PubMed HealthSearch

Biomedical subjects

S J Kaus

Publications and source records attributed to S J Kaus.

2 recordsLinked to original sources

Sevoflurane depresses myocardial contractility less than halothane during induction of anesthesia in children.

BACKGROUND: Cardiovascular stability is an important prerequisite for any new volatile anesthetic. We compared echocardiographically derived indices of myocardial contractility during inhalation induction with sevoflurane and halothane in children. METHODS: Twenty children were randomized to receive either halothane or sevoflurane for inhalation induction of anesthesia. No preoperative medications were given. Myocardial contractility was evaluated at baseline and at sevoflurane and halothane end-tidal concentrations of 1.0 minimum alveolar concentration (MAC) and 1.5 MAC. RESULTS: There were no differences between groups in patient age, sex, physical status, weight, or height. Equilibration times and MAC multiples of sevoflurane and halothane were comparable. Vital signs remained stable throughout the study. Left ventricular end-systolic meridional wall stress increased with halothane but remained unchanged with sevoflurane. Systemic vascular resistance decreased from baseline to 1 MAC and 1.5 MAC with sevoflurane. Halothane depressed contractility as assessed by the stress-velocity index and stress-shortening index, whereas contractility remained within normal limits with sevoflurane. Total minute stress and normalized total mechanical energy expenditure, measures of myocardial oxygen consumption, did not change with either agent. CONCLUSIONS: Myocardial contractility was decreased less during inhalation induction of anesthesia with sevoflurane compared with halothane in children. Although the induction of anesthesia with sevoflurane or halothane was equally well tolerated, the preservation of myocardial contractility with sevoflurane makes it an attractive alternative for inducing anesthesia in children.

Anesthesia, Inhalation

Malignant hyperthermia.

Major advances have occurred in the management of MH since this disorder was first described. Despite the initially high mortality, deaths secondary to MH have dramatically decreased over the past 15 years, which is due in large part to the discovery of efficacious therapy. It is also a result of ever-increasing awareness and appreciation of the syndrome by physicians, other health care providers, and patients. Research has provided many answers to questions about the pathologic mechanisms of this disorder, and an animal model exists for testing new therapies; however, many questions remain. It is hoped that future investigations such as advances in genetic mapping may provide a specific, noninvasive method of predictive testing. It is possible that a complete understanding of MH and its mechanisms could teach us more about the ways anesthetic agents work. For now, identifying individuals at risk, rigorously avoiding exposure to potential anesthetic triggering agents in MH-susceptible patients, and promptly recognizing and treating unexpected MH episodes are the primary means of reducing morbidity and mortality from MH. Interested and informed clinicians and families are the patient's best allies against MH.

Adolescent