Celal Bayar University, School of Medicine, Department of Anaesthesiology and Reanimation, Manisa, Turkey*Corresponding author
Accepted for publication: May 30, 2002
![]() |
Abstract |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
Br J Anaesth 2002; 89: 6557
Keywords: complications, bradycardia; heart, arrhythmia, bradycardia; surgery, laryngoscopy
![]() |
Introduction |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
We describe two episodes of severe bradycardia in the same patient during general anaesthesia, the second of which was managed with a pacemaker.
![]() |
Case report |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
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 fluticasone 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 µg. 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% sevoflurane 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 µg. 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 |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
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 patients 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 dual-chamber 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.
![]() |
References |
---|
![]() ![]() ![]() ![]() ![]() ![]() |
---|
2 Kinsella SM, Tuckey JP. Perioperative bradycardia and asystole: relationship to vasovagal syncope and the Bezold-Jarish reflex. Br J Anaesth 2001; 86: 85968
3 Sheldon R. Role of pacing in the treatment of vasovagal syncope. Am J Cardiol 1999; 84: 2636
4 Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: a useful test for investigating unexplained syncope. Lancet 1986; 1: 13525[ISI][Medline]
5 Mark AL. Cardiopulmonary baroreflexes 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 Marfil 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[Medline]