lable at ScienceDirect

Heart & Lung 42 (2013) 462e464

Contents lists avai

Heart & Lung

journal homepage: www.heartandlung.org

Cardiogenic shock following electro-cardioversion of new onset atrial flutter

M. Usman Khan, MD a, Rami N. Khouzam, MD, FACC, FACP, FASNC, FASE, FSCAI a,*, Heena Khalid, MD b,Riaz Baqir, MD, FACC, FACP c, Marriyam Moten, MDd

aDivision of Cardiovascular Diseases, Department of Internal Medicine, University of Tennessee Health Science Center Memphis, 6283 Common Oaks Crt # 106,Memphis, TN 38120, USAbDepartment of Internal Medicine, University of Tennessee Health Science Center Memphis, TN, USAcDepartment of Cardiology, Via Christie Medical Center Pittsburg, KS, USAdDepartment of Cardiology, Kansas City Veterans Affair Medical Center Kansas, MO, USA

a r t i c l e i n f o

Article history:Received 13 May 2013Received in revised form14 July 2013Accepted 22 July 2013Available online 19 August 2013

Conflicts of interest: All authors have none to declar* Corresponding author. Tel.: þ1 901747 5805, þ1 51

901 747 5805.E-mail address: khouzamrami@yahoo.com (R.N. K

0147-9563/$ e see front matter � 2013 Elsevier Inc.http://dx.doi.org/10.1016/j.hrtlng.2013.07.007

a b s t r a c t

Transient hypotension and atrial stunning are known complications of electro-cardioversion forsupra-ventricular tachyarrhythmias, however, a clinically significant cardiac failure is extremely rare inthis setting.

We, herein, present a 77-year-old African American male who underwent electro-cardioversionfollowing an unremarkable transesophageal echocardiogram (TEE) for a symptomatic atrial flutter of anew onset. Immediately post-cardioversion, he suffered severe hypotension with a depressed LV systolicfunction. IV dobutamine stabilized his blood pressure.

� 2013 Elsevier Inc. All rights reserved.

Introduction

Electro-cardioversion (ECV) is life-saving when applied in ur-gent circumstances.1 Although ECV appears fairly simple, seriousconsequences might occur, especially if inappropriately per-formed.1 Thromboembolism, supra- and ventricular arrhythmias,bradycardia and conduction abnormalities, myocardial necrosis,myocardial dysfunction, transient hypotension, pulmonary edemaand skin burns are known complications of the procedure.1e5

A global LV dysfunction due tomyocardial stunningmay be seenin patients with cardiac arrest who have undergone successfulcardiopulmonary resuscitation.1 However, a clinically significantcardiac failure post-ECV performed for atrial arrhythmias is highlyuncommon. Herein, we report a unique case of cardiogenic shockpost-ECV in a patient with new onset atrial flutter.

Case report

A 77-year-old African American male presented with new onsetof intermittent dyspnea for 1 month. He denied any chest pain,palpitations, dizziness or edema. His past medical history was un-remarkable. His home medications consisted of baby aspirin,

e.6 780 3762 (mobile); fax: þ1

houzam).

All rights reserved.

multivitamin and fish oil. Physical exam revealed an averagelooking male in mild distress. His vitals included pulse 150/minregular, BP 135/95 sitting, RR 18/min. Rest of his physical examwasunremarkable. His blood counts, metabolic profile and TSH werewithin normal limits. An electrocardiogram revealed atrial flutter ata rate of around 300/min with 2:1 AV conduction (Fig. 1). His heartrate was controlled with intravenous (IV) cardizem and he wasstarted on IV heparin infusion.

A transthoracic echocardiogram (TTE) revealed a good leftventricular (LV) systolic function and normal sized atria withoutany thrombi (Fig. 2). Later, following confirmation on trans-esophageal echocardiogram (TEE), hewas cardioverted successfullyby a single 100 J synchronized direct current (DC) monophasicshock (Fig. 3). Immediately thereafter, his BP dropped to70/30 mm Hg and he started experiencing apneic spells. IV fluidbolus minimally helped BP but markedly raised his jugular venouspressure and caused bilateral basal rales. A limited bedside TTErevealed a severely depressed LV systolic function (Fig. 4). He wasstarted on IV dobutamine which stabilized his blood pressure afterseveral hours and later patient was discharged in a stable condition.His repeat TTE 3 months later showed a preserved LV function.

Discussion

Global left ventricular dysfunction due to myocardial stunningseen in patients with cardiac arrest post cardiopulmonary resus-citation is related in part to defibrillation.1 Xie et al showed thatthe severity of post-resuscitation myocardial dysfunction is

Fig. 1. 12 lead EKG showing atrial flutter (pre-cardioversion).

Fig. 2. Pre-cardioversion: 2D-echocardiogram; 4 chambers view: diastolic (left upper quadrant), systolic (right upper quadrant), parasternal long axis view: diastolic (left lowerquadrant), systolic (right lower quadrant).

Fig. 3. 12 lead EKG showing normal sinus rhythm (post-cardioversion).

M.U. Khan et al. / Heart & Lung 42 (2013) 462e464 463

Fig. 4. Post-cardioversion: 2D-echocardiogram; 4 chambers view: diastolic (left upper quadrant), systolic (right upper quadrant), parasternal long axis view: diastolic (left lowerquadrant), systolic (right lower quadrant).

M.U. Khan et al. / Heart & Lung 42 (2013) 462e464464

related to the magnitude of the electrical energy of the deliveredshock in Sprague-Dawly rats.2 Similarly, Tang et al found thatbiphasic waveform defibrillation with a fixed energy of 150 Jproved to be as effective as conventional monophasic dampedsine waveform defibrillation for restoration of spontaneous cir-culation, with significantly lower delivered energy. This wasassociated with significantly less severity of post-resuscitationmyocardial dysfunction.3

The mechanism by which these electrical shocks produce injuryis only partially understood and may include pathological pro-cesses implicated in tachycardia induced cardiomyopathy such asmyocyte and extracellular matrix remodeling, and abnormalities ofcardiac calcium regulation.4 Free ascorbyl radicals are generatedafter defibrillation with electrodes applied directly to the epicar-dium.4 Their concentration in coronary sinus blood is also increasedin direct proportion to the delivered energy.4 These free radicalsmay explain damaged sarcolemma and mitochondria, calciumoverload, impaired mitochondrial function and cellular oxidativemetabolism, and cellular swelling.4 ACE inhibitors may attenuatefree radical generation.4

The transient atrial contractile dysfunction after cardioversion,known as atrial stunning, can occur whether sinus rhythm isrestored spontaneously, by external or internal DC (electric) car-dioversion or by antiarrhythmic medications.5 The duration of the

left atrial dysfunction appears to be related in part to the durationof atrial fibrillation/flutter.5 Although transient hypotension andatrial stunning are known complications of ECV, a clinically sig-nificant cardiac failure is highly uncommon post-cardioversion inatrial tachyarrhytmias. Hence our case highlights an uncommonphenomenon where a commonly performed procedure can resultin a clinically significant complication. It further highlights the needfor further studies to identify patients at risk of having clinical heartfailure post-cardioversion.

References

1. Kern KB, Hilwig RW, Rhee KH, et al. Myocardial dysfunction after resuscitationfrom cardiac arrest: an example of global myocardial stunning. J Am Coll Cardiol.1996;28(1):232.

2. Xie J, Weil MH, Sun S, et al. High-energy defibrillation increases the severity ofpostresuscitation myocardial dysfunction. Circulation. 1997;96(2):683.

3. Tang W, Weil MH, Sun S. Low-energy biphasic waveform defibrillation reducesthe severity of postresuscitation myocardial dysfunction. Crit Care Med. 2000Nov;28(11 suppl):N222eN224.

4. Pagan-Carlo LA, Garcia FA, Hutchison JL, Buettner GR, Kerber RE. Captoprillowers coronary venous free radical concentration after direct current cardiacshocks. Chest. 1999;116:484e487.

5. Grimm RA, Stewart WJ, Maloney JD, et al. Impact of electrical cardioversion foratrial fibrillation on left atrial appendage function and spontaneous echocontrast: characterization by simultaneous transesophageal echocardiography.J Am Coll Cardiol. 1993;22(5):1359.