Lidocaine-Related Increase in Defibrillation Threshold

With the growing reliance on the implantable cardioverter defibrillator (ICD) for the primary treatment of life-threatening ventricular arrhythmias, interactions between these devices and antiarrhythmic drugs has assumed increased clinical importance. The effects of antiarrhythmic drugs on defibrillation threshold (DFT) have been investigated [1]. Lidocaine, a commonly used antiarrhythmic drug, has generally been reported to increase DFT (requires more energy to defibrillate the heart) on a concentration-dependent basis in experimental animal preparations [2,3], but there are relatively little data available regarding the effects of lidocaine on DFT in humans. We describe a major increase in DFT that occurred in a patient who received 100 mg of intravenous (IV) lidocaine to attenuate the pain during the injection of an IV anesthetic during routine ICD implantation. Case Report A 59-yr-old man with coronary artery disease and moderately severe left ventricular dysfunction was referred for ICD implantation after electrophysiologic study revealed an easily inducible, rapid, sustained, monomorphic ventricular tachycardia. Implantation was performed with sedation provided by IV midazolam (7 mg), fentanyl (100 micro g), and droperidol (0.75 mg). The initial DFT was determined to be 15 joules using a stepdown approach from 20 joules with a transvenous lead system (Endotak C; Guidant Corp., Cardiac Pacemakers, St. Paul, MN) and a biphasic waveform. Brief general anesthesia was then induced with 200 mg of propofol administered IV with 100 mg of lidocaine. The pulse-generator pocket was constructed in the subcutaneous tissue superficial to the rectus sheath, and the lead was tunneled to the pocket and connected to the pulse generator. A total of 10 mL of 1% lidocaine was used for local infiltration during the procedure. During subsequent device testing, a 30-J biphasic shock was insufficient to defibrillate the patient in two consecutive trials, and a biphasic 34-J "rescue" shock was required to restore normal sinus rhythm. Subsequently, the implant team discovered that IV lidocaine had been administered. Serum lidocaine concentration, drawn 30 min after the 100-mg bolus of lidocaine, was 3.8 micro g/mL (therapeutic range 1.5-5.0 micro g/mL). After allowing an additional 30 min for the serum lidocaine concentration to dissipate, repeat testing revealed a biphasic DFT of 10 J. The patient has done well since that time and has been successfully defibrillated by his device on several occasions. Discussion The major finding in the present case report is that lidocaine, when administered IV for the purpose of preventing discomfort associated with the administration of IV propofol, can significantly increase DFT and have potentially important clinical consequences. Given the time course of the events (30-J shocks that failed twice and a subsequent DFT of 10 J after sufficient time had elapsed to allow the serum lidocaine concentration to decrease), we believe it unlikely that our findings are artifactual. In this case, the knowledge that lidocaine can increase DFT prevented unnecessary revision of the lead system. Like many other antiarrhythmic medications, lidocaine increases DFT, usually in a dose-related manner [2]. Echt et al. [4] obtained DFT in 16 patients before and after the administration of a 200 to 250-mg loading dose of lidocaine followed by a 3-mg/min maintenance infusion. They found that 7 of 8 patients with a serum lidocaine concentration increased >or=to5 micro g/mL had a significant increase in DFT. In contrast, DFT increased in only two patients with lower serum concentrations, although in those two patients, it increased to 25 and 30 J. The maximum output of most commercially available ICDs is 30-34 J. In our case, the blood sample was drawn 30 minutes after the lidocaine bolus had been administered, therefore, it is probable that the serum concentration was considerably higher at the time of the failed shocks. Assuming that lidocaine is eliminated by first-order kinetics with a half-life of 120 minutes, the estimated initial lidocaine concentration would be approximately 4.8 micro g/mL at the time of the failed shocks and 3.2 micro g/mL one hour later, when repeat DFT testing was successful. Propofol is an IV general anesthetic that has become increasingly popular recently because of rapid induction and emergence with few side effects [5]. One of the major drawbacks in the use of propofol is the pain associated with IV administration. Accordingly, it has become customary to administer propofol in conjunction with a local anesthetic, most often lidocaine [5,6]. Although the effects of propofol on DFT have not been fully elucidated, the lack of problems in direct current cardioversion in patients treated with propofol [7] suggests that it is unlikely to have played a role in our findings. Based upon our experience, it would be prudent to use IV lidocaine with caution in patients with ICDs. The dramatic increase in DFT encountered in our patient was most probably secondary to the large (1.4 mg/kg) dose of lidocaine administered and appears less likely with the use of smaller doses (0.1-0.2 mg/kg), which are still sufficient to minimize pain [5]. Alternatively, patients should be cautioned about the possibility of brief pain, and propofol should be administered through large-bore catheters using a free-flowing IV line. For patients known to have a low pain threshold, pentothal or metoclopramide, which have also been reported to attenuate the local discomfort of propofol injection, may be added to the infusion [8,9]. Our findings have another potentially important implication: lidocaine is recommended by the American Heart Association (Guidelines for Advanced Cardiac Life Support) for use in patients with persistent ventricular fibrillation [10]. Our experience and other published data [2-4] suggest that this recommendation should be reevaluated.