Predictions of blood volume (BV) assume the existence of a constant ratio between BV and body weight or surface area (SA). We examined the validity of this assumption by calculating BV from plasma volume and body hematocrit in 160 normal volunteers whose weights ranged from -38.7 to 210.8% of desirable weight (assessed by a modification of the Metropolitan Life Insurance Company Desirable Weight tables). BV is not a constant fraction of body weight or SA in this population. Its prediction from such constant ratios results in a large error of estimate which is systematically biased with respect to height and weight. BV prediction from the observed regressions of the parameter on weight and SA reduces the error substantially but remains biased with respect to height. BV prediction from the subject's degree of deviation from desirable weight affords a smaller error of estimate which is apparently free from systematic bias.

As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11±3 to 63±15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urnary sodium excretion (r = -0.768, r = -0.726, respectively; P < 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (a = 5) achieved neutral balance, while the second (a = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses.

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