Valvular+Disease

Valvular Disease


 * __Aortic Stenosis__** - the most common valvular disease in the U.S.

Normal Values
 * Aortic Valve (AV) diameter = 1.9 - 2.3 cm
 * AV area = 2 - 4 cm 2
 * Left Ventricular Outflow tract (LVOT) = 2.2 cm __+__ 0.2 cm

[|Aortic Valve Diagram]

//Pathophysiology of AS//
 * Like atherosclerosis, Calcific AV disease is a disease continuum characterized by increased mechanical stress leading to disruption of endothelial cells and subsequent lipoprotein deposition, chronic inflammation and cusp calcification
 * Progressive Valve thickening and well as leaflet immobility and outflow obstruction finally occur due to the calcification.
 * Intraventricular systolic pressure increases to preserve forward flow amidst the progressive outflow obstruction. This increased pressure, in turn leads to concentric hypertrophy/ stiff ventricles.
 * **impaired lusitropy impedes EARLY ventricular filling, making atrial kick critical for adequate filling, and therefore, stroke volume (atrial contraction can be responsible for 30-40% LVEDV)**
 * **Moreover, capillary density is often inadequate for hypertrophic muscle, and coronary perfusion pressure is decreased (as occurs with increased intraventricular pressures)**
 * Contractility is preserved and EF is maintained until late in the disease course.
 * Signs and symptoms occur when the orifice < 0.8 cm 2
 * angina (35%) mortality within 5 yrs without AVR
 * Syncope (15%) mortality within 3 yrs without AVR
 * Dyspnea (50%) mortality within 2 yrs without AVR

Pressure Volume loop for AS

[|Pressure volume loop and legend for AS]

Anesthetic Goals in AS
 * maintenance of adequate ventricular volume and sinus rhythm is crucial
 * Hypotension must be prevented, if it occurs it must be corrected promptly
 * It can lead to decrease in Coronary Perfusion and further hypotension
 * Avoid Bradycardia and Tachycardia
 * Bradycardia increases time in diastole but not SV (stiff ventricles). It is also a cause of hypotension
 * Ischemia
 * can be due to elevated LV vol. While LV vol is critical to preserve, sometimes nitroglycerine can be titrated for minimal reductions in LV vol to improve Coronary perfusion (CPP = Aortic Diastolic pressure - LVEDP)


 * __Aortic Insufficiency__**
 * results from either
 * Abnormal cusp AV cusp motion -OR-
 * Annular Dilation
 * If acute, then the cause is either:
 * 1) aortic dissection
 * 2) trauma
 * 3) bacterial endocarditis

//Pathophysiology of AI//
 * Fundamental principle is diastolic blood flow from aorta to Ventricle
 * Whereas in AS has primarily Pressure overload, AI has both Pressure **AND**Volume overload

Chronic AI Acute AI Pressure Volume Loop in Aortic Insufficiency
 * minimal change in pressure can lead to drastic changes in filling volume
 * Over time, Pressure and volume lead to eccentric hypertrophy
 * Despite enormous increases in LVEDV, LVEDP remains within normal limits
 * MVO2 (myocardial oxygen demand) does not increase greatly b/c work for muscle shortening is low
 * Unlike chronic AI, nml size ventricle is not accustomed to large volumes, so acute rise in LVEDP
 * Contractility becomes impaired as LVEDP rises
 * Severe CHF is the clinical cardinal sign
 * Compensatory mechanisms include tachycardia and peripheral vasoconstriction

[|Pressure Volume loop for AI and Legend] Anesthetic Goals in AI
 * 1) Main goal is to limit LV wall stress!
 * Full - maintain preload
 * Mildly vasodilated - with nitroprusside - promotes forward flow
 * Modestly Tachycardic (controversial) - heart rate probably does not affect forward or regurgitant flow
 * tachycardia allows less diastolic runoff into LV -> less wall tension
 * it also increases DBP, in turn increasing CPP and offsetting the increase in MVO2
 * Special considerations during Coronary Bypass
 * when crossclamping the aorta, normally cardioplegia is injected into aortic root and enters coronaries and produces diastolic arrest
 * with AI, Cardioplegia will regurgitate into LV, increasing wall tension and worsen ischemia. Therefore, Cardioplegia must be injected directly into coronary ostia

- causes:
 * __Mitral Valve Stenosis__**
 * Rhematic Fever (Rare in U.S) - chronic inflammation leads to valve damage decades after initial insult
 * Atherosclerosis associated mitral annular calcification

Pathophysiology
 * Progressive decrease in Mitral Valve area leads to an increased pressure gradient, and decreased LV filling (in turn reducing stroke volume)
 * LV dysfunction ensues because of increased afterload (reflex peripheral vasoconstriction) and from decreased SV (from preload).
 * Gorlin's Formula (rearranged):
 * LAP = LVDP + (flow / {K x MVA}) 2
 * flow or Cardiac output therefore is directly proportional to increases in left atrial pressure
 * Elevated LAP is reflected by upstream vasculature (pulm artery, right ventricle etc)
 * Once pulmonary HTN has developed, operative risk is now increased (12% v. 3-8%)



[|Mitral Valve stenosis pressure-volume loop and legend]

Anesthetic Goals in MS
 * Avoid tachycardia - pre-op B-blockers, and achieve depth of anesthesia to block adrenergic response
 * This is done to avoid increasing CO and therefore LAP which could lead to R heart failure, Pulm HTN, decreased LV filling which could inturn lead to hypotension
 * Prevent pulmonary vasoconstriction - avoid hypoxemia, hypercarbia and acidosis.
 * Hypotension - although Contractility is usually preserved in MV stenosis, it is usually prudent to pick a + inotrope such as ephedrine or epi because pure vasoconstrictors (phenylephrine) can cause pulmonary vasoconstriction. Moreover, Hypovolemia is often not the cause of hypotension in MV stenosis.