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Severe bradycardia during general anaesthesia

References
1 Ostrzega E, Mehra A, Widerhorn J, et al. Evidence of increased incidence of arrhythmias during pregnancy: a study of 104 pregnant women with symptoms of palpitations, dizziness or syncopy. J Am Coll Cardiol 1999; 19: 125A 2 Sibai BM, Frangieh A. Maternal adaptation to pregnancy. Curr Opin Obstet Gynecol 1995; 7: 4206 3 Drugs Facts and Comparisons. St Louis, MO: Facts and Comparisons, 1997 4 Joglar JA, Page RL. Treatment of cardiac arrhythmias during pregnancy: safety considerations. Drug Safety 1999; 20: 8594 5 Committee on drugs. Transfer of drugs and other chemicals into human milk. Pediatrics 1994; 93: 13750 6 Hantler CB, Wilton NC, Knight PR. Comparative effects of halothane, enurane, and isourane on atrioventricular conductivity and subsidiary pacemaker function in dogs. Anesth Analg 1994; 79: 4559 7 Atlee JL, Malkinson CE. Potentiation by thiopental of 8 9 10 11 12

halothaneepinephrine-induced arrhythmias in dogs. Anesthesiology 1982; 57: 2858 Kowey PR, Marinchak RA, Rials SJ, Bharucha DB. Classication and pharmacology of antiarrhythmic drugs. Am Heart J 2000; 140: 1220 Finfer SR. Pacemaker failure on induction of anaesthesia. Br J Anaesth 1991; 66: 50912 Domino KB, Smith TC. Electrocautery-induced reprogramming of a pacemaker using a precordial magnet. Anesth Analg 1983; 62: 60912 Bierman PQ, Roche DA, Carlson LG. Abnormal permanent pacemaker inhibition by a magnet: a case study. Heart Lung 1993; 22: 14850 Lockhart EM, Penning DH, Olufolabi AJ, Bell EA, Booth JV, Kern FH. SvO2 monitoring during spinal anesthesia and cesarean section in a parturient with severe cyanotic congenital heart disease. Anesthesiology 1999; 90: 12135

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British Journal of Anaesthesia 89 (4): 6557 (2002)

Anaesthetic management of severe bradycardia during general anaesthesia using temporary cardiac pacing
V. Toprak*, A. Yentur and M. Sakarya
Celal Bayar University, School of Medicine, Department of Anaesthesiology and Reanimation, Manisa, Turkey
*Corresponding author
There are few reports of management of severe bradycardia with temporary cardiac pacing. We describe a 65-yr-old female patient who developed bradycardia and hypotension on two occasions during general anaesthesia for laryngoscopy. The rst episode was treated with atropine, ephedrine, and colloid infusion and the second with a temporary pacemaker and ephedrine. Br J Anaesth 2002; 89: 6557 Keywords: complications, bradycardia; heart, arrhythmia, bradycardia; surgery, laryngoscopy Accepted for publication: May 30, 2002

Excessive vagal activity, which causes severe bradycardia and hypotension, can be life threatening. The trigger can be painful stimulation of the bronchial, pharyngeal, laryngeal, or oesophageal mucosa.1 Prompt treatment is needed with urgent restoration of venous return by leg elevation, head down tilt, and i.v. uids, and the use of anticholinergic and sympathomimetic drugs.2 A pacemaker should be con-

sidered for patients with vasovagal syncope which is frequent and does not respond to medical treatment. The use of a temporary pacemaker for patients who develop bradycardia during general anaesthesia is controversial.3 We describe two episodes of severe bradycardia in the same patient during general anaesthesia, the second of which was managed with a pacemaker.

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Toprak et al.

Case report
The patient was a 65-yr-old female who weighed 59 kg. She was admitted to hospital to have direct laryngoscopy and vocal cord biopsy, because of a history of hoarseness. This was to be carried out under general anaesthesia. She gave a history of a myomectomy under general anaesthesia in 1970, which was uneventful, and asthma for the last 25 yr. Her medications were N-acetyl cysteine and an inhaler of uticasone propionate. She was given 5 mg diazepam by mouth before going to the operating theatre. She was monitored with non-invasive arterial pressure, electrocardiogram, and pulse oximetry. Her heart rate was 68 beats min1 and arterial pressure 115/78 mm Hg. Anaesthesia was induced with propofol 150 mg, followed by vecuronium 6 mg and fentanyl 200 mg. After the trachea had been intubated with a microlaryngeal tube, her heart rate was 76 beats min1 and arterial pressure was 136/82 mm Hg. Anaesthesia was maintained with 2% sevourane in nitrous oxide/oxygen, and the patient was positioned slightly head up to facilitate direct laryngoscopy. Sinus rhythm was present throughout the episode. Immediately after direct laryngoscopy by the surgeon, the heart rate suddenly decreased to 28 beats min1. Despite withdrawal of the laryngoscope, bradycardia persisted. Atropine 0.5 mg was given i.v., but the heart rate remained slow and the arterial pressure was 55/28 mm Hg. A further dose of atropine 0.5 mg i.v. had no effect but ephedrine 10 mg i.v. caused the heart rate to increase to 72 beats min1. Hypotension persisted and was treated with infusion of 500 ml of hydroxyethyl starch. Arterial blood gas and serum electrolyte measurements were normal. After 12 min the patient became cadiovascularly stable. The operation was postponed, and the patient recovered without sequelae. Subsequent cardiac examination was normal. Six months later the same patient returned for treatment of nasal polyps, by nasal endoscopy. Her hoarseness had resolved with medical therapy. On careful questioning the patient gave a history of attacks of syncope or pre-syncope for 40 yr. A cardiologist suggested a head-up tilt test, and that a temporary pacemaker should be used. Tilting head up to 60 for 45 min4 had no effect. For the second operation, she was given diazepam 5 mg by mouth. After applying non-invasive cardiovascular monitors a temporary pacemaker3 (Dispomedia) was inserted via the femoral vein to the apex of the right ventricle, and set at 60 beats min1. Before induction of anaesthesia her heart rate was 66 beats min1 and the arterial pressure was 125/66 mm Hg. Anaesthesia was induced with etomidate 18 mg, followed by vecuronium 6 mg and fentanyl 250 mg. After tracheal intubation, the heart rate decreased. The pacemaker became active and at the same time the arterial pressure was noted to be 76/40 mm Hg. After ephedrine 10 mg i.v., the heart rate was 68 beats min1 and the arterial pressure 106/58 mm Hg. The remainder of the surgery and anaesthesia was uneventful. The pacemaker

was withdrawn the day after surgery. The patient recovered completely and left hospital after 3 days.

Discussion
During anaesthesia, changes of heart rate may suggest changes in the depth of anaesthesia, changes in vagal activity, or the effects of drugs or possible hypoxia. Simple vagal reactions usually respond to when the stimulus is stopped. Here, the vagal response was excessive and severe hypotension persisted despite stopping the laryngoscopy. Tilt-table testing may be useful in the diagnosis of vasovagal syncope, and can guide treatment. However the tilt-table test is positive in only 75% of patients with classic vasovagal syncope. The sensitivities of the various test methods vary widely and they are only 7580% reproducible, suggesting that they may give an incorrect diagnosis.3 However, as tilt-table testing is the only investigation that can precipitate a typical attack that can be directly observed, it is taken as the `gold standard' for the diagnosis of vasovagal syncope.4 Clinically, syncope associated with autonomic dysfunction tends to be most frequent early in the day, and is more likely after a period of bed rest, after vigorous exercise, or during drug treatment that can reduce central circulatory volume. Unlike vasovagal faints, these episodes of syncope are not associated with bradycardia, sweating, or marked pallor.5 Our patient's clinical presentation, and the absence of predisposing factors such diabetes mellitus led us to think she had a vasovagal response rather than autonomic dysfunction. Treatment of vasovagal syncope with a pacemaker is controversial.6 Vasovagal syncope can be aborted by dualchamber pacing, and if syncope does occur, pacing can prolong consciousness.7 However, in a report of 22 patients with neurocardiogenic syncope, pacing failed to prevent a decrease in arterial pressure during bradycardia caused by tilt testing.8 Temporary pacing is most commonly used to treat symptomatic bradycardia for short periods, either before a permanent pacemaker or when the bradycardias is not persistent.3 6 There are few reports of temporary pacing for general anaesthesia.9 We suggest that as well as drug treatment, temporary pacing is a useful form of treatment for this condition.

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References
1 Hosie L, Wood JP, Thomas AN. Vasovagal syncope and anaesthetic practice. Eur J Anaesth 2001; 18: 55457 2 Kinsella SM, Tuckey JP. Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold-Jarish reex. Br J Anaesth 2001; 86: 85968 3 Sheldon R. Role of pacing in the treatment of vasovagal syncope. Am J Cardiol 1999; 84: 2636

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Severe bradycardia during general anaesthesia

4 Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: a useful test for investigating unexplained syncope. Lancet 1986; 1: 13525 5 Mark AL. Cardiopulmonary baroreexes in humans. In: Shepherd JI, Abboud FM, eds. Handbook of Physiology, Section 2: The Cardiovascular System, Vol. III. Bethesda, MD: American Physiological Society, 1983; 795813 6 Haye S, David L. Pacemakers. In: Topol Eric J, ed. Textbook of Cardiovascular Medicine. Philadelphia: Lippincott-Raven Publishers, 1998; 18791911

7 Glikson M, Espinoza RE Hayes DL. Expanding indications for permanent pacemakers. Ann Intern Med 1995; 123: 44351 8 Sra JS, Jazayeri MR, Avitall B, et al. Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystole. N Engl J Med 1993; 328: 1085 9 Fuentes Rodriguez R, Sebastianes Marl MC, Mato Ponce M, Morales Guerrero J, Torres Morera LM. Preoperative prophylactic pacemakers: apropos of their indication in a disputed case. Rev Esp Anestesiol Reanim 2001; 48: 3841

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