Case 4--2000. A systematic approach to intraoperative transesophageal echocardiographic evaluation of the mitral valve apparatus with anatomic correlation.
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Aged↗
Biomedical subjects
B A Bollen
Publications and source records attributed to B A Bollen.
QT interval changes following neck dissection. A stratified prospective study.
Studies from Europe have suggested that neck dissection, especially right radical neck dissection, causes a dangerous prolongation of the QT interval. Sudden cardiac arrest due to QT prolongation has been reported following right radical neck dissection. We investigated the prevalence of QT interval prolongation following neck dissection. Electrocardiogram tracings from 45 patients who underwent different combinations of neck dissection were studied. Preoperative and postoperative tracings were interpreted by a cardiologist blinded to the patient identification of each tracing. There were 28 unilateral neck dissection patients and 17 bilateral neck dissection patients eligible for analysis. There were 7 patients in the classic right radical neck dissection group, and only 3 of these had no neck dissection on the left. Comparisons of preoperative versus postoperative corrected QT interval for all subjects did not indicate a significant change. Stratification by neck dissection type (radical, modified or selective, and carotid artery resection) or by side dissected (left, right, or both) also showed no significant differences. No malignant arrhythmias were encountered. Thus, in contrast to the European experience, our findings show no significant predictable change in the QT interval after any of the combinations of neck dissection. Head and neck surgeons should be aware of the possibility of postoperative QT interval prolongation following neck dissection, although in the absence of other risk factors it appears to be a rare occurrence.
Analysis of Variance↗
Halothane relaxes preconstricted small and medium isolated porcine coronary artery segments more than isoflurane.
To compare the putative vasodilatory effects of isoflurane versus halothane on porcine coronary arteries, we studied the capacity of isoflurane and halothane to relax K(+)-constricted (30 mM) small (0.5-1.0 mm outside diameter [OD]) and medium (1.0-1.5 mm OD) porcine coronary arteries with use of in vitro tension recording. We also examined the effect of the dihydropyridine calcium channel agonist BAY K8644 on previously constricted epicardial porcine coronary artery segments in the presence of halothane or isoflurane. Our purpose was to determine (a) whether anesthetic effect on coronary arteries varied with arterial diameter, and (b) whether halothane and isoflurane inhibited BAY K8644-induced contraction of coronary vessels. Small and medium porcine coronary artery segments were constricted with K+ (30 mM) and the resulting contraction was allowed to stabilize. This was followed by exposure to 0.5%, 1.0%, 2.0%, and 3.0% isoflurane or halothane and the resultant tension was again measured. Potassium-induced contractions were significantly relaxed by halothane in small coronary artery segments at 0.5%, 1.0%, 2.0%, and 3.0% and in medium coronary artery segments at 1.0%, 2.0%, and 3.0%. Potassium-induced contractions were significantly reduced by isoflurane only at 3.0% in both small and medium coronary artery segments. Halothane caused significantly more relaxation of both small and medium porcine coronary arteries previously constricted with K+ (30 mM) than did isoflurane. There were no significant differences in coronary artery response to isoflurane or halothane with respect to coronary artery diameter. These experiments indicate that in porcine coronary arteries greater than 0.5 mm OD, studied in vitro after K(+)-induced contraction, isoflurane was not a potent coronary vasodilator.(ABSTRACT TRUNCATED AT 250 WORDS)
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
Halothane relaxes previously constricted human epicardial coronary artery segments more than isoflurane.
To compare the vasodilatory effects of isoflurane versus halothane on coronary arteries in vitro, we studied the capacity of isoflurane and halothane to relax resting and previously constricted human coronary artery segments with use of in vitro tension recording. Human epicardial coronary artery segments (1.5-2.0 mm outside diameter) were obtained from hearts excised from recipient patients at time of heart transplantation. The effects of 0.5%, 1.0%, 2.0%, and 3.0% isoflurane or halothane on resting coronary artery segments stretched to their optimal resting tension were determined. Next, after removal of anesthetic from the bathing solution, the segments were constricted with K+ (60 mM), and this contraction was allowed to plateau. The arteries were then again exposed to isoflurane or halothane at 0.5%, 1.0%, 2.0%, and 3.0% concentrations. Isoflurane and halothane had no effect on noncontracted coronary artery segments stretched to their optimal resting tension. Halothane caused significant relaxation of K(+)-induced (60 mM) contractions at 2.0% and 3.0% but not at lower concentrations. Isoflurane did not cause significant relaxation of K(+)-induced (60 mM) contractions at any concentration studied. Our studies indicate that under the conditions studied, isoflurane at clinically relevant concentrations is not a significant coronary dilator.
Coronary Vessels↗
Halothane relaxes previously constricted isolated porcine coronary artery segments more than isoflurane.
Coronary vasodilation by halothane and isoflurane were compared using in vitro tension recording. Porcine left anterior descending coronary arterial segments (1.5-2.0 mm o.d.) were constricted with either K+ (30 mM) or prostanoid U44069 (6 X 10(-7) M) in the absence of other drugs or anesthetics. Following stabilization of constriction, arteries were exposed to halothane or isoflurane at 0.5, 1.0, 1.5, 2.0, and 3.0% concentrations. K+ (30 mM) induced constriction was reduced by halothane at 1.5, 2.0, and 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced at 0.5, 1.0, 1.5, 2.0, and 3.0%. K+ (30 mM) induced constriction was reduced by isoflurane only at 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced by isoflurane only at 2.0 and 3.0%. U44069 induced constriction was more susceptible than K+ induced constriction to relaxation by halothane or isoflurane. Halothane was more potent than isoflurane as a direct relaxant of porcine epicardial left anterior descending arterial segments previously constricted with K+ (30 mM) or U44069 (6 X 10(-7) M).
Animals↗
The QT interval following carotid artery resection.
BACKGROUND: Right radical neck dissection has been shown to prolong the QT interval, reportedly caused by surgical trauma to the cervical autonomic system, which may result in malignant ventricular arrhythmias. Carotid artery resection would be expected to be more likely to cause dangerous arrhythmias. METHODS: We prospectively studied eight patients with electrocardiograms before and after carotid resection. Four patients had left-sided procedures and four patients had right-sided procedures. In addition, 11 patients were studied retrospectively. QT intervals were normal in all patients preoperatively. RESULTS: Preoperative corrected QT intervals (QTc) were in the normal range used by our institution for all eight patients in the prospective group. There were no significant QTc changes after either left-sided or right-sided carotid resection. However, the retrospective group did show significant changes in QTc following right carotid resection (n = 5), but not left resection (n = 6). CONCLUSIONS: EKG changes associated with carotid resection may not be uniform and may depend on surgical technique or specific anatomic factors. Controlled prospective studies are needed to confirm the prevalence of QT interval changes in radical neck surgery.
Adult↗