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Year : 2011  |  Volume : 55  |  Issue : 4  |  Page : 378-380  

Anaesthetic management of Wolff-Parkinson-White syndrome for hysterectomy

1 Department of Anaesthesiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Maternal and Reproductive Health, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Consultant Gynaecology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication13-Sep-2011

Correspondence Address:
Sandeep Sahu
Department of Anaesthesiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.84866

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Wolff-Parkinson-White syndrome (WPW) is an uncommon cardiac disorder having an aberrant pathway between atria and ventricles. We are reporting a known case of WPW syndrome for hysterectomy under combined spinal epidural anaesthesia. Management of the present case is an important pearl to revisit management of WPW syndrome. The perioperative management should be tailored according to the nature of surgery and the clinical presentation of the patient.

Keywords: Combined spinal epidural block, re-entral phenomenon, regional anaesthesia, Wolff-Parkinson-White syndrome

How to cite this article:
Sahu S, Karna ST, Karna A, Lata I, Kapoor D. Anaesthetic management of Wolff-Parkinson-White syndrome for hysterectomy. Indian J Anaesth 2011;55:378-80

How to cite this URL:
Sahu S, Karna ST, Karna A, Lata I, Kapoor D. Anaesthetic management of Wolff-Parkinson-White syndrome for hysterectomy. Indian J Anaesth [serial online] 2011 [cited 2021 Jul 30];55:378-80. Available from: https://www.ijaweb.org/text.asp?2011/55/4/378/84866

   Introduction Top

Wolff-Parkinson-White (WPW) syndrome is a pre-excitation syndrome caused due to a pathway known as "bundle of Kent", which is an aberrant pathway between atria and ventricles, bypassing the normal atrioventricular (AV) conduction. [1],[2] The AV node utilises a calcium-dependent slow inward current, while the accessory pathway utilises 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. Anaesthetic drugs and techniques tend to change the physiology of AV conduction. Therefore, management of the present case is an important pearl to revisit management of WPW syndrome.

   Case Report Top

A 45-year-old female, a known case of WPW syndrome, presented with complaints of excessive bleeding per vagina and weakness, for which surgery was planned. She was diagnosed to have dysfunctional uterine bleeding and planned for total abdominal hysterectomy. The patient gave history of having repeated episodes of palpitations and syncope in the past. She was asymptomatic presently, with good exercise tolerance (8 METS) and was on tab. diltiazem 120 mg OD for last 2 years. The general and systemic examination was within normal limits with regular pulse rate of 74/ min and BP of 124/80 mm Hg. Her haemoglobin was 7.8 g/ dl because of active and excessive bleeding, and so surgery was planned. Rest of the investigations were in normal ranges. Electrocardiograph (ECG) showed decreased PR interval (<120 ms), delta waves (slurred upstroke of QRS), wide QRS and associated ST and T wave changes. The 2D-echocardiography (ECHO) showed normal vulvular and ventricular functions with ejection fraction 60%.

The patient was counselled and reassurance was given. On the night before the surgery, tab. lorazepam 2 mg and tab. ranitidine 150 mg were given at 10 p.m. with advice to continue diltiazem. In the operation theatre, 12-lead ECG was connected with other routine monitoring. After 2% xylocard (Astra Zeneca pharma Ltd, Bangalore) local infiltration, IV access, USG-guided radial artery cannulation (for invasive arterial pressure monitoring) and right internal jugular vein cannulation (for central venous pressure measurement and fluid management) was secured. Availability of anti-arrhythmics like diltiazem, adenosine, procainamide, lignocaine, phenylephrine, and amiodarone, inotropes, infusion pumps and defibrillator was confirmed.

The patient was preloaded with colloid tetrastarch (130/0.4) 250 ml slowly over 15 min. Combined spinal epidural was inserted under all aseptic precautions in L3-4 space using needle through the needle technique (18 g Tuohy's/27 g Whitacare needle). In subarachnoid space, 1.2 ml of 0.5% bupivacaine with 25 μg fentanyl was injected. Level of sensory block achieved was T8. O 2 was administered with Hudson's mask at 6 l/min. After 1 hour, epidural bolus was started with 0.25% bupivacaine 8 ml with 2 μg/ml fentanyl, and then 5 ml/hour infusion was given for the maintenance. After initial epidural bolus dose, there was one episode of hypotension, up to 84/42 mm Hg, which was managed successfully with one IV bolus dose of 50 μg phenylephrine. The total duration of surgery was 2 hours. Meanwhile, the patient received 1.5 l of Ringer's lactate and 500 ml of tetrastarch colloid. Total blood loss and urine output were 200 and 600 ml, respectively. Postoperatively, the patient was monitored in the ICU for 24 hours. Patient controlled epidural analgesia (PCEA) was provided with PCEA pump using 0.125% bupivacaine with 2 μg/ml fentanyl (6 ml/hour continuous infusion, 2 ml demand dose, interval 5 min, max 4 doses/hour). Postoperative convalescence period was uneventful. After 8 days of uneventful hospital stay, the patient was discharged on medical management for WPW syndrome.

   Discussion Top

In WPW syndrome, two common life-threatening arrhythmias that occur are atrial fibrillation which may lead to ventricular fibrillation and circus re-entrant tachycardias causing paroxysmal supraventricular tachycardia (PSVT) or ventricular tachycardia (VT). [3] The VT is very difficult to treat and may even be life threatening. Patients with either arrhythmia can present with rapid heart rate starting and stopping abruptly or may even give history of palpitation, dyspnoea, angina pain, anxiety, fatigue or polyuria. There have been reports of unmasking of WPW syndrome under either general or regional anaesthesia. Its means that the patient was asymptomatic with normal ECG preoperatively and under anaesthesia re-entrant arrhythmia gets unmasked with clinical symptoms and ECG changes suggestive of WPW syndrome. [4]

In addition to the classical WPW syndrome, there exist subgroups of patients who are said to have the WPW pattern. These patients have a surface ECG tracing similar to that of WPW syndrome but are asymptomatic. [5] It is worthwhile to elicit history of the above symptoms in patients showing a WPW configuration on surface ECG. This is because asymptomatic patients with intermittent pre-excitation require no treatment. Prospective electrophysiological (EP) studies have demonstrated that there is very low risk (<10%) for development of tachycardia in these patients. Further, no clinical or EP characteristic clearly identifies patients likely to develop atrial fibrillation and sudden cardiac death. [6]

Anaesthetic drugs tend to change the physiology of AV conduction. These two pathways may thus be differently affected by drugs, changes in EP milieu and autonomic tone during anaesthesia. Conduction via the accessory pathway may occur only intermittently when a permissive environment is present. Managing the case with thorough preoperative evaluation is important. If the patient is symptomatic, it is advisable to achieve heart rate control preoperatively, as was done in our patient, with diltiazem. If the patient is asymptomatic, then risk of arrhythmias perioperatively is very less. In general anaesthesia, it is pivotal to avoid light planes and drugs that can precipitate tachycardia (like atropine, glycopyrrolate, ketamine) resulting in PSVT or atrial fibrillation. Opioids like fentanyl, benzodiazepines including midazolam have been found to have no effect on the EP effects of the accessory pathway. [4],[6]

Regional anaesthesia has significant advantage over general anaesthesia as multidrug administration, laryngoscopy stimulation, intubation and light planes leading to sympathetic stimulations are avoided. Epidural anaesthesia is preferred to spinal due to controlled and segmental block with better haemodynamic stability. [7] Subarachnoid block with low-dose bupivacaine supplemented with opioids provides rapid onset with decreased risk of hypotension. There are references showing disappearance of delta waves after propofol administration, making it the drug of choice for induction. [8] Isoflurane and sevoflurane have been found to have no effect on AV node conduction and this may make these agents preferable to halothane for maintenance of cardiostability under anaesthesia after the manifestation of the WPW pattern. Isoflurane in addition has been found to increase accessory pathway refractory period unlike halothane that has no such effect. [9] Vecuronium, due to its cardio stable effect, may be preferred over pancuronium. Of the newer muscle relaxants, cis-atracurium may be the agent of choice because of its high autonomic safety ratio and absence of histamine release. Mivacurium, if available, would be an acceptable choice as reversal of neuromuscular blockade using neostigmine and atropine is not required. [10]

We opted for combined spinal epidural anaesthesia for our patient, thereby ensuring reliable, rapid onset, prolonged duration, and stable haemodynamics with better postoperative pain management. Adequate preloading was done to maintain atrial filling and decrease the need of sympathomimetics which may trigger tachycardia. The single episode of hypotension after epidural supplementation was managed successfully with phenylephrine that treats hypotension without increasing the heart rate in patients of WPW syndrome. [11] We were prepared to manage arrhythmias with drugs like lignocaine, procainamide, diltiazem, adenosine and defibrillator, if needed. Postoperatively, the PCEA ensured better patient comfort, analgesia and early ambulation.

Despite taking all precautions, if atrial fibrillation occurs, the treatment principle is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway, and thus, the ventricular rate. This is in direct contradiction to the goal of treatment of non-WPW atrial fibrillation, which is to slow the refractory period of the AV node. If PSVT is precipitated, then vagal manoeuvres should be tried initially. In haemodynamically stable patients, lignocaine or adenosine can be administered intravenously to break a re-entrant tachycardia. [11] 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. Diltiazem also converts PSVT to normal sinus rhythm by interrupting the re-entry circuit in AV nodal re-entrant tachycardias and WPW syndrome. If haemodynamically unstable, then direct current cardioversion may be needed for atrial fibrillation. Digitalis and verapamil are strictly contraindicated in patients with pre-excited atrial fibrillation or flutter with rapid conduction over an accessory pathway. [12],[13]

In conclusion, our case report demonstrates that a diagnosed case of WPW syndrome can be managed uneventfully under combined spinal epidural anaesthesia. We recommend regional anaesthesia with adequate preloading and treatment of any precipitating factors like hypotension with phenylephrine. We also emphasise the importance of thorough preoperative evaluation, meticulous intraoperative monitoring for atrial and ventricular arrhythmias, and preparedness for the treatment of such conditions in case they develop.

   References Top

1.Wolff L, Parkinson J, White PD. Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. 1930. Ann Noninvasive Electrocardiol 2006;11:340-53.  Back to cited text no. 1
2.Nishikawa K, Mizoguchi M, Yukioka A, Asada A, Fujimori M. Concealed Wolff-Parkinson-White syndrome detected during spinal anaesthesia. Anaesthesia 1993;48:1061-4.  Back to cited text no. 2
3.Rahul S, Patel R, Dewoolkar. Anaesthetic management of WPW Syndrome. Internet J of Anaesthesiology 2007;11:2.  Back to cited text no. 3
4.Chhabra A, Trikha A, Sharma N. Unmasking of benign Wolff-Parkinson-White syndrome under general anaesthesia. Indian J Anaesthesia 2003;47:208-11.  Back to cited text no. 4
5.Yee R, Klein GJ, Guiraudon GM. The Wolff-Parkinson-White syndrome. In: Zipes DP, Jalife J editors. Cardiac Electrophysiology, 2 nd Ed. Philadelphia, London, Toronto, Montreal, Sydney, Tokyo: WB Saunders Company; 1995. p. 1199-214.  Back to cited text no. 5
6.Wellens HJ, Smeets JL, Gorgels AP, Gorgels AP, Farre J. Wolff-Parkinson-White Syndrome. In: Mandel WJ editor. Cardiac Arrhythmias. 3 rd Ed. Philadelphia: J B Lippincott Company; 1995. p. 389-413.  Back to cited text no. 6
7.Okamoto T, Minami K, Shiraishi M, Ogata J, Shigematsu A. Repeated SVT in asymptomatic patients with WPW syndrome during cesarean delivery. Can J Anaesth 2003;50:752-3.  Back to cited text no. 7
8.Seki S, Ichimiya T, Tsuchida H, Namiki A. A case of normalization of Wolff-Parkinson-White syndrome conduction during propofol anaesthesia. Anesthesiology 1999;90:1779-81.  Back to cited text no. 8
9.Sharpe MD, Dobkowski WB, Murkin JM, Klein G, Guiraudon G, Yee R. The electrophysiologic effects of volatile anaesthetics and sufentanil on the normal atrioventricular conduction system and accessory pathways in Wolff-Parkinson-White Syndrome. Anesthesiology 1994;80:63-70.  Back to cited text no. 9
10.Savarese JJ, Caldwel JE, Lien CA, Miller RD. Pharmacology of muscle relaxants and their antagonists. In: Miller RD editor. Anaesthesia 5 th ed. Philadelphia, London, Toronto, Montreal, Sydney, Tokyo, Edinburgh: Churchill Livingstone; 2000.p. 412-90.  Back to cited text no. 10
11.Jacobson L, Turnquist K, Masleys S. WPW syndrome: termination of paroxysmal supraventricular tachycardia with phenylephrine. Anaesthesia 1985;40:657-60.  Back to cited text no. 11
12.Robbins K, Lyons G. Supraventricular tachycardia in pregnancy. Case Reports. Br J Anaesth 2004;92:140-3.  Back to cited text no. 12
13.Van ziil DH, Dyer A, Scott Millar RN, James MF. Supraventricular tachycardia during spinal anaesthesia for cesarean section. Int J Obstet Anesth 2001;10:202-5.  Back to cited text no. 13

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