Department of Anesthesiology, Seoul National University Hospital, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, Korea
Corresponding author. E-mail: limyjin@snu.ac.kr
Accepted for publication: October 9, 2002
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Abstract |
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Br J Anaesth 2003; 90: 3914
Keywords: anaesthesia, general; surgery, cardiovascular; complications, coronary vasospasm
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Introduction |
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The carotid sinus, located at the bifurcation of carotid arteries, has an important role in the baroreceptor reflex. Carotid sinus massage can cause cardiac vagal activity, which can cause CAS.8 We present a case of CAS during an operation for modified radical neck dissection under general anaesthesia, which recurred in association with carotid sinus stimulation. We present ECG and coronary angiogram results that confirmed this diagnosis. To our knowledge, this is the first case report to describe CAS evoked by carotid sinus stimulation during general anaesthesia.
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Case report |
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In the operating room, the patients arterial pressure (AP) was 145/75 mm Hg and heart rate (HR) was 75 beats min1. Anaesthesia was induced with fentanyl 100 µg, propofol 120 mg and vecuronium 10 mg. After intubation, anaesthesia was maintained with nitrous oxide (50%), oxygen (50%) and isoflurane (0.52.0 vol %). Ninety minutes after induction, ST-segment elevation in lead II, not preceded by changes in HR or AP (HR 85 beats min1, AP 120/70 mm Hg), was noted suddenly on the ECG monitor. The ST-segment alterations subsided completely in 5 min without treatment. Forty minutes later, an identical ECG change of marked ST-segment elevation, lasting only 1 min (HR 90 beats min1, AP 110/69 mm Hg), occurred again during retraction of the tissues surrounding the mass. PaCO2 (42 mm Hg), PaO2 (203 mm Hg), haematocrit (36%) and plasma potassium concentration (4.2 mmol litre1) were within normal limits. We suspected that the ST-segment elevation and carotid sinus stimulation were related. The carotid sinus was compressed for 10 s by steady finger pressure after removal of the neck mass. About 1 min later, the same ECG change of ST-segment elevation and QRS widening appeared (Fig. 1A) without any associated changes in HR or AP (HR 84 beats min1, AP 122/55 mm Hg). The entire episode lasted 5 min and resolved spontaneously (Fig. 1B). Thirty minutes later, during skin closure, marked ST-segment elevation, mimicking intraventricular conduction delay or ventricular rhythm, occurred again (Fig. 1C), with a slight decrease in HR (from 88 to 80 beats min1) and AP (from 94/70 to 86/50 mm Hg). The elevated ST-segment began to decline immediately after giving lidocaine 1% 80 mg i.v. A continuous infusion of nitroglycerine (1 µg kg1 min1) was started. The entire episode lasted 5 min. A 12-lead ECG, taken immediately after operation, showed normal sinus rhythm, and cardiac enzyme measurements, including creatine kinase and lactate dehydrogenase, were within normal limits.
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Discussion |
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General anaesthesia can be a triggering event for CAS, although CAS during anaesthesia is a rare event.911 This case is unique in that the typical ECG changes of variant angina were provoked by surgical manipulation of the carotid sinus during general anaesthesia.
Sympathovagal imbalance caused by sudden increases in parasympathetic tone was thought to be the triggering factor for CAS in this patient. Previous studies have shown that the increased parasympathetic activity can trigger the development of coronary vasospasm.35 The carotid sinus reflex is a baroreceptor-mediated reflex that responds rapidly, a maximum response often being observed even in the first cardiac cycle after carotid sinus stimulation.12 The reflex does not continue for more than 20 s because of parasympathetic withdrawal and the return of sympathetic discharge. Nishizaki and colleagues8 showed that carotid sinus massage in an awake patient without significant coronary artery stenosis could provoke CAS on angiography in approximately 2.5 min with a short period of bradycardia. In our case, about 1 min elapsed from the carotid sinus stimulation to the appearance of ST-segment elevation, and bradycardia was not noted. Thus, in our case, involvement of reflex sympathetic activity in response to enhanced parasympathetic activity2 68 could have been a predominant mechanism.
In summary, we describe a case of CAS associated with carotid sinus stimulation during general anaesthesia in a patient with variant angina. Because of the possibility of fatal arrhythmias and myocardial ischaemia, early recognition of CAS-induced ST-segment elevation and prompt initiation of nitroglycerine infusion is indicated.
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References |
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