The editorial emphasizes that safe anesthesia for cardiac patients relies on understanding pathophysiology and pharmacology rather than adhering to a specific "cardiac anesthetic" regimen.
In 1969, Lowenstein et al. [1] published a paper in the New England Journal of Medicine on the use of "morphine anesthesia" for patients undergoing cardiac valvular replacement. Since that time there has been a school of thought that anesthesia for cardiac patients should be radically different from that for other patients. The paper by Mora et al. in this issue of Anesthesia & Analgesia [2] makes the point that widely disparate anesthetic maintenance regimens can be safely used in cardiac patients. Although patients were indeed given a large dose of fentanyl for induction of anesthesia, the remainder of the anesthetic was managed in more conventional ways by supplementation with either enflurane, fentanyl, propofol, or thiopental. Noticeably absent was supplementation with midazolam and sufentanil. Nonetheless, the point is that drugs with very different sites and mechanisms of action can be given to achieve the same hemodynamic and other efficacy end-points during cardiac anesthesia. The same drugs are used in patients undergoing noncardiac surgery. There need not be any dogma concerning an ideal or specific regimen required to safely anesthetize patients with known heart disease. Anesthetics used in noncardiac surgical patients are safe and efficacious in cardiac surgical patients. We might have concluded this from a host of papers in the literature that have each shown how a particular "recipe" works very well in the highly monitored cardiac patient. On the other hand, we might have inferred this from the enormous clinical experience of using a wide variety of anesthetic techniques in patients who undergo noncardiac surgery, many of whom most certainly have ischemic heart disease because of its prevalence in our society. We thus conclude that there is no such entity as a "cardiac anesthetic." What is required to anesthetize patients with ischemic heart disease is knowledge of the pathophysiology of the disease and of the clinical pharmacology of any number of anesthetic vasoactive drugs at the practitioner's disposal. The paper by Mora et al. [2] makes another point. When one examines outcome after a cardiac operation, clinical end-points should be chosen that truly distinguish one anesthetic from another. For example, eye opening during emergence from anesthesia occurs earlier in patients whose anesthesia is maintained with propofol. This fact is not surprising, because the literature is replete with information on this subject. If the objective is to see patients awaken sooner after anesthesia than later, propofol would logically be chosen over thiopental for repeated administration during maintenance of anesthesia. On the other hand, when the end-point is discharge from the intensive care unit (ICU), we see no difference between the group given a shorter lasting anesthetic and the group given a longer lasting one. Is this because there is some delayed awakening in the propofol group? Of course not; the end-point of ICU discharge is dependent on a host of other overriding variables, most of which occur during the postanesthetic course. It is therefore of little value to use ICU discharge as an outcome end-point unless the anesthetic continuum is maintained in the ICU differently. For example, if the question is whether propofol used as an adjunct to anesthesia and sedation in the ICU allows earlier discharge than some alternative pharmacologic approach, then the ICU sedation regimen should be part of the study. This brings us to the final point. Mora et al. conclude that shorter acting anesthetics have a role in cardiac anesthesia. We agree, of course, but we also would add that it may be more important how the drugs are administered than which ones are used. For example, the overall efficacy of an anesthetic may be quite different when it is given by continuous infusion rather than by repeated bolus administration. We would argue that if the goal is to maintain a stable level of anesthesia a continuous infusion of intravenous drugs should be given--whether with short- or long-acting intravenous drugs, or for maintenance of anesthesia or ICU sedation [3]. If continuous infusions are properly titrated during and after the case, patients will have a smooth emergence that is governed more certainly by the pharmacokinetics and pharmacodynamics of the drug. This adage applies to cardiac and noncardiac patients alike, which is where we began.
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Reves et al. (1995) studied this question.
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