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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

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pregnancy: safety considerations. Drug Safety 1999; 20: 8594

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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

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8 Kowey PR, Marinchak RA, Rials SJ, Bharucha DB. Classication

and pharmacology of antiarrhythmic drugs. Am Heart J 2000;

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9 Finfer SR. Pacemaker failure on induction of anaesthesia. Br J

Anaesth 1991; 66: 50912

10 Domino KB, Smith TC. Electrocautery-induced reprogramming

of a pacemaker using a precordial magnet. Anesth Analg1983; 62:

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pacemaker inhibition by a magnet: a case study. Heart Lung1993;

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12 Lockhart EM, Penning DH, Olufolabi AJ, Bell EA, Booth JV, Kern

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

Anaesthetic management of severe bradycardia during generalanaesthesia 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 atro-

pine, ephedrine, and colloid infusion and the second with a temporary pacemaker and ephe-

drine.

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.

Severe bradycardia during general anaesthesia

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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 andan 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 min 1.

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 min

1

. Before induction ofanaesthesia 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 min 1

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. Simplevagal 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% reprodu-

cible, 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 dysfunc-

tion 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 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

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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4 Kenny RA, Ingram A, Bayliss J, Sutton R. Head-up tilt: a useful

test for investigating unexplained syncope. Lancet 1986; 1:

13525

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JI, Abboud FM, eds. Handbook of Physiology, Section 2: The

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Physiological Society, 1983; 795813

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Publishers, 1998; 18791911

7 Glikson M, Espinoza RE Hayes DL. Expanding indications for

permanent pacemakers. Ann Intern Med 1995; 123: 44351

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with drug therapy in the treatment of neurocardiogenic

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