**11. Impact of arterio-venous hemodialysis fistula**

In dialysis patients, one can assume the relationship between CHF and recent AVF formation in slight reduction of cardiac output, absence of pulmonary hypertension and other causes of heart failure progression (severe CHD, cardiomyopathy).

After AVF formation, peripheral vascular resistance decreases rapidly, leading to compensatory increase of cardiac output and possibly to acute CHF decompensation. Because of the increase of blood inflow to the heart, the diastolic size of the left ventricleand pulmonary pressure increase [114]. Subsequently, progressing myocardial hypertrophy and dilatation of heart cavities cause diastolic LV dysfunction and CHF development [115]. Pulmonary hypertension, found in 40–50% of patients on HD [116], joins soon after AVF formation and is associated with the size of arterio-venous shunt [117]. The inadequate pulmonary vasodilation in response to the AVF-induced increase in blood flow rate is thought to be caused by decreased NO synthesis in the endothelium or accumulation of uremic NO inhibitors, such as asymmetric dimethyl arginine [118].

#### *Cardiorenal Syndrome in Patients on Renal Replacement Therapy DOI: http://dx.doi.org/10.5772/intechopen.100493*

In all patients on regular HD, AVF with a large shunt should be considered as a factor aggravating the CHD and CHF development. Normalization of blood flow in AVF can lead to delay in cardiovascular pathology progression. In peripheral bypass syndrome, blood flow and perfusion in the limb distal to the fistula reduce dramatically because of shunt redistribution of blood flow. Less known is coronary bypass syndrome, where left-sided AVF, bypassing the left internal thoracic artery, reduces coronary blood flow, which can lead to myocardial ischemia, especially during the HD session [119].

After the AVF formation, the blood volume increases to maintain a higher cardiac output and can be complicated by severe (refractory) hypertension. In several "preload (end-diastolic pressure)-dependent" dialysis patients, poorly controlled dialysis-induced hypotension accompanies inter-dialysis hypertension in the first 15–20 min of HD even with moderate volumes of UF. Among other complications, fistula infection with outcome in progressing CHF and thromboembolic syndrome provokes prognostically unfavorable bacterial endocarditis.

Thus, AVF, being essentially an iatrogenic vascular anomaly formed to treat HD, can contribute to cardiac mortality. The negative effect of AVF on cardiovascular mortality is directly proportional to blood flow in the fistula and severity of initial cardiovascular pathology. Thus, AVF should not be used in patients with LV ejection fraction <40% and significant pulmonary hypertension. Therefore, the AVF formation should be preceded by cardiac assessment (ECG and Echo-CG monitoring) involving a consultation with a cardiologist.

AVF formation should be planned 2–3 months before the expected start of HD. It is unwise to form AVF a year or more before the start of HD and at Hb levels >12 g/dL because of high risk of fistula thrombosis. Blood flow in the fistula should be targeted at 400–600 ml/min; for blood flow over 800 ml/min, surgical reduction of arterio-venous blood shunt is reasonable. Ultrasonography, venography, and arteriography (fistulography) are used to monitor AVF.

In patients with refractory CHF, CHD with unstable angina, coronary or peripheral bypass syndrome, or severe pulmonary hypertension, AVF ligation with transfer to CAPD is indicated. In endocarditis after removal of infected AVF is recommended temporary transfer of a patient with HD to CAPD or low-flow dialysis, increasing the effectiveness of antibiotic therapy, followed by prosthetic heart valves insertion. PD can be used also for the period of standard AVF formation and maturation instead of AVF with excessive shunt.
