Abstract

Intravenous lidocaine was evaluated as an anesthetic adjunct and its hemodynamic effects compared to those of morphine sulfate. Forty patients undergoing surgery for coronary artery bypass or aortic valve replacement for moderate aortic stenosis were randomly assigned to one of two groups. Patients in group 1 received a total dose of 2 mg/kg of morphine sulfate while those in group 2 received 21 mg/kg of lidocaine. In addition, patients in both groups were given 0.6 mg/kg of diazepam and 50% N2O in oxygen. Peak plasma lidocaine levels in group 2 occurred following sternotomy. Electroencephalo-graphic evidence of seizure activity was absent at this time. Indices of myocardial performance (cardiac index, stroke work index) were depressed following induction of anesthesia and remained depressed up to institution of cardiopulmonary bypass in patients given lidocaine. Arterial blood pressure changed minimally. In contrast, patients given morphine demonstrated an increase in cardiac index and left ventricular stroke work index following tracheal intubation. Arterial blood pressure and systemic vascular resistance initially decreased following induction of anesthesia and increased with tracheal intubation in patients receiving morphine sulfate. Arterial blood pressure, stroke work index, and systemic vascular resistance increased further in these patients while cardiac index returned to control values during the period of surgical stimulation. Electrocardiographic changes indicative of myocardial ischemia did not differ in the two groups. The relationship between myocardial oxygen supply and demand, as reflected by the rate pressure product and endocardial viability ratio indices, was, however, adversely affected during surgical stimulation in the patients given morphine. Lidocaine produced stable clinical anesthesia without large fluctuations in hemodynamic function. In contrast to morphine, lidocaine depressed the hypertensive and tachycardic responses to surgery, thus favorably influencing the balance between myocardial oxygen supply and demand.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.