Biomedical Engineering Reference
In-Depth Information
160
+50% afterload
140
120
control
100
-50%
80
60
40
20
0
40
60
80
Ventricular Volume V LV [ml]
100
120
FIGURE 4.52 Left ventricular pressure-volume work loops computed for the complete human circulation
model (Figure 4.50) for control and varied afterload, achieved by changing both systemic (
R SA ) and pulmonic
(
R PA ) peripheral resistances
50 percent.
venous return due, for example, to gravity via head-down tilt. Preload may also change
with total blood volume, which may, for example, decrease as the direct consequence of
hemorrhage, or change with renal regulation.
Figure 4.52 shows work loops computed for the left ventricle in the complete circulation
model for three different values of afterload, achieved by varying both systemic peripheral
resistance,
R PA . Stroke volume is inversely related to
peripheral resistance, but the Frank-Starling mechanism partially compensates. For increased
afterload, smaller SV results in increased filling for the subsequent beat, and this increased
EDV moderates the reduction in SV. This compensatory mechanism is more pronounced in
the full circulation model than for the isolated left ventricle (Figure 4.49). Afterload com-
monly increases in the natural system via increased aortic pressure with increased systemic
vascular resistance. The latter occurs, for example, when arterial vessel diameter is reduced
associated with chronic hypertension. Afterload also increases with aortic valve stenosis, the
narrowing of the valve orifice.
The interdependence of preload and afterload is manifested in treatment of heart failure
with vasodilator drugs. These drugs decrease afterload, allowing the ventricle to eject blood
more rapidly via muscle's force-velocity relation, which increases stroke volume. As SV
increases, less blood remains to fill the ventricle for the next beat, but this decrease in
EDV is less than the reduction of ESV, resulting in a net increase in stroke volume.
The heart's contractile state may be changed by varying the parameter
R SA , and pulmonic peripheral resistance,
in the model
(Eq. (4.75)). Figure 4.53 shows left ventricular work loops for such variations in inotropy,
executed by changing the contractile parameter
c
for each of the four heart chambers.
Increased inotropy causes an increase in stroke volume, with a decrease in end-systolic volume
due to the more strongly contracting heart. End-diastolic volume decreases a small amount
c
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