Ventricular function in surgical patients.
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Biomedical subjects
Publications and source records attributed to A J Crumbley.
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Although left ventricular (LV) function appears altered by severe hemorrhagic shock (HS), the mechanisms of this dysfunction have been difficult to characterize. Depression in the LV function curve could be caused by altered diastolic or systolic function. It has been difficult to assess the systolic function, but the use of the rate and load independent index of contractility, Emax (the slope of the end-systolic pressure-dimension relationship), offers a new approach to the quantification of systolic mechanical performance. Emax and the LV diastolic pressure-strain relationship were measured in 15 chronically instrumented dogs by sonomicrometric and micromanometric techniques. Gradual LV unloading was obtained from transient vena caval occlusion. After control study, each dog underwent 2 hours of HS (mean aortic pressure 40 mm Hg), followed by reinfusion of all shed blood. Upon reinfusion, Emax was not decreased; however, all dogs had a significant decrease in LV compliance. During the next 4 days, the LV compliance of the eight survivors progressively returned toward control, while Emax remained stable. All seven nonsurvivors demonstrated progressive loss of LV compliance, and Emax was significant decreased prior to death. Cardiac contractility appeared improved immediately after shock, but a consistent decrease in compliance was observed. Reversal of abnormal diastolic function was demonstrated in all survivors and progressive depression in all nonsurvivors. Depression in systolic function was observed only in nonsurvivors immediately prior to death.
The clinical diagnosis of acute deep thrombophlebitis of the lower extremities is notoriously grossly inaccurate, even in experienced hands. Phleborheography (PRG) is one of the noninvasive diagnostic methods developed to make diagnosis accurate, noninvasive, and easily reproducible. The records of the first 272 patients studied by this method at South Fulton Hospital were examined, beginning June 1977 and ending August 1979. In those patients who had PRG and radiologic phlebography, the two methods were compared. Phlebography was considered as the standard for comparison. There were 36 patients who had both studies performed. Of the 36 patients studied, the PRG and the x-ray studies agreed in 34. Both were normal in 21 patients; and in 13 patients both were abnormal and in agreement. The studies did not agree in two of the 36 patients. There were none where the PRG was normal and the x-ray abnormal, and two where the PRG was abnormal and the x-ray normal. The diagnostic accuracy of a normal PRG in this study was 100 per cent, with no false-negatives. There were two false-positives with an accuracy of 87 per cent. The overall accuracy was 94 per cent. There were no complications.
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We report the case of a heart transplant patient whose cyclosporine clearance decreased by more than 50% after the institution of amiodarone therapy. This interaction necessitated a significant dosage reduction to maintain cyclosporine concentrations within the therapeutic range. To investigate the mechanism of the interaction, a cyclosporine-lipoprotein-binding determination was performed. The results suggest that drug displacement from competitive lipoprotein-binding sites is not responsible for the alterations in cyclosporine pharmacokinetics. Clearance data suggests, however, that the primary mechanism for the interaction is the inhibition cyclosporine metabolism by the cytochrome P-450 system. This report emphasizes the importance of reevaluating therapeutic drug regimens when new agents are added to prevent complications caused by drug interactions. If amiodarone and cyclosporine must be used concomitantly, cyclosporine levels must be monitored frequently, in anticipation of this interaction.