AORTIC STENOSIS
DIAGNOSTIC PROCEDURES:
Echocardiogram Electrocardiogram
Chest X-ray Exercise Stress Test
CT Scan Cardiac Test
Cardiac Catheterization
MEDICAL MANAGEMENT:
(M) Anti-arrhythmic
(M) Blood Thinners
(M) Antibiotics
(M) Hypertensive Medications
TREATMENT MODALITIES:
(T) Lifestyle changes
(T) Oxygen Therapy
(Nd) Impaired gas exchange r/t
ventilation-perfusion imbalance as
evidenced by dyspnea and syncope
(N) Assess the patient’s VS, especially
the O₂ saturation and respiration
characteristics at least every 4 hours.
(N) Administer supplemental oxygen
as prescribed
(N) Administer medications as
prescribed
Prognosis is good with immediate
treatment especially with surgical
treatment. Poor prognosis may
occur otherwise and may lead to
complications and worse, death.
RISK FACTORS:
-this is the narrowing of the orifice between the left ventricle and aorta
Degenerative
Congenital heart disease
Congenitally malformed valve
Syncope on
exertion/dyspnea
Angina on
exertion/chest pain
(Nd) Acute pain r/t decreased
myocardial flow as evidenced by pain
scale of 8 out of 10
(N) Monitor VS every 5 minutes during
initial angina attack.
(N) Instruct the patient to notify nurse
immediately when chest pain occurs.
(N) Place patient at complete rest
during anginal episode.
- Older age
- DM
- High cholesterol
Calcium build up on the valve
- Hypertension
Rheumatic fever
- Chronic kidney disease
COMPLICATIONS:
Wear-and-tear of moving valve over many years - Heart failure - Bleeding
disrupts valve endothelium and underlying matrix - Stroke - Arrhythmia
- Blood clots - Death
Fibrosis and calcification of aortic valve SURGICAL MANAGEMENT:
(S) Aortic Valve repair
(S) Balloon valvuloplasty
Impeded blood flow through aortic valve (S) Aortic valve replacement
(S) Transcatheter aortic valve replacement
Left ventricle contracts harder to pump blood
across the stenotic valve A stiff, hypertrophied LV and the high LV
pressure both make the LV harder to fill
High LV- aorta pressure gradient drives blood into the aorta,
initially maintaining cardiac output-over time, forceful contraction Decreased cardiac output
of the LV causes concentric LV myocardial hypertrophy
Pressure overload in the LV backs
up into the lung vasculature
Left atrium dilates and hypertrophies
as a result of pressure overload
Pulmonary congestion
Cardiac output becomes more relient on
atrial filling of LV Transudation of fluid through alveolar walls into
outer spaces
If atrial fibrillation develops, carbon dioxide
decreases
Diffuse crackles on
Dyspnea
auscultation