Page 741 - Cardiac Nursing

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C HAPTER 2 9 / Acquired Valvular Heart Disease 717
rather than replacement. For discussion of surgical options, refer stenosis becomes severe, left ventricular systolic function may also
to the section on surgical intervention for mitral regurgitation. decline, resulting in CHF.
Angina may result even in the absence of CHD because of an
Prognosis imbalance in myocardial oxygen supply and demand. Myocardial
oxygen demand is increased secondary to increased left ventricu-
MVP is usually a benign condition and most patients remain lar wall stress and muscle mass. Myocardial oxygen delivery is re-
asymptomatic for their entire lives. Patients with progressive duced as a result of decreased coronary perfusion pressure.
and symptomatic mitral regurgitation should be considered for Syncope or near syncope can result secondary to reduced cere-
mitral valve repair. In a small subset of patients, sudden cardiac bral perfusion pressure, inappropriate left ventricular baroreceptor
death may occur secondary to arrhythmias. Patients with MVP response, or arrhythmia. Orthostatic blood pressure changes may
and history of syncope, prolonged QT interval, palpitations, or occur during exertion when arterial pressure drops because of sys-
dizziness should have further evaluation with arrhythmia mon- temic vasodilation in the setting of a fixed cardiac output. In-
itoring. creased left ventricular pressure may result in inappropriate
baroreceptor response. Development of atrial fibrillation with
rapid ventricular response may produce light-headedness or syn-
cope due to loss of atrial kick and decline in cardiac output. Syn-
AORTIC STENOSIS cope at rest may be due to transient ventricular fibrillation that
spontaneously converts. 10
Cause
Aortic stenosis is characterized by obstruction of the left ventricular Clinical Manifestations
outflow tract. Most commonly, left ventricular outflow obstruction
is valvular, but it may be either supravalvular or subvalvular. Aortic Patients with mild-to-moderate aortic stenosis are usually asymp-
stenosis is a gradually progressive disease that may have a long tomatic. As severe aortic stenosis develops, the most common ini-
asymptomatic phase often lasting for decades that is then followed tial symptom is dyspnea on exertion, followed by angina and near
by a much shorter symptomatic phase with severe narrowing of the syncope or syncope. CHF also may occur as a result of ventricular
aortic valve orifice. 37 The age at which aortic stenosis becomes dysfunction or increasing mitral regurgitation. Less commonly,
symptomatic is determined by the underlying cause. Aortic stenosis sudden death, probably caused by ventricular fibrillation, may be
occurring from 1 to 30 years of age usually represents congenital the presenting clinical feature.
aortic stenosis. Aortic stenosis presenting at the ages of 40 to
60 years is primarily rheumatic in origin or secondary to calcific Physical Assessment
aortic stenosis in a congenitally bicuspid aortic valve. In patients
past the age of 60 to 70 years, calcific degenerative stenosis is the Aortic stenosis is most readily detected by auscultation of its clas-
most prevalent cause. Of the causes of aortic stenosis, senile/degen- sic mid-systolic (systolic ejection) murmur (see Table 29-3). As
erative calcific aortic stenosis is most common. aortic stenosis progresses, the murmur peaks progressively later in
systole and decreases in intensity as cardiac output falls. The mur-
mur often radiates to one or both carotids. The murmur may be
Pathology diminished at the base of the heart and radiate to the apex, which
may be incorrectly thought to be mitral regurgitation (Gallavardin
In senile/degenerative calcific aortic stenosis, cumulative wear and
phenomenon). An S 4 gallop is usually present. The point of max-
tear leads to calcification on an otherwise normal aortic valve. Cal-
imal intensity is sustained but may not be displaced. Blood pres-
cific deposits prevent the cusps from opening normally in systole,
sure is normal-to-hypertensive until late in the disease progress.
resulting in stenosis. Risk factors for the development of calcific
Jugular venous pressure is normal in most patients except in pa-
aortic stenosis include male sex, elevated lipoprotein(a), height
tients with severe aortic stenosis associated with heart failure. Re-
(inverse relation), hypertension, smoking, elevated low-density
duction in stroke volume and cardiac output may cause dimin-
lipoprotein cholesterol, raised serum calcium, raised serum creati- ished carotid upstrokes and late systolic peak (tardus) in severe or
nine, and diabetes. 38 In patients with congenitally bicuspid aortic
critical aortic stenosis.
valves, abnormal flow through the valve leads to calcium deposi-
tion and restriction of cusp opening.
Diagnostic Tests
Pathophysiology Echocardiography is the principal modality used to diagnose and
quantify aortic stenosis. Aortic valve pressure gradient can be
Aortic stenosis typically progresses over a period of years. As the measured, aortic valve area calculated, pulmonary artery pressures
valve cusps become less mobile, the valve orifice decreases in size, estimated, and left ventricular function and hypertrophy can be
resulting in an increasingly higher left ventricular systolic pressure evaluated. Echocardiography is the most important diagnostic im-
necessary to eject blood across the stenosed valve. Increased left aging technique used to diagnose and follow aortic stenosis. 12
ventricular afterload results first in compensatory concentric left Cardiac catheterization is performed in patients with aortic
ventricular hypertrophy. Although initially adaptive in aortic stenosis primarily to rule out concomitant CHD. Left ventricu-
stenosis, left ventricular hypertrophy leads to decreased ventricu- lography can quantify the left ventricular ejection fraction. The
lar compliance and diastolic dysfunction. With the increased pres- transvalvular gradient can be established by direct pressure meas-
sure gradient, blood from the left ventricle is ejected back into the urement. Right heart catheterization can better quantify pul-
left atrium worsening underlying mitral regurgitation. As aortic monary artery pressures and cardiac output.