Abdominal Venous Congestion

WRF often complicates the trajectory of ADHF within the first couple of days of hospitalization and is a strong predictor of adverse outcome [11]. Historically, a poor forward flow (low cardiac output) has been considered as the main hemodynamic infliction in heart failure resulting in a progressive decline of kidney function. However, growing evidence supports the role of systemic congestion (backward failure) in the development of WRF in patients admitted with ADHF. In a prospective series of 145 heart failure patients with a reduced ejection fraction (left ventricular ejection fraction = 20 ± 8%) central venous pressure was the cardiac hemodynamic variable with the strongest association with WRF during the treatment of ADHF (see Fig. 13.2), hereby outperforming cardiac index [12].

In patients with increased right sided filling pressure, abdominal venous congestion will be universally present. This as the venous compartment ensures venous return. Therefore, venous pressures in the abdominal compartment should be higher than in the right atrium [13]. The abdominal venous compartment consists of both the splanchnic veins draining in the portal vein and passing through the liver eventually draining via the hepatic veins in the inferior vena cava. Additionally, the retroperitoneal inferior vena cava directly drains venous blood originating from the kidneys. In normal physiologic circumstances the splanchnic venous system serves as a vehicle for returning venous blood to the heart, but also guards the heart against under-filling by maintaining a reservoir function [14, 15]. Indeed, some of the volume in the splanchnic veins does not contribute to central venous pressure (unstressed volume). However, it can be recruited, such as in situations of bleeding, by α-adrenergic mediated venoconstriction. In heart failure, several alterations occur at this level, and chronic neurohormonal activation can result in chronic sodium and water retention, hereby expanding the splanchnic venous reservoir [1]. However, overzealous plasma volume expansion (which is mainly buffered in the splanchnic venous system) can result in a lower compliance of the splanchnic veins resulting in abdominal venous congestion. Furthermore chronic adrenergic activation might also directly result in venoconstriction as the splanchnic veins are highly innervated with α-adrenergic receptors [16]. Therefore, even without an increase in plasma volume, abdominal congestion can occur due to splanchnic venoconstriction. In the setting of ADHF, a high adrenergic tonus will often lead to vasoconstriction of the arterioles of the splanchnic system (often measured as a high systemic vascular resistance [SVR]), which results in a passive recoil force in the splanchnic venous, further enhancing abdominal venous congestion in addition to direct venoconstriction [16]. Interestingly, abdominal venous congestion might be earlier detectable than a rise in cardiac filling pressures in the patient on the verge of decompensation [17]. More recently, progressive (abdominal) venous congestion has been shown to impede renal venous outflow (Fig. 13.3), which is associated with a reduced natriuretic renal response in patients with heart failure. Renal venous outflow abnormalities can manifest, even before a rise in cardiac filling pressures are noted [17].

Extrinsic Kidney and Kidney Outflow Compression

In addition to a poor trans-renal pressure gradient mediated by backward failure (high venous outflow pressures) and forward cardiac failure (low kidney perfusion pressure), extrinsic kidney compression can result in further WRF in heart failure patients [6]. Importantly, the kidney is an encapsulated organ so intra-renal interstitial fluid built-up will further increase the parenchymateous pressures. Indeed, as earlier alluded to, an increased IAP is strongly associated with WRF, and reductions in IAP are associated with improvement in renal function (measured as a decline in plasma creatinine). A high IAP can mechanically obstruct the glomerular filtration force [2, 3]. The perfusion pressure of the abdomen is an important determinant of the perfusion of the visceral organs. Abdominal perfusion pressure (APP) is calculated as mean arterial pressure (MAP) minus the obstruction to venous outflow by the IAP. Elevated IAP induced kidney function is proposedly mediate by a low renal perfusion pressure and low renal filtration gradient (FG). The filtration gradient is the mechanical force across the glomerulus and equals the difference between the glomerular filtration pressure (GFP) and the proximal tubular pressure (PTP) [2, 3]. In the presence of an elevated IAP, PTP may be assumed to be equal to IAP and GFP is equated as MAP minus IAP. Therefore, the FG = GFP-PTP or FG = MAP – 2x IAP. During decongestive therapy in patients with ADHF, both a reduction in IAP and an increase in FG results in an improvement of serum creatinine [8].

Bowel Wall Congestion – Altered Pharmacology and Inflammation

During ADHF increased hydrostatic venous pressures in the abdomen result in net more filtration at the level of the microcirculation [1]. This can result in the formation of bowel wall edema, if lymphatic reabsorption forces are overwhelmed. Several observational studies in heart failure patients with reduced ejection fraction have shown that patients with high right atrial pressure often manifest with increased bowel wall thickness on abdominal ultrasound. It is well recognized that such formation of abdominal congestion is associated with a reduced appetite and a sensation of abdominal satiety [18, 19]. Furthermore, it is well documented that in the presence of abdominal edema the uptake of oral loop diuretics become less predictable. This results in a reduced bio-availability of loop diuretics in the circulation and potentially leading to incessant congestion. Furthermore, the villi in the bowel wall are very sensitive to changes in blood flow due to the countercurrent system in their arteriovenous supply. Therefore, a state of low cardiac output and venous congestion often results in villi tip ischemia, which is associated with increased bowel wall permeability. This lead to translocation of gram-negative bacteria that normally only reside in the bowel lumen. These gram negative bacteria carry lipopolysaccharides (LPS) on their cell walls, which activate the immune system [18, 19]. Hereby contributing to the overall state of inflammation often seen in heart failure. Interestingly, in patients with cirrhosis, the LPS-induced endotoxicity is strongly associated with the development of hepatorenal syndrome [20].

Relieving Congestion During ADHF

As increased filling pressures (congestion) drive the progression of the disease in ADHF and strongly determine symptoms, the goal of therapy should be to completely relief congestion [21]. Lingering congestion following discharge is one of the strongest predictors of adverse outcome following a heart failure hospitalization. Furthermore, hemoconcentration (a marker of relieving excessive plasma volume) is associated with improved outcome in ADHF [22]. As earlier alluded to, increased venous filling pressures can occur both if the increased plasma volume overshoots the splanchnic venous buffering capacity or due to a reduced compliance of the splanchnic venous system. With the former mechanism often being labeled volume overload and the latter mechanism being labeled volume misdistribution. Clearly in clinical practice both these mechanisms (plasma volume expansion and reduced venous capacitance) overlap and contribute to the presence of congestion. If the ADHF-patient clearly manifest with signs of volume overload (e.g. weight gain, pleural effusion, peripheral edema, ascites, ..), than the goal of therapy should be to completely get rid of excessive volume. Loop diuretics remain the cornerstone of diuretic therapy in AHF, with almost 90% of patients receiving intravenous loop diuretics in the ADHERE database [23]. Furthermore, in 63% of patients, loop diuretics are the sole drug therapy being used to combat AHF [23]. In the DOSE trial, no difference was seen between continuous versus bolus infusion. However, patients receiving a high dose of furosemide (median dose of 773 mg vs 358 mg over 72 hours), demonstrated a trend towards faster dyspnea relief and a significantly higher net fluid and weight loss [24]. Adjusting the employed dose of loop diuretics is often necessary when a low glomerular filtration rate is present, with higher doses needed in this setting. Furthermore, recently it has been illustrated that early initiation of loop diuretics might be associated with better outcome [25]. In the case of severe abdominal congestion loop diuretics should be administered intravenous as bowel congestions make oral absorption of loop diuretics less predictable. However, a fair proportion of patients do not attain decongestion despite therapy with a loop diuretic. In these patients it is less clear if further loop diuretic dose uptitration or combinational diuretic therapy should be employed. Several additional agents with a diuretic property such as thiazides, high dose mineralocorticoid receptor antagonists, acetazolamide or sodium glucose linked transporters can be used. A detailed description of their use spans beyond the scope of this chapter.

When volume redistribution is driving congestion, the goal of therapy should be to enhance venous capacitance function and lower cardiac filling pressures [26]. To achieve this goal a combination of vasodilators and lower doses of intravenous diuretics are often employed. Again a detailed discussion spans beyond the scope of the chapter but have been published previously.

Reducing IAP Specifically

In case of the presence of ascites with an elevated IAP, paracentesis has been shown to effectively reduce the volume overload in third space while at the same time resulting an improvement in renal function. One small hypothesis generating study documented that reduction of ascites true either paracentesis of ultrafiltration resulted in a reduction in IAP which was associated with an improvement in renal function [8]. These strategies might be important in patients who exhibit a progressive increase in IAP during the ADHF hospitalization, as these patients are extremely vulnerable to WRF. A therapeutic flowchart to the approach of elevated IAP in ADHF is reflected in Fig. 13.4.

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