Estimated central blood volume in cirrhosis

The estimated central blood volume (i.e., blood volume in the heart
cavities, lungs and central arterial tree) was determined by
multiplying cardiac output by circulatory mean transit time in 19
patients with cirrhosis and compared with sympathetic nervous
activity and circulating level of atrial natriuretic factor.
Arterial norepinephrine level, an index of overall sympathetic
nervous activity (3.08 nmol/L in patients vs. 1.36 nmol/L in
controls; p < 0.01) was negatively correlated (r = -0.54, p <
0.01) with estimated central blood volume (mean = 23 ml/kg in
patients vs. 27 ml/kg in controls; p < 0.05). Similarly, renal
venous norepinephrine level (an index of renal sympathetic tone;
4.26 nmol/L in patients vs. 1.78 nmol/L in controls; p < 0.01)
was inversely correlated with estimated central blood volume (r =
-0.53, n = 18, p < 0.02). No significant correlation could be
established between arterial atrial natriuretic factor level (8.9
pmol/L in patients vs. 9.6 pmol/L in controls; not significant) and
estimated central blood volume. Hemodynamic values were
subsequently modified with oral propranolol (80 mg). During
-adrenergic blockade, the mean estimated central blood volume was
not altered significantly, except in six patients who exhibited
decreases in mean arterial blood pressure (85 to 69 mm Hg; n = 6)
and decreases in mean estimated central blood volume (23.2 to 20.6
ml/kg; n = 6, p < 0.05). Slight increases were observed in mean
right atrial pressure (2.2 to 3.7 mm Hg; n = 14, p < 0.05); this
change was positively correlated with the change in estimated
central blood volume (r = 0.44, n = 14, p = 0.06). In conclusion,
reduced estimated central blood volume probably unloads volume
receptors and baroreceptors, thus provoking enhanced overall and
renal sympathetic nervous activity and thereby contributing to
increased water and salt retention in cirrhosis. During -adrenergic
blockade estimated central blood volume changes correlated with
alterations in preload and afterload. These findings indicate that
central circulatory and arterial underfilling is a key element of
the hemodynamic derangement observed in cirrhosis.