Summary: Stimulation of the sympathetic nervous system associated with tracheal intubation causes corrected QT (QTc) interval prolongation. We postulated that the use of remifentanil during induction of anaesthesia might prevent this. Sixty unpremedicated, ASA grade 1 patients were selected and randomly allocated to receive either saline (group S), remifentanil 0.5 μg.kg ⁻¹ (group R 0.5) or remifentanil 1.0 μg.kg ⁻¹ (group R1.0) 1 min before laryngoscopy. The QTc interval was significantly prolonged immediately following intubation in group S and group R0.5, but it remained stable in group R1.0, compared with the QTc interval just before laryngoscopy. It is concluded that the administration of remifentanil 1.0 μg.kg ⁻¹ before intubation can prevent the prolongation of the QTc interval associated with tracheal intubation during induction of anaesthesia with sevoflurane.

Background. Chronic treatment with renin-angiotensin system (RAS) antagonists frequently causes deleterious hypotension during anaesthesia. We compared the effects of angiotensin II receptor antagonists (ARA) and angiotensin-converting enzyme inhibitors (ACEI) on neurohormonal levels and haemodynamics during cardiopulmonary bypass (CPB). Methods. Forty-four patients undergoing mitral valvular surgery who were treated with either ARA (ARA group, n=14) or ACEI (ACEI group, n=15) over 12 weeks or who were not treated with any RAS antagonist (control group, n=15) were enrolled. The plasma levels of epinephrine, norepinephrine, arginine vasopressin (AVP) and angiotensin II, and haemodynamic variables were measured before (T1) and 15 min after (T2) the start of CPB, before aortic unclamping (T3) and at skin closure (T4). Mean arterial pressure (MAP) was maintained above 60 mm Hg with phenylephrine administration during CPB. Results. The plasma epinephrine, norepinephrine, AVP and angiotensin II levels increased during CPB in all groups. Compared with the control group, the AVP level was lower at T1 in the ARA group and at T2 in the ARA and ACEI groups. The angiotensin II level was higher at T1, T2 and T3 in ARA group compared with ACEI and control groups. There were no significant differences in the epinephrine and norepinephrine levels among the three groups. The amount of administered phenylephrine during CPB was greater and MAP was lower in the ARA group compared with the ACEI and control groups. Conclusions. Chronic ARA treatment resulted in more profound hypotension than ACEI treatment during CPB, and this may be associated with the blockade of angiotensin II receptors by ARA.