The main proposed mechanism of diuretic resistance in the context of decompensated HF is the increased renal vein pressure which decreases arteriovenous pressure gradient, with a parallel increase in the interstitial pressure within the kidney, thereby decreasing renal blood flow, ultrafiltration pressure and GFR [4]. Congestion also worsens diuretic resistance by decreasing intestinal absorption, and because of a stimulation of the SNS and RAAS systems. Moreover, worsened liver function in patients with right heart failure and congestion leads to hypoalbuminemia which can increase resistance to furosemide the most commonly used diuretic [5].

In patients without significant diuretic resistance, increased doses of diuretics may temporarily increase urine output succeeding in resolution of congestion. However, neurohormonal mechanisms involving continued activation of the SNS and RAS can maintain diuretic resistance at a high level so that a sustainable equilibrium cannot be achieved in out-of-hospital settings. Intravenous loop diuretics at high doses and combination of different diuretics often aid in overcoming the obstacle of resistance [5]. In case of low cardiac output and low blood pressure the use of inotropes and vasospastic drugs, often in combination, should be also considered. Ultrafiltration comes as the last resort but its use is limited due the potential further hemodynamic instability. When ultrafiltration rate significantly exceeds the plasma refill rate, there is intravascular volume depletion which in preload dependent HF patients can decrease cardiac output with detrimental effects for the patient. Continuous ultrafiltration, on the other hand, exerts a minimum impact on hemodynamic status and tissue perfusion as the low and continuous ultrafiltration rate contributes to the maintenance of the necessary preload and thus cardiac output. Furthermore, ultrafiltration prevents neurohormonal activation and could possibly reduce diuretic resistance [3].

In the RAPID-CHF trial 40 patients were evaluated and ultrafiltration resulted to higher weight loss than diuretic therapy with low complication risk. In the UNLOAD trial, 200 patients were randomized to either ultrafiltration or diuretic therapy. Ultrafiltration was associated with a significantly greater fluid removal, fewer hospitalizations for HF and lower readmission rate than diuretic therapy [6].  In the CARRESS-HF trial 188 patients with acute HF decompensation, congestion and worsened renal function were assigned to either pharmacologic treatment or ultrafiltration. The main findings were a similar weight loss with fewer complications in the pharmacologic treatment group than the ultrafiltration group [7].  However, in CARRESS-HF trial the average furosemide dose was relatively low at 120mg per day, while only 20% were on MRAs, indicating low diuretic resistance of the study population. Real world retrospective 10-year study which included 335 consecutive patients has shown superiority of the readmission rates compared to the data from the randomized trials, which could be attributed to the adjustable ultrafiltration rate and personalized ultrafiltration protocol [8].

According to the available data and experience, continuous ultrafiltration could be considered in patients with congestion refractory to intravenous diuretics and diuretic combinations, low urine output (<100ml), impaired renal function, compromised function of the right ventricle and frequent hospitalizations for decompensated HF. Termination of the procedure is indicated after clinical resolution of congestion and after either persistent elevation of creatinine by more than 1mg/dl compared to baseline or persistent hemodynamic instability [3].

This case demonstrated an impressive response to this method which most importantly was retained long term. Contrary to the main studies of UF in this case a combination of low dose of IV furosemide was sustained during the UF procedure, which resulted to great volume loss through UF and increased urine output resulting from decongestion of the kidney and the resulting decrease of diuretic resistance. The continuing application of the method supported loss of high volumes in short therapy duration, preserving cardiac output, as the degrees of hemoconcentration, venous saturation and arterial blood pressure were constantly monitored, and ultrafiltration rate and output were modified accordingly. However, it should be noted that despite the right ventricular systolic dysfunction and the prominent right heart failure patient had equal interventricular pressures, due to the Eisenmenger physiology as the right to left intra – atrial shunt, that contributed on the maintenance of cardiac output.