Biomedical Engineering Reference
In-Depth Information
The simulation results are as shown in
Figs. 2.2-26-
2.2-28. The right and left ventricular pressures are as
shown in Fig. 2.2-26
.
The blood volumes in the right and left heart:
Notice that there is an increase in left ventricular
pressure, while the right ventricular pressure is not af-
fected. The coarctation causes an increase in left ven-
tricular pressure as blood encounters greater resistance.
By the time the blood has passed through the capillaries
and pooled during venous return, the pressure drop
caused by the coarctation is diminished. The same anal-
ysis could be traced in reverse over the pulmonary circuit.
These results suggest that a small change in re-
sistance (that is, conductance) affected pressures
throughout the body. However, the PHYSBE system is
somewhat limited in that a pressure differential of 15
mmHg between the right and left arms suggests the
narrowing of the artery (
Braunwald, 1988
). This in-
cipient coarctation could not be modeled by PHYSBE,
as the arms as well as the legs are lumped into one
subsystem each.
2.2.7.2 Aortic stenosis
Aortic stenosis is a condition where deposits on the aortic
valve cause it to become narrowed or blocked. As
a result, the valve is unable to open properly, and blood
flow out of the left ventricle into the aorta is reduced,
causing the left ventricle to work harder to compensate
and ensure that the body receives the necessary blood
supply (Texas Heart Institute, 2004).
There are numerous causes of this condition, including
congenital defects, rheumatic fever, and calcification on
the aortic valve. A small percentage of people are born
with two cusps on their aortic valve instead of three and,
as a result of wear and tear over the years, the valve may
become calcified or scarred, or its motility may be re-
duced. Rheumatic fever also damages the cusps of the
aortic valve, causing the edges of the cusps to fuse to-
gether. As a person ages, the collagen in his/her body,
including in the cusps of the aortic valve, is destroyed,
and calcium deposits form. The calcium deposits on the
valve reduce the cusps' motility and therefore increase
the resistance of the blood flow. Symptoms resulting
from a stenosis include fainting, shortness of breath,
heart palpitations, angina, and coughing (Texas Heart
Institute, 2004).
The increased resistance at the aortic valve results in
an increase in left ventricular pressure and a decrease in
aortic pressure. Severe stenosis results in decreased
stroke volume, increased afterload, and increased end
systolic volume. If the model of aortic stenosis is accu-
rate, then the simulation results should mimic these
pressure changes as shown in
Fig. 2.2-29
.
Figure 2.2-27 Blood volume simulation results, left and right
heart.
The blood pressure before and after the coarctation:
Example 2.2.9 Simulink model of aortic valve stenosis.
Modify the Simulink implementation of PHYSBE to
model an aortic valve stenosis and predict the effect on
blood pressure and volume in the heart.
Figure 2.2-28 Blood pressure simulation results, before and
after coarctation.
