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CARDIOVASCULAR ANESTHESIA

The Effects of Acute Normovolemic Hemodilution on Left Ventricular Systolic and Diastolic Function in the Absence or Presence of ß-Adrenergic Blockade in Dogs

Department of Anesthesiology, Tokushima University School of Medicine, Tokushima, Japan

Address correspondence and reprint requests to Junpei Nozaki, MD, Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. Address e-mail to jnozaki{at}clin.med.tokushima-u.ac.jp

Acute normovolemic hemodilution (ANH) increases cardiac output because of a reduction in blood viscosity and enhancement of left ventricular (LV) contractility. The status of LV function, especially LV diastolic function during ANH, remains controversial. We therefore examined LV systolic and diastolic function during ANH. Sixteen dogs were anesthetized with isoflurane in the absence (Group 1) and presence (Group 2) of ß-adrenergic blockade (propranolol 1 mg/kg). LV contractility was quantified by the slope (M_w) of the stroke work and end-diastolic volume relation. Diastolic function was evaluated with the time constant of LV relaxation (T), chamber stiffness constant (K_c), peak LV diastolic filling rate during early filling (peak E) and atrial contraction (peak A), and ratio of peak E to peak A (E/A). Normovolemic exchange of blood (50 mL/kg) for 6% hydroxyethyl starch (ANH50) significantly increased M_w in Group 1 but not in Group 2. In both groups, ANH50 significantly decreased T. ANH50 significantly increased peak E in both groups and peak A in Group 1, and it did not change the E/A ratio or K_c in either group. ANH causes positive inotropic effects and enhances diastolic function without ß-blockade. Even after ß-adrenergic blockade, ANH improves diastolic function through the reduction of LV ejection impedance.

IMPLICATIONS: Acute normovolemic hemodilution enhances LV (left ventricular) diastolic function by alterations in the LV loading condition produced by hemodilution, which mainly contributes to a compensatory increase in cardiac output.

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