The Mechanisms of Hyperkinetic Circulation in Chronic Anemia

It has been well known that the hemodynamic characteristic of chronic anemia is "hyperkinetic circulation" (high cardiac output state). However, the mechanisms of the enhanced left ventricular (LV) performance have not been clearly defined. The several factors may contribute to increase cardiac output (CO) ; an increase in preload, a decrease in afterload, an increase in myocardial contractility and an increase in heart rate (HR). We studied 62 patients with chronic anemia, and analysed the parameters of LV function. In the analyses Wezler's method was used. Systolic time intervals were also measured. Total blood volume (TBV) and circulation time (CT) were measured with evance blue, and TBV/CT was used as an index of preload. Total peripheral resistance (TPR) was used as an index of afterload. LV contractility was evaluated by ET/PEP, preload-LV performance (TBV/CT-CO) relations, afterload-LV performance (TPR-CO) relations, and force-velocity (1/TPR-SV/ET) relations. When the cases were classified in 3 groups by the grade of anemia, CO were increased along with the aggravation of anemia. In the mild (Mi) group (Hb≧10mg/dl) CO was within normal limits, in the moderate (Mo) group (10>Hb≧6 mg/dl) CO was enhanced due to the increase in SV, and in the severe (S) group (Hb<6 mg/dl) the increase in CO became more remarkable, which was caused by the increase in HR; the hyperkinetic circulation in Mo group was preload-dependent, and that in S group positive chronotropic effect took part in. The regression line of TBV/CT-CO relation in Mo group showed y=8.7x+4.5 (r=0.48, p<0.05). The evaluation of LV contractility revealed that this mechanism didn't participate clinically in the CO increase ; in TPR-CO relations, which is both preload-dependent and contractility-dependent, the regression line of Mo and S group shifted more upwards than that of Mi group, but in 1/TPR-SV/ET relation, which is contractility-dependent, the regression lines of 3 groups of anemia were quite similar to normal one. The values of ET/PEP were equal in 3 groups of anema. Thus, we concluded that the hyperkinetic circulaition in the moderate grade of anemia is caused by Frank-Starling mechanism, and with the progresses of the severity it becomes more remarkable by the participation of the chronotropic reserve. The contributin of positive inotropism was unclear clinically.