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Atrial flutter: the dangers of cardioversion
International Journal of Cardiology 81 (2001) 93–95 www.elsevier.com / locate / ijcard
Letter to the Editor
Atrial flutter: the dangers of cardioversion C. Charalambous, R.A. Malik*, M. Davies, A.M. Heagerty University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester M13 9 WL, UK Received 16 May 2001; accepted 16 July 2001
1. Introduction Exacerbation or development of pulmonary oedema is a recognised complication during cardioversion of atrial fibrillation or flutter to sinus rhythm by countercurrent electric shock [1]. We report a case of development of acute intractable pulmonary oedema and death following cardioversion of atrial flutter by overdrive atrial pacing.
2. Case history A 67-year-old man with a previous myocardial infarction, CABG and paroxysmal atrial flutter was admitted with palpitations and shortness of breath. A 12-lead electrocardiogram showed atrial flutter at a rate of 130 / min, and a chest radiograph demonstrated cardiomegaly (CTR-17 / 32) and an echocardiogram demonstrated a left ventricular ejection fraction of 40%. Amiodarone 200 mg daily and Verapamil (40 mg tds) achieved control of his ventricular rate (72 / min) (Fig. 1a). On discharge the patient stopped his medication, and presented 5 days later in atrial flutter, with a ventricular rate of 144 / min (Fig. 1b), and a chest radiograph which demonstrated pulmonary oedema. Amiodarone (200 mg daily) and Frusemide (80 mg daily) were recommenced, his pulmonary oedema resolved, but he remained in atrial flutter at a *Corresponding author. Tel.: 144-161-276-4406; fax: 144-161-2744740. E-mail address: [email protected] (R.A. Malik).
ventricular rate of 100 / min. He was cardioverted to sinus rhythm at a rate of 80 bpm with atrial overdrive pacing. However, within 5 h of cardioversion he became extremely dyspnoeic with a regular pulse (96 / min) (Fig. 1c), reduction in oxygen saturation 70–80% on 10 l of oxygen (Fig. 2). He developed florid pulmonary oedema confirmed on a chest radiograph. A myocardial infarction screen was negative. Despite extensive pharmacological intervention (i.v. Frusemide 300 mg, Metolazone 5 mg, Enalapril 30 mg, Nitrocine 192 mg daily), he deteriorated and died 6 days later from intractable heart failure.
3. Discussion Atrial fibrillation / flutter is the commonest sustained cardiac rhythm disorder [2]. Pharmacological ventricular rate control forms the mainstay of therapy, however increasing attention is focusing on non-pharmacological interventions to restore sinus rhythm and include direct cardioversion, atrial overdrive pacing or catheter ablation with permanent pacing [3]. Pulmonary oedema following cardioversion of atrial tachyarrhythmias to sinus rhythm by electrical counter shock has been reported previously and attributed to electric current induced myocardial damage [1]. We report the development of intractable heart failure following cardioversion of atrial flutter to sinus rhythm by overdrive atrial pacing, indicating that restoration of sinus rhythm rather than the electric shock may be the cause of the haemodynamic
0167-5273 / 01 / $ – see front matter 2001 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00532-0
94
C. Charalambous et al. / International Journal of Cardiology 81 (2001) 93 – 95
Fig. 1. ECG traces — lead II. (a) Controlled atrial flutter on Amiodarone and Verapamil. (b) Fast atrial flutter prior to overdrive pacing. (c) Controlled sinus rhythm post atrial overdrive pacing.
deterioration. The underlying mechanism for this is unclear. Atrial tachyarrhythmias are associated with cytosolic calcium overload of atrial myocytes and desensitization of the contractile machinery with
resultant atrial hypocontractility following restoration of sinus rhythm in animals with atrial fibrillation [4]. This may be compensated to some extent by fast atrial contraction [4]. However, restoration of sinus
Fig. 2. Plot of heart rate and oxygen saturation illustrating the reversion to sinus rhythm associated with the acute reduction in oxygen saturation secondary to intractable heart failure.
C. Charalambous et al. / International Journal of Cardiology 81 (2001) 93 – 95
rhythm with accompanied atrial hypocontractility may result in significant haemodynamic compromise and intractable pulmonary oedema. In such a situation there may be a case for temporarily pacing the atria at a higher rate (120–140) to maintain increased atrial output to prevent the development of acute pulmonary oedema or alleviate it once established.
References [1] Resnekov L, Medonald L. Pulmonary oedema following treatment of arrhythmia’s by direct current countershock. Lancet 1965;1:506– 8.
95
[2] Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart study. Circulation 1998;98:946–52. [3] Foran J, Rowland E. Pacing therapy to prevent atrial fibrillation. Br J Cardiol 2000;7:411–8. [4] Leistad E, Aksner G, Verburg E, Christiansen G. Atrial contractile dysfunction after short term atrial fibrillation is reduced by verapamil but increased by BAY K8644. Circulation 1996;93:1747–54.
Letter to the Editor
Atrial flutter: the dangers of cardioversion C. Charalambous, R.A. Malik*, M. Davies, A.M. Heagerty University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester M13 9 WL, UK Received 16 May 2001; accepted 16 July 2001
1. Introduction Exacerbation or development of pulmonary oedema is a recognised complication during cardioversion of atrial fibrillation or flutter to sinus rhythm by countercurrent electric shock [1]. We report a case of development of acute intractable pulmonary oedema and death following cardioversion of atrial flutter by overdrive atrial pacing.
2. Case history A 67-year-old man with a previous myocardial infarction, CABG and paroxysmal atrial flutter was admitted with palpitations and shortness of breath. A 12-lead electrocardiogram showed atrial flutter at a rate of 130 / min, and a chest radiograph demonstrated cardiomegaly (CTR-17 / 32) and an echocardiogram demonstrated a left ventricular ejection fraction of 40%. Amiodarone 200 mg daily and Verapamil (40 mg tds) achieved control of his ventricular rate (72 / min) (Fig. 1a). On discharge the patient stopped his medication, and presented 5 days later in atrial flutter, with a ventricular rate of 144 / min (Fig. 1b), and a chest radiograph which demonstrated pulmonary oedema. Amiodarone (200 mg daily) and Frusemide (80 mg daily) were recommenced, his pulmonary oedema resolved, but he remained in atrial flutter at a *Corresponding author. Tel.: 144-161-276-4406; fax: 144-161-2744740. E-mail address: [email protected] (R.A. Malik).
ventricular rate of 100 / min. He was cardioverted to sinus rhythm at a rate of 80 bpm with atrial overdrive pacing. However, within 5 h of cardioversion he became extremely dyspnoeic with a regular pulse (96 / min) (Fig. 1c), reduction in oxygen saturation 70–80% on 10 l of oxygen (Fig. 2). He developed florid pulmonary oedema confirmed on a chest radiograph. A myocardial infarction screen was negative. Despite extensive pharmacological intervention (i.v. Frusemide 300 mg, Metolazone 5 mg, Enalapril 30 mg, Nitrocine 192 mg daily), he deteriorated and died 6 days later from intractable heart failure.
3. Discussion Atrial fibrillation / flutter is the commonest sustained cardiac rhythm disorder [2]. Pharmacological ventricular rate control forms the mainstay of therapy, however increasing attention is focusing on non-pharmacological interventions to restore sinus rhythm and include direct cardioversion, atrial overdrive pacing or catheter ablation with permanent pacing [3]. Pulmonary oedema following cardioversion of atrial tachyarrhythmias to sinus rhythm by electrical counter shock has been reported previously and attributed to electric current induced myocardial damage [1]. We report the development of intractable heart failure following cardioversion of atrial flutter to sinus rhythm by overdrive atrial pacing, indicating that restoration of sinus rhythm rather than the electric shock may be the cause of the haemodynamic
0167-5273 / 01 / $ – see front matter 2001 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 01 )00532-0
94
C. Charalambous et al. / International Journal of Cardiology 81 (2001) 93 – 95
Fig. 1. ECG traces — lead II. (a) Controlled atrial flutter on Amiodarone and Verapamil. (b) Fast atrial flutter prior to overdrive pacing. (c) Controlled sinus rhythm post atrial overdrive pacing.
deterioration. The underlying mechanism for this is unclear. Atrial tachyarrhythmias are associated with cytosolic calcium overload of atrial myocytes and desensitization of the contractile machinery with
resultant atrial hypocontractility following restoration of sinus rhythm in animals with atrial fibrillation [4]. This may be compensated to some extent by fast atrial contraction [4]. However, restoration of sinus
Fig. 2. Plot of heart rate and oxygen saturation illustrating the reversion to sinus rhythm associated with the acute reduction in oxygen saturation secondary to intractable heart failure.
C. Charalambous et al. / International Journal of Cardiology 81 (2001) 93 – 95
rhythm with accompanied atrial hypocontractility may result in significant haemodynamic compromise and intractable pulmonary oedema. In such a situation there may be a case for temporarily pacing the atria at a higher rate (120–140) to maintain increased atrial output to prevent the development of acute pulmonary oedema or alleviate it once established.
References [1] Resnekov L, Medonald L. Pulmonary oedema following treatment of arrhythmia’s by direct current countershock. Lancet 1965;1:506– 8.
95
[2] Benjamin EJ, Wolf PA, D’Agostino RB, Silbershatz H, Kannel WB, Levy D. Impact of atrial fibrillation on the risk of death: the Framingham Heart study. Circulation 1998;98:946–52. [3] Foran J, Rowland E. Pacing therapy to prevent atrial fibrillation. Br J Cardiol 2000;7:411–8. [4] Leistad E, Aksner G, Verburg E, Christiansen G. Atrial contractile dysfunction after short term atrial fibrillation is reduced by verapamil but increased by BAY K8644. Circulation 1996;93:1747–54.