TY - JOUR
T1 - Haemodialysis arteriovenous access - A prospective haemodynamic evaluation
AU - Ori, Y.
AU - Korzets, A.
AU - Katz, M.
AU - Perek, Y.
AU - Zahavi, I.
AU - Gafter, U.
PY - 1996/1
Y1 - 1996/1
N2 - Background. Factors affecting cardiac function in dialysis patients include arterial blood pressure, anaemia, intravascular volume, and the arteriovenous (a-v) access. Cardiac failure has been directly attributed to dialysis a-v access in several cases. The contribution of the a-v access to cardiac performance has been tested, in the past, by a short manual compression on the fistula, but this technique has obvious limitations. Methods. The present study examined prospectively the effect of dialysis a-v access on both cardiac function and various hormonal responses. Ten patients (age, mean ± SD, 59.6 ± 12.3) with end-stage renal failure being prepared for chronic dialysis therapy were included. All patients underwent an echocardiographic study before and 2 weeks after the creation of the a-v access. Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA), and plasma aldosterone were measured at the same time periods. Results. Following the creation of the a-v fistula or graft, shortening fraction increased by 15.8 ± 6.3% (P < 0.01), stroke volume increased by 21.9 ± 5.3% (P < 0.01), ejection fraction increased by 10.6 ± 4.5% (P < 0.02), cardiac output increased by 19.0 ± 6.9% (P < 0.02), and cardiac index increased by 18.3 ± 7.1% (P = 0.05). Systemic vascular resistance decreased by 23.5 ± 7.1% (P < 0.01). There was no change in blood pressure, heart rate, weight, haemoglobin or serum creatinine. ANP increased by 83.7 ± 17.0% following the a-v access operation (P < 0.001), PRA decreased by 41.2 ± 10.0% (P < 0.05), and plasma aldosterone did not change. None of the patients developed overt high-output cardiac failure. Conclusions. This study shows that at least in the short term following the creation of a dialysis a-v access, a mild state of volume overload develops, which is offset by the 'unloading' effect of the decreased peripheral vascular resistance; the latter is probably mediated by secretion of ANP in response to atrial stretching.
AB - Background. Factors affecting cardiac function in dialysis patients include arterial blood pressure, anaemia, intravascular volume, and the arteriovenous (a-v) access. Cardiac failure has been directly attributed to dialysis a-v access in several cases. The contribution of the a-v access to cardiac performance has been tested, in the past, by a short manual compression on the fistula, but this technique has obvious limitations. Methods. The present study examined prospectively the effect of dialysis a-v access on both cardiac function and various hormonal responses. Ten patients (age, mean ± SD, 59.6 ± 12.3) with end-stage renal failure being prepared for chronic dialysis therapy were included. All patients underwent an echocardiographic study before and 2 weeks after the creation of the a-v access. Plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA), and plasma aldosterone were measured at the same time periods. Results. Following the creation of the a-v fistula or graft, shortening fraction increased by 15.8 ± 6.3% (P < 0.01), stroke volume increased by 21.9 ± 5.3% (P < 0.01), ejection fraction increased by 10.6 ± 4.5% (P < 0.02), cardiac output increased by 19.0 ± 6.9% (P < 0.02), and cardiac index increased by 18.3 ± 7.1% (P = 0.05). Systemic vascular resistance decreased by 23.5 ± 7.1% (P < 0.01). There was no change in blood pressure, heart rate, weight, haemoglobin or serum creatinine. ANP increased by 83.7 ± 17.0% following the a-v access operation (P < 0.001), PRA decreased by 41.2 ± 10.0% (P < 0.05), and plasma aldosterone did not change. None of the patients developed overt high-output cardiac failure. Conclusions. This study shows that at least in the short term following the creation of a dialysis a-v access, a mild state of volume overload develops, which is offset by the 'unloading' effect of the decreased peripheral vascular resistance; the latter is probably mediated by secretion of ANP in response to atrial stretching.
KW - Arteriovenous access
KW - Atrial natriuretic peptide
KW - Cardiac function
KW - Cardiac output
KW - Fistula
KW - Haemodialysis
UR - http://www.scopus.com/inward/record.url?scp=0030069837&partnerID=8YFLogxK
U2 - 10.1093/ndt/11.1.94
DO - 10.1093/ndt/11.1.94
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AN - SCOPUS:0030069837
SN - 0931-0509
VL - 11
SP - 94
EP - 97
JO - Nephrology Dialysis Transplantation
JF - Nephrology Dialysis Transplantation
IS - 1
ER -