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NDT Advance Access originally published online on January 31, 2006
Nephrology Dialysis Transplantation 2006 21(5):1305-1311; doi:10.1093/ndt/gfk070
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Dialysis and Transplantation

Norepinephrine-induced vasoconstriction results in decreased blood volume in dialysis patients

Robert W. Nette1, Eric H. Y. Ie1, Wim B. Vletter2, Rob Krams3, Willem Weimar1 and Robert Zietse1

1 Department of Internal Medicine, 2 Department of Cardiology and 3 Department of Biomedical Engineering, Erasmus MC, Rotterdam, The Netherlands

Correspondence and offprint requests to: Robert Zietse, MD, Erasmus MC, Department of Internal Medicine, PO Box 2040, 3000 CA Rotterdam, The Netherlands. Email: r.zietse{at}erasmusmc.nl



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. Hypotension during haemodialysis results from an inadequate cardiovascular response to ultrafiltration-induced hypovolaemia. It has been suggested that plasma volume could be increased as a result of systemic vasoconstriction.

Methods. We studied the effect of a norepinephrine (NOR) infusion (30 min), compared with no infusion, on relative blood volume (RBV) in six haemodialysis patients. During infusion we measured RBV, systolic blood pressure (SAP), heart rate (HR), stroke volume index (SI), total peripheral resistance (TPRI), ejection fraction (EF), inferior vena cava diameter (VCD) and core temperature.

Results. At the end of the NOR infusion, we observed a significant increase in TPRI (47±47% vs 4±17%; P<0.01) and SAP (27±12% vs 0±8%; P<0.01). Norepinephrine-induced vasoconstriction resulted in a significant decrease in RBV (–9±3% vs 0±1%; P<0.01). No significant changes were seen in SI (–4±21% vs 0±8%), HR (–5±19% vs –4±5%), EF (7±14% vs –2±10%), VCD or temperature.

Conclusions. We conclude that norepinephrine-induced vasoconstriction results in a decrease in RBV. This indicates that improved haemodynamic stability during haemodialysis through vasoconstriction can be accompanied by a decrease in RBV and that part of the variability in blood volume may be due to changes in arterial tone. Such changes must be taken into account if RBV measurements are used to improve the haemodynamic tolerance of dialysis.

Keywords: blood volume monitoring; haemodialysis; relative blood volume; vasoconstriction



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 References
 
Hypotension is a major complication during haemodialysis (HD) [1]. Decreased plasma volume preservation, due to the fluid withdrawal from the intravascular space and a delay in plasma refilling by ultrafiltration, combined with inadequate compensatory vasoconstriction, are directly responsible for this phenomenon [2,3]. The relative blood volume (RBV) can be derived from percentual changes in total protein concentration, measured in the arterial blood line. Blood volume monitoring (BVM) allows us to adjust the ultrafiltration rate to changes in RBV during HD [4].

An increase in peripheral arterial resistance can increase venous return by means of the DeJagher–Krogh phenomenon [5–7]. Due to passive recoil, venous capacity is decreased and sequestered blood is translocated back to the heart. When arterial resistance is increased, flow and intracapillary pressure are reduced and vascular refilling is increased. Moreover, it was suggested that arterial vasoconstriction increases blood volume [8–10]. However, evidence for a positive correlation between changes in total blood volume and peripheral resistance has never been found. In contrast, there is evidence suggesting an inverse relationship between the total blood volume and peripheral resistance. In non-dialysis patients, plasma volume decreased as a result of an adrenergic-induced vasoconstriction [11–14]. Additionally, both during diffusive dialysis and glucose infusion, procedures in which vascular resistance is decreased, we observed a concomitant increase in RBV [15,16]. The use of a lower dialysate temperature increases peripheral resistance, but decreases RBV [17].

In order to clarify the relationship between vascular resistance and RBV, we studied the effect of norepinephrine-induced vasoconstriction, compared with no infusion, on RBV in six dialysis patients. During the infusion, we measured RBV, blood pressure, stroke volume index (SI), ejection fraction (EF), heart rate (HR), inferior vena cava diameter (VCD) and body temperature (T body).



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 References
 
Patients
We studied six patients requiring chronic HD. None of the patients had severe valvular heart disease, heart failure (>NYHA class I) or arrhythmias. All medication was stopped on the day of the investigation. In the patients using beta-blockers, this medication was withdrawn 2 days before the experiment. The ethical review committee of our hospital approved the study and written informed consent was obtained from all patients.

Study design
Each patient was studied during two dialysis sessions, which were performed on the same day of the week. On arrival, the patients were weighed and were placed in a dialysis chair, where they rested for 30 min (t = –30). During the study, the patients remained supine and no food or beverages were provided throughout the experiment. The patients were connected to the extracorporeal circuit (Fresenius 4008H machines with Fresenius F60-S polysulphone artificial kidneys and BVM/BTM arterial and venous lines; Fresenius MC, Bad Homburg, Germany). During connection to the dialysis circuit, the priming volume of saline was discarded. At the start of this procedure, blood was drawn from the access for laboratory measurements. Blood flow was set at 250 ml/min. Neither diffusive dialysis (dialysate flow = 0 ml/min) nor ultrafiltration (ultrafiltration rate = 0 ml/h) were performed throughout the investigation. After the patient was connected to the dialysis circuit, RBV, systolic (SAP), diastolic (DAP) and mean arterial (MAP) blood pressures and HR were measured continuously throughout the experiment. At the start of the experiment (t = 0), echocardiography was performed to obtain stroke volume, EF and VCD. Directly after these measurements (t = 0), either norepinephrine (NOR) was infused (for 30 min) or a control experiment was performed in which no infusion was given (CONT). NOR was given intravenously at an initial dose of 0.02 µg/kg/min. This was increased by 0.03 µg/kg/min every 5 min until after 20 min a maximum dose of 0.14 µg/kg/min was reached or until SAP was raised by >30%. The infusions and control experiments were performed in random order and the patient was blinded to the nature of the infusion. At 10 and 30 min (t = 10 and t = 30) after the start of the NOR infusion, or at the comparable moments for the CONT experiments, a second and third echographic measurement was done. Body temperature measurements were also performed. After these measurements, the infusion was stopped and the study was ended. For safety reasons, dialysis was started ≥10 min after the infusion was discontinued, in order to allow the haemodynamic effects of the previous infusion to wear off.

Measurements
RBV was measured continuously throughout the experiment by means of a blood volume monitor (BVM; Fresenius, Bad Homburg, Germany). The BVM measures the total protein concentration in the arterial bloodline, which is the sum of haemoglobin and plasma proteins in the vascular space. Changes in total protein concentration during dialysis are used to estimate changes in RBV. This method has a very good agreement with a standard reference method involving calculation of RBV from serial measurements of haemoglobin levels (SD = 1.7%, r>0.96) and allows precise and reliable measurement of RBV [4]. SAP, DAP, MAP and HR were measured continuously throughout the experiment by the Finapres device (Ohmeda 2300; Englewood, CO, USA), using the middle finger of the non-fistula arm. This device measures the blood volume under an infrared plethysmograph. When blood volume is kept constant at a set point value by controlling the cuff pressure, SAP and HR can be calculated from these changes in cuff pressure. This method has been validated in many studies against invasive blood pressure measurements [18]. Echocardiograms were obtained using an ultrasound machine (Sonos 5500; Hewlett Packard Medical Products, Boston, MA, USA). The volume of the left ventricle was calculated from a two-dimensional parasternal view. Endocardial borders of these views were digitally traced at the end of systole and diastole and their volume was calculated. Stroke volume was calculated as the difference between end-diastolic and end-systolic volume. A mean stroke volume of five consecutive beats was taken. SI was calculated from stroke volume and body surface area, which was calculated from weight and height, according to the Dubois formula [19]. Directly after each echocardiography, VCD was measured by ultrasonography. The longitudinal axis of the inferior vena cava was used to measure its diameter at inspiration and at end-expiration, exactly 2 cm below the diaphragm.

Directly after each ultrasonography, SAP, DAP and MAP were also measured by an oscillometric device (Accutor 3; Datascope Co., Paramus, NJ, USA). Total peripheral resistance index (TPRI) was calculated from MAP, measured by datascope, and cardiac index (CI). Using an ear thermometer, T body was measured after each ultrasonography.

Statistical analysis
Haemodynamic data are given as means±SD. Differences between NOR and CONT experiments were tested with analysis of variance with repeated measurements. When yielding a significant F-ratio, multiple comparisons were made using the Student–Neuman–Keuls test. The Graphpad Prism software program was used to perform these calculations. A P-value of <0.05 was assumed to indicate statistical significance.



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 References
 
Patients
Six dialysis patients, five males and one female, participated in the study (mean time on dialysis: 2.6 years; range: 1.5–4 years; Table 1). The median age of the subjects was 53 years (range: 35–62 years; Table 1). Median residual diuresis was 252 ml (range: 0–950 ml; Table 1). Three patients had a diuresis of <5 ml/day, while the other three had a diuresis of ≥500 ml/day. Two patients with diabetes were included and two patients had hypertensive nephrosclerosis. All patients had received treatment with one or more antihypertensive agents prior to dialysis. Mean dry weight was 70.6±12.9 kg and interdialytic weight gain was comparable in the two sessions (3.6±1.4 vs 3.6±2.3 kg, P = NS; Table 1).


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  		Table 1. Characteristics of the patients

 
Baseline values
At baseline, no differences were found in laboratory data between the CONT and the NOR sessions (Table 2). SAP tended to be lower at the start of the NOR experiment, but this did not reach statistical significance (139±35 vs 165±23 mmHg; Table 3). Datascope blood pressure measurements were comparable to the Finapres measurements (SAP; 142±34 vs 165±24 mmHg for NOR and CONT, respectively).


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  		Table 2. Baseline laboratory data

 

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  		Table 3. Baseline haemodynamics

 
HR, SI and TPRI were comparable in both experiments (75±17 vs 78±12 bpm, 20±3 vs 18±6 ml/min/m2 and 6154±1486 vs 6940±3215 dynes s m2/cm5, respectively; Table 3).

T body, VCD and EF were comparable between both groups (36.3±1.0 vs 36.9±0.9°C, 13±4 vs 13±3 mm and 47±17% vs 42±7%, respectively; Table 3).

Response to norepinephrine
The patients tolerated the infusion of NOR well, with minor complaints of anxiety and no palpitations. All patients completed the protocol.

After 10 min of infusion, SAP was increased in the NOR group and RBV was decreased as compared with baseline (SAP +12±10% and RBV –3±2%, P<0.05; Table 4, Figure 1). HR, MAP, SI and TPRI did not change significantly (Table 4, Figures 1 and 2).


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  		Table 4. Haemodynamic changes during sessions in the control and the norepinephrine groups

 

Figure 1
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  		Fig. 1. Comparison of RBV, SAP, DAP and HR during a 30 min norepinephrine infusion (NOR) and during a control experiment in which no infusion was given. Norepinephrine infusion resulted in a marked decrease in RBV.

 

Figure 2
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  		Fig. 2. Comparison of CI, TPRI, EF and temperature (Temp) during a 30 min norepinephrine infusion (NOR) and during a control experiment in which no infusion was given. Norepinephrine resulted in an increase in TPRI.

 
At 30 min, SAP, MAP and DAP were increased during the NOR infusion, both compared with baseline and compared with the CONT experiment (SAP +24±15%, MAP +24±17%, DAP 18±12%, P<0.05; Table 4, Figure 1). TPRI increased as compared with baseline (47±47%; P<0.05), whereas in the CONT experiment TPRI did not change significantly (4±17%, P = NS; Table 4, Figure 2).

No significant changes in SI (–4±21% vs 0±8%), HR (–5±19% vs –4±5), EF (7±14% vs –2±10), CI (–10±21% vs –3±6%), VCD (0±3% vs 0±3 mmHg) and T body (–1±1% vs 0±2%) were observed between both experiments (Table 4, Figures 1 and 2). During the NOR infusion, RBV decreased significantly (–9±3% vs 0±1%, P<0.001; Table 4, Figure 1). In the NOR group, RBV decreased in all patients and no relation was found between the decrease in RBV and the patient characteristics, such as the amount of volume overload. The increase in TPRI did not result from cooling of blood by the extracorporeal circuit, as T body did not decrease significantly (–1±1 vs 0±2°C).



   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
References
 
This study demonstrates that norepinephrine infusion results in a direct and substantial decrease in RBV, in patients on HD. The observed decrease in RBV during the NOR infusions could be either due to a relative increase in the erythrocyte cell mass or to a decrease in the total amount of plasma fluid.

Circulating erythrocytes are not uniformly distributed throughout the body and Mitra et al. [20] have demonstrated that the relationship between systemic and whole-body haematocrit is not constant during ultrafiltration. However, as the haematocrit of the peripheral vascular beds is much lower than that of the large vessels [21,22], during vasoconstriction, blood with a relatively low erythrocyte content is shifted to the large vessels; hence, the arterial bloodline in which RBV is measured. This would result in an increase in RBV, rather than a decrease. Therefore, it is unlikely that this mechanism could explain the observed decrease in RBV. Alternatively, central erythrocyte cell mass could be increased by splenic contraction. We did not measure changes in splenic diameter in this study. However, previous studies showed that the spleen does not serve as an important reservoir for red blood cells in humans and this phenomenon could account for a minor increase in RBV only (1–2%) [23,24].

Changes in plasma volume can be explained by Starling's law, which determines the fluid shift between the vascular and the interstitial compartments. This shift depends on changes in hydrostatic and oncotic capillary pressure and on the filtration coefficient of the capillary basement membrane [25]. Reduced perfusion of capillary beds during arteriolar constriction, leading to a decrease of the vascular surface area, could explain the norepinephrine-induced decline in RBV [26]. A decrease in perfused vascular beds could also increase hydrostatic capillary pressure in the remaining vascular beds. This, in turn, could lead to a decreased vascular refilling and a lower blood volume. On the other hand, constriction of veins could also contribute to the decrease in RBV. When vasoconstriction is more pronounced at the venular than at the arteriolar end of the capillaries, intracapillary hydrostatic pressure would rise. This would favour a shift of fluid from the intravascular to the interstitial compartment [27].

The results of our study are in accordance with most previous studies in which the effect of norepinephrine on plasma volume was studied in non-dialysis patients or animals [11–14].

In one study, central erythrocyte cell mass increased. However, this study was done in dogs, in which the spleen is a far more important red blood cell reservoir [11]. In another study, a norepinephrine-induced increase in peripheral resistance caused no significant change in plasma volume, although haematocrit was increased in three out of four patients [13]. This experiment differs from ours in that norepinephrine was given for 6 h, while in our experiment norepinephrine was given for only 30 min. It is known that, in response to prolonged norepinephrine infusion, cardiac output increases and, consequently, peripheral resistance decreases, due to the release of endogenous epinephrine [27]. This could diminish the increase in RBV. Moreover, when using a mechanical oscillator technique for the measurement of the blood density, acute haemoconcentration was observed in response to injection of norepinephrine in splenectomized cats, which resembled that following the administration of angiotensin, while acetylcholine produced acute haemodilution [28].

Many other studies also indicate that blood volume increases after a decrease in total peripheral resistance by arterial vasodilatation [29–32] and that vasodilatation is inversely related to the change in central venous pressure [33]. Indeed, the inverse relationship between peripheral resistance and plasma volume in essential hypertension is well documented [34]. Nevertheless, the conviction that increased vascular resistance increases plasma volume in dialysis patients is widely held [8–10].

The results of our study have major implications for the interpretation of measurements and the applications of a biofeedback control system in order to prevent dialysis-related hypotension. When performing manoeuvers to improve vascular stability during dialysis through increased vasoconstriction, such as isolated ultrafiltration, or using a lower dialysate temperature, the decrease in RBV will be greater. Also, the critical RBV, at which hypotension occurs, may be lowered [17,33]. Thus, our study helps to explain the findings of Schneditz et al. [17] who described improved haemodynamic stability during cold dialysis, in spite of a greater reduction in RBV. Differences in arteriolar tone may also explain the observed variability in RBV during HD and the difficulties to observe a critical value at which hypotension occurs [35].

Norepinephrine-induced vasoconstriction may reflect only part of the haemodynamic response during dialysis, as the adaptive response to extracellular fluid reduction is more complex than solely increased sympathetic activity [9]. However, this study does provide the first direct evidence for an adverse effect of vasoconstriction on blood volume preservation in HD patients.

We conclude that a norepinephrine-induced increase in total peripheral resistance results in a decrease in RBV. This indicates that the improved haemodynamic stability during HD through vasoconstriction can be accompanied by a decrease in RBV and that part of the variability in RBV may be due to changes in arterial tone. Such changes must be taken into account if RBV measurements are used to improve the haemodynamic tolerance of dialysis.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

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Received for publication: 6. 9.05
Accepted in revised form: 22.12.05


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