- Email: [email protected]
Intraoperative cardiac arrest in acquired long QT syndrome
British Journal of Anaesthesia 102 (4): 503–5 (2009)
doi:10.1093/bja/aep038
Case Report
Intraoperative cardiac arrest in acquired long QT syndrome S. Dolenska* Department of Anaesthetics, William Harvey Hospital, Kennington Road, Ashford, Kent TN24 8NU, UK *E-mail: [email protected] A healthy female sustained a life-threatening arrhythmia and cardiac arrest while undergoing routine surgery under general anaesthesia. Resuscitation was prolonged but successful, with a complete neurological recovery. Br J Anaesth 2009; 102: 503–5
Accepted for publication: January 12, 2009
A 35-yr-old healthy female presented for routine septoplasty and grommet insertion under general anaesthesia. She had a history of mild asthma and allergy to penicillin, but had undergone three uneventful general anaesthetics previously. A preoperative ECG showed sinus rhythm (heart rate 69 beats min21), a normal corrected QT interval (QTc) 346– 388 ms, and biphasic T waves in leads II, III, aVR, aVF, and V3 – V6. No premedication was given. Anaesthesia was induced using fentanyl 100 mg and propofol 200 mg and a reinforced laryngeal mask airway inserted. The surgeon then applied 1 ml of 25% cocaine paste (250 mg) to the nostrils. Anaesthesia was maintained with spontaneous respiration of nitrous oxide 60% in oxygen and sevoflurane 2 – 3%; ondansetron 4 mg and diclofenac 75 mg were also administered i.v. The surgeon injected 5 ml of lidocaine 2% with epinephrine 1 in 80 000 (i.e. lidocaine 100 mg and epinephrine 60 mg) intranasally. At this time, heart rate was 42 beats min21, arterial pressure 124/80 mm Hg, end-tidal sevoflurane concentrations equivalent to 1.6 MAC, and end-tidal CO2 6.7 kPa. Immediately after the injection, ventricular tachycardia (VT) occurred without any prior warning extrasystoles, progressing rapidly to ventricular fibrillation (VF) associated with apnoea. Cardiopulmonary resuscitation (CPR) was commenced immediately including tracheal intubation and artificial ventilation with oxygen 100%; two other anaesthetists and several operating department technicians attended. A DC biphasic shock of 200 J was administered within 2 min and a perfusing rhythm (rapid supraventricular rhythm) occurred after a second DC shock, within 7 min of the onset of cardiac arrest. Cardiac massage was discontinued as there was a palpable pulse and spontaneous
respiratory efforts, but after a further 5 min a tachycardia recurred (180 beats min21) which converted to VF. CPR was continued for a further 30 min, including five DC shocks of 360 J, four boluses of epinephrine 1 mg plus an infusion of epinephrine when return of spontaneous circulation occurred, and atropine 3 mg (for severe bradycardia after one cycle of resuscitation). Arterial blood gas analysis showed normal pH, base excess, glucose, sodium and lactate concentrations; arterial PO2 was 3.5 kPa and serum potassium 3.1 mmol litre21. Potassium chloride infusion was requested but was not administered immediately because of a delay in preparation. Telephone advice regarding the possibility that cocaine was the cause of the arrhythmia (at that time a perfusing rhythm), given by a technician operating the Toxbase database, was to give verapamil 5 – 10 mg i.v. over 2 – 3 min, sodium bicarbonate 50 mmol twice as required, and lidocaine 50– 100 mg bolus followed by an infusion of 4 mg kg21 over 30 min. In accordance with this advice, we administered two doses of lidocaine 100 mg, one of which was effective in restoring the spontaneous circulation after the fourth defibrillation, and two doses of bicarbonate 50 mmol. Amiodarone 300 mg was administered instead of verapamil as the rhythm was ventricular and the problem was hypotension, not hypertension. After stabilization, the patient was transferred to ICU. On admission, arterial PO2 was 25 kPa (FIO2 0.5), serum potassium concentration 3.0 mmol litre21, calcium 2.0 mmol litre21, and magnesium 0.78 mmol litre21. These electrolyte abnormalities were corrected and magnesium also administered i.v. Artificial ventilation was continued until the following day when the trachea was extubated. There were no neurological sequelae and the
# The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected]
Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
Keywords: complications, arrhythmia; sympathetic nervous system, epinephrine; toxicity, local anaesthetics
Dolenska
patient recovered fully. Corrected QT interval was prolonged (QTc 559 ms) for 48 h, but then normalized again. A cardiologist diagnosed a long QT syndrome and offered the patient an implantable cardioverter-defibrillator. However, the patient has declined this at present and was discharged on bisoprolol maintenance therapy.
Discussion
504
Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
The sequence of events in this case suggests a causal relationship between the injection of lidocaine with epinephrine and the onset of the arrhythmia, after recent injection of high-dose cocaine and during volatile-based general anaesthesia and mild hypercarbia. The working diagnosis at the time was cocaine-induced arrhythmia and the subsequent diagnosis of acquired LQTS was based on the markedly prolonged postoperative QTc, supported by the preoperative T wave changes. It is not possible to establish retrospectively whether the presenting arrhythmia was torsades de pointes or not, as no record of it was retained on the anaesthetic monitor. The dose of cocaine was high (250 mg), but the dose of epinephrine was fairly small (60 mg) and the pattern of development was unusual in that there was no warning arrhythmia before the onset of VT, as would be expected in the case of a cocaine-induced or exacerbated arrhythmia. It is possible that the arrhythmia provoked by the cocaine was very coarse VF or monomorphic VT, thus unrelated to the long QT syndrome diagnosed later, though the tachycardia was not uniform as would be the case in the monomorphic type. By the time the defibrillator trolley (which documents the trace) arrived, the rhythm was confirmed as VF. LQTS may be congenital (incidence 1:3000) or acquired (incidence slightly more common). A prolonged QT interval is a feature of the congenital type only and the ECG may be normal before presentation in the acquired form. The hallmark arrhythmia of LQTS is torsades de pointes, that is, polymorphic VT with a constantly changing electrical axis. This may be self-terminating but can convert to VF. Many drugs used by anaesthetists are potential triggers for the malignant arrhythmias which occur with LQTS.1 2 Cocaine and epinephrine are major triggers for torsades de pointes and also for monomorphic VT and VF. Acquired LQTS and torsades de pointes have previously been reported during general anaesthesia, all in older patients with predisposing factors (electrolyte disturbances and ischaemic heart disease) or already confirmed LQTS.3 – 5 In several cases, torsades de pointes was selfterminating after correcting the precipitating problem. In our patient, there was no history or symptoms of ischaemic heart disease or other predisposing factors and the only indication of abnormality was the preoperative ECG changes. Biphasic T waves can occur in LQTS, but are not pathognomonic2 and the patient had undergone general anaesthesia several times previously without incident. On later examination of the previous anaesthetic records,
which were not available at the time of this procedure, no major triggers of torsades de pointes were administered. During this case, several potential triggers of acquired LQTS were administered (cocaine, epinephrine, ondansetron, amiodarone, and possibly sevoflurane). Some authors believe that volatile anaesthetic agents contribute to the development of torsades de pointes.1 2 Sevoflurane has been suggested as a trigger in congenital LQTS,6 as it prolongs the QT interval.7 However, sevoflurane does not increase the transmural distribution of repolarization (the period between the peak of the T wave and its end) and therefore is unlikely to be torsadogenic.8 Ondansetron also prolongs the QT interval,9 but torsades de pointes has not been reported in association with ondansetron during general anaesthesia. Cardiac arrest in this case was prolonged, possibly because the high circulating epinephrine concentrations may have contributed to the spontaneous degeneration into the malignant arrhythmia after the two successful shocks. Hypokalaemia may have also contributed, though there was no reason to suspect this before surgery and sinus rhythm was restored before the serum potassium concentration had been normalized. Amiodarone is the treatment of choice of shock-resistant arrhythmias in the ALS guideline, but it is a known torsadogenic agent.1 2 In our patient, it did not prevent successful defibrillation and return of spontaneous circulation. It is also possible that lidocaine absorbed from the mucosa initially helped to restore a perfusing rhythm. IV lidocaine has been successfully used for resuscitation in congenital LQTS;8 it shortens the QT interval and may be particularly effective in torsades de pointes induced by drugs including cocaine. For a full list of drugs implicated in the long QT syndrome, see http://www.torsades.org. Recommended treatments for torsades de pointes which is not self-terminating or proceeds to cardiac arrest include magnesium sulphate, correction of hypokalaemia, transvenous pacing, or defibrillation if the patient is pulseless or haemodynamically unstable. We followed the universal European Resuscitation Council algorithm for pulseless shockable rhythms, including the administration of epinephrine, albeit ( purposefully) less frequently than advised. The European Resuscitation Council does not advise dose reduction or omission of epinephrine in the case of cocaine-induced arrhythmias in the pulseless VT/ VF algorithm.10 Cocaine overdose was noted as a relative contraindication for the use of epinephrine in the 2000 Resuscitation Council (UK) Advanced Life Support manual and this will be re-visited for the 2010 European Resuscitation Council guidelines ( personal communication, Dr J. Nolan). In summary, this case highlights that acquired long QT syndrome can present spontaneously during anaesthesia, in association with factors which may precipitate arrhythmias. In addition, high-dose cocaine administered with systemic (as opposed to topical) epinephrine in ENT surgery has potential risks. Furthermore, epinephrine administered
Intraoperative cardiac arrest in acquired long QT syndrome
systemically as part of the ALS algorithm may not be helpful in the management of cocaine-induced arrhythmias.
Acknowledgements I would like to thank Dr Judith Banks for her help with the resuscitation and with preparation of the manuscript.
References 1 Hunter JD, Sharma P, Rathi S. Long QT syndrome. Contin Educ Anaesth Crit Care Pain 2008; 8: 67 – 70 2 Booker PD, Whyte SD, Ladusans EJ. Long QT syndrome and anaesthesia. Br J Anaesth 2003; 90: 349 – 66 3 Abe K, Takada K, Yoshiya I. Intraoperative torsade de pointes ventricular tachycardia and ventricular fibrillation during sevoflurane anesthesia. Anesth Analg 1998; 86: 701 – 2 4 Lustik SJ, Eichelberger JP, Chibber AK, Bronsther O. Torsade de pointes during orthoptic liver transplantation. Anesth Analg 1998; 87: 300 – 3
5 Soroker D, Ezri T, Szmuk P, Merlis P, Epstein M, Caspi A. Perioperative torsade de pointes ventricular tachycardia induced by hypocalcemia and hypokalemia. Anesth Analg 1995; 80: 630 – 3 6 Katz RI, Quijano I, Barcelon N, Bianceaniello T. Ventricular tachycardia during general anesthesia in a patient with congenital long QT syndrome. Can J Anaesth 2003; 50: 398 –403 7 Kleinsasser A, Loeckinger A, Lindner KH, Boehler M, Puehringer F. Reversing sevoflurane-associated QTc prolongation by changing to propofol. Anaesthesia 2001; 56: 248 – 50 8 Whyte SD, Sanatani S, Lim J, Booker PD. A comparison of the effect on dispersion of repolarization of age-adjusted MAC values of sevoflurane in children. Anesth Analg 2007; 104: 277 – 82 9 Charbit B, Albaladejo P, Funck-Brentano C, Legrand M, Samain E, Marty J. Prolongation of QTc interval after postoperative nausea and vomiting treatment by droperidol or ondansetron. Anesthesiology 2005; 102: 1094 – 100 10 Nolan JP, Deakin CD, Soar J, Bo¨ttiger BW, Smith G. Available from www.erc.edu (accessed October 13, 2008) Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
505
doi:10.1093/bja/aep038
Case Report
Intraoperative cardiac arrest in acquired long QT syndrome S. Dolenska* Department of Anaesthetics, William Harvey Hospital, Kennington Road, Ashford, Kent TN24 8NU, UK *E-mail: [email protected] A healthy female sustained a life-threatening arrhythmia and cardiac arrest while undergoing routine surgery under general anaesthesia. Resuscitation was prolonged but successful, with a complete neurological recovery. Br J Anaesth 2009; 102: 503–5
Accepted for publication: January 12, 2009
A 35-yr-old healthy female presented for routine septoplasty and grommet insertion under general anaesthesia. She had a history of mild asthma and allergy to penicillin, but had undergone three uneventful general anaesthetics previously. A preoperative ECG showed sinus rhythm (heart rate 69 beats min21), a normal corrected QT interval (QTc) 346– 388 ms, and biphasic T waves in leads II, III, aVR, aVF, and V3 – V6. No premedication was given. Anaesthesia was induced using fentanyl 100 mg and propofol 200 mg and a reinforced laryngeal mask airway inserted. The surgeon then applied 1 ml of 25% cocaine paste (250 mg) to the nostrils. Anaesthesia was maintained with spontaneous respiration of nitrous oxide 60% in oxygen and sevoflurane 2 – 3%; ondansetron 4 mg and diclofenac 75 mg were also administered i.v. The surgeon injected 5 ml of lidocaine 2% with epinephrine 1 in 80 000 (i.e. lidocaine 100 mg and epinephrine 60 mg) intranasally. At this time, heart rate was 42 beats min21, arterial pressure 124/80 mm Hg, end-tidal sevoflurane concentrations equivalent to 1.6 MAC, and end-tidal CO2 6.7 kPa. Immediately after the injection, ventricular tachycardia (VT) occurred without any prior warning extrasystoles, progressing rapidly to ventricular fibrillation (VF) associated with apnoea. Cardiopulmonary resuscitation (CPR) was commenced immediately including tracheal intubation and artificial ventilation with oxygen 100%; two other anaesthetists and several operating department technicians attended. A DC biphasic shock of 200 J was administered within 2 min and a perfusing rhythm (rapid supraventricular rhythm) occurred after a second DC shock, within 7 min of the onset of cardiac arrest. Cardiac massage was discontinued as there was a palpable pulse and spontaneous
respiratory efforts, but after a further 5 min a tachycardia recurred (180 beats min21) which converted to VF. CPR was continued for a further 30 min, including five DC shocks of 360 J, four boluses of epinephrine 1 mg plus an infusion of epinephrine when return of spontaneous circulation occurred, and atropine 3 mg (for severe bradycardia after one cycle of resuscitation). Arterial blood gas analysis showed normal pH, base excess, glucose, sodium and lactate concentrations; arterial PO2 was 3.5 kPa and serum potassium 3.1 mmol litre21. Potassium chloride infusion was requested but was not administered immediately because of a delay in preparation. Telephone advice regarding the possibility that cocaine was the cause of the arrhythmia (at that time a perfusing rhythm), given by a technician operating the Toxbase database, was to give verapamil 5 – 10 mg i.v. over 2 – 3 min, sodium bicarbonate 50 mmol twice as required, and lidocaine 50– 100 mg bolus followed by an infusion of 4 mg kg21 over 30 min. In accordance with this advice, we administered two doses of lidocaine 100 mg, one of which was effective in restoring the spontaneous circulation after the fourth defibrillation, and two doses of bicarbonate 50 mmol. Amiodarone 300 mg was administered instead of verapamil as the rhythm was ventricular and the problem was hypotension, not hypertension. After stabilization, the patient was transferred to ICU. On admission, arterial PO2 was 25 kPa (FIO2 0.5), serum potassium concentration 3.0 mmol litre21, calcium 2.0 mmol litre21, and magnesium 0.78 mmol litre21. These electrolyte abnormalities were corrected and magnesium also administered i.v. Artificial ventilation was continued until the following day when the trachea was extubated. There were no neurological sequelae and the
# The Author [2009]. Published by Oxford University Press on behalf of The Board of Directors of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected]
Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
Keywords: complications, arrhythmia; sympathetic nervous system, epinephrine; toxicity, local anaesthetics
Dolenska
patient recovered fully. Corrected QT interval was prolonged (QTc 559 ms) for 48 h, but then normalized again. A cardiologist diagnosed a long QT syndrome and offered the patient an implantable cardioverter-defibrillator. However, the patient has declined this at present and was discharged on bisoprolol maintenance therapy.
Discussion
504
Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
The sequence of events in this case suggests a causal relationship between the injection of lidocaine with epinephrine and the onset of the arrhythmia, after recent injection of high-dose cocaine and during volatile-based general anaesthesia and mild hypercarbia. The working diagnosis at the time was cocaine-induced arrhythmia and the subsequent diagnosis of acquired LQTS was based on the markedly prolonged postoperative QTc, supported by the preoperative T wave changes. It is not possible to establish retrospectively whether the presenting arrhythmia was torsades de pointes or not, as no record of it was retained on the anaesthetic monitor. The dose of cocaine was high (250 mg), but the dose of epinephrine was fairly small (60 mg) and the pattern of development was unusual in that there was no warning arrhythmia before the onset of VT, as would be expected in the case of a cocaine-induced or exacerbated arrhythmia. It is possible that the arrhythmia provoked by the cocaine was very coarse VF or monomorphic VT, thus unrelated to the long QT syndrome diagnosed later, though the tachycardia was not uniform as would be the case in the monomorphic type. By the time the defibrillator trolley (which documents the trace) arrived, the rhythm was confirmed as VF. LQTS may be congenital (incidence 1:3000) or acquired (incidence slightly more common). A prolonged QT interval is a feature of the congenital type only and the ECG may be normal before presentation in the acquired form. The hallmark arrhythmia of LQTS is torsades de pointes, that is, polymorphic VT with a constantly changing electrical axis. This may be self-terminating but can convert to VF. Many drugs used by anaesthetists are potential triggers for the malignant arrhythmias which occur with LQTS.1 2 Cocaine and epinephrine are major triggers for torsades de pointes and also for monomorphic VT and VF. Acquired LQTS and torsades de pointes have previously been reported during general anaesthesia, all in older patients with predisposing factors (electrolyte disturbances and ischaemic heart disease) or already confirmed LQTS.3 – 5 In several cases, torsades de pointes was selfterminating after correcting the precipitating problem. In our patient, there was no history or symptoms of ischaemic heart disease or other predisposing factors and the only indication of abnormality was the preoperative ECG changes. Biphasic T waves can occur in LQTS, but are not pathognomonic2 and the patient had undergone general anaesthesia several times previously without incident. On later examination of the previous anaesthetic records,
which were not available at the time of this procedure, no major triggers of torsades de pointes were administered. During this case, several potential triggers of acquired LQTS were administered (cocaine, epinephrine, ondansetron, amiodarone, and possibly sevoflurane). Some authors believe that volatile anaesthetic agents contribute to the development of torsades de pointes.1 2 Sevoflurane has been suggested as a trigger in congenital LQTS,6 as it prolongs the QT interval.7 However, sevoflurane does not increase the transmural distribution of repolarization (the period between the peak of the T wave and its end) and therefore is unlikely to be torsadogenic.8 Ondansetron also prolongs the QT interval,9 but torsades de pointes has not been reported in association with ondansetron during general anaesthesia. Cardiac arrest in this case was prolonged, possibly because the high circulating epinephrine concentrations may have contributed to the spontaneous degeneration into the malignant arrhythmia after the two successful shocks. Hypokalaemia may have also contributed, though there was no reason to suspect this before surgery and sinus rhythm was restored before the serum potassium concentration had been normalized. Amiodarone is the treatment of choice of shock-resistant arrhythmias in the ALS guideline, but it is a known torsadogenic agent.1 2 In our patient, it did not prevent successful defibrillation and return of spontaneous circulation. It is also possible that lidocaine absorbed from the mucosa initially helped to restore a perfusing rhythm. IV lidocaine has been successfully used for resuscitation in congenital LQTS;8 it shortens the QT interval and may be particularly effective in torsades de pointes induced by drugs including cocaine. For a full list of drugs implicated in the long QT syndrome, see http://www.torsades.org. Recommended treatments for torsades de pointes which is not self-terminating or proceeds to cardiac arrest include magnesium sulphate, correction of hypokalaemia, transvenous pacing, or defibrillation if the patient is pulseless or haemodynamically unstable. We followed the universal European Resuscitation Council algorithm for pulseless shockable rhythms, including the administration of epinephrine, albeit ( purposefully) less frequently than advised. The European Resuscitation Council does not advise dose reduction or omission of epinephrine in the case of cocaine-induced arrhythmias in the pulseless VT/ VF algorithm.10 Cocaine overdose was noted as a relative contraindication for the use of epinephrine in the 2000 Resuscitation Council (UK) Advanced Life Support manual and this will be re-visited for the 2010 European Resuscitation Council guidelines ( personal communication, Dr J. Nolan). In summary, this case highlights that acquired long QT syndrome can present spontaneously during anaesthesia, in association with factors which may precipitate arrhythmias. In addition, high-dose cocaine administered with systemic (as opposed to topical) epinephrine in ENT surgery has potential risks. Furthermore, epinephrine administered
Intraoperative cardiac arrest in acquired long QT syndrome
systemically as part of the ALS algorithm may not be helpful in the management of cocaine-induced arrhythmias.
Acknowledgements I would like to thank Dr Judith Banks for her help with the resuscitation and with preparation of the manuscript.
References 1 Hunter JD, Sharma P, Rathi S. Long QT syndrome. Contin Educ Anaesth Crit Care Pain 2008; 8: 67 – 70 2 Booker PD, Whyte SD, Ladusans EJ. Long QT syndrome and anaesthesia. Br J Anaesth 2003; 90: 349 – 66 3 Abe K, Takada K, Yoshiya I. Intraoperative torsade de pointes ventricular tachycardia and ventricular fibrillation during sevoflurane anesthesia. Anesth Analg 1998; 86: 701 – 2 4 Lustik SJ, Eichelberger JP, Chibber AK, Bronsther O. Torsade de pointes during orthoptic liver transplantation. Anesth Analg 1998; 87: 300 – 3
5 Soroker D, Ezri T, Szmuk P, Merlis P, Epstein M, Caspi A. Perioperative torsade de pointes ventricular tachycardia induced by hypocalcemia and hypokalemia. Anesth Analg 1995; 80: 630 – 3 6 Katz RI, Quijano I, Barcelon N, Bianceaniello T. Ventricular tachycardia during general anesthesia in a patient with congenital long QT syndrome. Can J Anaesth 2003; 50: 398 –403 7 Kleinsasser A, Loeckinger A, Lindner KH, Boehler M, Puehringer F. Reversing sevoflurane-associated QTc prolongation by changing to propofol. Anaesthesia 2001; 56: 248 – 50 8 Whyte SD, Sanatani S, Lim J, Booker PD. A comparison of the effect on dispersion of repolarization of age-adjusted MAC values of sevoflurane in children. Anesth Analg 2007; 104: 277 – 82 9 Charbit B, Albaladejo P, Funck-Brentano C, Legrand M, Samain E, Marty J. Prolongation of QTc interval after postoperative nausea and vomiting treatment by droperidol or ondansetron. Anesthesiology 2005; 102: 1094 – 100 10 Nolan JP, Deakin CD, Soar J, Bo¨ttiger BW, Smith G. Available from www.erc.edu (accessed October 13, 2008) Downloaded from http://bja.oxfordjournals.org/ at NERL on May 12, 2015
505