Aortic Stenosis

• Valvular AS should be distinguished from nonvalvular forms of LV outflow obstruction, including

congenital supravalvular stenosis and subvalvular membrane, ridge or tunnel stenosis, and dynamic
subvalvular LV outflow obstruction in HOCM
• The normal AVA is 2.5-3.5 cm2. AS is not usually of hemodynamic significance until the valve
area is ↓ to 25% of normal. mild 1.5 to 3.0 cm2, moderate 1.0 to 1.5 cm2, severe <1.0 cm2. With
normal CO, severe AS →mean transvalvular pressure gradient 50 mm Hg.
• Transvalvular gradients are affected by flow, so patients may have low gradients despite severe AS
if there is LV systolic dysfunction.
• therapeutic decisions typically are based on the presence of symptoms in the setting of significant
aortic stenosis, categorization of disease as mild, moderate, or severe is of lesser clinical
importance.
Etiology congenital (bicuspid), rheumatic, or senile degenerative (calcific) in origin.
History long latent period >30 yrs
• The three classic symptoms associated with aortic stenosis are dyspnea, angina pectoris, and
syncope. (life expectancy < 5 yrs)
• Dyspnea due to↑ in LVDP, LA, and pulmonary venous pressures.
• Angina occurs without CAD resulting from ↑ O2 demand from ↑ LV mass and ↑ intracavitary
pressures in the setting of a fixed blood supply and from ↓ coronary flow due to progressive
outflow obstruction.
• Syncope may be caused by peripheral vasodilation with exertion, with ↑ in peripheral oxygen
requirement in the setting of a fixed CO.
• Later →↓in CO→ CHF( fatigue, weakness, and peripheral cyanosis). Peripheral edema,
hepatomegaly, and ascites may occur as a result of RV failure secondary to pul HTN. A fib is a late
manifestation of pure AS, and its presence without other symptoms of advanced disease should
suggest the possibility of concomitant mitral valve disease.
• P/E :The classic murmur of aortic stenosis is a harsh, low-pitched, crescendo–decrescendo systolic
ejection murmur, which radiates from the base of the heart into the carotids.
• Laboratory Findings:ECG: LVH, CXR: Cardiomegaly, Echo
Hemodynamic management:
Preload: ↑,
Contractility: maintain, avoid myocardial depressant drugs,
R&R: maintain NSR, avoid brady or tachycardia,
Afterload: avoid ↓ SVR
• neuroaxial anesthesia the epidural is better than spinal, → less ↓ in SVR by titrating the LA.
• Consider antibiotics prophylactic coverage in a Pt with AS.
• In severe AS with LV dysfunction consider AVR, Balloon valvuloplasty, or IABP
• Monitors: consider TEE, PAC.