By N. Ghista Dhanjoo, Eddie Yin-kwee Ng
For the 1st time, this worthy e-book exhibits how cardiac perfusion and pumping could be quantified and correlated. Self-contained and unified in presentation, the reasons within the compendium are specified adequate to seize the reader s interest and entire sufficient to supply the heritage fabric to discover additional into the topic. Mathematically rigorous and clinically orientated, the booklet is a huge source for biomedical engineers, cardiologists, cardiac surgeons and clinicians. for college kids, it truly is an amazing textbook for senior-level classes in cardiovascular engineering.
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Extra info for Cardiac perfusion and pumping engineering
8. Simulated blood ﬂow waveforms in subepicardial, midmyocardial, and subendocardial arterioles. Note that there is systolic reverse ﬂow in deeper myocardium, while systolic forward ﬂow in superﬁcial portion. The amount of diastolic ﬂow component is larger in deeper portion. 17 In subendocardium, two-peaked systolic retrograde ﬂow with predominant diastolic ﬂow was simulated, as seen in our in vivo visualization experiments (see Fig. 3). The subepicardial arteriolar ﬂow exhibited two peaked forward ﬂows, one during systole and the other during diastole, consistent with our experimental data except a sharp and short dip during isovolumic contraction phase, probably due to local muscle strain.
Schematic diagram of experimental apparatus for ventricular mechanics modeling. The system contains a force transducer (1), a linear motor for applying mechanical deformations (2), an optical transducer to measure the muscle length (3), and a sustenance system (4) with the bath for muscle perfusion and platinum electrodes connected to the electronic generator (5). Measurement and control devices are interfaced with a computer (6). the actual length into chamber radius. The chamber volume (V ) of the ventricle was calculated as: V = 4 3 πR .
H was calculated as: ∆H = (H1 − H2 )/H1 × 100%, where H1 and H2 are the values of LV wall region thickness corresponding to the beginning and the end of diastole. 89%, which is less than normal (∼40%39 ). Figure 6 shows the distribution of ∆H in the LV wall for both IHD and the relatively normal heart. The distribution of regional ∆H to total LV wall elasticity seems fairly uniform as opposed to the pathologic LV, where it is not. For this example, the CVs of ∆H for the pathologic and relatively healthy heart are 61% and 24%, respectively.
Cardiac perfusion and pumping engineering by N. Ghista Dhanjoo, Eddie Yin-kwee Ng