Peters did not measure effective arterial blood volume (EABV); he invented it. He reasoned that a normal kidney in a patient with congestive heart failure (CHF) will relentlessly retain salt to the point where it kills the patient. Normal kidneys retain salt when volume is contracted. But all the measurable volume compartments in patients with CHF are expanded – blood volume, interstitial volume, extracellular volume. So Peters said that the volume compartment that was contracted was EABV. It’s essentially the degree of arterial filling or organ perfusion. Its contraction is discerned by history and other markers or poor organ perfusion such as low urinary Na concentration, high renin, high aldosterone, high vasopressin, etc. All the markers for a low EABV are presented in the paper under the features of CHF. EABV is expanded in patients with renal disease when the disease causes primary salt retention. The example I used in the paper is a patient with salt retaining acute glomerulonephritis.

A lot of investigators failed to make the distinction between EABV and other volume compartments and accordingly got into trouble. The problem of cirrhotic edema is a good example of this failure to understand EABV on the part of some investigators who tried to argue that volume was expanded early in the course of this disease.

Please answer me this question: How did Peters measured the EABV? which animal model and under which circumstances he discovered a low EABV in CHF?