Cardiac mechanoenergetic cost of elevated plasma viscosity after moderate hemodilution

Abstract

The purpose of this study was to investigate how plasma viscosity affects cardiac and vascular function during moderate hemodilution. Twelve anesthetized hamsters were hemodiluted by 40% of blood volume with two different viscosity plasma expanders. Experimental groups were based on the plasma expander viscosity, namely: high viscosity plasma expander (HVPE, 6.3 mPa · s) and low viscosity plasma expander (LVPE, 2.2 mPa · s). Left ventricular (LV) function was intracardiacally measured with a high temporal resolution miniaturized conductance catheter and concurrent pressure-volume results were used to calculate different LV indices. Independently of the plasma expander, hemodilution decreased hematocrit to 28% in both groups. LVPE hemodilution reduced whole blood viscosity by 40% without changing plasma viscosity, while HVPE hemodilution reduced whole blood viscosity by 23% and almost doubled plasma viscosity relative to baseline. High viscosity plasma expander hemodilution significantly increased cardiac output, stroke volume and stroke work compared to baseline, whereas LVPE hemodilution did not. Furthermore, an increase in plasma viscosity during moderate hemodilution produced a higher energy transfer per unit volume of ejected blood. Systemic vascular resistance decreased after hemodilution in both groups. Counter-intuitively, HVPE hemodilution showed lower vascular resistance and vascular hindrance than LVPE hemodilution. This result suggests that geometrical changes in the circulatory system are induced by the increase in plasma viscosity. In conclusion, an increase in plasma viscosity after moderate hemodilution directly influenced cardiac and vascular function by maintaining hydraulic power and reducing systemic vascular resistance through vasodilation.

Fig. 1

Hemodilution protocol. Baseline characterization was performed before hemodilution. 40% blood volume was exchanged with test solutions (HVPE; viscosity = 6.3 mPa s or LVPE; viscosity = 2.2 mPa s). Observation period was 1 hour after exchange. Hct, hematocrit; BL, baseline; HD, hemodilution.

Fig. 2

Mean arterial pressure (MAP) measured at baseline (BL), at 0, 15, 30 and 60 minutes after hemodilution (HD0, HD15, HD30, HD60). †, p < 0.05 compared to baseline. ‡, p < 0.05 between groups at specific time points.

Fig. 3

Relation between end-systolic pressure (P_es) and end-systolic volume (V_es) during hemodilution. The insert presents the end-systolic elastance (E_es) determined from the slope of the linear relationship between P_es and V_es. Solid lines are the linear regression for each experimental group (LVPE: P_es = 2.77 (V_es) + 74.04, r = 0.97; HVPE: P_es = 1.67 (V_es) + 96.08, r = 0.77).

Fig. 4

(A) Systemic vascular resistance (SVR) at each time point after hemodilution; (B) Systemic vascular hindrance (SVH) at last time point; and (C) The work done by the heart per stroke volume (SW/SV ratio) at each time point after hemodilution. The baseline mean and standard deviation for i) systemic vascular resistance is 9 + 2 mmHg·min·ml⁻¹, and ii) stroke work per stroke volume is 108 + 5 mmHg. Broken lines represent the values at baseline. †, p < 0.05 compared to baseline within a same group. ‡, p < 0.05 between groups at a specific time point.

Fig. 5

Equivalent wall shear rate (WSR) and wall shear stress (WSS) in an HVPE group relative to an LVPE group. The WSS ratios are based on apparent blood viscosity (WSS_Blood) and plasma 3 viscosity (WSS_Plasma).

Fig. 6

Hydraulic power (MAP × CO) against normalized stroke work per stroke volume (SW/SV). The second factor contributing to the determination of systemic hydraulic power is the left ventricular afterload.