(S-234) Suzuki, T., Monday 9:15
TITLE: SUSCEPTIBILITY TO VENTRICULAR ARRHYTHMIA DURING INDUCTION OF ANESTHESIA DIFFERS BY INDUCTION AGENT: PROPOFOL VS. THIOPENTAL
AUTHORS: Takashi Suzuki, MD1, Tetsushi Katayama, MD2, Toshio Maeda, MD1, Yutaka Masuda, MD1, Akiyoshi Hosoyamada, MD1
AFFILIATION: 1Showa University School of Medicine, Tokyo, Japan; 2Tokyo Kyosai Hospital, Tokyo, Japan.
INTRODUCTION: Previous work has shown that the QT interval varies from lead to lead of the surface ECG. QT dispersion (QTd) is defined as the difference between the maximum and minimum QT intervals in each of the standard 12- leads. This may give an indirect measure of the underlying inhomogeneity of myocardial repolarization, believed to be ventricular arrhythmogenesis, and a prediction marker for sudden cardiac death.
METHODS: Forty-eight ASA 1 or 2 patients, aged 40 yr or older, undergoing elective surgery, randomly received 2mg/kg propofol (P, n=24, 59±10yr) or 5mg/kg thiopental (T, n=24, 58±10yr) as induction agents. Patients with arrhythmia, diabetes, or receiving medication known to alter QT interval were excluded. All participants received 1mg vecuronium (VCB) as the priming dose. P or T was administered over 30sec, followed by the remaining dose of VCB. The tracheal intubation was done after 1 min of manual ventilation with oxygen through a mask. Anesthesia was maintained with 2-4% sevoflurane (dial setting) and 66% N2O in oxygen for initial 5 min. The ECGs were recorded using a machine capable of simultaneous 12-leads acquisition at 50mm/s and 1mv/2cm, before induction (BL), immediately before intubation (preT), 2.5 min after intubation (2.5T), and 5 min after intubation (5T). One observer blinded to other data measured QT intervals. Each QT interval was corrected for the patient's heart rate: QTc = QT/square root of the preceding RR (sec). QTc dispersion (QTcd) was also calculated. Data were analyzed by Student's t test and ANOVA. Statistical significance was assumed at p<0.05.
RESULTS: No significant demographic differences existed between the two groups. The T group had a significantly greater mean QTd at 2.5T, QTcd at 2.5T, and QTcd at 5T compared with the corresponding BL value(68±25vs.92±36, p<0.05; 77±27vs.114±43, p<0.001; 77±27vs.95±32, p<0.01). The P group had a significantly lesser mean QTd at preT compared with the BL value(77±19vs.65±24, p<0.05). The enlargements in QT(c)d at 2.5T and 5T were also seen in the P group, but these changes were not significant. At 2.5T, QTcd in the T group was significantly greater than that of the P group (114±43vs.92±29: p<0.05). (Data were expressed with mean±SD and msec.)
CONCLUSION: This study shows that anesthetic induction with P results in less susceptibility to ventricular arrhythmia than that with T, although QT(c)d is not yet fully recognized as a true marker of ventricular arrhythmogenesis.
REFERENCE:
Br Heart J 1994; 71:508-510.