Hyponatremia: terminology and more

Karen Yeates and associates1 are to be commended for their concise, pragmatic and expert update on hyponatremia. However, they implicitly endorse a previously described concept — low effective circulating volume2 — which is offered to account for why sodium retention in heart failure persists despite established volume overload. In fact, this concept is physiologically unsound.

First, the circulating volume comprises plasma volume plus interstitial volume, the 2 major components of extracellular volume (also known as sodium space). Since this volume is not further partitioned either anatomically or physiologically, it is “effective” in its entirety and is expanded in heart failure. Thus, the qualifier “effective” is inapplicable overall, and the adjectives “low” and “contracted” are inapplicable in the context of heart failure.

Second, although it has been fashionable to dismiss the role of low cardiac output in heart failure, it is in fact the central pathophysiologic element “not only of advanced heart failure (systolic and/or diastolic) but also of the earliest stages of the underlying ventricular dysfunction, long before heart failure is symptomatic or detectable at the bedside.”3Indeed, low cardiac output is the driving force for virtually the entire heart failure syndrome, including persistent sodium retention despite established hypervolemia,3 neurohormonal hyperactivation (in a futile attempt to preserve cardiac output, but at the expense of further cardiac and vascular dysfunction)3 and elevation of natriuretic peptides and troponins. Neglect of this reality has fostered the conceptual aberration “low effective circulating volume”3^,4 and the proliferation of various models of heart failure (each further obscuring the central role of low cardiac output3) and has delayed elucidation of the true pathophysiology of diastolic heart failure and several other issues related to heart failure in general.3^,4

This might be mere pedantry were it not for the risk that use of the term “low effective circulating volume” poses to patients. Advanced congestive heart failure typically presents with high venous pressure — jugular or pulmonary or both — and frequently with high renal function indices (blood urea nitrogen and creatinine). High renal function indices in this setting, in the absence of another explanation, are too often perceived as a sign of hypo-volemia, despite clearly elevated venous pressure. The natural therapeutic response, which in fact is potentially countertherapeutic if not hazardous, would be to attenuate any pre-existing regimen or to supplement circulatory volume.

In cases of advanced heart failure, the cardiac output (Starling) curve commonly exhibits a “descending limb” effect, whereby therapeutic lowering of venous pressure actually increases cardiac output.5^,6^,7 Thus, aggressive diuretic therapy not only alleviates the congestive phenomena as expected, but also (by increasing cardiac output and hence renal perfusion), typically and dramatically lowers the renal function indices. Indeed, the notion that excessive venous pressure must be maintained to preserve cardiac output in heart failure has long been dispelled; it is only when venous pressure falls below a value approximately 50% greater than the upper limit of the normal range that cardiac output begins to further decline.7

I would respectfully suggest that the term “low effective circulating volume” be expunged from the heart failure lexicon. Not only is it physiologically unsound, but it also invites the misperception that high renal function indices in advanced congestive heart failure are a sign of extracellular volume contraction.

Philip Andrew Watertown, NY