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Valvular Stenosis
Aortic Stenosis and Mitral Stenosis
| Question | Answer |
|---|---|
| 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
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