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Electrical storm and termination with propofol therapy: A case report
International Journal of Cardiology 128 (2008) e6 – e8 www.elsevier.com/locate/ijcard
Letter to the Editor
Electrical storm and termination with propofol therapy: A case report Siva K. Mulpuru a,⁎, Darshan V. Patel b , Sabrina L. Wilbur b , Balendu C. Vasavada b , Tejani Furqan b a
Department of Internal Medicine, Long Island College Hospital, NY, United States b Division of Cardiology, Long Island College Hospital, NY, United States Received 27 February 2007; accepted 19 May 2007 Available online 13 August 2007
Keywords: Propofol; Defibrillator; Electrical storm
1. Introduction Approximately 50 to 70% of the patients treated with implantable cardioverter defibrillator (ICD) receive device based therapy within first 2 years following implantation [1]. However, a few patients receive multiple appropriate shocks during a short period of time. Electrical storm (ES) is a syndrome of recurrent ventricular tachycardia or fibrillation occurring two or more times in a 24 h period and usually requires electrical cardioversion or defibrillation [2]. We describe an elderly patient who presented with ES that did not respond to conventional medications like metoprolol, amiodarone and lidocaine. It was successfully terminated with Propofol infusion therapy. 2. Case report A 76 year old Caucasian male presented to the emergency room with multiple ICD discharges for 1 day. The discharges started when he was sleeping and continued till the following morning. He denied any chest pain, shortness of breath on presentation. He was noted to have incessant polymorphic ventricular tachycardia (VT) with QT prolongation (Fig. 1). He was given amiodarone, lidocaine, and metoprolol with little response in the emergency room. He was electively intubated for air way protection due to altered mental status. His electrolytes were replaced and he was immediately transferred to the cardiac catheterization lab for a diagnostic angiogram. ⁎ Corresponding author. 94 Amity St Apt 4E, Brooklyn NY 11201. Tel.: +1 718 928 5013; fax: +1 718 928 1300. E-mail address: [email protected] (S.K. Mulpuru). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.05.052
His past medical history includes recent ST elevation myocardial infarction with four vessel bypass, mitral valve replacement and a MAZE procedure. He had severe dilated ischemic cardiomyopathy with an ejection fraction of 30%, longstanding diabetes, hypertension and dyslipidaemia. During the post operative period he had cardiac arrest requiring placement of a dual chamber ICD (Entrust, Medtronic, USA). He quit smoking many years ago and denied any alcohol or drug use. His home medications included amiodarone, digoxin, furosemide, spironolactone, metoprolol, aspirin, coumadin, atrovastatin and rosiglitazone. He was initially sedated with midazolam with little effect and later was switched over to propofol. VT as well as ICD discharges subsided after the patient was started on propofol drip. The diagnostic angiogram showed occlusion of the proximal anastomosis of the RCA (right coronary artery) graft which was opened and he had a balloon pump to improve myocardial perfusion. ICD interrogation suggested that he received a total of 61 appropriate shocks (Fig. 2) before propofol therapy and the device was reprogrammed for a higher rate and a tighter AV (atrio-ventricular) delay for overdrive suppression of paroxysmal VT. He had a protracted recovery complicated by sternal wound infection but was eventually discharged home to lead a functional life. 3. Discussion Propofol is a substituted isoprophylphenol, short acting general anesthetic agent that acts through its interactions with gamma-amino butyric acid receptors. In human electrophysiological studies propofol has been shown to have no direct effect on the sino-atrial activity, intra-atrial
S.K. Mulpuru et al. / International Journal of Cardiology 128 (2008) e6–e8
e7
Fig. 1. EKG showing AV sequential pacing followed by VT.
activity or atrio-ventricular conduction [3] (Table 1). The cardiovascular effects of propofol are due to modulation of the autonomous nervous system. The decrease in heart rate and mean arterial pressure seen with propofol are due to central vagotonic effects, resetting of baroreflexes and also due to inhibition of sympathetic activity. The bradyarrythmias and heart blocks seen with propofol are likely explained by an increased sensitivity to parasympathetic stimulus due to reduction in sympathetic tome [4].
Ventricular tachycardia is the recorded arrhythmia in 90% of electrical storms. Precipitating factors could only be found in 36% of the cases [5]. Patients presenting with low ejection fraction and chronic renal insufficiency are more likely to experience electrical storms. ES usually presents 6 months after ICD implantation. There is conflicting evidence on the effect of ES on mortality in the ICD recipients. However it has a huge psychological impact on patients in addition to increasing the ICD related treatment costs. New ischemia,
Fig. 2. ICD interrogation showing delivery of 61 shocks.
e8
S.K. Mulpuru et al. / International Journal of Cardiology 128 (2008) e6–e8
Table 1 Propofol and effects on the human heart Effects of propofol on the cardiac conducting system. ❖ In guinea pigs propofol reduces atrial rate and reduces AV conduction through M2 muscarinic receptor mechanism. ❖ In pigs, the sinus node and His-Purkinje system functions are depressed but there is no effect on AV node, or on the conduction of atria or ventricular tissue. ❖ In dogs there is no direct effect on the conduction system if complete autonomic blockade is implemented. ❖ In humans there is no direct effect on the SA node activity, intra-atrial or AV conduction. ❖ Propofol elevates defibrillation thresholds in humans and prolongs QT interval.
electrolyte abnormalities, metabolic profile, cardiac decompensation, and autonomic nervous system input alter the conduction properties of the myocardium and are involved in initiation of arrhythmia. Increased sympathetic activation has been implicated in the generation of electrical storm whereas sympathetic blockade has been shown to prevent VF and sudden death. Although beta-blocker and anti-arrhythmics are the main stay of therapy catheter ablation has been successfully used to treat ES. 4. Conclusion Propofol therapy in our patient was associated with both conversion as well as suppression of ventricular arrythmias.
To our knowledge this is the second reported case of successful treatment of ES with propofol. We believe that the anti-arrhythmic effects of propofol are due to the reduction in sympathetic tone. References [1] Credner SC, Klingenheben T, Mauss O, Sticherling C, Hohnloser SH. Electrical storm in patients with transvenous implantable cardioverterdefibrillators: incidence, management and prognostic implications. J Am Coll Cardiol 1998;32(7):1909–15. [2] Dorian P, Cass D. An overview of the management of electrical storm. Can J Cardiol 1997;13(Suppl A):13A–7A. [3] Burjorjee JE, Milne B. Propofol for electrical storm; a case report of cardioversion and suppression of ventricular tachycardia by propofol. Can J Anaesth 2002;49(9):973–7. [4] Romano R, Ciccaglioni A, Fattorini F, et al. Effects of propofol on the human heart electrical system: a transesophageal pacing electrophysiologic study. Acta Anaesthesiol Scand 1994;38(1):30–2. [5] Brigadeau F, Kouakam C, Klug D, et al. Clinical predictors and prognostic significance of electrical storm in patients with implantable cardioverter defibrillators. Eur Heart J 2006;27(6):700–7.
Letter to the Editor
Electrical storm and termination with propofol therapy: A case report Siva K. Mulpuru a,⁎, Darshan V. Patel b , Sabrina L. Wilbur b , Balendu C. Vasavada b , Tejani Furqan b a
Department of Internal Medicine, Long Island College Hospital, NY, United States b Division of Cardiology, Long Island College Hospital, NY, United States Received 27 February 2007; accepted 19 May 2007 Available online 13 August 2007
Keywords: Propofol; Defibrillator; Electrical storm
1. Introduction Approximately 50 to 70% of the patients treated with implantable cardioverter defibrillator (ICD) receive device based therapy within first 2 years following implantation [1]. However, a few patients receive multiple appropriate shocks during a short period of time. Electrical storm (ES) is a syndrome of recurrent ventricular tachycardia or fibrillation occurring two or more times in a 24 h period and usually requires electrical cardioversion or defibrillation [2]. We describe an elderly patient who presented with ES that did not respond to conventional medications like metoprolol, amiodarone and lidocaine. It was successfully terminated with Propofol infusion therapy. 2. Case report A 76 year old Caucasian male presented to the emergency room with multiple ICD discharges for 1 day. The discharges started when he was sleeping and continued till the following morning. He denied any chest pain, shortness of breath on presentation. He was noted to have incessant polymorphic ventricular tachycardia (VT) with QT prolongation (Fig. 1). He was given amiodarone, lidocaine, and metoprolol with little response in the emergency room. He was electively intubated for air way protection due to altered mental status. His electrolytes were replaced and he was immediately transferred to the cardiac catheterization lab for a diagnostic angiogram. ⁎ Corresponding author. 94 Amity St Apt 4E, Brooklyn NY 11201. Tel.: +1 718 928 5013; fax: +1 718 928 1300. E-mail address: [email protected] (S.K. Mulpuru). 0167-5273/$ - see front matter © 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2007.05.052
His past medical history includes recent ST elevation myocardial infarction with four vessel bypass, mitral valve replacement and a MAZE procedure. He had severe dilated ischemic cardiomyopathy with an ejection fraction of 30%, longstanding diabetes, hypertension and dyslipidaemia. During the post operative period he had cardiac arrest requiring placement of a dual chamber ICD (Entrust, Medtronic, USA). He quit smoking many years ago and denied any alcohol or drug use. His home medications included amiodarone, digoxin, furosemide, spironolactone, metoprolol, aspirin, coumadin, atrovastatin and rosiglitazone. He was initially sedated with midazolam with little effect and later was switched over to propofol. VT as well as ICD discharges subsided after the patient was started on propofol drip. The diagnostic angiogram showed occlusion of the proximal anastomosis of the RCA (right coronary artery) graft which was opened and he had a balloon pump to improve myocardial perfusion. ICD interrogation suggested that he received a total of 61 appropriate shocks (Fig. 2) before propofol therapy and the device was reprogrammed for a higher rate and a tighter AV (atrio-ventricular) delay for overdrive suppression of paroxysmal VT. He had a protracted recovery complicated by sternal wound infection but was eventually discharged home to lead a functional life. 3. Discussion Propofol is a substituted isoprophylphenol, short acting general anesthetic agent that acts through its interactions with gamma-amino butyric acid receptors. In human electrophysiological studies propofol has been shown to have no direct effect on the sino-atrial activity, intra-atrial
S.K. Mulpuru et al. / International Journal of Cardiology 128 (2008) e6–e8
e7
Fig. 1. EKG showing AV sequential pacing followed by VT.
activity or atrio-ventricular conduction [3] (Table 1). The cardiovascular effects of propofol are due to modulation of the autonomous nervous system. The decrease in heart rate and mean arterial pressure seen with propofol are due to central vagotonic effects, resetting of baroreflexes and also due to inhibition of sympathetic activity. The bradyarrythmias and heart blocks seen with propofol are likely explained by an increased sensitivity to parasympathetic stimulus due to reduction in sympathetic tome [4].
Ventricular tachycardia is the recorded arrhythmia in 90% of electrical storms. Precipitating factors could only be found in 36% of the cases [5]. Patients presenting with low ejection fraction and chronic renal insufficiency are more likely to experience electrical storms. ES usually presents 6 months after ICD implantation. There is conflicting evidence on the effect of ES on mortality in the ICD recipients. However it has a huge psychological impact on patients in addition to increasing the ICD related treatment costs. New ischemia,
Fig. 2. ICD interrogation showing delivery of 61 shocks.
e8
S.K. Mulpuru et al. / International Journal of Cardiology 128 (2008) e6–e8
Table 1 Propofol and effects on the human heart Effects of propofol on the cardiac conducting system. ❖ In guinea pigs propofol reduces atrial rate and reduces AV conduction through M2 muscarinic receptor mechanism. ❖ In pigs, the sinus node and His-Purkinje system functions are depressed but there is no effect on AV node, or on the conduction of atria or ventricular tissue. ❖ In dogs there is no direct effect on the conduction system if complete autonomic blockade is implemented. ❖ In humans there is no direct effect on the SA node activity, intra-atrial or AV conduction. ❖ Propofol elevates defibrillation thresholds in humans and prolongs QT interval.
electrolyte abnormalities, metabolic profile, cardiac decompensation, and autonomic nervous system input alter the conduction properties of the myocardium and are involved in initiation of arrhythmia. Increased sympathetic activation has been implicated in the generation of electrical storm whereas sympathetic blockade has been shown to prevent VF and sudden death. Although beta-blocker and anti-arrhythmics are the main stay of therapy catheter ablation has been successfully used to treat ES. 4. Conclusion Propofol therapy in our patient was associated with both conversion as well as suppression of ventricular arrythmias.
To our knowledge this is the second reported case of successful treatment of ES with propofol. We believe that the anti-arrhythmic effects of propofol are due to the reduction in sympathetic tone. References [1] Credner SC, Klingenheben T, Mauss O, Sticherling C, Hohnloser SH. Electrical storm in patients with transvenous implantable cardioverterdefibrillators: incidence, management and prognostic implications. J Am Coll Cardiol 1998;32(7):1909–15. [2] Dorian P, Cass D. An overview of the management of electrical storm. Can J Cardiol 1997;13(Suppl A):13A–7A. [3] Burjorjee JE, Milne B. Propofol for electrical storm; a case report of cardioversion and suppression of ventricular tachycardia by propofol. Can J Anaesth 2002;49(9):973–7. [4] Romano R, Ciccaglioni A, Fattorini F, et al. Effects of propofol on the human heart electrical system: a transesophageal pacing electrophysiologic study. Acta Anaesthesiol Scand 1994;38(1):30–2. [5] Brigadeau F, Kouakam C, Klug D, et al. Clinical predictors and prognostic significance of electrical storm in patients with implantable cardioverter defibrillators. Eur Heart J 2006;27(6):700–7.