Normal EABV exists when the ratio of cardiac output to peripheral resistance maintains venous return and cardiac output at normal levels.
EABV can be reduced, therefore, by factors which reduce actual arterial blood volume (hemorrhage, dehydration), increase arterial vascular capacitance (cirrhosis, sepsis) or reduce cardiac output (congestive heart failure).
EABV can be reduced in the setting of low, normal, or high actual blood volume.
Whenever EABV falls, the kidney is triggered to retain sodium and water.
[1] In cases of edema, increases in extracellular fluid (ECF) is associated with a corresponding decrease in EABV.