CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
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diastolic pressure increase the aortic pulse
pressure. The regurgitation, which takes place
as the ventricle relaxes and fills, causes a dias-
tolic murmur, which is louder early in diastole
(decrescendo murmur).
Because of the backward flow of blood
from the aorta into the left ventricle, there
is no true phase of isovolumetric relaxation
(see Fig. 9.13, right panel). Instead, the left
ventricle begins to fill with blood from the
aorta before the mitral valve opens. Once
the mitral valve opens, ventricular filling
occurs from the left atrium; however, blood
continues to flow from the aorta into the
ventricle throughout diastole because aortic
pressure is higher than ventricular pressure
during diastole. This greatly enhances ven-
tricular filling (end-diastolic volum e), which
activates the Frank-Starling mechanism to
increase the force of contraction and stroke
volume as shown by the increased width of
the
pressure-volume
loop.
With
chronic
aortic
regurgitation,
the
ventricle
remod-
els by dilating, which increases compliance.
This helps the ventricle to accommodate the
large increase in volume without excessive
increases in end-diastolic pressure. As long
as the ventricle is not in failure, normal end-
systolic volumes can be sustained; however,
the end-systolic volume increases when the
ventricle goes into systolic failure. Because
the
aortic valve never
completely closes,
blood will always be m oving across the valve
depending on the aortic and left ventricular
pressure difference. Consequently, there is no
true isovolumetric phase at the beginning of
diastole or systole. W hen the ventricle first
begins to contract, blood continues to enter
the ventricle from the aorta until the ventric-
ular pressure exceeds the aortic pressure. It
is important to note that the stroke volume,
calculated from the difference between the
end-diastolic and end-systolic volumes, is
increased. However, the net stroke volume
into the aorta (net forward flow in the aorta)
is lower than normal. For example, assume
that stroke volume is normally 70 mL. During
aortic regurgitation, the stroke volume calcu-
lated from the end-diastolic and end-systolic
volumes may be 120 mL. If half of that stroke
volume flows backward into the ventricle
(regurgitant fraction = 0.5), then the net out-
ward stroke volume will be 60 mL, which is
smaller than normal.
In summary, aortic valve insufficiency is
characterized by an increase in aortic pulse
pressure, a diastolic murmur, increased stroke
volume but reduced net aortic flow, ventricu-
lar dilation, no true isovolumetric phases,
increased
ventricular
filling pressure,
and
increased left atrial and pulmonary vascular
pressures.
MITRAL VALVE REGURGITATION
In mitral valve regurgitation, blood flows
backward into the left atrium as the left
ventricle contracts. This leads to a large
increase in the
v
wave of the left atrial pres-
sure tracing (Fig. 9.14, left panel) and the
generation of a systolic murmur that spans
briefly beyond S2. Ventricular systolic and
aortic pressures decrease if the net ejec-
tion of blood into the aorta is significantly
reduced.
There are several important changes in the
left ventricular pressure-volume loop in the
presence of mitral insufficiency (Fig. 9.14,
right panel). First, there is no true isovolumet-
ric phase at the beginning of systole. As soon
as the ventricle begins to contract and develop
pressure, blood begins to flow across the mitral
valve and back into the left atrium. Mitral
regurgitation reduces the afterload on the left
ventricle (total outflow resistance is reduced),
which causes stroke volume to be larger and
end-systolic volume to be smaller than nor-
mal; however, end-systolic volume increases if
the heart goes into systolic failure in response
to chronic mitral regurgitation. Because the
mitral valve is never completely closed, blood
flows back into the left atrium as long as intra-
ventricular pressure is greater than left atrial
pressure; therefore, there is no true phase of
isovolumetric
relaxation.
During
diastole,
the elevated pressure within the left atrium is
transmitted to the left ventricle during filling
so that left ventricular end-diastolic pressure
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