EditorWe wish to report a case of etomidate reverting ventricular tachycardia to sinus rhythm. Although there have been several case reports and studies demonstrating the antiarrhythmic affects of propofol13 this has not been true of etomidate.
A 59-yr-old man presented to the emergency department with a 2 h history of central chest pain radiating to the left arm and palpitations. He denied any symptoms of shortness of breath, nausea or vomiting. He had no history of ischaemic heart disease but was taking irbesartan for hypertension. He had no other past medical history. He was an ex-smoker having stopped 30 yr previously.
On examination he was orientated with no clamminess or pallor. His pulse rate was 180 beats min1 with a blood pressure of 140/100 mm Hg. On auscultation, heart sounds and breath sounds were normal with no added sounds. An initial 12-lead ECG demonstrated a supra-ventricular tachycardia with a rate of 180 beats min1 and evidence of ischaemic change posteriorly. A 300 mg bolus of amiodarone i.v. failed to produce a response. Systolic arterial pressure remained stable at 140 mm Hg. Subsequently, i.v. adenosine was administered in increasing doses of 6 and 12 mg to no effect. By this time the 12-lead ECG had changed showing a rate of 200 beats min1 and broadening complexes suggestive of ventricular tachycardia (VT). The blood pressure had now fallen to 96/50 mm Hg so the decision was made to cardiovert and anaesthetic assistance was sought.
Owing to the ingestion of solid food 3 h previously, the anaesthetic plan was for a rapid sequence induction with cricoid pressure and tracheal intubation followed by cardioversion. After pre-oxygenation, cricoid pressure was applied and anaesthesia was induced with etomidate. After etomidate 14 mg, it was noted that the rhythm had converted to sinus.
As the patient had been rendered apnoeic, succinylcholine 100 mg was given and the trachea intubated. The tracheal tube was subsequently removed with the patient fully awake in the right lateral position. His blood pressure was 127/87 mm Hg and sinus rhythm persisted at a rate of 90 beats min1. Owing to the presence of chest pain and the electrocardiographic evidence of a posterior infarct, the patient was thrombolysed with tenectaplase and transferred to the coronary care unit.
Cricoid pressure was applied in this case but this was away from the site used for carotid sinus massage. Carotid sinus massage had not been attempted before the need for urgent cardioversion but it is unlikely to have a role in terminating VT in any case.
There have been several reports of the antiarrhythmic properties of propofol in the literature including the conversion of fast atrial fibrillation to sinus rhythm,1 the resolution and suppression of VT2 and in the termination of SVT.3 However, there have been no such reports in the literature regarding etomidate. Isolated heart studies have, however, demonstrated a decrease in heart rate and atrioventricular conduction time with etomidate.4
Dartford, UK
References
1 Miro O, de la Red G, Fontanelo J. Cessation of paroxysmal atrial fibrillation during acute intravenous propofol administration. Anesthesiology 2000; 92: 910[ISI][Medline]
2 Burjorjee JE, Milne B. Propofol for electrical storm; a case report of cardioversion and suppression of ventricular tachycardia by propofol. Can J Anaesth 2002; 49: 9737
3 Kannan S, Sherwood N. Termination of supraventricular tachycardia by propofol. Br J Anaesth 2002; 88: 8745
4 Stowe DF, Bosnjak ZJ, Kampine JP. Comparison of etomidate, ketamine, midazolam, propofol and thiopental on function and metabolism of isolated hearts. Anesth Analg 1992; 74: 54758[Abstract]
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