Objectives: The purpose of this study was to determine if long-term pharmacotherapy mediated changes in intravascular plasma and blood volumes in patients with chronic heart failure (CHF).
Background: Intravascular fluid volume expansion is an acute compensatory adaptation to ventricular dysfunction in patients with CHF. To our knowledge there are no reports on plasma and blood volume measures in clinically stable patients with CHF receiving standard pharmacotherapy. Such information may provide a better understanding of the clinical hallmarks of heart failure.
Methods: Plasma volume (PV) and blood volume (BV) were measured in 12 patients (62.8 +/- 8.2 years old, 175.2 +/- 6.8 cm, 96.2 +/- 18.2 kg, peak oxygen consumption (VO2max) 15.2 +/- 3.3 ml/kg per min) with CHF secondary to coronary artery disease (left ventricular ejection fraction 31.2 +/- 9.7, New York Heart Association functional class 2.5 +/- 0.5) and seven healthy subjects (71.7 +/- 5.3 years old, 177.1 +/- 10.8 cm, 84.4 +/- 11.7 kg, VO2max 26.0 +/- 6.5 ml/kg per min) 3 to 4 h after eating and after supine rest using the Evan's blue dye dilution technique. Venous blood samples were collected before blue dye infusion and analyzed for hematocrit (corrected 4% for trapped plasma and venous to whole body hematocrit ratio) and hemoglobin.
Results: Hematocrit was 36.6 +/- 3.5% and 37.4 +/- 1.1%, and hemoglobin was 15.4 +/- 1.9 and 16.2 +/- 1.4 g/dl for patients with CHF and control subjects, respectively. Absolute PV was 3489.3 +/- 655.0 and 3728.7 +/- 813.2 ml, and absolute BV was 5,496.8 +/- 1,025.4 and 5,942.4 +/- 1,182.2 ml in patients with CHF and control subjects, respectively. Relative PV was 34.1 +/- 12.9 versus 44.5 +/- 9.0 ml/kg (p < or = 0.05), and relative BV was 58.5 +/- 12.3 versus 70.8 +/- 12.6 ml/kg (p < or = 0.05) in patients with CHF and control subjects, respectively.
Conclusions: Our data indicate significantly lower intravascular volumes in patients with CHF than in control subjects, indicating a deconditioned state or excessive diuresis, or both. The contracted PV and BV may contribute to exercise intolerance, shortness of breath and chronic fatigue, secondary to reduced cardiac output or regional blood flow, or both.