Transcript AORTIC STENOSIS - Ravenwood-PA

AORTIC STENOSIS
BY
EPIFANI D. ARMEDILLA
OBJECTIVES
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Review the anatomy and physiology of the
cardiovascular system
Describe the pathophysiology of aortic stenosis
Identify the causes of aortic stenosis
Recognize the signs and symptoms of aortic
stenosis
Discuss the imaging studies used in detecting
the severity of aortic stenosis
Review the treatment for aortic stenosis
The Cardiovascular System
AORTIC STENOSIS
Obstruction of blood flow across
the aortic valve during left
ventricular systole
AORTIC STENOSIS
Causes of Aortic Stenosis
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Congenital
Rheumatic fever
Degenerative calcification of the aortic cusps –
most common
Obstructive infective vegetations
Paget’s disease of the bone
Systemic lupus erythematous
Rheumatoid disease
Irradiation
Congenital AS
Calcified AS
Senile or degenerative AS
Aortic Stenosis
Clinical Findings in Aortic Stenosis
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Typical murmur and thrill for slightly narrowed,
thickened, or roughened valves
Systolic ejection murmur at the aortic area transmitted
to the neck and apex for mild or moderate cases
Palpable left ventricular heave or thrill, a weak to absent
aortic second sound, or reversed splitting of the second
sound are present in severe cases of AS because of
prolonged ejection time
S4 is common and reflects increased atrial contribution
to ventricular filling
Symptoms of Aortic Stenosis
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AS is asymptomatic until the valve orifice has
narrowed to approximately 0.5 cm²/m² body
surface area of adults
Patients remain asymptomatic for a long period
of time
The condition is first diagnosed based on
detection of a systolic murmur on auscultation
that can be explained by the gradual process of
obstruction
Three Cardinal Symptoms of AS
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Exertional dyspnea
Exertional angina
Exertional syncope
Exertional Dyspnea
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Is a result of elevation of the pulmonary
capillary pressure secondary to reduced
compliance and/or LV dilatation
Exertional Angina
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Usually develops later and reflects an imbalance
between the augmented myocardial oxygen
requirements and reduced oxygen availability
Exertional Syncope
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Caused by arrhythmias (usually ventricular tachycardia
and bradycardias), hypotension, or decreased cerebral
perfusion resulting from increased blood flow to
exercising muscles without compensatory increase in
cardiac output
Imaging Studies
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ECG
Chest radiography
Echocardiography
Dobutamine echocardiography
Cardiac catheterization
ECG
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LV hypertrophy – classic finding
Other nonspecific changes are left atrial
enlargement, left axis deviation, and left
bundle-branch block
Not a reliable test because of the wide
variations seen in AS and other cardiac
conditions
ECG – LV Hypertrophy
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Large S wave in V1
Large R wave in V5
Chest Radiograph
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Normal or enlarged
cardiac silhouette
Calcification of aortic
valve
Dilatation and
calcification of
ascending aorta
Arrow points out dilated shadow
of the ascending aorta
Echocardiography
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Useful in assessing the
severity of AS, the degree
of coexisting aortic
regurgitation, LV size and
function
Helpful in estimating
pulmonary systolic
pressure and in
identifying other cardiac
abnormalities
TEE – displays the
obstructive orifice
extremely well
TEE
Dobutamine Echocardiography
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Indicated in patients with moderate aortic
stenosis and LV dysfunction to predict the
reversibility of LV dysfunction after AVR
Pts. With AS, LV dysfunction, and relatively low
gradients have better outcome when
management decisions are based on the results
of dobutamine echocardiogram
(Schwammenthal, et al, 2001)
Cardiac Catheterization
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Indicated for hemodynamic evaluation whenever there is
discrepancy between the clinical picture and
echocardiography
Indicated for young, asymptomatic patients with
noncalcific congenital AS, to define the severity of
obstruction to LV outflow
Indicated for patients in whom it is suspected that the
obstruction to LV outflow may not be at the aortic valve
but rather in the sub or supra-valvular regions
Also indicated to evaluate the coronaries in AS patients
at risk for coronary artery disease
Grading of Aortic Stenosis
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The aortic valve area must be reduced to
one-fourth of its normal size before
significant changes in the circulation occur
AS is graded based on the aortic valve
area
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Mild - >1.5 cm²
Moderate – 1.1 to 1.5 cm²
Severe - <0.75 to 1 cm²
Management of Aortic Stenosis
Pharmacological Management
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Medical treatment has no role in
preventing the progression of the disease
process
But with the onset of LV systolic
dysfunction, the use of inotropic agent
may be advocated
Surgical Management
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AVR is indicated for symptomatic patients
AVR improves survival in patients with
depressed as well as normal LV function
The risks of surgery and prosthetic valve
complications outweigh the benefits of
preventing sudden cardiac death and
prolonged survival in asymptomatic
patient
Types of Valves
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Bioprosthesis
(Porcine)
Mechanical (St. Jude)
Homograft
Porcine valve
Bioprosthesis vs. Mechanical Valves
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Bioprosthesis valves are less durable than mechanical valves and
begin to deteriorate after 5-6 years; usually do not require longterm coagulation
Mechanical valves are durable but require lifelong anticoagulation to
control thromboembolism
Mechanical valve was associated with significantly lower 15 year
mortality compared with bioprosthesis valve (66% vs. 79%)
(Hammermeister, et al, 2000).
Mechanical valves are less obstructive than stented bioprosthesis
valves of the same size (Bech-Hanssen, et al, 1999).
Despite a better survival rate with mechanical valve, the choice of
valve should be tailored to the patient’s needs.
References
Alpert, J. T. (Ed.). (2001). The AHA Clinical Cardiac Consult. Philadelphia:
Lippincott Williams & Wilkens.
Bech- Hassen, O., Caidahl, K., Wall, B., Myken, P., Lason, S., & Wallentin, I.
(1999). Influence of aortic valve replacement, prosthesis type, and size of functional
outcome and ventricular mass in patients with aortic stenosis. Journal of Thoracic
Cardiovascular Surgery. 118(1):57-65.
Braunwald, E., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., &
Jameson, J. L. (2001). Harrison’s 15th Edition Principles of Internal Medicine. New York:
McGraw-Hill.
Hammersmeister, K., Sethi, G. K., Henderson, W. G., Grover, F. L., Oprian, C., &
Rahimtoola, S. H. (2000). Outcome 15 years after valve replacement with a mechanical
versus a bioprosthetic valve: Final report of the Veterans Affairs Ramdomized trials.
Journal of American Cardiology. 36:1152-1158.
Martin, L. & Coulden, R. (1999). Cardiac radiology: valvular heart disease.
Clinics of North America. 37(2):319-338.
Munt, B. (1999). Physical examination in valvular aortic stenosis: correlation
with stenosis severity and prediction of clinical outcome. American Heart Journal.
137(2):298-306.
Nowrangi, S. K., Connolly, H. M., Freeman, W. K., & Click, R. L. (2001). Impact
of intraoperative transesophageal echocardiography among patients undergoing aortic
valve replacement for aortic stenosis. Journal of American Society of Echocardiography.
14(9):863-6.
Otto, C. M. (1999). Valvular Heart Disease. Philadelphia: W. B. Saunders
Company.
Tierney, Jr., L. M., McPhee, S. J., & Papadakis, M. A. (2002). Current Medical
Diagnosis & Treatment: 2002. (41st Ed.). New York: Lange Medical Books/McGraw-Hill.
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