Abstract

[2]. Furthermore, a paradoxical increase in blood Introduction pressure during ultrafiltration in HD patients can occur in the presence of overhydration [3]. Overhydration The oscillation of the fluid state in anuric patients is can lead to a wide spectrum of cardiac changes dependent on the type of dialysis, which has to mimic depending on the pre-existing cardiac state: hypercirexcretory renal function. Typically, in haemodialysis culation, characterized by an increased cardiac output, (HD), patients’ fluid state is in a continuous disequilibcan be one sequela. Another reaction pattern can be rium characterized by a rapid reduction during dialysis cardiac dilatation, characterized by increases in the and a slow increase between dialysis sessions. Maxima diameters of the vena cava, right atrium, left atrium and minima of the cyclic fluctuations of body water and right and left ventricles [4]. (and sodium) are determined by the physician’s preIn some patients with end-stage renal failure, cardiac scription (target weight) and by the drinking and enlargement associated with a reduced left ventricle eating habits of the patients (pre-dialysis weight). Both (LV ) function can be present without other evidence extremes of fluid state have to be compensated by the of hyperhydration. Initiation of dialysis and water cardiovascular system of dialysis patients, which freremoval to normovolaemia can regress cardiac quently is in an abnormal state. Typical cardiovascular dilatation and restore normal cardiac function. complications can occur originating from all three Symptoms of hypovolaemia most frequently occur determinants: dialysis target weight can be erroneous during or immediately post-haemodialysis and ultraand the mode of the dialysis technique can be inadfiltration. Although plasma volume is an integral part equate; the fluid intake of the patients may overwork of the extracellular volume and the equilibrium the cardiovascular compensation capacity; and, finally, between the two compartments establishes eventually, a pathological cardiovascular system responds refilling of plasma volume takes some time and clearly differently to the stress of fluid fluctuation. depends on the degree of overhydration [5,6 ]. Primarily with high ultrafiltration rates, as necessitated Fluid-dependent signs and symptoms in short dialysis sessions, vascular underfilling can lead to ventricular underfilling and eventually to dialysis hypotension [7]. Thus, dialysis hypotension need not In chronic dialysis patients without acute disease, some necessarily be a consequence of hypovolaemia and an signs and symptoms occur at distinct phases of the incorrectly defined dialysis target weight. The same is fluid cycle. However, all signs and symptoms can have true for symptoms such as muscle cramps. On the a multi-factorial origin, and only in the case of other hand, suddenly occurring fatigue, low blood regression after fluid correction do they appear to be pressure, cramps and hypotension can be taken as specifically volume related. In the pre-dialysis phase, hypovolaemic signs when the dialysis schedule has not a patient frequently is hyperhydrated, which can been altered and has been tolerated without symptoms translate into sudden dyspnoea during exercise, while during preceding sessions. recumbent or while sitting, and this can culminate in The incidence of dysvolaemic periods in dialysis pulmonary oedema. Ankle or tibial oedema can be patients is virtually unknown. By clinical standards, present. Hypervolaemia is not the only cause of arterial only about half of the patients are in a state of hypertension in dialysis patients, albeit that it is the normohydration, about one-third are hypovolaemic most important and most frequent. It has been shown that salt loading increases the arterial pressure of and a quarter are hypervolaemic (Table 1). Whether patients with renal failure in contrast to healthy persons dysvolaemia is an independent risk factor in the pro[1], and that systolic blood pressure is significantly gnosis of dialysis patients still awaits further elucidaincreased during hypervolaemic periods in HD patients tion. There are three lines of indirect evidence that this may well be the case: Kramer et al. published data from the (at that time still incomplete) EDTA registry Correspondence and offprint requests to: Dr V. Wizemann, J.-S. Bachstrasse 40, D-35392, Giessen, Germany. of increased mortality in dialysis patients with excess

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