CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
223
VALVE DISEASE
N ormal valve function as described in Chapter 4
is characterized as having (1) low pressure
gradients across the valve as blood flows
through the orifice and (2) unidirectional
flow. These normal features are altered when
heart valves function abnormally. When this
occurs, net ventricular outflow can decrease,
leading to a fall in cardiac output and clinical
signs of heart failure.
There are two general categories of valve
defects: stenosis and insufficiency. Valve
stenosis results from a narrowing of the
valve orifice. Fibrosis, often accompanied
by calcification, causes the valve leaflets
to thicken so that they cannot open fully,
which decreases cross-sectional area of the
open orifice. Furthermore, the valve cusps
can fuse
together, which prevents them
from fully opening. Congenital valve defects
can also produce stenosis. Valve regurgita-
tion (insufficiency) occurs when the valve
leaflets do not completely seal when the
valve is closed; this causes blood to flow
backward (regurgitate) into the proximal
chamber. Both of these valve defects alter
intracardiac pressures and volumes during
the cardiac cycle.
Valve defects produce murmurs that can
be heard with a stethoscope. A murmur is a
rumbling or rasping sound caused by vibra-
tions generated by the abnormal movement of
blood within or between cardiac chambers, or
by turbulent flow within the pulmonary artery
or aorta just distal to the outflow valve. If a
murmur is heard during systole between the
first (S1) and second (S2) heart sounds, it is
termed a systolic murmur. If it is heard dur-
ing diastole (between S2 and S1), it is termed
a diastolic murmur. The sound intensifies
with increasing flow and turbulence across
the valve.
The
following
sections
describe
pres-
sure and volume changes that occur during
valve
stenosis
and
regurgitation.
Because
valve disease is generally a chronic problem,
neurohumoral activation and cardiac remod-
eling occur in an attempt to maintain normal
cardiac output and arterial pressure. These
compensatory
responses
include
systemic
vasoconstriction,
increased
blood
volume,
and increased heart rate and inotropy Cardiac
remodeling involves hypertrophy or dilation,
depending on the valve defect. When these
compensatory mechanisms fail to maintain
cardiac output and arterial pressure within
normal limits (termed “decompensation”),
the patient develops symptoms of heart fail-
ure as described in the previous section.
The following discussion examines cardiac
changes during valve disease in the absence of
significant heart failure at rest, therefore rep-
resenting compensated conditions.
Valve Stenosis
Stenosis can occur at either an
outflow
valve (aortic or pulmonic valve) or inflow
valve (mitral or tricuspid valve). Stenosis
increases the resistance to flow across the
valve, which causes a high pressure gradi-
ent across the valve. The pressure gradient
across a valve is the pressure difference on
either side of the leaflets as blood is flowing
through the valve. For the aortic valve, the
pressure gradient is the left ventricular pres-
sure minus the aortic pressure; for the mitral
valve, the pressure gradient is the left atrial
pressure minus the left ventricular pressure.
In normal valves, the pressure gradient is
only a few mm Hg when blood is flowing
across the open valve.
The
following equation
is
the general
hemodynamic expression that relates pressure
gradient (AP), flow (F), and resistance (R)
under laminar, nonturbulent flow conditions:
AP = F ■
R
A reduced valve orifice increases the resist-
ance to flow across the valve because resist-
ance is inversely related to the radius (r) of
the valve orifice to fourth power (equiva-
lent to valve orifice area [A] to the second
power because A = n r2) (see Chapter 5).
Therefore, the above equation can also be
expressed as:
AP ~
_F_
A2
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