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U N I T 5
Circulatory Function
persons with advanced aortic stenosis and is similar to
that observed in CAD. Dyspnea, marked fatigability,
peripheral cyanosis, and other signs of heart failure
usually are not prominent until late in the course of
the disease. Syncope (fainting) is most commonly due
to the reduced cerebral circulation that occurs during
exertion when the arterial pressure declines conse-
quent to vasodilation in the presence of a fixed cardiac
output.
AorticValve Regurgitation.
Aortic valve regurgitation
or aortic insufficiency is the result of an incompetent
aortic valve that allows blood to flow back to the left
ventricle during diastole (see Fig. 19-15). As a result,
the left ventricle increases its stroke volume to accom-
modate blood entering from the pulmonary veins in
addition to the volume of blood leaking back through
the regurgitant valve. This defect may result from con-
ditions that cause scarring of the valve leaflets or from
enlargement of the valve orifice to the extent that the
valve leaflets no longer meet. There are various causes
of aortic regurgitation, including rheumatic fever, idio-
pathic dilation of the aorta, congenital abnormalities,
infective endocarditis, and Marfan syndrome. Other
causes include hypertension, trauma, and failure of a
prosthetic valve.
Acute aortic regurgitation is characterized by a
sudden, large regurgitant volume to a left ventricle of
normal size that has not had time to adapt to the vol-
ume overload. It is caused by disorders such as infec-
tive endocarditis, trauma, or aortic dissection. Using
the Frank-Starling mechanism, the heart responds by
increasing heart rate, but the compensatory mechanisms
fail to maintain the cardiac output. As a result, there
is severe elevation in left ventricular end-diastolic pres-
sure, which is transmitted to the left atrium and pulmo-
nary veins, culminating in pulmonary edema. A decrease
in cardiac output leads to sympathetic activation and a
resultant increase in heart rate and peripheral vascular
resistance that cause the regurgitation to worsen. Death
from pulmonary edema, ventricular arrhythmias, or
circulatory collapse is common in severe acute aortic
regurgitation.
Chronic aortic regurgitation, which usually has a
gradual onset, represents a condition of combined left
ventricular volume and pressure overload. As the valve
deformity increases, regurgitant flow into the left ventri-
cle increases, diastolic blood pressure falls, and the left
ventricle progressively enlarges or eccentrically hyper-
trophies. Hemodynamically, the increase in left ven-
tricular volume results in the ejection of a large stroke
volume that usually is adequate to maintain the forward
cardiac output until late in the course of the disease.
Most persons remain asymptomatic during this com-
pensated phase, which may last decades. The only sign
for many years may be a soft systolic aortic murmur.
As the disease progresses, signs and symptoms of
left ventricular failure begin to appear. These include
exertional dyspnea, orthopnea, and paroxysmal noc-
turnal dyspnea. In aortic regurgitation, failure of aortic
valve closure during diastole causes an abnormal drop
in diastolic pressure. Because coronary blood flow is
greatest during diastole, the drop in diastolic pressure
produces a decrease in coronary perfusion. Although
angina is rare, it may occur when the heart rate and
diastolic pressure fall to low levels. Persons with severe
aortic regurgitation often complain of an uncomfort-
able awareness of heartbeat, particularly when lying
down, and chest discomfort due to pounding of the
heart against the chest wall. Tachycardia, occurring
with emotional stress or exertion, may produce pal-
pitations, head pounding, and premature ventricular
contractions.
The major physical findings relate to the widening
of the arterial pulse pressure, a hallmark of chronic
aortic regurgitation. The pulse has a rapid rise and fall
(Corrigan pulse), with an elevated systolic pressure and
low diastolic pressure owing to the large stroke volume
and rapid diastolic runoff of blood back into the left
ventricle. Korotkoff sounds may persist to zero, even
though intra-arterial pressure rarely falls below 30 mm
Hg.
37
The large stroke volume and wide pulse pres-
sure may result in prominent carotid pulsations in the
neck, throbbing peripheral pulses, and a left ventricular
impulse that causes the chest to move with each beat.
The hyperkinetic pulse of more severe aortic regurgita-
tion, called a
water-hammer pulse,
is characterized by
distention and quick collapse of the artery. On ausculta-
tion, the turbulence of flow across the aortic valve dur-
ing diastole produces a high-pitched or blowing sound.
Diagnosis andTreatment
Valvular defects usually are detected through cardiac
auscultation (i.e., heart sounds). Echocardiography
provides a means of visualizing valvular motion, pat-
terns of flow, and closure patterns. Pulsed Doppler
ultrasonography provides a semiquantitative or quali-
tative estimation of the severity of transvalvular gra-
dients, right ventricular systolic pressure, and valvular
regurgitation. Color flow Doppler provides a visual
pattern of flow velocities over the anatomic 2-D echo-
cardiographic image. This allows for demonstration
of turbulence from stenotic and regurgitant valves.
Transesophageal echocardiography with Doppler ultra-
sonography is used to obtain echocardiographic data
when surface sound transmission is poor, particularly of
the AV valves and prosthetic heart valves. Cardiac cath-
eterization may be used to further describe the effects
of the defect.
The treatment of valvular defects consists of medical
management of heart failure and associated problems
and surgical valve repair or replacement, if warranted
by the extent of deformity. Valvular replacement with
a prosthetic device or a homograft usually is reserved
for severe disease because the ideal substitute valve has
not as yet been developed. Percutaneous balloon valvu-
loplasty involves the opening of a stenotic valve by guid-
ing an inflated balloon through the valve orifice. The
procedure is done in the cardiac catheterization labora-
tory and involves the insertion of a balloon catheter into
the heart through a peripheral blood vessel.
