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Copyright © Medical Economics Publishing Co., Inc.
Volume 64(1)
January 2001
pp 58-64
Aortic valve replacement
[CE Articles]
BAPTISTE, MARIA M. RN, MSN, APN,C
Section Editor(s): Vernarec, Emil
Abstract
From hospital to home care, patients receiving prosthetic valves benefit from
nurses who understand their condition and know the essentials for avoiding
complications of the procedure- and the anticoagulant therapy they may be on
for a lifetime.
FIGURE Symptomatic aortic valve dysfunction has an ominous endpoint: heart
failure. Replacing the damaged valve before the patient reaches that stage is a
lifesaving intervention.
Figure. No caption available.
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Many of these patients, however, will need anticoagulation therapy for the rest
of their lives to prevent thrombus formation. Anticoagulant therapy itself
poses a risk of major bleeding. The key to minimizing both risks is patient
adherence to medication, diet, and medical follow-up. Their importance can't
be overemphasized.
This article reviews the causes and clinical manifestations of aortic valve
dysfunction, highlights key points on managing patients who receive valve
replacement, and describes how nurses-from hospital to office to home carecan promote the best outcomes by educating patients in their care.
When aortic valves malfunction
Aortic valve dysfunction usually results from one of two major conditions:
aortic stenosis, in which the orifice of the aortic valve narrows and can't open
completely, or aortic regurgitation, in which the leaflets of the aortic valve
cannot close completely.
A healthy aortic valve opens during systole to allow oxygenated blood into
systemic circulation and closes during diastole to prevent the backflow of
blood into the left ventricle. But if the aortic valve is stenotic, blood flow is
obstructed and the heart must work harder to maintain adequate circulation.
This leads to a decrease in stroke volume-the amount of blood that is ejected
with each beat.
To compensate for the decrease, ventricular systolic pressure increases to push
the volume of blood into the circulation. The strain on the left ventricle
gradually leads to hypertrophy, then to diastolic dysfunction as the atrium
meets resistance when it tries to fill the stiff, thickened left ventricle, and,
eventually, to congestive heart failure. Aortic stenosis can lead to sudden
cardiac death.
In aortic regurgitation (sometimes called aortic insufficiency), the stroke
volume increases to compensate for the volume of blood leaking back into the
left ventricle. This added work causes the heart to enlarge and the left ventricle
to dilate, making the heart's pumping action less effective.
The stroke volume falls, resulting in hypotension and syncope as a result of
decreased cardiac output. The heart becomes congested, causing peripheral
and pulmonary edema. The end result: The heart can no longer meet the
cardiovascular and oxygenation needs of the body.
The most common cause of stenosis is calcification of the aortic leaflets,
particularly in patients older than 60 years of age.1 In patients up to age 30,
aortic stenosis usually results from an abnormal congenital bicuspid or
tricuspid aortic valve. The cause of stenosis in patients between the ages of 40
and 60 is usually rheumatic fever, damage to the heart's connective tissue as a
complication of a group A streptococcal upper respiratory infection, or
calcification of a congenital bicuspid aortic valve.
Aortic regurgitation, on the other hand, is usually a result of rheumatic fever,
endocarditis, or a congenital bicuspid aortic valve. Another possible cause is
aortic root dilation associated with Marfan's syndrome, rheumatic arthritis,
ankylosing spondylitis, or syphilis.2
Clinical manifestations of aortic valve disease
If symptomatic, patients with aortic valve disease present with chest pain,
shortness of breath, dizziness, and syncope as a result of diminished blood
flow to the brain. The signs and symptoms that distinguish aortic stenosis and
aortic regurgitation are listed in the box at right.
Box 1. Signs and symptoms
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These patients require immediate assessment of their airway, circulation, and
mental status function, and they need to be treated clinically until a definitive
diagnosis is made and other diseases are ruled out. The patient history should
include description of the chest pain and related symptoms, the frequency and
duration of the episodes, what activity precipitates the symptoms, and which
interventions alleviate them.
The standard tests for diagnosing aortic valve dysfunction include
electrocardiogram, two-dimensional echocardiogram, cardiac catheterization,
and chest X-ray.1 In patients with aortic stenosis, the EKG would reveal signs
of left ventricular hypertrophy and ST-T wave changes consistent with left
ventricular strain. The 2-D echocardiogram will show leaflet thickening,
movement restriction, left ventricular hypertrophy, and an increase in pressure
gradient (the speed at which blood is ejected from a narrowing valve).
Cardiac catheterization is performed to measure pulmonary artery pressures
and cardiac output. Chest X-ray may reveal a normal to enlarged heart, a
calcified aortic valve, and dilation of the aorta, depending on the severity of
the disease.1
In patients with aortic regurgitation, the EKG typically shows a left ventricular
hypertrophic pattern-indicated by exaggerated R waves and prolonged QRS
duration-and the chest X-ray shows an enlarged left ventricle. The
echocardiogram would reveal the presence of valvular disease and may
identify the cause of the regurgitant valve. Like aortic stenosis, cardiac
catheterization is done to assess the severity of disease.
Managing patients with valve dysfunction
Patients with aortic stenosis who are asymptomatic are treated with
prophylactic antibiotics and given serial echocardiograms every six to 12
months.3 Serial echocardiograms serve as a guide for appropriate surgical
intervention. Stenosis patients should be taught to recognize the signs and
symptoms of cardiac decompensation-a stage at which the heart is unable to
provide adequate blood circulation.
The symptoms include dyspnea, shortness of breath, decreased exercise
tolerance, chest pain, and episodes of syncope or near syncope. The use of
beta-blockers, diuretics, nitrates, and ACE inhibitors in these patients should
be used with caution because such medications may further decrease cardiac
output.4
Patients with previously undiagnosed aortic stenosis who present with
advanced or symptomatic disease require aortic valve replacement. Both
mechanical and biologic tissue valves (bioprosthetics) are available. Without
valve replacement, the mortality rate for those with congestive heart failure or
those who have had a syncopal episode is 50% over two to three years.1 Poor
surgical candidates may undergo percutaneous balloon valvuloplasty to reopen the stenotic valve, which provides short-term relief until they are stable
enough for replacement.
The management of patients with chronic aortic regurgitation consists of
prophylactic treatment with antibiotics, reduction of ventricular afterload with
vasodilators such as nifedipine (Adalat, Procardia), and serial
echocardiograms every six to 12 months.1 Patients with chronic regurgitation
should have a valve replacement before they develop left ventricular
dysfunction, and before the heart's ejection fraction falls below 55%. Valve
replacement is also indicated for symptomatic patients with an ejection
fraction greater than 55%.1
Patients with acute aortic regurgitation as a result of endocarditis are likely to
be in an advanced state of heart failure, since a compensatory mechanism for
the newly regurgitant valve would not have developed yet. These patients
frequently arrive at the ED with severe shortness of breath, tachycardia, and
decreased cardiac output.
If surgery is indicated, the patient should be treated with antibiotics for at least
48 hours before-hand and may need to be started on nitroprusside sodium
(Nitropress) to decrease preload and afterload.4
Avoiding complications after valve replacement
Complications of replacing the aortic valve include rejection of the prosthesis,
early and late prosthetic endocarditis, mechanical valve malfunction, and
hemolytic anemia. For patients with suspected prosthetic valve endocarditis, a
surgical consult is imperative. Replacing the infected valve while the patient is
on antibiotic therapy has been shown to decrease mortality.5
Early prosthetic endocarditis occurs within 40 to 60 days of valve
replacement. It is usually caused by staphylococci, streptococci, or
enterococci. The mortality rate ranges from 20% - 70%.1 Signs and symptoms
include fever, a new and previously undiagnosed heart murmur, signs of heart
failure, and development of thrombus or embolism. IV antibiotic therapy with
vancomycin hydrochloride (Vancocin) and gentamicin sulfate (Garamycin) is
the standard treatment.6
However, both vancomycin and gentamicin can have toxic effects on the
kidneys and the nerves that affect hearing and balance (ototoxicity). Clinicians
should therefore know the patient's baseline renal function and monitor blood
urea nitrogen (BUN) and creatinine levels daily, as well as the antibiotics'
peak and trough levels. Tell patients to notify staff of tinnitus.
Late prosthetic endocarditis has signs and symptoms similar to those of early
infection but occurs more than 60 days after surgery. It is usually due to
infection from staphylococci, streptococci, fungi, or gram-negative bacterial
organisms.
Bacterial infections are treated with vancomycin and gentamicin. If the
infection is caused by staphylococci susceptible to methicillin sodium
(Staphcillin), nafcillin sodium (Unipen) may be used in place of vancomycin.
Infections caused by candida or aspergillus require IV antifungal treatment
with amphotericin B (Fungizone) with or without fluconazole (Diflucan).6
Preventing thrombosis
Valvular disease and subsequent valve replacement put the patient at risk for
the development of what's known as Virchow's triad: stasis of blood flow,
tissue damage, and increased hypercoagulability, which contribute to the
formation of clots. To the body, mechanical or prosthetic valves are foreign
materials susceptible to fibrin and platelet aggregation; suture material and
damage to the endothelium also are factors. For this reason, patients require
anticoagulation therapy, initially with heparin and then long-term with
warfarin sodium (Coumadin).7
IV heparin is administered immediately following surgery to minimize the risk
of thrombus formation. An initial bolus of 80 units/kg followed by an infusion
of 18 units /kg/hour has been found to be most effective.8
The patient's activated partial thromboplastin time (APTT) should be
measured every six hours after the start of the infusion and the dose adjusted
as needed, until an APTT of 46 - 70 seconds is achieved. This is followed by
daily APTT measurement while the patient remains on heparin.
The patient should be monitored for signs of internal bleeding by testing stool
guaiac, hematocrit, and platelet levels.9 Look also for increased bruising,
hematuria, and tarry stools. Patients on heparin should be told not to use
razors, hard toothbrushes, and sharp items.
Patients are also started on oral warfarin as early as a day after surgery to
minimize the formation of clots. Warfarin works by blocking the enzymatic
reduction of vitamin K. This action, in turn, reduces the quantity of circulating
coagulation factors by 30% - 50%, and also reduces the activity of each factor
by 10% - 14%.7
Precautions are needed with warfarin therapy
Patients who have received bioprosthetic valves and who do not have atrial
fibrillation or other comorbidities usually require 12 weeks of warfarin
therapy. Life-long therapy is required for those who receive a mechanical
valve and for patients who have atrial fibrillation or other conditions that could
promote clot formation.10
Even with anticoagulation therapy, patients have up to a 2% risk of a
thromboembolic event, and up to a 7% risk of bleeding within the first days
after surgery.11
Monitoring is critical, since too low a level of anticoagulation for even a brief
period of time can result in the formation of a clot on the prosthetic valve,
which may break away when warfarin levels are increased to a therapeutic
range.7 Monitoring the blood is especially important during the first three
months after valve replacement, when anticoagulation control is difficult to
manage.12
Warfarin therapy is monitored by measuring prothrombin time (PT). Initially,
testing should take place every week to ensure that therapeutic levels have
been achieved, and then every one to two months and as needed if there have
been changes in diet or episodes of bleeding. The standard measure of PT is
the internationalized normalization ratio (INR).
According to the American College of Chest Physicians, the recommended
therapeutic INR range for patients with mechanical prosthetic valves is
between 2.5 and 3.5.13 The optimal range for INR, however, remains
controversial.
One retrospective study found that patients on anticoagulation therapy who
suffered a stroke had an average INR of 2.8, well within that therapeutic
range.13 A second study found that bleeding increased at an INR greater than
2.5.14 Other research suggests that an INR as low as 2.0 to 3.0 provides
protection against clot formation, with less risk of bleeding.10
For these reasons, the therapeutic INR range should be individualized
according to the type of mechanical replacement, the presence of other
conditions such as atrial fibrillation, the patient's age, and his history of
thrombus formation and stroke.
In addition to anticoagulation therapy, some patients are given antiplatelet
therapy with either aspirin or dipyridamole (Persantine), especially those with
co-existing cardiac comorbidities such as atrial fibrillation or previous
thrombus formation.10 But adding an antiplatelet agent may increase the risk
of bleeding.
Other prescription and over-the-counter medications affect warfarin levels and
can therefore increase or decrease warfarin's anticoagulant effects. (See the box
on page 61.) So caution and monitoring are essential if any new medications
are added or dosages of existing medications changed-including OTC
medications.
Box 2. Commonly used drugs that increase warfarin activity
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That's one of the reasons why safe and effective anticoagulant therapy calls for
aggressive patient education about the value and the risks of a lifelong
regimen following valve replacement. The box at left suggests key points to
emphasize when counseling patients. Following through with vigilant
monitoring, continuous assessment, and effective patient education is the key
to helping these patients reduce their risk of hemorrhage or a debilitating, lifethreatening thromboembolic event.
Box 3. Anticoagulation therapy: Get patients involved at the
start
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REFERENCES
1. LeDoux, D. (2000). Acquired valvular heart disease. In S. L. Woods, E. S. Froelicher, & S. U.
Motzer (Eds.), Cardiac nursing (pp. 699-718). Philadelphia: Lippincott Williams & Wilkins.
[Context Link]
2. Massie, B. M., & Amidon, T. M. (1998). Heart in L. M. Tierney, Jr., S. J. McPhee, & M. A.
Papadakis (Eds.), Current medical diagnosis and treatment (pp. 333-429). Stamford. CT: Appleton
& Lange. [Context Link]
3. Carabello, B. A. (1997). Timing of valve replacement in aortic stenosis: Moving closer to
perfection. Circulation, 95(9), 2260. [Medline Link] [Context Link]
4. Logan, P., Ruddy-Stein, Y. A., & Staudenmayer, C. B. (1999). Principles and practice for the
acute care nurse practitioner (pp. 641-671). Stamford, CT: Appleton & Lange. [Context Link]
5. John, M. D., Hibberd, J., et al. (1998). Staphylococcus aureus prosthetic valve endocarditis:
Optimal management and risk factors for death. Clinical Infectious Disease, 26(9), 1302. [Context
Link]
6. Gilbert, D., Moellering, R. C., & Sande, M. (1999). The Sanford guide to antimicrobial therapy
(29th ed.), (p. 22). Vienna, VA: Antimicrobial Therapy, Inc. [Context Link]
7. Tiede, D. J., Nishimura, R. A., et al. (1998). Modern management of prosthetic valve
replacement. Mayo Clin. Proc., 73(7), 665. [Medline Link] [BIOSIS Previews Link] [Context Link]
8. Ferri, F. F. (1998). Practical guide to care of the medical patient (pp. 922-923). St. Louis:
Mosby. [Context Link]
9. Gahart, B. L., & Nazareno, A. R. (1999). 1999 intravenous medications (pp. 446-450). St. Louis:
Mosby. [Context Link]
10. Turpie, A. G. (1997). Safer anticoagulation therapy after heart valve replacement:
Recommendations for less intense regimens. Postgrad. Med., 101(3), 85. [Medline Link] [CINAHL Link]
[Context Link]
11. Cannegieter, S. C., Torn, M., & Rosendaal, F. R. (1999). Oral anticoagulant treatment in
patients with mechanical heart valves: How to reduce the risk of thromboembolic and bleeding
complications. J. Intern. Med., 245(4), 369. [Medline Link] [BIOSIS Previews Link] [Context Link]
12. Speight, J., & Cooper, G. L. (1997). Anticoagulant control in the first three months after
mechanical heart valve replacement. Internstional Journal of Clinical Practice, 51(7), 427. [Context
Link]
13. Bussey, H. I., & Lyons, R. M. (1998). Controversies in antithrombotic therapy for patients with
mechanical heart valves. Pharmacotherapy, 18(3), 45. [Medline Link] [Context Link]
14. Milano, A., Guglielmi, C., et al. (1998). Valve-related complications in elderly patients with
biological and mechanical aortic valves. Ann. Thorac. Surg., 66(6 Suppl), S82. [Context Link]
Continuing Education Test #570: "Aortic valve replacement"
OBJECTIVES After reading the article you should be able to:
1. Compare and contrast the clinical manifestations of aortic stenosis and
aortic regurgitation.
2. Compare and contrast the management of aortic stenosis and aortic
regurgitation.
3. Develop a plan of care for the patient with aortic valve replacement.
Circle the one best answer for each question below. Transfer your answers
to the card that follows page 84. Save this sheet to compare your answers
with the explanations you'll receive. Or, take the test online at
www.rnweb.com .
1. Patients who have aortic valve replacement should be told to control
intake of vitamin K because it:
a. Has an additive effect with warfarin.
b. Counteracts the effects of warfarin.
c. Increases the risk of hemorrhage.
d. Impairs the liver's ability to clear warfarin from the body.
2. The most common cause of aortic stenosis in adults older than 60 years
of age is:
a. Rheumatic fever.
b. Congestive heart failure.
c. Calcification of aortic leaflets.
d. Abnormal congenital bicuspid aortic valve.
3. Which statement is NOT true about aortic regurgitation?
a. It can lead to sudden cardiac death.
b. It can be a result of endocarditis.
c. Peripheral and pulmonary edema result from aortic regurgitation.
d. The leaflets of the aortic valve can't close completely.
4. Standard testing for diagnosing aortic valve dysfunction includes:
a. Cardiac catheterization.
b. CT scan.
c. Complete blood count.
d. Tilt table test.
5. Which of the following is NOT usually seen on the chest X-ray of a
patient with aortic stenosis?
a. A calcified aortic valve.
b. A normal to enlarged heart.
c. An enlarged left ventricle.
d. Dilation of the aorta.
6. Patients with aortic stenosis who are asymptomatic are:
a. Told to decrease salt intake.
b. Given an annual EKG.
c. Scheduled for valve replacement.
d. Treated with prophylactic antibiotics.
7. Which is NOT a complication of aortic valve replacement?
a. Hemolytic anemia.
b. Congestive heart failure.
c. Rejection of the prosthesis.
d. Early and late prosthetic endocarditis.
8. Diuretics must be used cautiously in the patient with asymptomatic
aortic stenosis because these medications:
a. Decrease cardiac output.
b. May cause dehydration.
c. Result in electrolyte depletion.
d. Cause wide fluctuations in blood pressure.
9. The management of patients with chronic aortic regurgitation includes
all of the following EXCEPT:
a. Angioplasty.
b. Vasodilators.
c. Prophylactic antibiotics.
d. Serial echocardiograms.
10. Patients with chronic aortic regurgitation should have valve
replacement before:
a. Congestive heart failure develops.
b. Preload and afterload are increased.
c. The ejection fraction falls below 55%.
d. Right ventricular dysfunction develops.
11. Early prosthetic endocarditis usually occurs within how many days
after valve replacement?
a. 10 to 14 days.
b. 21 to 28 days.
c. 40 to 60 days.
d. 90 to 120 days.
12. Patients receiving gentamicin sulfate (Garamycin) for early prosthetic
endocarditis should be closely monitored for:
a. Hyperglycemia.
b. Tinnitus.
c. Drug rash.
d. Elevated liver enzymes.
13. Patients who have aortic valve replacement initially receive
anticoagulation with heparin and then are given:
a. Aspirin.
b. Vitamin K.
c. Warfarin sodium (Coumadin).
d. No further medication.
14. Patients on anticoagulation therapy following aortic valve
replacement are at what risk for a thromboembolic event?
a. Up to 2%.
b. 3% - 5%.
c. 7% - 10%.
d. 12% - 15%.
15. Blood monitoring is especially important for the client after aortic
valve replacement for the first:
a. Month.
b. Three months.
c. Six months.
d. Year.
16. The recommended therapeutic international normalization ratio
(INR) range for patients with mechanical prosthetic valves is between:
a. 1.5 and 2.0.
b. 2.5 and 3.5.
c. 4.5 and 5.5.
d. 6.0 and 7.0.
17. All of the following drugs have a major effect on increasing warfarin
activity EXCEPT:
a. Cimetidine (Tagamet).
b. Clofibrate (Atromid-S).
c. Ketoconazole (Nizoral).
d. Rifampin (Rifadin).
18. Patients who are symptomatic from aortic valvular disease present
with:
a. Cough.
b. Chest pain.
c. Peripheral edema.
d. Orthostatic hypotension.
Credit will be granted for this unit through January 2003. It was prepared by
Nancy Clarkson, BS, MEd, RNC, and Anne Robin Waldman, RN,C, MSN,
AOCN. Approved for Texas type I credit. Iowa Provider #191.
KEY WORDS: anticoagulant therapy; aortic stenosis; aortic regurgitation;
cardiovascular procedures; valve replacement