Anesthetic management in a patient with Wolff-Parkinson-White syndrome for laparoscopic cholecystectomy.

Wolff-Parkinson-White syndrome is an electrophysiological disorder of heart. Patients with such disorder may be asymptomatic or present with cardiac symptoms like palpitation and dyspnea. These patients may present with serious cardiac complication like atrial fibrillation and PSVT intraoperatively. We report a case of a 30-year-old female with WPW syndrome posted for laparoscopic cholecystectomy under general anesthesia. We took all the precautions necessary to avoid tachycardia and arranged drugs necessary to treat any complications together with stringent monitoring which is very important for favorable outcome in these patients. Management of the case offers an opportunity to relearn the important considerations on WPW syndrome.

INTRODUCTION

Wolff-Parkinson-White syndrome or pre-excitation syndrome, as it is called, is an electrophysiological disorder of heart with an incidence of 0.9 to 3% of the general population.[1] Patients with WPW syndrome can be asymptomatic or may present with cardiac symptoms such as palpitation or dyspnea on exertion. Patient's history and the classic electrocardiograph (ECG) findings, which show shortened PR interval, delta waves, and widened QRS complex,[12] confirm the diagnosis. Other findings may be ST depression and associated atrial fibrillation. These patients may or may not be on cardiac drugs. Considering the rarity of the case and paucity of data available for the management of such cases under general anesthesia for laparoscopic surgery, we take this as an opportunity to relearn the steps needed for successful anesthetic management.

CASE REPORT

A 30-year-old female weighing 45 kg was posted for laparoscopic cholecystectomy for calculus cholecystitis. While the patient was asymptomatic during examination, she gave history of frequent palpitation, which gets spontaneously remitted on rest; the general and systemic examination was within normal limits with a regular heart rate of 88/min and BP of 108/78. Her 12 lead ECG was suggestive of WPW syndrome with shortened PR interval and presence of “delta” wave, [Figure 1] the 2D ECHO showed normal valvular and ventricular size and function with ejection fraction of 62%. Complete cardiology evaluation was done including 24 hours Holter monitoring which showed a brief and single event of arrhythmia, for which no intervention was required [Figure 2].

Figure 1

Preoperative resting ECG showing short PR interval, slurred QRS complex “Delta wave”

Figure 2

Preoperative holter monitoring showing short PR interval, wide and slurred QRS complex “delta wave” and an episode of arrhythmia

The goal during perioperative management of anesthesia was to avoid any factor that increases sympathetic activity such as pain, anxiety, fear, stress response of intubation/extubation, lighter plane of anesthesia, hypovolemia,[3] and avoiding premedication with anticholinergic drugs.

Patient was adequately counseled and reassured. Premedication with tab alprazolam 0.5 mg and tab ranitidine 150 mg was given in the night before and morning of surgery.

In the theatre, patient was attached to 12 lead ECG, Bispectral index along with other routine monitoring. Drugs which were kept ready included adenosine, esmolol, lignocaine, procainamide, and defibrillator, to tackle any episode for re-entrant tachycardia and atrial fibrillation. Under lignocaine 2% infiltration, IV catheter, radial artery and central venous access was secured. We gave inj. fentanyl 2 mcg/kg preoperatively and preoxygenated the patient with 100% oxygen for 3 minutes prior to induction with titrating dose of propofol; after induction, anesthetic depth was maintained by adding isoflurane to the patient, prior to laryngoscopy and intubation 10% lignocaine spray was used to anesthetize the airway. Postintubation sympathetic response was observed with rise in a heart rate and blood pressure with ECG showing prominent “delta waves” and shortened PR interval; after stabilization of vitals, we started a background infusion of propofol at the rate of 25 mcg/kg/min and maintained BIS between 40-60 levels throughout surgery by titrating isoflurane concentration. We observed that propofol infusion gradually reduced delta wave, with normalization of QRS complex and PR interval [Figure 3].

Figure 3

Intraoperative ECG showing normalization of PR interval and QRS complex

While creating carbopneumoperitonium for surgery, care was taken to slowly increase the IAP (intra-abdominal pressure), keeping the upper limit of IAP within 12 mm Hg, and EtCO2 between 35-40 mm of Hg. Further putting the patient in trendelenburg position had no effect on the ECG rhythm.

The case proceeded uneventfully and after completion of surgery, residual carbon dioxide in the peritoneal cavity was carefully removed by the surgeon. While the patient was still under anesthesia and paralysis, gentle suctioning under direct vision was done and size 3 Proseal LMA was inserted behind the endotracheal tube (Bailey's Maneuver), the cuff of the Proseal LMA was inflated prior to removal of endotracheal tube,[4] isoflurane and propofol was then stopped and residual neuromuscular blockage was reversed with neostigmine and glycopyrrolate. After the return of consciousness with ability to follow verbal commands and generation of adequate tidal volume along with BIS showing >90 values, the LMA was removed and patient was kept on mask ventilation. Prophylaxis against PONV was taken intraoperatively and patient was sent to recovery room for monitoring of vitals. Patient was successfully managed with the above technique and comfortably shifted to ward.

DISCUSSION

Many literatures describe about cases of WPW syndrome where patient remains asymptomatic throughout life, but such patients are always at a risk of PSVT or atrial fibrillation during perioperative period. The typical ECG findings are short PR interval (0.12 sec or less), prolong QRS complex (0.11 sec or more), and slurred QRS wave known as “delta wave”.

The AV node utilizes a calcium-dependent slow inward current, while the accessory pathway utilizes a sodium-dependent fast inward current for electrical impulse transmission. The lack of physiological delay in transmission of the sinus impulse via the abnormal path results in short PR interval, and ventricular excitation being a composite of the two impulses results in a fusion beat seen as a “delta wave” and short PR interval with prolonged QRS complex. Anesthetic drugs and techniques tend to change the physiology of AV conduction.[5] For general anesthesia, thiopentone is safe but propofol is preferred, as it has no effect on the refractory period of accessory pathway. Atropine, glycopyrrolate, and ketamine precipitate tachycardia, therefore should be avoided. Isoflurane and sevoflurane have no effect on AV node conduction and provide the optimal hemodynamic status. Fentanyl provides adequate hemodynamic stability. Vecuronium and rocuronium are cardio stable muscle relaxants preferred over pancuronium and atracurium.[3] In our case, after induction of anesthesia with titrated dose of propofol, we started background infusion of propofol at the rate of 25 mcg/kg/min and found that there was normalization of PR interval and reduction of wide QRS complex. Sumhiko Seki et al.,[6] in his case report, mentioned about such normalization with propofol infusion, although no electrophysiological study was done to prove its efficacy.

Traditionally, WPW syndrome is classified in two types, Type A and type B. On ECG, Type A resembles right bundle branch block with right ventricular hypertrophy and posterior myocardial infarction, whereas type B resembles left bundle branch block with left ventricle hypertrophy.[7] The most important complications occurring in these patients are PSVT and atrial fibrillation, the occurrence of supraventricular tachycardia, also described as re-entrant tachycardia or circus movement tachycardia, is the result of premature activation of ventricle as a result of anomalous AV conduction via accessory pathway directly from the atrium to the ventricle. In most cases, this pathway is the “kent” pathway. The cardiac anomaly most frequently associated with this problem is Ebstein's anomaly.[7] If PSVT is precipitated, then vagal maneuvers should be tried initially. In hemodynamically stable patients, lignocaine or adenosine 6-12 mg or beta blockers (Esmolol, 50-300 μg/kg/min IV) can be administered intravenously to break a re-entrant tachycardia. Class-I anti-arrhythmic drugs such as disopyramide and procainamide can be used. These drugs block transmission via the accessory pathway by blocking fast sodium channel.[5]

Patient with this anomaly, depending upon the symptoms and underlying mechanism, are started with propranolol, or procainamide or quinidine. When supraventricular tachycardia occurs with normal QRS complex, propranolol should be used because it depresses the AV conduction. Digitalis is contraindicated in these patients as it tends to accelerate conduction through accessory pathway. In urgent situations with supraventricular tachycardia with extreme rapid response, especially with atrial fibrillation and atrial flutter, DC shock is the treatment of choice. Patients developing AF with hemodynamic stability should be treated pharmacologically, whereas hemodynamically unstable patients should be treated by cardio version with 150-200 J.[3]

In patients in whom extubation response can be detrimental, tracheal extubation under deep anesthesia may reduce the incidence and degree of these complications; however, tracheal extubation under deep anesthesia may often cause airway obstruction and risks an unprotected airway. Meanwhile, LMA insertion after tracheal extubation may minimize the stress response while providing a patent airway during emergence from anesthesia (Bailey procedure).[5]