Aortic Stenosis

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.

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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.