1 Cardiology, Swiss Cardiovascular Centre and 2 Department of Anaesthesiology, University Hospital of Bern, CH-3010 Bern, Switzerland *Corresponding author
Accepted for publication: May 14, 2002
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Abstract |
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Br J Anaesth 2002; 88: 51923
Keywords: agonists, adrenergic; complications, hypertension; heart, arrhythmia, tachycardia; spinal cord, sensory block; veins, complications
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Introduction |
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We describe two cases of coronary artery spasm induced by ephedrine given for treatment of a vasovagal reaction at the placement of a spinal anaesthetic in young women who had minimal cardiovascular risk factors and angiographically normal coronary arteries.
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Case 1 |
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The ECG 1 h after the event showed diffuse ST-segment depression, and transthoracic echocardiography revealed a moderately-to-severely impaired left ventricular systolic function (ejection fraction 40%), with mild mitral regurgitation, akinesia of the basal segments and apical hypercontractility. The ECG had returned to normal 8 h later, whereas the troponin-I concentration rose from 4.7 µg litre1 (2.5 h after the event) to a peak of 29.5 µg litre1 8 h later (normal range <0.6). Total CK and CK-MB mass peaked at 268 units litre1 (normal range <167) and 18.9 µg litre1 (normal range <4.0), respectively, 11 h after the event, consistent with non-Q-wave myocardial infarction. Coronary angiography performed the next day revealed normal coronary arteries. Global left ventricular systolic function was normal (EF 64%), but hypokinesia of the anterobasal, inferobasal and lateral wall segments was noted, and left ventricular end diastolic pressure was increased (22 mm Hg). An echocardiography performed on the 4th day showed normalization of left ventricular systolic function, with a small pericardial effusion. The patient underwent uneventful surgery under general anaesthesia 3 months later.
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Case 2 |
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The ECG 90 min after the event showed ST-segment depression in V3 and V4, but the chest x ray showed cardiomegaly and right-sided pulmonary oedema. Echocardiography revealed a slightly diminished left ventricular systolic function (EF 55%), with akinesia of the basal segments and apical hypercontractility, and moderate mitral regurgitation. Troponin-I and total CK concentration peaked at 25.8 µg litre1 and 185 units1, respectively, 10 h after the event, consistent with minimal non-Q-wave myocardial infarction. Coronary angiography performed the next day revealed normal coronary arteries. The left ventricular systolic function was slightly depressed (EF 50%) with hypokinesia of the anterobasal, inferobasal and lateral wall segments, and the left ventricular end diastolic pressure was increased (22 mm Hg). An echocardiography performed on the 4th day showed normalization of left ventricular systolic function, with only minimal mitral regurgitation. The patient underwent uneventful surgery under general anaesthesia 3 months later. The correct ephedrine concentration was confirmed by the hospital pharmacy in the remainder of the liquid from the ephedrine syringe used in this patient and the possibility of contamination with other substances was excluded.
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Discussion |
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In Case 1 the sitting position was maintained for a few minutes in order to complete epidural catheter fixation despite the patients complaint of nausea and dizziness. The decrease of heart rate and arterial pressure was aggressively treated with ephedrine assuming a rapidly increasing level of spinal block. However, the level of the block recorded immediately after the event was only T8. She was not hypotensive and only slightly bradycardic at the onset of symptoms, although her heart rate decrease from 80 to 55 beats min1 was abrupt. Many of the reported cases of asystole under spinal anaesthesia occurred within seconds of the abrupt onset of bradycardia, suggesting a cardiac reflex induced by an acute drop in right-sided cardiac filling pressure.16 17 Because of this and another case report,18 the early use of ephedrine is recommended (treat the downward trend) in our department. In retrospect this patients symptoms were more likely to have been vasovagal in origin and the dose of ephedrine excessive. The use of the sitting position for easier siting of combined spinalepidural analgesia may have further increased the risk of a vasovagal episode.5
In Case 2, a clearly anxious patient with a history of vasovagal syncope and some vasovagal reaction even before the start of the procedure, exhibited a rather high level of spinal block that was well tolerated until she was turned to a lateral position. In contrast to the first patient, she was administered a larger volume of i.v. fluid and kept in the right lateral position for at least 15 min after the onset of symptoms. This explains why the subsequent pulmonary oedema was predominantly on the right side. As in the first patient the initial symptoms of fainting were treated first with ephedrine and not atropine. Nevertheless, the patient developed severe bradycardia and hypotension on moving her from the supine to the right lateral position.
We can only speculate as to the pathophysiological mechanism causing myocardial ischaemia, diastolic dysfunction, pulmonary oedema and infarction associated with the transient regional left ventricular dysfunction. A predominant vagal tone, as occurred in both of our patients, may induce multivessel coronary vasospasm.4 A decreased sympathetic tone caused ST-segment depression in women during Caesarean section under spinal anaesthesia.19 Intracoronary injection of acetylcholine is used as a diagnostic test to identify patients with coronary artery spasm, which supports the pathogenic role of predominant vagal tone.20 21 In a recent study on dobutamine stress echocardiography22 the pure ß-stimulator, dobutamine, induced coronary vasospasm in patients with coronary spastic angina inducible by intracoronary acetylcholine.
Other explanations are less likely. Myocardial ischaemia secondary to a massively increased oxygen demand associated with sinus tachycardia and severe hypertension after administration of atropine and ephedrine is unlikely. In young patients with excellent exercise tolerance and angiographically normal coronary arteries, such periods of hypertension, even when preceded by hypotension, are usually well tolerated and have not been reported to be associated with regional wall abnormalities. Even less likely as an explanation would be acute thrombus formation in normal coronary arteries with spontaneous lysis, since the regional distribution of the stunned myocardium would require several coronary arteries to be affected.
Anaesthetists are more and more reluctant to use vagolytic drugs prophylactically, in order not to mask the tachycardia induced by accidental i.v. injection of an epinephrine-containing test dose, and also because the tachycardia induced by atropine is considered potentially harmful in elderly patients. Moreover vasovagal syncope occurring during placement of i.v. lines or regional blocks is considered a harmless and mostly spontaneously resolving event. Vasovagal fainting is associated with an increased vagal, and a decreased sympathetic, activity explaining bradycardia and hypotension, respectively.5 Kinsella and Tuckey5 therefore suggest ephedrine as the logical first-line drug treatment of bradycardia during spinal anaesthesia, whereas others recommend atropine first and then ephedrine.3
In order to prevent fatal cardiac arrest under spinal anaesthesia early aggressive treatment of bradycardia and hypotension with fluids, atropine, ephedrine and eventually epinephrine is recommended. How early, at what dose and what intervals the drugs are to be administered must be decided by the attending anaesthetist. Whereas administering too little, too late may lead to asystole, too much, too early may lead to arrhythmia and coronary vasospasm with infarction, as in our two cases. Furthermore, although the ephedrine doses as administered in our patients seem to be large, similar doses were investigated for prophylactic use without serious side effects.23 24
The important parasympathetic predominance in two young, anxious women may have increased the risk for coronary vasospasm that was then induced by, retrospectively, too large a dose of ephedrine, administered under the assumption of a rapidly increasing level of spinal block. Prior administration of atropine, especially to the first patient who was not hypotensive at the onset of the symptoms, might have prevented the coronary vasospasm.
We conclude that a delay of immediate supine placement of a patient suffering from vasovagal symptoms during placement of neuraxial block in the sitting position may not be compensated by increasing the dose of - and ß-adrenergic drugs. In the light of unopposed vagal predominance predisposing to coronary vasospasm, even in young healthy patients, the previously suggested sequence of first injecting atropine and then ephedrine in the case of bradycardia with or without hypotension under spinal anaesthesia is further corroborated.
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Acknowledgement |
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References |
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