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Valvular Stenosis

Aortic Stenosis and Mitral Stenosis

QuestionAnswer
What are 3 ways to be diagnosed with Aortic Stenosis Congenital, Rheumatic Fever, Degenerative
What 3 deformities occur with rheumatic fever leading to AS Progressive cusp fibrosis, Fusion of aortic commissures, Valve calcification possible
Two degenerative diseases leading to AS Cusp fibrosis and calcification
When is AS considered to be critical When valve is 0.7 cm^2 or less
What is the normal aortic size 2.6-3.5 cm^2
What pressures do you look at to detect AS AS= LVs > AOs
What is the normal aortic pressure 120 / 80
What are hemodynamic effects of Aortic Stenosis High LV systolic and low aortic systolic pressures
Pullback Method Average of LV Systole and AO Systole used to determine gradient
When is the Pullback Method not accurate? In the presence of ectopy or catheter whip at point of pullback
What are AS systolic effects on the heart LV hypertrophy (thickening of wall without increasing diameter of chamber) occurs in chronic state
What does decreased perfusion result in increased preload and systemic afterload
What is effect of AS on coronary perfusion? Decreased perfusion. Coronary arteries take off from each side of the aorta.
Aortic stenosis effect on O2 supply/demand Increased demand and decreased supply. Heart is trying to compensate
AS effect on pulmonary afterload Increase in ventricular afterload, a decrease in stroke volume, and an increase in end-systolic volume.
What happens when afterload increases There is an increase in end-systolic volume and a decrease in stroke volume.
What is Afterload The "load" (resistance) that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure
Frank-Starling Law The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. The greater the stretch the greater the contraction.
Systolic effects of valvular heart disease ***LOCO*** Low cardiac output/ low stroke volume * Syncope * Increased systemic afterload (increased resistance)
Diastolic effects of valvular heart disease Increased preload * Dyspnea * Heart Failure * Pulmonary edema * Pulmonary effusion * Murmurs * Lower extremity edema * Hypertrophy, dilatation
What can occur with A-fib in Valvular Heart Disease Sudden cardiac death
Two methods to measure AS Pullback and Simultaneous
Simultaneous Method Direct evaluation of AO and LV systole using either LV/AO or LV/FA (femoral artery)
If you are to use the LV/FA in the simultaneous method to measure AS, what must you first determine Determine difference between AO and FA, then factor in the gradient when measuring LV/FA
What gradient is used to measure AS in the Simultaneous Method Peak-to-peak, not average (mean) gradient
If you encounter ectopy when determining AS gradient, which method would you use to avoid error Simultaneous Method
How many transducers needed to measure AS in the Simultaneous method Two
Which treatment is optimal for AS Surgical. AO valve repair or replacement. Aortic Commissurotomy
What percutaneous replacement for AS is now approved by FDA Bovine valve on stent
Which provides better long term results? Cardiac Catheterization intervention or surgical valve repair Surgical. AOV Repair or replacement.
What is the final outcome if AS not treated and becomes critical? Sudden death syndrome
Left ventricular systolic pressure greater than aortic systolic pressure Aortic Stenosis
When does stenosis show When valves are open
What is the primary cause of MS Rheumatic fever
What are some causes for MS Congenital defects, calcium accumulation in the mitral annulus and degeneration
When is mitral valve area considered critically tight 1.0 cm^2 or less
What is the normal size of the MV 4-6 cm^2
Factors determining hemodynamic effects of MS *Severity of obstruction, the tighter the valve the greater the effect. ** Heart rate and rhythm (development of A-Fib likely) *** Severity of secondary pulmonary factors such as pulmonary vascular resistance
Decreased mitral valve area results in Increased LA pressures and LA enlargement
Increased right heart pressures in later stages Dyspnea and pulmonary edema
Effect of MS Decreased LV preload, decreased SV and decreased CO
If cardiac output decreases what subsequently happens to afterload increase in systemic afterload
HR increases in MS as a compensatory factor Exacerbates problem by increasing LA pressures
Treatment of MS Medical, Surgical, and Cath lab
What would constitute medical treatment for MS *Anti-coagulation ** Diuretics *** Avoid exercise (no CO available-using up more O2 than supply available) ****Improve contractility
Surgical treatment of MS **Mitral commissurotomy (cut open leaflets) ***Replacement of MV (open heart surgery)
Cath lab treatment of MS Mitral valvuloplasty - balloon inflated to tear commissures open
What hemodynamic pressures would you look at to determine MS? PCW Mean and LVEDP. These numbers should be =
PCW Mean not equal to LVEDP MS
Created by: CVTMom