Download Advances in Biomedical Engineering. Volume 3 by J.H.U. Brown, J.F. Dickson PDF

By J.H.U. Brown, J.F. Dickson

ISBN-10: 0120049031

ISBN-13: 9780120049035

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097\ ot 5. Effects of Cardiac and Vascular Parameters The description of the vascular portion of Beneken's model will be given in Section ΙΙΙ,Β. Here, let us examine the effects of changing the maximum shortening velocity, Vc max , the heart rate, /, and the arterial resistance, Ra) parameters. Figure 24B plots cardiac output (F) against F cma x under two different heart rates (Beneken, 1965). When the heart rate is 72 beats/min, the effect of increasing Vcm&x is very slight, but decreasing it to one-half the normal (N) reduces the cardiac output considerably.

K. (min 5 1 -y* '· r~ ^Z ^ [ -8D| 100 100 T j 5Fi <^ 1 ,P "Ϊ SV2 Γ^Ί V CiDSL I 0 N -ι f«72 min 1 w»H 1 11 1 0 :N ν r, * MXN F I G . 24. (A) Effect of changing the maximum shortening velocity of the contractile element, F c m a x (abscissa), on various hemodynamic variables. The change is normalized with respect to the normal value (the arrow N). The test was performed in Beneken's model of the entire circulatory system—that is, with the mechanical circulatory loop closed. (B) Effect of changing F c m a x on cardiac output, F, at two different heart rates.

23 is characterized by a fall with time in contrast to a continued rise in the former. A corresponding difference exists in the aortic flow curves seen in the two models. The aortic flow in Beneken's model is a triangle in shape, whereas that of Robinson's model is more complex, being precipitously cut off at the end of systole. It is probably fair to judge that Robinson's model contracts too slowly relative to the assigned fixed duration of systole, whereas in Beneken's model the contractile force develops much more quickly.

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