Decreased bispectral index as an indicator of syncope before hypotension and bradycardia in two patients with needle phobia
N. N. Win,
H. Kohase*,
T. Miyamoto and
M. Umino
Section of Anesthesiology and Clinical Physiology, Department of Oral Restitution, Division of Oral Sciences, Graduate School, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, Japan 113-8549
Corresponding author: e-mail: hkohase.anph@tmd.ac.jp
Accepted for publication: May 8, 2003
 |
Abstract
|
---|
We report two cases who exhibited a decrease in their bispectral index (BISTM) score, associated with syncope during venipuncture in patients with suspected needle phobia. In case 1, the reduction in BIS score occurred during the development of hypotension and bradycardia and may well have been caused by cerebral hypoperfusion. In case 2, the patient lost consciousness with decreasing BIS score before hypotension and bradycardia; this patients condition could not be completely explained by cerebral hypoperfusion as a result of a vasovagal reflex because the patients blood pressure and heart rate remained normal during the syncopal episode.
Br J Anaesth 2003; 91: 74952
Keywords: brain, syncope; complications, injection phobia; monitoring, bispectral index
 |
Introduction
|
---|
The bispectral index (BISTM) is currently used to monitor the depth of sedation or general anaesthesia.1 Fainting or vasovagal syncope before the induction of anaesthesia is not uncommon.2 3 We report two cases of syncope accompanied by decreased BIS score before sedation in patients with suspected needle phobia.
 |
Case reports
|
---|
Case 1
A 27-yr-old male, weighing 62 kg, was scheduled to undergo dental implantation. He had a history of fainting during a phlebotomy procedure and an anxiety disorder. A psychiatrist had prescribed fluvoxamine maleate (50 mg twice daily), a potent and selective serotonin reuptake inhibitor, for the treatment of this anxiety disorder. The patient had been taking this medicine for 5 yr before the scheduled dental implantation. Propofol sedation with local anaesthesia was planned for dental implantation because of his past history. Before the commencement of sedation and the surgical procedure, the patient was lying on a dental chair. A vital signs monitor (Lifescope®; Nihon Kohden, Tokyo, Japan) was used for routine monitoring, including blood pressure, arterial oxygen saturation and an electrocardiogram (ECG). The sensors of the BIS monitor (Aspect A2000; Aspect Medical Systems, Newton, MA, USA) were placed on the forehead in accordance with instructions. Just before venipuncture, he had a heart rate of 96 beats min1, an arterial blood pressure (BP) of 135/67 mm Hg, a respiratory rate (RR) of 14 bpm, a pulse oximeter reading (SpO2) of 98% and a BIS score of 95. During venipuncture, the patient complained of nausea and dizziness. He had a weak arterial pulse, he was sweating and his breathing was irregular and shallow. At this time his heart rate was 35 beats min1, BP 78/30 mm Hg and SpO2 83%. Immediately after the onset of the bradycardia and hypotension, the BIS score decreased to 42 (Fig. 1) and the patient lost consciousness. Immediately, we administered 100% oxygen, raised his legs, infused i.v. fluid and i.v. atropine 0.5 mg. After about 2 min, the patient had recovered from the syncopal attack. His heart rate, BP, SpO2 and BIS score returned to normal levels. Immediately after recovery, propofol sedation was started. The heart rate, BP and SpO2 remained stable and normal and the BIS score ranged between 70 and 90 during sedation.

View larger version (19K):
[in this window]
[in a new window]
|
Fig 1 Decreased bispectral index (BIS) followed by hypotension in case 1. A=decrease in BIS score to 42; B=venipuncture; C=nausea and dizziness; D=hypotension and bradycardia; E=atropine sulphate and propofol.
|
|
Case 2
A 29-yr-old male, weighing 56 kg, visited our hospital for tooth extraction. He had a history of two experiences of abnormal emotional upset during injection of local anaesthesia for a dental procedure and at venipuncture for fluid infusion. Tooth extraction was planned under local anaesthesia and i.v. sedation with propofol. The heart rate, BP, SpO2 and BIS were monitored in the same manner as in Case 1. Before sedation, his BP was 130/70 mm Hg, heart rate 80 beats min1, RR 16 bpm, SpO2 98% and BIS score 98. The first attempt at venipuncture was not successful. A transient decrease in SpO2 (92%) associated with breath-holding was observed during the second venipuncture but the RR and SpO2 recovered to 18 bpm and 96% respectively. Immediately after the second venipuncture, the patient complained of an unpleasant feeling and lost consciousness. At that time, his pulse was regular with an adequate volume and a rate of 68 bpm. The BIS score decreased to 35 when the fainting episode occurred, although the heart rate and BP were maintained at 70 beats min1 and 130/80 mm Hg respectively. Shortly thereafter, a seizure of the entire body occurred and continued for a few minutes. By the end of the seizure, the BIS had increased to 98. After this, bradycardia and hypotension developed, but the BIS score remained between 95 and 98 (Fig. 2). During the entire episode, the SpO2 and RR ranged between 92 and 98% and 16 and 20 bpm, respectively. The patient was treated by raising his legs, infusing dextrose saline i.v. and the i.v. administration of atropine 0.5 mg. Sedation with propofol was started a few minutes after the syncope and seizure episodes had ended, when the patients consciousness level, BP, heart rate, SpO2 and BIS score had returned to normal. There were no abnormal events, and BP, heart rate and SpO2 were stable and within normal ranges during sedation. The BIS score was between 60 and 80 during sedation.

View larger version (18K):
[in this window]
[in a new window]
|
Fig 2 Decreased bispectral index (BIS) before hypotension and bradycardia in case 2. A=decrease in BIS score to 35; B=venipuncture; C=seizure; D=hypotension and bradycardia; E=atropine sulphate and propofol.
|
|
 |
Discussion
|
---|
Although the BIS is not a specific index of consciousness, it correlates with wakefulness,4 learning5 and the conscious processing of information.6 In the present cases, BIS changes were recognized by chance during syncope. Anxiety, fear and pain associated with dental treatment may evoke physiological, behavioural, motor or cognitive changes. In case 1, the patient had a past history of a fainting attack during a phlebotomy, while Case 2 had a history of injection and venipuncture phobia. According to the classification of the American Psychiatric Association, both cases were classified as blood-injury-injection phobias.7 Syncope is a sudden transient loss of consciousness that may be the result of cardiovascular, neurological, metabolic or psychological disorders, or iatrogenic events.8 Among these disorders, vasovagal syncope (also called neurocardiogenic syncope or neurally mediated syncope) has been reported as the cause of over half of dental office emergencies.9 Though vasovagal syncope tends to occur when the subject is in a standing position, it can also occur when the subject is in a supine position.2 3 10 In the present cases, both patients fainted while in a supine position. In Case 1, pain, anxiety and fear at venipuncture triggered an intense parasympathetic state leading to bradycardia and hypotension. Bradycardia and hypotension probably caused cerebral hypoperfusion, resulting in a syncopal attack.8 11 De creased BIS was accompanied by cerebral hypoperfusion in case 1, as in other reported cases.12 13
The second case shows that syncope and a decreased BIS score can be caused by factors other than cerebral hypoperfusion. The patient lost consciousness with a rapidly decreasing BIS score immediately after venipuncture, although BP, heart rate and SpO2 remained normal. Hyperventilation, hysteria and other forms of psychogenic unresponsiveness14 15 are possible causes of the seizure and syncope. However, our patient did not hyperventilate and recovered from the syncopal attack and seizure with no postictal signs or symptoms of epilepsy. The reduction in the BIS score was not due to seizure because the decrease in the index occurred before the muscle contraction and was not influenced by abnormal electrical discharges in the brain. The BIS score increased after the seizure, probably as a result of electromyographic activity arising from the muscle contractions.1 16 The syncopal episode was brought on by an intense emotional experience, consisting of anxiety, fear and pain at the time of venipuncture; the episode was considered to result from centrally mediated vasovagal syncope. Thus, the cortical processing of emotional fear, stress and pain appears to have been conveyed to the medullary cardiovascular centre through the limbic system. The limbic system is known to be concerned with emotions, and stimulation of the limbic sympatho-inhibitory centre causes hypotension and bradycardia in some animal species.17 18 Mercader and colleagues19 observed an increase in EEG slow-wave activity and delta waves during syncope and in patients before syncopal episodes. These EEG wave changes were associated with the onset of bradycardia, hypotension and clinical symptoms.19 Unfortunately, we were unable to analyse EEG components.
Whatever the case, the BIS observed in both cases was caused by syncope, reflecting centrally mediated brain activity in response to emotional stress and pain.
Syncope and a decrease in BIS may precede hypotension and bradycardia in patients with needle phobia.
 |
References
|
---|
1 Rampil IJ. A primer for EEG signal processing in anesthesia. Anesthesiology 1998; 89: 9801002[ISI][Medline]
2 Hampl KF, Schneider MC. Vasovagal asystole before induction of general anaesthesia. Eur J Anaesthesiol 1994; 11: 1313[ISI][Medline]
3 Keane TK, Hennis PJ, Bink-Boelkens MT. Non-drug related asystole associated with anesthetic induction. Anaesthesia 1991; 46: 389[ISI][Medline]
4 Barnett TP, Johnson LC, Naitoh P, et al. Bispectral analysis of electroencephalogram signals during waking and sleeping. Science 1971; 172: 4012[ISI][Medline]
5 Leslie K, Sessler DI, Schroeder M, Walters K. Propofol blood concentration and the bispectral index predict suppression of learning during propofol/epidural anesthesia in volunteers. Anesth Analg 1995; 81: 126974[Abstract]
6 Kearse LA, Rosow C, Zaslavsky A, et al. Bispectral analysis of the electroencephalogram predicts conscious processing of information during propofol sedation and hypnosis. Anesthesiology 1998; 88: 2534[ISI][Medline]
7 American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th Edn. Washington, DC: American Psychiatric Association, 1994
8 Martin RB. Anxiety, its manifestation and role in the dental patient. Dent Clin North Am 1995; 39: 52339[Medline]
9 Malamed SF. Managing medical emergencies. J Am Dent Assoc 1993; 124: 4053
10 Verril PJ, Aelling WH. Vasovagal faint in the supine position. Br Med J 1970; IV: 348
11 Hunt M. Syncope. In: Rosen P, Barkin R. Emergency Medicine: Concepts and Clinical Practice, 4th Edn. St Louis: Mosby-Year Book, 1998; 157082
12 Engl MR. The changes in bispectral index during a hypovolemic cardiac arrest. Anesthesiology 1999; 91: 19479[ISI][Medline]
13 Merat S, Levecque J-P, Le Gulluche Y, Diraison Y, Brinquin L, Hoffmann J-J. BIS monitoring may allow the detection of severe cerebral ischemia. Can J Anaesth 2001; 48: 10669[Abstract/Free Full Text]
14 Krumholz A. Nonepileptic seizures: diagnosis and management. Neurology 1999; 53 (5 Suppl 2): S7683[ISI][Medline]
15 Chabolla DR, Krahn LE, So EL, Rummans TA. Psychogenic nonepileptic seizures. Mayo Clin Proc 1996; 71: 493500[ISI][Medline]
16 Bruhn J, Bouillon TW, Shafer SL. Electromyographic activity falsely elevates the bispectral index. Anesthesiology 2000; 92: 14857[ISI][Medline]
17 Kinsella SM, Tuckey JP. Perioperative bradycardia and asystole: relationship to vasovagal syncope and the BezoldJarisch reflex. Br J Anaesth 2002; 86: 85968[CrossRef][ISI]
18 VanLieshout JJ, Wieling W, Karemaker JM, Eckberg DL. The vasovagal response. Clin Sci 1991; 81: 57586[ISI][Medline]
19 Mercader MA, Varghese PJ, Potolicchio SJ, Venkatraman GK, Lee SW. New insights into the mechanism of neurally mediated syncope. Heart 2002; 88: 21721[Abstract/Free Full Text]