Scott Merrick

Postoperative myocardial ischemia. Therapeutic trials using intensive analgesia following surgery

Recent data suggest that postbypass and postoperative myocardial ischemia are related to adverse cardiac outcome following myocardial revascularization. Therapeutic trials to suppress postoperative ischemia are warranted. Because anesthetics can suppress a variety of physiologic responses to stress as well as myocardial ischemia intraoperatively, we examined whether use of intensive analgesia in the stressful postoperative period could decrease postoperative ischemia. In 106 patients undergoing elective myocardial revascularization, we standardized the anesthetic prior to bypass (sufentanil 5-10 micrograms/kg [induction] and 4.2-6.0 micrograms.kg-1.h-1 [infusion] supplemented with up to 0.5 mg/kg of diazepam). During bypass, patients were randomly assigned to receive either morphine sulfate (group M, n = 54, up to 2 mg/kg) or sufentanil (group S, n = 52, 1 microgram/kg and 1 microgram.kg-1.h-1). In the intensive care unit (ICU), group M received low-dose analgesia (morphine sulfate 1-10 mg intravenously every 30 min, average dose = 2.2 +/- 2.1 mg/h), while group S continued to receive intensive analgesia (infusion of sufentanil at 1 microgram.kg-1.h-1). Both groups received supplemental midazolam in the ICU (group M = 1.1 +/- 1.1 mg/h; group S = 0.6 +/- 0.6 mg/h; P = 0.01). All analgesic and sedative-hypnotic medications were discontinued at 18 hours following myocardial revascularization. Using continuous two-channel electrocardiographic (ECG) monitoring (CC5 and CM5), we documented and characterized ECG changes consistent with ischemia during the preoperative, intraoperative (pre- and postbypass), and postoperative (on- and off-treatment) periods. The total ECG monitoring time was 8,486 h, averaging 81 h per patient. During the prebypass (anesthetic control) period, groups M and S had a similar incidence, but group S episodes were more severe: maximum ST-segment change (median), S versus M: -1.8 mm versus -1.4 mm (P = 0.04). During the postbypass period, both groups had a similar incidence of ischemia, but episodes in group S were less severe: maximum ST-segment change, S versus M: -1.8 mm versus -2.7 mm (P = 0.0005). During the ICU-on-therapy period, the incidence of ischemic episodes was less in group S patients, and the severity was less: area-under-the-ST-time curve, S versus M: -21 mm.min versus -161 mm.min (P = 0.05). After discontinuation of the drug regimen in the ICU, the incidence and severity of ischemic episodes was similar. The incidence of hypotension, hypertension, and tachycardia was similar in both groups in both the intraoperative and ICU periods.(ABSTRACT TRUNCATED AT 400 WORDS)

Improved evaluation of the location and mechanism of mitral valve regurgitation with a systematic transesophageal echocardiography examination.

UNLABELLED Mitral regurgitation (MR) is a major determinant of outcome in cardiac surgery. The location and mechanism of mitral lesions determine the approach to various repairs and their feasibility. Because of incomplete evaluations or change in patient condition, detailed intraoperative transesophageal echocardiography (TEE) examination of the mitral valve may be required. We hypothesized that a systematic TEE mitral valve examination would allow precise identification of the anatomic location and mechanism of MR in patients undergoing mitral surgery. We designed a systematic mitral valve examination consisting of six views: five-chamber, four-chamber, two-chamber anterior, two-chamber mid, two-chamber posterior and short-axis. We used this examination prospectively in 13 patients undergoing mitral valve surgery for severe MR and compared the results with the surgical findings. We then retrospectively interpreted 11 similar patients who had undergone intraoperative TEE studies before this examination. TEE correctly diagnosed the mechanism and precise location of pathology in 12 of 13 patients in the prospective group, but in only 6 of 10 patients in the retrospective group. TEE also correctly identified 75 of 78 mitral segments (96%) as being normal or abnormal. In the retrospective group, only 42 of 60 segments (70%) were correctly identified (P < 0.001). We conclude that this systematic TEE mitral valve examination improves identification of mitral segments and precise localization of pathologies and may also improve the diagnosis of the mechanism of MR. IMPLICATIONS In this article, we describe how a systematic examination of the mitral valve by using transesophageal echocardiography allows identification of the different segments of the mitral valve, precise localization of pathology, and helps to diagnose the mechanism of mitral regurgitation. This is important in determining an approach to mitral valve repair and its feasibility.

Use of recombinant factor VIIa as a rescue treatment for intractable bleeding following repeat aortic arch repair

Hemorrhage, refractory to aggressive conventional therapy, at a rate of 16 L/hr following separation from cardiopulmonary bypass for aortic arch repair, was controlled with a dose of 90 microg/kg of recombinant factor VIIa, repeated once after 2 hours.

Rapid atrial pacing for detecting provokable demand ischemia in anesthetized patients.

A stress test that can be performed intraoperatively might be valuable for cardiac risk stratification in patients needing urgent noncardiac surgery and for early evaluation of coronary reserve in patients undergoing aortocoronary bypass surgery.Therefore, we evaluated the sensitivity and safety of rapid atrial pacing combined with electrocardiography and transesophageal echocardiography for inducing and detecting provokable demand ischemia in 20 anesthetized patients with multivessel coronary artery disease. Rapid atrial pacing induced ST segment changes or new segmental wall motion abnormalities (SWMA), which were defined as evidence of induced ischemia in 15 of the 20 patients. Unexpectedly, the new SWMA normalized during the first beat after abrupt cessation of pacing in three patients who did not show any ST segment changes. Simultaneously, left ventricular preload was severely decreased during pacing and recovered to baseline immediately when pacing was abruptly discontinued. Rapid atrial pacing was safe in all patients, but the target heart rate could not be achieved because of heart block or arterial hypotension in 4 of the 20 patients. These findings raise the question of whether rapid atrial pacing is the most appropriate approach for inducing provokable demand ischemia in anesthetized patients. However, its potential usefulness for predicting adverse cardiac outcomes has not been evaluated and would require larger studies. In addition, the immediate normalization of new SWMA after abrupt cessation of pacing in some patients calls into question the validity of new SWMA as evidence of myocardial ischemia when left ventricular preload is severely decreased. (Anesth Analg 1997;84:1180-5)