Abstract

T HE USE OF ketamine in anesthesia for patients who have coronary artery disease (CAD) might seem unreasonable because ketamine can cause tachycardia, hypertension, and excess inotropy.‘~’ However, in combination with a variety of agents including droperidol,’ diazeparnt~” midazolam,” fentanyl,“‘~” and sufentanil,” ketamine provides effective anesthesia with minimal hemodynamic effects. For example, in diazepam-premeditated adult patients having similar demographics to coronary artery bypass graft (CABG) patients, ka most reports describe an uneventful postoperative course after ketamine.4~7.“‘.“.“.‘5 Ketamine as the anesthetic for thoracic surgery did result in some dreams, but was well accepted by patients,” and ketamine also is well accepted for awake analgesia.‘” After cardiac surgery, patients usually are sedated and mechanically ventilated postoperatively to allow rewarming and to establish that hemostasis and hemodynamics” are acceptable before full awakening and extubation. Under these circumstances, dysphoric emergence related to ketamine is unlikely because the patient is also sedated with an opioid or a benzodiazepinc. A more obscure concern is that ketamine, which when used alone may increase the cerebral blood volume (CBV), may also exacerbate the strokes that occur during CABG surgery. It seems that the majority of perioperative strokes during CABG surgery are related to embolization.‘” Watershead infarctions. at one time thought to be related only to hypoperfusion, arc now recognized as caused by embolization in some cases.” One might suppose that, as a consequence of embolization, edema and a mass effect might occur while ketamine was still affecting the CBV. The circumstances of ketamine use during CABG surgery, however, should prevent increases in intracranial pressure (ICP). These circumstances include concomitant use of benzodiazepines or potent opioids,“’ controlled ventilation” with moderate hyperventilation postbypass used pri-

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