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NDT Advance Access originally published online on November 29, 2007
Nephrology Dialysis Transplantation 2008 23(4):1355-1361; doi:10.1093/ndt/gfm805
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Acute effects of low and high intravenous doses of furosemide on myocardial function in anuric haemodialysis patients: a tissue Doppler study

Shirley Yumi Hayashi1,3,4, Astrid Seeberger3, Britta Lind2, Sigurd Gunnes2, Anders Alvestrand3, Marcelo Mazza do Nascimento4, Bengt Lindholm4 and Lars-Åke Brodin1,2

1 Department of Medical Engineering, Royal Institute of Technology, Stockholm 2 Department of Clinical Physiology, Karolinska Institute, Karolinska University Hospital at Huddinge, Sweden 3 Division of Renal Medicine 4 Division of Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Karolinska University Hospital at Huddinge, Stockholm, Sweden

Astrid Seeberger, Division of Renal Medicine K56, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Karolinska University Hospital at Huddinge, 141 86 Stockholm, Sweden. Tel: +46-8-58587616; Fax: +46-8-711-4742; E-mail: astrid.seeberger{at}ki.se



   Abstract
Top
 Abstract
Introduction
 Methods
 Statistical analysis
 Results
 Discussion
 References
 
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.

Keywords: anuria; colour tissue Doppler velocity imaging echocardiography; furosemide; haemodialysis; systolic function



   Introduction
Top
 Abstract
 Introduction
Methods
 Statistical analysis
 Results
 Discussion
 References
 
Patients with end-stage renal disease (ESRD) who are not able to decrease fluid intake run the risk of developing acute pulmonary oedema. In patients with residual renal function, the use of furosemide may relieve the symptoms of this life-threatening complication. In patients without residual renal function, it is unclear whether furosemide, a diuretic drug inhibiting the Na+, K+, 2CL– cotransporter in the renal tubular system, is efficacious.

In patients with preserved renal function, furosemide has been shown to induce a rapid vascular effect, besides its effect on diuresis. Venous capacitance increases, which results in a decrease in preload [1]. In anuric patients, diverging results have been found. In a study by Kohn et al. [2] who investigated 10 patients with end-stage renal failure with occlusive rheography, a low intravenous dose of furosemide caused augmented venous pooling in the leg. In another study investigating 11 functionally anephric hypertensive patients, furosemide induced a rapid and short-term decrease in peripheral vascular resistance demonstrated by an increase in forearm blood flow [3]. In contrast, furosemide did not change venous capacitance in five anephric patients studied by Johnston et al. [4].

There are few studies concerning central haemodynamic effects of furosemide in ESRD patients. Schmieder et al. [5] who used infusion of indocyanine-green dye for measurements of cardiac output noted an almost immediate but short-term decrease in central blood volume and stroke volume after the infusion of a low dose of intravenous furosemide in 10 haemodialysis (HD) patients. Dikshit et al. [1] investigated three patients who had developed congestive heart failure and acute renal failure after myocardial infarction, using the balloon catheter technique. In these patients, furosemide lowered left ventricular filling pressure.

According to our knowledge, there are no previous studies that have used echocardiographic techniques in order to answer the question whether furosemide can improve central haemodynamics in anuric patients. Therefore, we studied acute cardiac effects of low and high doses of furosemide in HD patients, using conventional echocardiography and a more sensitive echocardiography technique, colour tissue velocity imaging (TVI), that allows non-invasive and quantitative evaluations of left ventricle (LV) and right ventricle (RV) function, including measurements of isovolumetric contraction (IVC) and LV filling pressure [6–8].



   Methods
Top
 Abstract
 Introduction
 Methods
Statistical analysis
 Results
 Discussion
 References
 
Patients and study design
All ESRD patients at the Karolinska University Hospital Huddinge who were treated with HD three times a week for more than 3 months, and who had no residual renal function and no clinical evidence of severe valvular heart disease, ischaemic heart disease, symptoms of congestive heart failure (New York Heart Association (NYHA) classes III and IV) or pericardial disease were asked to participate in the present study. Nineteen patients agreed and were studied with conventional echocardiography and TVI before a HD session after a long interval (3 days), in the supine position after an overnight fast. All 19 patients had technically adequate echo Doppler images. One patient who developed nausea and vomiting during the study could not complete the investigation and was therefore excluded. Thus, the results of 18 patients were analysed. The causes of renal failure were nephrosclerosis in four patients, diabetes mellitus in five, chronic glomerulonephritis in three, crescentic nephritis in four and obstructive nephropathy in two. All medications were suspended 24 h before the investigation. We started the study by administering two low doses of furosemide (40 mg) given at 0 and 30 min to 12 patients [7 men, 5 women, mean age (61.5 ± 16 years)] assuming that even in the presence of advanced renal failure, a low dose of furosemide is sufficient to cause vascular effects. When interim results demonstrated a lack of vascular activity, we decided to use a single high dose of furosemide (250 mg) in six patients (five men, one woman, mean age 63.5 ± 3.5 years). We compared the baseline myocardial velocities with the velocities of 18 age- and sex-matched healthy controls (12 men, 6 women, mean age 62.1 ± 1.0 years).

The study was approved by the Ethics Committee of Karolinska University Hospital Huddinge, Stockholm, Sweden. The nature and the purpose of the investigation were explained to the subjects, who gave their informed consent. The investigation conforms with the principles outlined in the Declaration of Helsinki [9]

Echocardiography
Conventional two-dimensional echocardiography and colour TVI images were recorded immediately before (0 min) furosemide i.v. infusion in both groups. In the low-dose group, the ultrasound examination was repeated at 10, 20, 30, 40, 50 and 70 min after the first dose (dose 2 was administered at 30 min), and in the high-dose group at 10, 20, 30 and 40 min. The design of the study is shown in Figure 1.


Figure 1
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  		Fig. 1 Study design showing the doses of furosemide infusion and the period where the echocardiography measurements were done.

 
The images were recorded with a Vivid 7 (General Electric, Horten, Norway) linked to a PC workstation with tissue Doppler capabilities. American Society of echocardiography (ASE) guidelines were applied. All 2D and Doppler parameters were acquired and documented. At least three consecutive heartbeats in each view were acquired.

Standard echocardiography measurements, including left ventricular end diastolic and end systolic dimensions (LVEDd and LVESd), end-diastolic and systolic wall thickness of interventricular septum (IVSd and IVSs) and left ventricular posterior wall (PWTd and PWTs) were determined from the M-mode (MM) technique and LV outflow track. Ejection fraction (EF) was calculated using MM and Simpson methods and complemented by subjective visual estimation. Because EF could not be determined in four patients using the Simpson method, and no patient presented with regional contraction abnormalities, MM, which was possible to use for estimation of EF in all patients, was selected.

LV mass was calculated according to the modified Penn formula. LV hypertrophy was defined as LVMI >50 g/m2 in men and >47 g/m2 in women. Transmitral flow velocities were acquired using pulse wave Doppler. Diastolic function was assessed by determining the velocities of early (E) and late (A) diastolic transmitral flow, the ratio E-to-A (E/A). In addition, isovolumetric relaxation time (IVRT), deceleration time of E wave (Edec) and E', A' by tissue Doppler were measured. The status of the diastolic function at baseline was defined as follows: (1) relaxation disturbance (E/A<1, Edec >220 ms, IVRT >100 ms, E' <8 cm/s); (2) pseudonormal pattern (E/A >1, Edec <150 ms, IVRT < 100 ms, E'<8 cm/s); (3) restrictive pattern (E/A >2, Edec <150 ms, IVRT <60 ms, E'<8 cm/s) [10] (Figure 2). Cardiac output was determined by the pulsed Doppler technique.


Figure 2
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  		Fig. 2 Changes in the mitral flow velocity ratio (E/A) ratio during transition from normal diastolic function to severe dysfunction. Effect of preload and changes in the pressure difference between left atrium and left ventricle. In the presence of relaxation disturbances, volume overload increasing the transmitral pressure gradient can shift the pattern from relaxation disturbance to pseudonormal or restrictive pattern. When this augmented preload decreases, a shift in the opposite direction occurs, going back to a relaxation pattern [12].

 
Tissue Doppler
TVI is a relatively new echocardiography technique for measuring myocardial velocities, quantitatively and objectively, with lower interobserver variability [11]. It has been shown to be a reliable and accurate method in comparison with invasive methods to evaluate cardiac function. Regarding systolic velocities, IVC velocity (IVCv) correlated well with sonomicrometry and dP/dT [7], peak systolic velocity (PSv) with measurements of contraction in isolated muscle preparations [6] and strain rate (SR) with simultaneous invasive LV volume and pressure evaluation [7,12]. Regarding diastolic velocities, E/E' has a strong correlation with pulmonary capillary wedge pressure (PCWP) and with direct simultaneous high-fidelity measurements of LV filling pressure [8,13,14].

For the quantitative analysis of TVI, after completion of the conventional echocardiography, apical images (2 chambers, 3 chambers and 4 chambers) with more than 100 frames/s were acquired. Off-line measurements were performed. TVI was performed with a 2 mm sampling volume at the basal region from the apical views. Myocardial velocities recorded with TVI have five main components. These include systolic, early diastolic and late diastolic velocities (Figure 3). The global LV function was calculated from the average of the different LV wall velocities (infero-septal, antero-lateral, inferior, anterior, infero-lateral and antero-septal walls). Tissue Doppler from the apical 4-chamber view for lateral site was used to calculate the E/E' ratio as an estimator of LV filling pressure [8]. LV systolic myocardial function was evaluated by measuring IVCv, PSv, SR and total mitral annulus motion (MAM). RV systolic myocardial function was evaluated by measuring IVCv, PSv and SR in the RV free wall. LV and RV diastolic components measured were early diastolic filling velocity (E'), late diastolic filling velocity (A') and IVRT. The SR was estimated from a region of interest with a width of 14.5 mm. This spatial offset was selected as a compromise between acceptable signal-to-noise ratio and longitudinal resolution [15]. TVI acquisition of velocities was feasible in all patients. The average of different walls, in the majority six walls and in a minority four walls, was used to evaluate global function (Figure 3).


Figure 3
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  		Fig. 3 The C-echo and TVI parameters measured in the cardiac cycle. Cardiac cycle with changes in LA pressure, LV pressure, aortic pressure and ventricular volume. The systolic myocardial velocity shows two components, representing isovolumetric contraction (IVC) and systolic ejection phase (PSV). The diastolic components are very similar in appearance and timing to mitral flow velocities: an early diastolic myocardial velocity (E'), and a late diastolic myocardial velocity (A'). The maximal velocity of the positive IVCv and PSv during systole, the maximal velocity during early filling phase (E') and atrial contraction (A') were registered.

 


   Statistical analysis
Top
 Abstract
 Introduction
 Methods
 Statistical analysis
Results
 Discussion
 References
 
Data are expressed as the mean ± SD. Comparisons between baseline and measurements obtained after drug infusion were performed using ANOVA with the Turkey post hoc test. P < 0.05 was considered statistically significant.



   Results
Top
 Abstract
 Introduction
 Methods
 Statistical analysis
 Results
Discussion
 References
 
Conventional echocardiography and TVI at baseline
Compared with controls, the patient group had significantly lower IVCv (2.3 ± 1.0 versus 3.3 ± 0.9 cm/s, P < 0.01), PSv (4.5 ± 1.3 versus 5.9 ± 1.0 cm/s, P < 0.001), E' (5.1 ± 1.7 versus 7.2 ± 2.4 cm/s, P < 0.001) and A' (4.0 ± 1.9 versus 7.9 ± 2.3 cm/s, P < 0.0001), indicating the presence of LV dysfunction. All patients presented with high values of E/E' (>10), indicating a capillary wedge pressure of >12 mmHg [8].

In the group who received the repeated low dose of furosemide (40 + 40 mg), LVH was present in 66% of the patients. Diastolic function was abnormal in 11 of 12 patients. Relaxation disturbance was found in three patients, pseudonormal pattern in five patients and a restrictive pattern in three patients. LV dilatation was present in two patients.

In the group who received the high dose of furosemide (250 mg), LVH was present in all six patients. Diastolic function was abnormal in all patients. Relaxation disturbance was noted in two patients, pseudonormal pattern in three and restrictive pattern in one patient. LV dilatation was present in one patient.

Effects of repeated low doses of furosemide (40 + 40 mg) and of a single high dose (250 mg)
Blood pressure
Neither repeated low doses nor high doses of furosemide were able to induce any significant changes in diastolic and systolic blood pressure or in heart rate, as shown in Table 1.


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  		Table 1 Clinical and conventional echocardiography parameters in the low and high group patients

 
Conventional echocardiography
Repeated low doses of furosemide were not able to cause any significant changes in systolic function, as measured by EF and % FS or in diastolic function evaluated by E, A and E/A. In addition, cardiac output remained unchanged. Even the high dose of furosemide failed to affect systolic and diastolic function and cardiac output as shown in Table 1.

TVI: global LV systolic function
TVI measurements of systolic function (IVCv, PSv, SR, MAM) (Table 2) did not change either in the low-dose group or in the high-dose group, indicating that furosemide was not able to influence LV global contraction and contractility.


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  		Table 2 TVI parameters of LV systolic function, LV diastolic function and LV filling pressure in the low and high group

 
TVI: global diastolic function
Neither repeated low doses nor a single high dose of furosemide could cause any significant changes in left ventricular filling pressure, as determined by the ratio E/E', or in diastolic filling dynamics evaluated by measurements of E', A', IVRT and E'/A'.

TVI parameters of RV contractile function
There were no significant changes in IVCv, PSv and SR in either group, showing that furosemide could not induce any significant changes in RV global contraction and contractility (Table 3).


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  		Table 3 TVI parameters of RV systolic and diastolic function in the low and high group

 
TVI parameters of global RV filling function
In both groups, no changes were found in E', A' and E'/A' after furosemide, indicating no changes in systemic venous return.



   Discussion
Top
 Abstract
 Introduction
 Methods
 Statistical analysis
 Results
 Discussion
References
 
The present study, which used both conventional echocardiography and a more sensitive method, TVI, showed that neither a repeated low dose nor a single high dose of furosemide was able to induce any significant changes in cardiac haemodynamics in anuric ESRD patients. This is in contrast to the findings in patients with preserved renal function and pulmonary oedema. In these patients furosemide causes a rapid venodilatory response, which starts before an effect on diuresis can be noted and which relieves the symptoms [1,16].

In order to be able to detect even minor changes in central cardiac haemodynamics induced by low and high doses of i.v. furosemide in anuric ESRD patients, we used not only conventional echocardiography, which is a more subjective and semiquantitative method [17] but also TVI. TVI is a quantitative and objective method, which can accurately evaluate the different phases of the cardiac cycle, including some parameters that previously could only be determined invasively [18]. Previous studies have demonstrated that it is a sensitive method for detecting myocardial ischaemia [19,20], finding subtle alterations in contractility induced by low doses of dobutamine [21] and for diagnosing new-onset congestive heart failure in patients with normal LV EF [22]. Therefore, TVI should be able to detect even more subtle changes in cardiac function induced by furosemide.

However, even with the use of this sensitive method we were not able to note any effects of furosemide on central haemodynamics. This contrasts with the results of previous studies performed in ESRD patients. In the first study, Schmieder et al. [5] administered an intravenous bolus injection of 60 mg furosemide to 10 HD patients. A significant 13% decrease in central blood volume was seen 5 min after the injection, indicating a redistribution of blood from the cardiopulmonary system to the periphery. However, already 10 min after the injection, blood volume had returned to baseline. As we measured the effects of furosemide 10 min after the administration, we cannot exclude a rapid and very short-term effect as reported by Schmieder et al. [5]. However, a response with such a short duration would not have any greater impact on the symptoms of anuric patients with acute pulmonary oedema.

In addition, there were important differences between the investigation by Schmieder et al. [5] and our study. The dialysis patients in their study were severely anaemic, which may influence the results, because anaemia induces a decrease in peripheral resistance and changes in cardiac structure and function. The patients in our study had haemoglobin concentrations within the target range of the K/DOQI guidelines. Schmieder et al. [5] also investigated the patients on a nondialysis day, whereas the patients in our study were studied immediately before dialysis when they were overhydrated.

In the second previous study, Dikshit et al. [1] investigated three anuric patients using the balloon catheter technique. After an intravenous dose of furosemide (0.5 to 1 mg/kg of body weight), left ventricular filling pressure decreased, a response that was not seen in our study. However, there are important differences between their and our patients. The patients investigated by Dikshit et al. [1] suffered from acute renal failure due to congestive heart failure after an acute myocardial infarction. Our patients had chronic kidney disease (CKD), a condition associated with changes in vascular morphology resulting in arterial stiffness [23] and endothelial dysfunction [24]. Therefore, CKD-associated morphological and functional changes in the vascular system may inhibit the vascular effects of furosemide.

There are three possible interpretations of our finding that central haemodynamics are unchanged after low and high intravenous doses of furosemide in anuric ESRD: (1) Furosemide may be unable to cause vascular effects in the presence of ESRD; (2) Furosemide may cause peripheral vascular effects in the presence of ESRD, but these are so subtle that they do not influence cardiac haemodynamics significantly; (3) although a recently published study showed that TVI was able to detect small changes in myocardial velocities during after-load reduction in hypertensive patients treated with valsartan [25], TVI may not be sensitive enough to detect very subtle changes in central haemodynamics. If this should be the case, the reasonable question is whether these very subtle changes are of clinical importance.

Regarding peripheral vascular effects of furosemide in ESRD patients, previous studies have shown contradictory findings. When five anephric patients [4] were investigated with venous plethysmography, an intravenous dose of 80 mg furosemide was not able to change venous capacitance. In addition, limb blood flow did not change in the anephric patients, whereas it decreased in healthy controls. In contrast, when Mukherjee et al. [3], who used the same plethysmographic method, administered a higher intravenous dose of furosemide (3 mg/kg) to 11 functionally anephric hypertensive patients, a short-term rise in forearm blood flow was seen, which was mediated by decreased peripheral vascular resistance.

In contrast to findings by Johnston et al. [4] and by Mukherjee et al. [3], Schmieder et al. [5], who used other methods, intra-arterial pressure measurements and the indocyanine green dye technique demonstrated a significant furosemide-induced increase in total peripheral resistance.

Thus, previous studies concerning peripheral vascular effects of furosemide have shown diverging results, which may be due to differences in methods, vascular beds and patients investigated. Our study was not designed to measure peripheral vascular effects of furosemide. However, the absence of changes in systolic and diastolic blood pressure in the presence of unchanged cardiac pressures and function argues against more significant and general effects of furosemide in the peripheral vascular tree in ESRD patients.

In terms of limitations of our study, one should consider the following when interpreting the results. Our patients were overhydrated, which was demonstrated by high E/E' values, indicating a capillary wedge pressure >-12 mmHg (E/E' > 10) [8]. However, none of the patients suffered from acute pulmonary oedema. We cannot exclude the possibility that furosemide could induce very subtle changes in central haemodynamics that increase in parallel with the severity of overhydration and become measurable only in the presence of pulmonary oedema. However, in our opinion, it would be unethical to study an uncertain effect of furosemide in anuric patients with pulmonary oedema, which is a life-threatening complication, and withhold effective life-saving ultrafiltration.

In summary, to our knowledge, our study is the first to use a sensitive echocardiographic method, TVI, in order to answer an important clinical question whether intravenous furosemide is efficacious in anuric dialysis patients. Our results demonstrate a lack of activity of furosemide even when high intravenous doses are given. Therefore, there seems to be no reason to recommend the use of furosemide in anuric ESRD patients.

Conflict of interest statement. Bengt Lindholm is employed by Baxter Healthcare.



   References
Top
 Abstract
 Introduction
 Methods
 Statistical analysis
 Results
 Discussion
 References
 

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Received for publication: 21. 7.07
Accepted in revised form: 16.10.07


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