. A serious cause of panic attack. Case Rep Emerg Med. 2012; 2012:393275.
33. Burns E, Buttner R. Pre-excitation Syndromes. Life in the Fast Lane. https://litfl.com/pre-excitation-syndromes-ecg-library. Published Feb 8, 2021. Accessed March 7, 2021.
34. Prutkin JM. ECG Tutorial: Preexcitation Syndromes. UpToDate. https://www.uptodate.com/contents/ecg-tutorial-preexcitation-syndromes?search=ecg%20tutorial:%20preexcitation%20syndromes&source=search_result&selectedTitle=1~135&usage_type=default&display_rank=1. Published Dec 30, 2019. Accessed March 7, 2021.
35. Rienstra M, Hobbelt AH, Alings M, et al. Targeted therapy of underlying conditions improves sinus rhythm maintenance in patients with persistent atrial fibrillation: results of the RACE 3 trial. Eur Heart J. 2018;39:2987-2996.