T HE DOSE-RESPONSE curve for narcotic or opioid anesthesia is not linear but reaches a plateau beyond a certain plasma concentration.‘J In patients undergoing cardiac surgery, increasing the plasma concentration of fentanyl above 20 ng/mL had little effect on the incidence of hypertension following sternotomy or aortic dissection.2,3 Similarly, high-dose opioid anesthesia using sufentanil or alfentanil has not suppressed breakthrough hypertension.4v5 Episodes of patient awareness are associated with this anesthetic technique,6 and also time to extubation is prolonged. If increasing the dose of opioid does not produce better suppression of hemodynamic responses to noxious stimuli, it seems more appropriate that a smaller dose of opioid is used to provide analgesia and another agent to provide anesthesia. Providing unconsciousness and amnesia is essential during highly stressful cardiac surgery, and, because opioids, by the nature of their action, are not expected to produce these effects,’ the addition of a hypnotic drug to a moderate or balanced dose of opioid would seem to be a logical approach to anesthetizing patients. The application of balanced total intravenous anesthesia in the context of cardiac surgery has in the past been limited by the availability of agents that are pharmacokinetically suited to continuous infusion. The advent of new short-acting drugs means that the component of hypnosis, analgesia and reflex suppression can now be provided by infusions that are independently titrated. Analgesia is provided by either a continuous infusion or by intermittent injection of one of the opioids, but using much lower total doses. The adjuvants frequently used are midazolams or propofol.’ Although midazolam is a good sedative and provides amnesia, it does have hemodynamic side effects that may not be beneficial during anesthesia for cardiac surgery. Midazolam exerts its major hemodynamic effects at the peripheral level with a small decrease in systemic vascular resistance but marked venodilatation.8J0 By decreasing the venous return, preload is reduced, which may contribute to a fall in cardiac output and blood pressure. Maintenance of the cardiac output greatly depends on compensatory mechanisms such as increased baroreceptor activity, blood mobilization from the splanchnic area and increased sympathetic tone. In patients with hypovolemia, hypertension and P-adrenergic blockade, impairment of these compensatory mechanisms has been reported to induce serious hypotensive episodes.” These have been described in patients with severe noncardiac systemic illness, in whom midazolam