Biomedical Engineering Reference
In-Depth Information
Fig.
15.4
). The P-Ao had the highest mean and peak strain, followed by the LCCA,
BA, LAD, and LMCA. Conversely, the highest mean wall shear stress and mean
circumferential stress were in the LMCA, followed by the BA, LAD, LCCA, and
P-Ao. The coronary arteries exhibited realistic shapes and averages in the flow, pres-
sure, and strain waveforms. In addition, equal regional blood flows were obtained in
the left and right cerebral hemispheres, with mean and pulse pressure lower in the
cerebral arteries than in other areas of the vasculature. These results are summarized
in Fig.
15.4
and Table
15.2
.
Cardiac output would have decreased from 5 to 4.46 L/min after introducing the
75 % aortic coarctation if no changes were made in the lumped parameter heart
model. Increasing the maximum elastance of the heart from 1
.
25 to 1.52 mmHg/mL
maintained cardiac output at 5 L/min, but increased blood pressure in the entire
model (e.g., from 120
/
80 to
150
/
90 mmHg in the P-Ao). The pressure, flow, and
strain waveforms exhibited more oscillations in each vascular territory, possibly due
to the additional reflection site at the coarctation (Fig.
15.4
). Similar to the baseline
condition simulation, the P-Ao had the highest mean and peak strain, followed by
the LCCA, BA, LAD, and LMCA, all with values higher than in baseline conditions.
Interestingly, while the % increase in MAP was approximately the same throughout
the model; the % increase in pulse pressure was greatest in the P-Ao, followed by
the LCCA, BA, LAD, and LMCA (Table
15.3
). Whereas flow increased through
the LAD, LCCA, LMCA, and BA, it decreased in the P-Ao, thus indicating an
early redistribution of flow due to the increased resistance at the coarctation. This
redistribution also explained the smaller percentage increase in wall shear stress in
the P-Ao compared to the other vascular territories. Cardiac workload, as measured
by the area within the pressure-volume loop of the left ventricle, increased 17 %
from 8476 to 9890 mmHg/mL.
In the early arterial remodeling case, had the heart model not been modified,
the changes in arterial properties would have decreased cardiac output from 5 to
4.59 L/min. Additional cardiac compensation was thus introduced (e.g., increased
maximum elastance to 1.82 mmHg/mL) to maintain cardiac output at 5 L/min. This
change resulted in yet another increase in blood pressure throughout the model, with
aortic blood pressure reaching
≈
180
/
80 mmHg. Additional oscillations were seen
in the pressure, flow, and strain waveforms compared with those found in the acute
cardiac compensation stage (Fig.
15.4
). The P-Ao again had the highest mean and
peak strain, followed by the BA, LCCA, LMCA, and LAD. In this case, wall strain
returned to near baseline levels in the P-Ao, whereas strains in the LCCA and LAD
were approximately the same as for acute cardiac compensation despite the stiffen-
ing and thickening experienced by these arteries. Lastly, strains in the LMCA and
BA were higher than those seen with acute cardiac compensation due to the higher
mean and pulse pressures, but no changes in wall properties. The mean values of cir-
cumferential stress were between those for baseline and acute cardiac compensation
for the P-Ao, LCCA, and LAD, but higher in the basilar artery and LMCA. When
comparing acute cardiac compensation and early arterial remodeling, the % increase
in mean pressure was nearly identical throughout the entire model but the % increase
in pulse pressure differed regionally, see Table
15.3
. This finding emphasizes that
≈
