This document discusses aortic valve disorders such as stenosis and regurgitation. It begins by reviewing the anatomy of the aortic valve and the cardiac cycle. Aortic stenosis is defined as a narrowing of the aortic valve that obstructs blood flow from the left ventricle. Causes include bicuspid valves and age-related calcification. Pathogenesis involves hypertrophy of the left ventricle and reduced coronary blood flow. Symptoms are related to reduced cardiac output. Aortic regurgitation occurs when the aortic valve is incompetent and allows backflow during diastole. Causes may be congenital or from conditions like rheumatic heart disease. Chronic regurgitation can lead to left ventricular

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Aortic Valve Disorders
Hizbullah Khan
BScN, MScN
Asst. Professor (CNM)

2. Objectives
Review the valves of the heart
Discuss the disorders of Aortic valve
List the etiology of Aortic valve disorders
Explain the pathophysiology of Aortic stenosis and
regurgitation
Describe the signs and symptoms of Aortic stenosis and
regurgitation
Discuss briefly the management Aortic valve disorders.
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6. Aortic Valve Overview
The aortic valve is located between the LV and the
aorta.
It has three cusps and sometimes is referred to as
the aortic semilunar valve because its leaflets are
crescent or moon shaped.
The aortic valve has no chordae tendineae.
The two main coronary arteries are located behind
the aortic valve.
During the ejection phase (systolic) of the cardiac
cycle, blood moves forward into the aorta to the
systemic circulation.
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7. Aortic Valve Stenosis
Stenosis: It refers to narrowing
Valve orifice is smaller, impending the forward flow
of blood.
It is characterized by increased resistance to ejection
of blood from the LV into the aorta.
Aortic stenosis (AS) is narrowing of the aortic valve
resulting in obstruction of blood flow from the left
ventricle to the ascending aorta during systole
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8. CausesBicuspid aortic valve is the most common cause of aortic
stenosis in patients under age 65. People may also be born
with one (unicuspid) or four (quadricuspid) cusps, but these
are veryrare. About 2% of people are born with aortic valves
that have only two cusps (bicuspid valves). Progressive wear
and tear of such bicuspid valve leads to stenosis.
Senile calcific aortic stenosis (65 and over): With aging,
protein collagen of the valve leaflets is destroyed, and
calcium is deposited on the leaflets which reduces its
mobility with time.
Rheumatic heart disease 8

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10. Pathogenesis
As Aortic stenosis develops gradually, the LV has time to
adapt. With increased systolic pressure from obstruction,
the left ventricular wall becomes thicker, or hypertrophies.
This increase in wall thickness can maintain a normal
ejection fraction.
Little hemodynamic disturbance occurs as the valve area is
reduced by half its normal area (from a normal 3 to 4 cm2
to
1.5 to 2 cm2
).
Additional reduction/narrowing in valve area produces
severe obstruction to flow and pressure overload on LV.
At this point, the increased work of the heart begins to
exceed the coronary blood flow reserve, causing both
systolic and diastolic dysfunction and signs of heart failure
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11. Pathophysiology
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12. Clinical Manifestations
Exertional dyspnea, weakness, marked fatigability,
peripheral cyanosis and other signs of low CO.
Exertional Angina occurs in approximately two thirds of
people with advanced aortic stenosis
Syncope (fainting) is most commonly due to the reduced
cerebral circulation that occurs during exertion
Palpitation
Loud systolic ejection murmur
The hallmark finding is a crescendo-decrescendo ejection
murmur, heard best with the diaphragm of the
stethoscope at the right and left upper sternal border
when a patient who is sitting upright leans forward.
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13. Aortic Valve Regurgitation
Aortic valve regurgitation (or aortic regurgitation) is
the result of an incompetent aortic valve that allows
blood to flow back to the LV during diastole.
As a result, the LV must increase its stroke volume to
include blood entering from the lungs (through LA)
as well as that leaking back through the regurgitant
valve.
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14. Causes
Congenital heart valve disease.
Age-related changes to the heart.
Rheumatic heart disease (RHD) is associated with a
rigid and thickened valve that does not open or close
completely.
Infective endocarditis
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15. Pathophysiology
Acute aortic regurgitation is characterized by the
presentation of a sudden, large regurgitant volume to a
normal size LV that has not adapted to volume overload.
As a result, there is severe elevation in left ventricular
end-diastolic pressure, which is transmitted to the left
atrium and pulmonary veins, culminating in pulmonary
edema.
A decrease in cardiac output leads to sympathetic
stimulation 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.
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16. Pathophysiology
Chronic aortic regurgitation, usually has a gradual onset.
As the valve deformity increases, regurgitant flow into the
LV increases, the LV progressively enlarges, and the
diastolic blood pressure falls.
Hemodynamically, the increase in left ventricular 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
compensated phase, which may last decades. The only sign
for many years may be a soft systolic aortic murmur.
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18. Clinical Manifestations
Fatigue and weakness, especially when you increase
your activity level
Shortness of breath with exercise or when you lie
down
Swollen ankles and feet
 Palpitations
Signs of decreased cardiac output in later stages
Cardiac Murmurs
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19. Diagnosis
Echo
Echocardiography is used to assess the anatomy of
the aortic valve, the degree of stenosis/regurgitation.
It also allows evaluation of cardiac chamber size and
function.
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20. MANAGEMENT
Aortic Valve Replacement:
The diseased aortic valve is replaced with tissue or
metallic valve surgically.
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21. 1. Emanuel Rubin & John L. Farber, Essential Pathology,
Philadelphia, 1990.
2. Kumar, Vinay; Abbas, Abul K; Aster, Jon. (2009).
Robbins & Cotran pathologic basis of diseases (8th ed.).
St. Louis, Mo: Elsevier Saunders. ISBN 1-4160-3121-9.
3. Porth CM. Pathophysiology: Concepts of altered Health
States. 7th
edition; 2005. Lippincott Williams & Wilkins.
Reference
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