Background. Factors affecting: cardiac function in dialysis patients i
nclude arterial blood pressure, anaemia, intravascular volume, and the
arteriovenous (a-v) access. Cardiac failure has been directly attribu
ted 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 sh
ort manual compression on the fistula, but this technique has obvious
limitations. Methods. The present study examined prospectively the eff
ect of dialysis a-v access on both cardiac function and various hormon
al responses. Ten patients (age, mean+/-SD, 59.6+/-12.3) with end-stag
e renal failure being prepared for chronic dialysis therapy were inclu
ded. All patients underwent an echocardiographic study before and 2 we
eks after the creation of the a-v access. Plasma atrial natriuretic pe
ptide (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 f
raction 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), an
d plasma aldosterone did not change. None of the patients developed ov
ert high-output cardiac failure. Conclusions. This study shows that al
least in the short term following the creation of a dialysis a-v acce
ss, 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.