Volume and Pressure in Heart Failure: Complementary but not Two Sides of the Same Coin

Abstract

Objectives Assess the relationship of measured intravascular volume to resting right heart catheterization hemodynamics in patients with chronic heart failure (HF). Background The hemodynamic assessment of cardiac filling pressures (CVP, PCWP) has played a prominent role in evaluating volume status in patients with HF. And more recently implantable ambulatory hemodynamic monitoring devices (CIEDs) have been employed to guide out-patient volume management. But does pressure tell us about intravascular volume? Methods Total blood volume (TBV) was prospectively measured in patients with chronic HF (NYHA Class III-IV) using a standardized radiolabeled albumin indicator-dilution blood volume technique (BVA). These patients also underwent clinically indicated right heart catheterization (RHC) within 24 hours of BVA to assess cardiac and pulmonary hemodynamics most commonly as part of a pre-transplant/LVAD candidacy evaluation. Linear regression analyses were used to assess associations between variables. Results Sixty-three patients were evaluated (age 60±11 yrs., 73% male, LVEF 33±16%, mRAP 11±6mm Hg, PCWP 18±7mm Hg, dPAP 19±7mm Hg, C.I. 2.3±0.6, TBV 6.5±1.8L). Average BV was expanded above normal by +21% with range of −17% to +116% of normal. CVP (mRAP) and left-sided filling pressure (PCWP) were shown to have only limited association with quantitated TBV ( Fig. 1–2 ). Diastolic PAP was also weakly associated with volume status ( Fig 3 ). Conclusions Cardiac filling pressures have been used clinically as surrogate indicators of volume expansion and overload in patients with HF. However, the findings of this analysis reveal that neither CVP, PCWP, nor dPAP accurately reflect intravascular volume status. Patients with low filling pressures can have marked expansion of intravascular volume while patients with elevated filling pressures can have normal or even contracted volumes. Elevated central pressures may, therefore, reflect hemodynamic congestion but not necessarily clinical volume overload-related congestion. Thus, quantitative BV and cardiac hemodynamics provide complementary but different information - Pressure is not volume and volume is not pressure . This has implications for the approach to volume management and potentially patient outcomes.