Aquapheresis means taking away (aphairesis, gr.) water (aqua, lat.) from the body, with an objective to restore euvolemia in fluid overloaded patients. Fluid overload can be caused by numerous reasons, mainly by heart, liver and kidney diseases. Congestive heart failure (CHF) is the most common reason for severe hypervolemia. Out of 105 388 CHF patients in 274 hospitals, congestion was present in almost 90%. The most common co-morbid conditions were hypertension (73%), coronary artery disease (57%), and diabetes (44%). Interestingly, the evidence of mild or no impairment of systolic function was found in 46% of patients only. In-hospital mortality was 4.0% and the median hospital length of stay was 4.3 days (1). The reduction, or even total removal, of extra body fluid is crucial to the successful therapy of the acute decompensated heart failure (ADHF) in patients with advanced heart failure. This is usually achieved with the use of saluretics, usually furosemide, indapamide, or torasemide, given orally in outpatient settings. If the in-patient treatment for ADHF is needed, furosemide as intravenous bolus or infusion is the therapeutic gold standard.

ADHF is defined as rapid appearance or worsening of clinical symptoms resulting from systolic or diastolic heart dysfunction, cardiac rhythm disturbance, or inadequate pre- or afterload. It can present in patients with or without previous heart dysfunction, and both conditions lead to the impaired blood volume distribution (to the venous compartment – pulmonary or systemic). Typically, the body fluid volume is increased in patients with chronic heart failure, and normal in patients with no underlying heart disease. The use of diuretics, which is obligatory in ADHF and CHF, in patients presenting ADHF and no fluid retention needs very careful, individualized evaluation, to avoid further decrease in effective blood volume.

The most common factors that precipitate hospitalization for decompensated heart failure are (2):

• Noncompliance with medical regimen, sodium and/or fluid restriction.

• Acute myocardial ischemia.

• Uncorrected high blood pressure.

• Atrial fibrillation and other arrhythmias.

• Recent addition of negative inotropic drugs (e.g., verapamil, nifedipine, diltiazem, beta blockers).

• Pulmonary embolus.

• Nonsteroidal anti-inflammatory drugs.

• Excessive alcohol or illicit drug use.

• Endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism, hypothyroidism).

• Concurrent infections (e.g., pneumonia, viral illnesses).

The venous blood volume expansion, pulmonary and systemic (both, splanchnic and peripheral), typical of CHF, results from decreased cardiac output, vascular resistance or pathological flow between the cardiac cavities. Even if the effective blood volume (i.e. inside the big arterial vessels) in chronic heart failure has been well preserved, the venous compartment is enlarged, second to sodium and water retention resulting from renal hypoperfusion. The chronic renal hypoperfusion second to heart dysfunction (cardiorenal syndrome type II) triggers many adaptive mechanisms – activation of renin-angiotensin-aldosterone axis, vasopressin release, increased blood natriuretic hormone levels and many others. Fluid retention leads to the increased pre- or afterload, increased cardiac filling pressures, myocardiac distention and remodeling, which close the vicius circle of progressive heart injury (3), and further deteriorate renal filtration (GFR) (4). The last might also result directly from the increased splanchnic venous pressure (5). This remains true for the opposite situation, when the fluid retention is triggered by renal insufficiency.

It is well known the hemoconcentration resulting from intensive diuretic treatment correlates positively with reduction of GFR in CHF and the decreased post-hospital survival (6). The higher the dose of diuretics is needed for reducing hypervolemia the worse is the prognosis (7, 8). The reduction in GFR and the CHF are the well known independent risk factors for death in general population. The coexistence of the two is even more fatal (9), which clearly suggest, aggressive diuretic therapy resulting in worsening renal fuction should be avoided. Renal failure worsens prognosis in both, the systolic and the diastolic CHF, and the impact of renal failure is more visible in patients with preserved ejection fraction (10), and even more in those with coexisting anemia (11). The episode of ADHF further worsens post-hospital CHF patients’ survival, irrespective of renal failure (12). In-hospital mortality is increased and the length of stay prolonged in ADHF patients with renal failure (13). Interestingly, heart failure in patients on chronic hemodialysis is not a frequent cause of death, for it accounts for 7% of death only (14).

Worsening of renal insufficiency leads to less secretion of diuretics into the tubular fluid, so it requires an increase in the total dose of diuretic for an effective amount reaches its site of action (15). However, the diuretic-induced activation of the renin-angiotensin-aldosterone system, results in an increased sodium and water reabsorption through a variety of mechanisms. Hypertrophy of distal tubule epithelial cells results in greater sodium absorption distal to the loop of Henle, the site of action of loop diuretics (16). In patients with decompensated heart failure, venous pressure is also elevated, leading to decreased absorption of oral agents and decreased renal blood flow and consequently, renal sodium excretion (17).

In case the diuretic resistance ensues, due to renal injury or any other cause, the retained fluid can be rapidly removed from the body by inducing massive diarrhea, the use of vasopressin receptor antagonists (vaptans), which is still not well established, or by a well know mechanical, extracorporeal support which enables to control the volume and rate of water removal.

The first action on blood taken by the kidney is to separate plasma water in the renal glomerulus. Exactly the same process is mimicked by dialysers and hemofilters in a process driven by exerting the hydraulic pressure difference between blood and the contralateral side of the semipermeable filtration membrane. This convective technique became available to dialysis patients in mid-seventies of the past century. And from the very first moment it was clear the procedure could be usefull in treating decompensated heart failure (18). This convective process has to be individually tailored regarding the volume and rate of fluid removal. If it takes several hours (usually more than 6), and the rate of ultrafiltration is of maximum 0.16 ml/min/kg lean body mass (usually 500 ml/h in adults), the procedure is called slow continuous ultrafiltration (SCCUF). The higher ultrafiltration volumes and higher ultrafiltration rates cause hemoconcentration and call for intravenous infusion of crystalloids to prevent it. In such case the process is called hemofiltration (HF). The infusion of a substitution fluid is the only factor to differentiate SCUF and HF. The last one can last longer than 24 hours, which is known as continuous hemofiltration. It is usually performed on venous blood (continuous veno-veno hemofiltration, CVVH). Quick removal of relatively small amount of plasma water is called isolated ultrafiltration (IUF), to differentiate it from the ultrafiltration (UF) occurring during hemodialysis.

There are three types of engines enabling filtration – hemodialysis monitor to perform isolated ultrafiltration, continuous renal replacement therapy monitors to perform SCUF or CVVHF, and specialized ultrafiltration monitors to perform solely the SCUF. The last technology is currently commercially unavailable in Europe. All three techniques operate on venous blood, which means blood is taken from the splanchnic overloaded compartment and returned to it after the volume has been reduced by ultrafiltration. The access to venous blood to ensure sufficient extracorporeal blood flow is possible by insertion of a central catheter. Typically the 250-500 ml/h of water is removed, the blood flow varies 20-200 ml/min, and systemic coagulation is obtained with heparin infusion (1000 IU/h, adjusted accordingly to ACT). The volume of the In-circuit extracorporeal blood is small – 30-50 ml.