The Contribution of Local Factors to the Elevated Venous Tone of Congestive Heart Failure

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Abstract
Since the concept of an elevated venous tone in congestive heart failure (CHF) has been recently questioned, the venous volume of the elevated calf at a venous pressure of 30 mm Hg (VV[30]) was determined in 18 normal volunteers (N) and 10 CHF patients with a mercury-in-rubber strain gauge plethysmograph. CHF patients had a significantly lower VV[30] at rest and after intra-arterial phentolamine (2 mg) than normal subjects, suggesting that in these patients a state of peripheral venoconstriction existed (rest-N: 4.63±0.17, CHF: 1.7±0.23 ml/100 ml, P < 0.01; pre- and postphentolamine-N: 4.85±0.21 to 4.95±0.31, CHF: 2.26±0.29 to 2.68±0.38 ml/100 ml, P < 0.01). Of note is that alpha adrenergic blockade failed to increase VV[30] significantly in N, but did increase it in CHF (P < 0.05), suggesting that part of the decreased VV[30] in CHF in due to an augmented sympathoadrenal discharge. When sodium nitrite (30 mg) was given as a single intra-arterial injection before or after phentolamine or when given in four successive doses at 3-min intervals, the VV[30] of CHF patients was never increased to more than 3.62±0.42 ml/100 ml and was always less than N (P < 0.01). Importantly, VV[30] in CHF after these interventions was even significantly less than that of N before intervention (P < 0.05), suggesting that factors other than local active smooth muscle venoconstriction were operative in CHF to lower VV[30]. It is suggested that perhaps clinically undetectable edema and an elevated tissue pressure may account for these differences.