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


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