Background: In patients with pulmonary oedema and preserved renal function, furosemide has not only a renal, but also a vascular effect, causing a rapid fall in left ventricular filling pressure accompanied by an increase in venous compliance. Previous studies have shown conflicting findings regarding the vascular effects of furosemide in patients with end-stage renal disease (ESRD). The objective of our study was to investigate whether furosemide induces changes in central cardiac haemodynamics in anuric ESRD patients, using conventional echocardiography and colour tissue Doppler velocity imaging (TVI), a new quantitative and sensitive method.
Methods: Repeated low doses (40 mg followed by an additional dose of 40 mg after 30 min) of i.v. furosemide were administered to 12 (61.6 +/- 16 years, 7 men) and a high dose (250 mg) of i.v. furosemide to 6 (64.1 +/- 3.6 years, 5 men) clinically stable anuric haemodialysis (HD) patients. Conventional two-dimensional echocardiography and colour TVI images were recorded immediately before (0 min) the furosemide infusion in both groups, and in the group receiving the repeated low-dose infusion (at 0 and 30 min), 10, 20, 30, 40, 50 and 70 min after the administration of the first infusion. In the group receiving the single high dose of furosemide the ultrasound investigation was repeated 10, 20, 30 and 40 min after the infusion. The myocardial tissue velocities (v; cm/s) for isovolumetric contraction (IVC), peak systole (PS), early (E') and late (A') myocardial diastolic filling velocities were measured in the left ventricle (LV) at six sites (infero-septal, antero-lateral, inferior, anterior, infero-lateral and antero-septal walls) at the basal region. IVC time (IVCT), IV relaxation time (IVRT), PS time (PSt), RR interval, mitral annulus motion (MAM), strain rate (SR), left ventricular filling pressure (E/E') and cardiac output were also measured. The average of the different walls was used to evaluate global function. Right ventricle (RV) dynamics was evaluated from measurements of IVC velocity (IVCv), peak systolic velocity (PSv), E' and A' from the RV free wall.
Results: No significant changes in cardiac output, IVCv, PSv, SR, MAM, E', A', E'/A', IVRT and LV filling pressure were observed, indicating that neither 40 mg (plus additional 40 mg after 30 min) nor 250 mg of furosemide had any measurable effects on LV filling pressure and LV and RV systolic and diastolic function.
Conclusions: In anuric HD patients, low and high doses of furosemide had no significant effects on central cardiac haemodynamics. Therefore, the use of furosemide infusion in anuric ESRD patients with acute pulmonary oedema is not supported by the results of this study.