The intravenous administration of 50 mg of lidocaine as a single bolus to four patients with heart disease did not result in a significant change in cardiac output or left ventricular end-diastolic pressure (LVEDP). Two patients had moderate decrease in systemic arterial pressure which was not accompanied by symptoms, was of short duration, and did not require therapeutic intervention. Left ventricular function, as assessed by the relationship of changes in stroke volume index (SVI) and stroke work index (SWI) to changes in LVEDP, was not significantly affected nor was the maximum rate of rise of left ventricular pressure (dp/dt).
SUMMARYThe case of a 73-year-old white man with corrected transposition of the great vessels and associated mitral and mild aortic regurgitation is reported. The patient's survival was the longest of any patient with this defect reported to date. Although the condition is theoretically compatible with a normal life span, few patients with this lesion survive past 40 years of age because of associated congenital defects or the subsequent development of A-V valvular insufficiency or heart block, or both.
Additional Indexing Words:Mitral insufficiency
The effect of 250 mg of diphenylhydantoin, administered intravenously, on left ventricular function was determined during cardiac catheterization in nine patients with heart disease.
Five minutes after drug administration, left ventricular end-diastolic pressure rose in each patient from an average of 6.0 mm Hg to 10.0 mm Hg. Concurrently, stroke work and stroke power indices decreased in each patient by an average of 22.0% and 22.2%, respectively. Stroke volume index decreased in seven patients and maximum left ventricular dp/dt fell in eight patients. Over the next 25 minutes, all parameters returned to control values. Cardiac index was unchanged, whereas generally small and insignificant changes were observed in heart rate and systemic arterial pressure throughout the study.
Although this study has demonstrated that diphenylhydantoin depresses myocardial function, the effect may have limited clinical significance since it was relatively short-lived and did not reduce cardiac output or greatly elevate ventricular end-diastolic pressure. Furthermore, the absence of a significant systemic hypotensive effect is of distinct clinical importance.
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