AORTIC STENOSIS

NCM 112
TOPIC TO DISCUSS: • DEFINITION OF AORTIC
STENOSIS.
• PATHOPHYSIOLOGY.
• ASSESSMENT.
• MEDICAL/SURGICAL
MANAGEMENT.
• NURSING MANAGEMENT.

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Aortic Stenosis
Aortic valve stenosis is narrowing of the orifice between the left ventricle
and aorta. In adults, stenosis often is a result of degenerative calcifications.
Calcifications may be caused by proliferative and inflammatory changes
that occur in response to years of normal mechanical stress, similar to
changes that occur in atherosclerotic arterial disease. Age, diabetes,

hypercholesterolemia, hypertension, smoking, and elevated levels of low-

density lipoprotein cholesterol may be risk factors for degenerative calcific

changes of the valve (Mann et al., 2015). Congenital leaflet malformations

or an abnormal number of leaflets (i.e., one or two rather than three) may
be involved. Rheumatic endocarditis may cause adhesions or fusion of the
commissures and valve ring, stiffening of the cusps, and calcific nodules
on the cusps.

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Pathophysiology
Progressive narrowing of the valve orifice occurs, usually over several
years to several decades. The left ventricle overcomes obstruction to
emptying by contracting more slowly but with more power than normal,
forcibly squeezing blood through the smaller orifice. Obstruction to left
ventricular outflow increases pressure on the left ventricle, so the
ventricular wall hypertrophies. When these compensatory mechanisms of
the heart begin to fail, clinical signs and symptoms develop (Otto &
Bonow, 2013).

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Clinical Manifestations
Many patients with aortic stenosis are asymptomatic. When symptoms
develop, patients usually first have exertional dyspnea, caused by
increased pulmonary venous pressure due to left ventricular failure.
Orthopnea, PND, and pulmonary edema also may occur. Reduced blood
flow to the brain may cause dizziness and syncope. Angina pectoris is a
frequent symptom; it results from increased oxygen demand of the
hypertrophied left ventricle with decreased blood supply due to decreased
blood flow into the coronary arteries and decreased time in diastole for
myocardial perfusion. Blood pressure is usually normal but may be low.
Pulse pressure may be low (30 mm Hg or less) because of diminished
blood flow.

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Assessment and Diagnostic Findings
On physical examination, a loud, harsh systolic murmur may be heard over
the aortic area (i.e., right second intercostal space) and may radiate to the
carotid arteries and apex of the left ventricle. The murmur is low pitched,
crescendo–decrescendo, rough, rasping, and vibrating (Weber & Kelley,
2014). An S4 sound may be heard. If the examiner rests a hand over the
base of the heart (second intercostal space next to the sternum and above
the suprasternal notch) and up along the carotid arteries, a vibration may
be felt. The vibration is caused by turbulent blood flow across the
narrowed valve orifice. By having the patient lean forward during
auscultation and palpation, especially during exhalation, it is possible to
accentuate sounds of aortic stenosis (Weber & Kelley, 2014).

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 Echocardiography, cardiac MRI, and computed tomography (CT)
scanning are used to diagnose and monitor progression of aortic stenosis.
Patients with symptoms usually have echocardiograms every 6 to 12
months, and those without symptoms have echocardiograms every 1 to 5
years (Fuster et al., 2011; Nishimura et al., 2014). Evidence of left
ventricular hypertrophy may be seen on a 12-lead ECG and an
echocardiogram. After stenosis progresses to the point that surgical
intervention is considered, left-sided heart catheterization is necessary to
measure the severity of the valvular abnormality and to evaluate the
coronary arteries. Pressure tracings are taken from the left ventricle and
base of the aorta. The systolic pressure in the left ventricle is considerably
higher than that in the aorta during systole. Graded exercise studies (stress
tests) to assess exercise capacity are performed with caution for patients
with aortic stenosis because of the high risk of precipitating ventricular
tachycardia or fibrillation, and should not be performed on symptomatic
patients (Cohn, 2012; Mann et al., 2015; Nishimura et al., 2014).

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Prevention
Prevention of aortic stenosis is primarily focused on controlling risk
factors for proliferative and inflammatory responses—namely, through
treating diabetes, hypertension, hypercholesterolemia, and elevated
triglycerides and avoiding tobacco products. (See prevention of
endocarditis later in this chapter.)

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Medical Management
Medications are prescribed to treat dysrhythmia or left ventricular failure
(see Chapters 26 and 29). Definitive treatment for aortic stenosis is
surgical replacement of the aortic valve. Patients who are symptomatic and
are not surgical candidates may benefit from one- or two-balloon
percutaneous valvuloplasty procedures with or without transcatheter aortic
valve implantation (TAVI) as described later in the chapter.

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Nursing Management: Valvular Heart
Disorders
The nurse educates the patient with valvular heart disease about the
diagnosis, progressive nature of the disease, and treatment plan. The
patient is instructed to report new symptoms or changes in symptoms to
the primary provider. The nurse also educates the patient that an infectious
agent, usually a bacterium, is able to adhere to a diseased heart valve more
readily than to a normal valve. Once attached to the valve, the infectious
agent multiplies, resulting in endocarditis and further damage to the valve.
In addition, the nurse educates the patient about how to minimize the risk
of developing infective endocarditis (discussed later in this chapter).
The nurse measures the patient’s heart rate, blood pressure, and
respiratory rate, compares these results with previous data, and notes any
changes. Heart and lung sounds are auscultated and peripheral pulses
palpated. The nurse assesses the patient with valvular heart disease for the
following:

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Signs and symptoms of heart failure, such as fatigue, DOE, decreased activity tolerance, an increase in coughing,
hemoptysis, multiple respiratory infections, orthopnea, and PND (see Chapter 29) Dysrhythmias, by palpating the
patient’s pulse for strength and rhythm (i.e., regular or irregular) and asking whether the patient has experienced
palpitations or felt forceful heartbeats (see Chapter 26) Symptoms such as dizziness, syncope, increased weakness, or
angina pectoris (see Chapter 27) The nurse collaborates with the patient to develop a medication schedule and provides
education about the name, dosage, actions, adverse effects, and any drug–drug or drug–food interactions of prescribed
medications for heart failure, dysrhythmias, angina pectoris, or other symptoms. Specific precautions are emphasized,
such as the risk to patients with aortic stenosis who experience angina pectoris and take nitroglycerin. The venous
dilation that results from nitroglycerin use decreases blood return to the heart, thus decreasing cardiac output and
increasing the risk of syncope and decreased coronary artery blood flow. The nurse instructs the patient about the
importance of attempting to relieve the symptoms of angina with rest and
relaxation before taking nitroglycerin and to anticipate the potential adverse effects. In addition, the nurse educates the
patient to take a daily weight and report sudden weight gain, as defined by the primary provider (American Heart
Association, 2015). For example, in the past patients were instructed to call their primary providers if they gained 3 lb in
1 day or 5 lb in 1 week. Now weight gain parameters are more individualized to each patient. The nurse may assist the
patient with planning activity and rest
periods to achieve an acceptable lifestyle. Patients who experience symptoms of pulmonary congestion are advised to
rest and sleep sitting in a chair or bed with the head elevated. Care of patients treated with
valvuloplasty or surgical valve replacement is described later in this chapter.

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