**Abstract**

In patients with Congestive Heart Failure (CHF), neurohormonal activation leads to fluid overload that can be treated with high doses of furosemide unless diuretic resistance and hyponatremia develop. End-stage CHF, including patients with normal or slightly deteriorated kidney function, can resist medical treatment. In some cases of refractory CHF, ultrafiltration (UF) is required. To manage a refractory CHF population, extracorporeal UF is commonly used as an emergency treatment, but peritoneal UF should be considered a follow-up therapy option. This method offers potential advantages over extracorporeal therapies, including better preservation of residual renal function, tighter control of sodium balance, less neurohumoral activation, and the possibility of daily treatment in the home environment. Using glucose as an osmotic agent leads to the deterioration of the peritoneal membrane. The UF properties of icodextrin depend on the dwell time, whereby the maximum effect of icodextrin concerning glucose is achieved at a prolonged dwell time. Icodextrin may offer improved peritoneal membrane biocompatibility compared with conventional glucose-based dialysates by decreasing glucose exposure, iso-osmolarity, and reduced carbonyl stress. The proper anesthesia technique and surgical approach for peritoneal dialysis (PD) catheter placement in CHF patients must be based on the patient's characteristics, available equipment, and surgeon's experience. An open procedure using a transversus abdominis plane block for PD catheter placement in patients with CHF is strongly recommended.

**Keywords:** chronic heart failure, heart failure treatment, peritoneal catheter placement, peritoneal ultrafiltration, refractory chronic heart failure

### **1. Introduction**

Congestive Heart Failure (CHF) is a severe and common disease affecting up to 10% of adults. In patients with CHF, neurohormonal activation leads to fluid overload that can be treated with high doses of furosemide unless diuretic resistance and hyponatremia develop. End-stage CHF, including patients with normal or slightly deteriorated kidney function, can resist medical treatment. This patient group requires frequent hospitalizations for electrolyte imbalance dyspnea, orthopnea, and oliguria. In some cases of refractory CHF (RCHF), ultrafiltration (UF) is required. To manage an RCHF population, extracorporeal UF is commonly used as an emergency treatment, but peritoneal UF (PUF) should be considered a follow-up therapy option.

Schneierson first reported using PUF successfully in heart failure (HF) [1]. Mailloux et al. concluded that PUF may be helpful in cardiac patients with concomitant renal impairment, electrolyte imbalance, preparation for cardiac surgery, and rapid deterioration of a previously stable cardiac state [2]. It has been known that PUF does not alter the course of HF but improves the congestive condition by correcting electrolyte imbalance, re-responsiveness to diuretics, weight loss, and overall clinical improvement [2]. A prospective non-randomized study including 20 patients with New York Heart Association (NYHA) class IV showed regression to NYHA class I, left ventricular systolic function recovery, a significant reduction in hospitalization days, and first-year mortality lower than expected [3]. Another prospective nonrandomized study from 2010 enrolled 17 patients with RCHF initially treated with extracorporeal UF and PUF. All patients improved their NYHA functional status within the first 3 months, and hospitalization days significantly decreased after 1 year [4]. Using an intraperitoneal solution such as icodextrin promotes a slow and efficient PUF that cardiac patients tolerate better, is less invasive, improves residual renal function, and improves quality of life and clinical symptoms.

Therefore, proposing PUF for long-term outpatient treatment of RCHF seems reasonable.

### **2. Congestive heart failure**

HF or CHF is an inadequate ability of the heart to meet patients' metabolic demands. According to the current guidelines (European Society of Cardiology, 2021), it is defined as a complex clinical syndrome presenting with typical symptoms (fatigue, breathlessness, and ankle swelling) that can go together with signs (elevated venous pressure, pulmonary crackles, or peripheral edema). HF is caused by structural and/or functional heart abnormalities, which lead to high intracardiac pressures and/or reduced cardiac output [5].

The definition should involve elevated natriuretic peptide levels (brain natriuretic peptide—BNP, or N-terminal pro-brain natriuretic peptide—NTproBNP), which are a group of hormones produced by the myocardium cells and are released in the bloodstream in response to the wall stress [6].

The incidence of HF increases because of population aging and has become a leading cause of hospitalizations among patients over 65 [5].

Many conditions can cause HF. This includes high blood pressure, coronary artery disease (CAD), valvular heart disease (VHD), cardiomyopathies, arrhythmias, myocarditis, congenital heart disease, thyroid disease, chronic kidney disease (CKD), anemia, or toxic myocardium damage (alcohol, heavy metals, and chemotherapeutics).

*Advanced Treatment of Refractory Congestive Heart Failure by Peritoneal Ultrafiltration… DOI: http://dx.doi.org/10.5772/intechopen.114022*

### **2.1 Classification**

The most used HF classification is based on left ventricular ejection fraction (EF). There are traditionally three phenotypes: HF with reduced ejection fraction (EF ≤ 40, heart failure with reduced ejection fraction (HFrEF)), HF with a mildly reduced ejection fraction (EF 41–49%, heart failure with mildly reduced and preserved ejection fraction (HFmrEF)), and HF with preserved EF (EF ≥ 50%, HFpEF) (**Figure 1**). EF is usually obtained by echocardiography. The explanation for this classification lies in many clinical treatment trials that showed different outcomes and heterogeneity between phenotypes.

Classification based on symptom severity and physical activity is the NYHA classification. NYHA has four functional classes (I–IV). Patients in class I have no limitation of physical activities, and there are no HF symptoms in ordinary physical activity. In contrast, patients in NYHA class IV have severe symptoms at rest and during minimal activity (**Figure 2**).

There are two main presentations of HF: acute and chronic. Acute heart failure (AHF) is a rapid or gradual onset of symptoms that require medical attention and/ or hospitalization. AHF can be the new onset of HF (first manifestation, newly diagnosed) or, more often, decompensation of known chronic HF [5]. Besides left ventricular failure, there can be right ventricular failure (RVF). It is primarily due to left heart disease with secondary pulmonary hypertension, but there are some conditions in which RVF is isolated (arrhythmogenic right ventricular cardiomyopathy, RV myocardial infarction, etc.) [5].

Many HF patients worsen over time and progress into advanced HF. It is defined as persistent symptoms despite optimal therapy. Those patients often have systemic or peripheral congestion that requires high doses of diuretics or procedures like renal replacement therapy (RRT).

The incidence of advanced HF is increasing due to the aging of the population, a growing number, and better survival of HF patients. The criteria needed to define advanced HF include severe HF symptoms (NYHA III-IV) despite optimal medical therapy (OMT), severe cardiac dysfunction (defined by at least one of the following:


#### **Figure 1.**

*Chronic heart failure definition and classification based on ejection fraction.*


**Figure 2.**

*Chronic heart failure classification based on symptoms severity and physical activity.*

EF ≤ 30%, isolated RVF, severe and non-operable valve abnormalities, severe and non-operable congenital abnormalities, persistently high natriuretic peptides levels, and severe left ventricular diastolic dysfunction), episodes of congestion (systemic or pulmonary, requiring the use of high dose intravenous diuretics), attacks of low output states (requiring inotropes or vasoactive agents) or malignant arrhythmias causing more than one hospitalization in the last year, and severe impairment of exercise capacity (**Figure 3**). Further classification of advanced HF patients and assessment


#### **Figure 3.**

*Advanced heart failure definition creteria (ESC2021).*

of advanced therapy can be done using the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) profiles [5].

#### **2.2 Pathophysiology**

Pathophysiologically, HF is defined as the inability of the heart as a pump to maintain the metabolic needs of the human body (failure to maintain adequate cardiac output). In this context, HF can be divided into systolic and diastolic dysfunction and left-sided and right-sided HF.

The most common cause of systolic dysfunction is ischemic heart disease. Other causes include dilated cardiomyopathy, chronic volume and pressure overload, chronic pulmonary diseases, and heart rhythm disorders. Diastolic dysfunction is most commonly due to pressure overload conditions causing pathological hypertrophy, not allowing the ventricle to relax. Common causes include hypertension, aortic stenosis, hypertrophic, and restrictive cardiomyopathy [7]. Cardiac output results from stroke volume and heart rate. Stroke volume is dependent on cardiac contractility (the inotropic state of the heart), preload (stretching of the cardiac myocytes before contraction), and afterload (the pressure that the heart needs to overcome to eject blood) [8].

In systolic dysfunction, the cardiac contractility is impaired, causing a decrease in stroke volume and, subsequentially, a reduction in cardiac output, resulting in global hypoperfusion. At the same time, left ventricular end-diastolic pressure is elevated, resulting in increased left atrial pressure and causing a rise in pulmonary capillary pressure. These changes lead to pulmonary venous congestion.

Diastolic dysfunction is characterized by the inability of the left ventricle to adequately relax in diastole due to abnormal stiffness of the left ventricular wall. The result is an increased ventricular filling pressure with a subsequent increase in the pulmonary circulation pressure. Systolic function is usually maintained; however, in the setting of chronic pressure overload, it can also be impaired.

Right-sided HF is most commonly a result of left-sided HF; however, it can also develop as an isolated entity, secondary to pulmonary diseases ("cor pulmonale") and due to increased right ventricular afterload. The main clinical presentation, in this case, is systemic venous congestion with minimal to no pulmonary congestion [9].

#### **2.3 Prognostic factors**

Despite the new therapeutic options (mainly for HFrEF), HF remains a progressive disease with a poor prognosis and a five-year survival rate of nearly 50% [10].

Prognostic factors related to higher mortality rates are advanced age (especially >75 y/o), male sex, and comorbidities such as diabetes, CKD, peripheral artery disease, atrial fibrillation, higher body mass index (BMI), lower systolic blood pressure, and chronic obstructive pulmonary disease [11].

Studies have shown that the mortality rate also increases with the number and duration of hospitalizations for HF. Regarding EF, HFpEF patients generally have a better survival rate than HFrEF patients. Transition in EF can also occur, and patients who progress to a lower EF have worse outcomes than those who remain stable or progress to a higher EF [5].

Laboratory tests such as natriuretic peptides, C-reactive protein (CRP), and serum sodium levels are also helpful in assessing patient prognosis. Serial natriuretic peptide measurements are used not only as a diagnostic tool but also to determine the efficacy of HF treatment and to evaluate prognosis. Patients with elevated levels of NT-proBNP and CRP correlate with worse clinical outcomes than those without elevation of both markers. Hyponatremia (serum sodium level of less than 135 mmol/L) is linked with increased mortality rates in HF patients. Diabetes is associated with worse clinical outcomes and greater hospitalization rates [12].
