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Mitral Valve Disease

Mitral Valve Disease Lecture

Mitral Stenosis Abnormal thickening and restriction in mitral valve leaflet motion
Mitral regurgitation or insufficiency Abnormal retrograde flow across the valve
Combined valvular disease both mitral stenosis and regurgitation
What are the 3 basic forms of mitral valve disease? stenosis, regurgitation/insufficiency, combined valvular disease (both of the above)
Describe the structure of the normal mitral valve 2 leaflets (anterior and posterior), each divided into 3 segments. Each leaflet attached to papillary muscles by chordae tendinae; the junction between anterior and posterior leaflets with the valve annulus referred to as the commissures
What are the possible etiologies for mitral stenosis? congenital deformities, rheumatic valvular disease, dense mitral annular calcification, systemic disease (lupus, rheumatoid arthritis, carcinoid syndrome, etc), pseudo mitral stenosis
What is the most common cause of mitral stenosis? Rheumatic valvular disease
How does mitral annular calcification lead to stenosis? Calcification extends from the annulus to the leaflets, restricts leaflet motion
What is pseudo mitral stenosis? Mitral valve anatomically normal. Obstruction casued by extrinsic structure
How does rheumatic mitral stenosis arise? Long term sequelae from acute rheumatic fever
Rheumatic fever collagen vascular disorder which occurs following group A beta hemolytic streptococcal infections (strep throat); develops after several weeks after acute strep infection; involves joints, heart, CNS
What histological changes are seen rheyumatic fever? inflammation --> damage of collagen fibers + ground substance in connective tissue; thought to be mediated by cross reactivity of Ab against streptococcal membrane proteins and human tissue
How is rheumatic fever diagnosed? Modified jones Criterion (2 major criteria or 1 major and 2 minor criteria)
What are the major criteria in the modified jones criteion for the diagnosis of acute rheumatic fever carditis, polyarthritis, chorea, subcutaneous nodules, erythema margitanum
What are the minor criteria in the modified jones criteion for the diagnosis of acute rheumatic fever Arthralgia, fever, elevated ESR (erythrocyte sedimentation rate) or cRP (C-reactive protein), ECG: increased PR interval)
In rheumatic fever, how does carditis present? Can be myocarditis (inflammation of myocardium with ventricular dysfunction), pericarditis (inflammation of the pericardium with pericardial friction rub or effusion), or valvulitis (inflammation of the cardiac valves)
In rheumatic fever, how does polyarthritis present? Asymmetrical, migratory, polyarticular arthritis
In rheumatic fever, how does chorea present? Syndeham's chorea (aka St. Vitus's dance): choreiform activity with rapid uncoordinated, jerky movement of cae, hands, feet; thought to be caused by destruction of basal ganglions; resolves after several months of onset but may persist indefinitely
In rheumatic fever, how does sybcutaenous nodules present? Usually 0.5-2 cm movable, firm painless nodules which develop on extensor surfaces of joints, spinous processess and occiput
In rheumatic fever, how does erythema marginatum present? Evanescent (fading), erythematous (red), nonpruritic macular rash with serpinginous (creeping, wormlike) margins and clear center
Describe the changes in the heart + blood during the acute phase of rheumatic fever valve leaflet inflammation --> transient regurgitant murmurs and mid-diastolic murmurs (aka Carey-Coombs murmur) due to turbulent blood flow
Describe the changes in the heart + blood during the chronic phase of rheumatic fever progressive thickening + fibrosis of the mitral valve commissures, leaflets, and chordae leading to stenosis or a combination of stenosis and regurgitation
What would you expect to find on an echocardiograph of a patient with chronic rheumatic valvular disease? Abnormal thickening and calcification of the valve leaflets with restriction in leaflet excursion and thickening of the mitral subvalvular apparatus.
What event casues the c-wave? Mitral valve rebounds upon systole and deflects into left atrium, causing a deflection in the left atrial pressure tracing
What event is associated with the v-wave? Mitral valve reamins closed during systole-->as it fills (due to pulmonary venous inflow), pressure progressively rises
What even is responsible for the a-wave? Towards END of ventricular diastole, left atrial contraction occurs, creating a transient increase in lef-atrial pressure tracing
What hemodynamic changes do you see in patients with Mitral Stenosis? Transvalvular pressure gradient rises (due to decreased atrial outflow into ventricle)
What are the hemodynamic changes associated with chronic elevation in left aterial pressure on the rest of the cardiopulmonary system? Left atrium can't empty as well, and left atrial pressure rises to maintain forward flow to LV; Increased LA pressure --> pulmonary + RV hypertension + congestion-->reactive vasoconstriction in pre-capillary beds of lungs --> more RV enlargement
What symptoms do patients with mitral stenosis develop? Dyspnea and cough, orthopnea, chest pain, hoarseness, peripheral edema, fatigue, systemic thromboembolism
What symptoms of mitral stenosis develop as a result of pre-capillary block? Low CO: fatigue, exhaustion, weakness, tiredness; right sided failure edamn, hepatomegally, tricuspid insufficiency, cyanosis, large heart, mild jaundice, hoarseness
What symptoms of mitral stenosis develop as a result of post-capillary block? Dyspnea, orthopnea, pulmonary edema, hemoptysis, cough, left sided failure, small heart, pulmonary congestion, no edema
What auscoltatory findings would you find in patients with mitral stenosis? Mild: decresendo diastolic rumble (due to turbulence) with possible pre-systolic accentuation (due to atrial contraction); moderate: pan-diastolic rumble; progressive decrease in A2 to opening snap interval (OS not normally heard); soft S1, louder P2
What is the Gorlin formula? Square root (mitral valve pressure gradient) = (Cardiac Ouput) / (Mitral valve area * diastolic filling period * 44.3)
What conditions can lead to increased mitral valve gradients? Conditions that increased CO, higher heart rates (decrease diastolic filling period), increased catecholamine tone, and hyperthyroidism
How is mitral stenosis treated? Medical: volume management, rate control, and controlling coexisting medical conidtions. Surgical: percutaneous baloon valuloplasty, mitral valve commisurotomy, mitral valve replacement
Volume management of mitral stenosis Regulate oral fluid intake, restrict Na consumption; oral diuretics (furosemid); important in pregant women (increase in intravascular volume + CO)
Rate control management of mitral stenosis Rate control and (when possible) restoration of sinus rhythm; IMPORTANT for patients with tachyarrhytmias due to decrease in diastolic filling period and loss of atrial kick-->insufficient CO
How does percutaneous baloon valvuloplasty work? insert catheter into right atrium through venous sheath-->intratrial septum punctured using small needled catheter --> balloon on catheter advanced through to mitral valve area and inflated to increase area
Who are ideal candidates for balloon mitral valvuloplasty? younger patients with low valvuloplasty scores, no prior history of surgical commissurotomy, and no significant mitral regurgitation; provides good results (event free 5-7 years post procedure)
Mitral valve commissurotomy surgically separating mitral valve leaflets in regions of commissural fusion; done either on or off bypass
Mitral valve replacement With either mechanical (metallic) or bioprosthetic (porcine or bovine)valve
What are the etiologies for mitral valve regurgitation? Mitral valve prolapse, rheumatic valvular disease, endocarditis, dilated cardiomyopathy, cornoary ischemia, trauma, systemic diseases
How can mitral valve prolapse lead to mitral regurgitation? imperfect coaptation of the mitral leaflets
How can rheumatic valvular disease lead to mitral regurgitation? Fibrosis and tethering of the valve leaflets
How can endocarditis lead to mitral regurgitation? leaflet inflammation, obstruction of leaflet coaptation by large vegetations, or leaflet destruction in the form of flail leaflets, leaflet perforation and/or perivalvular abcessess
How can dilated cardiomyopathy lead to mitral regurgitation? dilation of the mitral valve annulus and/or apical displacement of the mitral leaflet coatpation poin due to enlargement of the ventricular cavity
How can coronary ischemia lead to mitral regurgitation? due to ischemically mediated papillary muscle dysfunction or (in infarction) papillary muscle rupture related to myocardial necrosis
How can trauma lead to mitral regurgitation? rupture of the papillary muscles
How can systemic disease lead to mitral regurgitation? Possible causes: carcinoid syndrome and collagen vascular diseases (cause fibrosis and deformity of the mitral valve)
Pathophysiology of acute Mitral Regurgitation Increased LV stroke Volume (with decrease forward flow and increased backward flow) --> increased LA pressure and increased pulmonary venous pressure (may cause pulmonary edema)
What changes do you expect to see in the left atrium with mitral regurgitation? Decrease LV end-systolic pressure, decreased LV systolic radius, decreased wall tension (Laplace's law), and increased extend and velocity of myofibril shortening
What changes are seen in pathophysiology of chronic MR? Left ventricular and atrial remodeling can occur to compensate --> eccentric ventricular hypertrophy --> increase in left ventricular volume; increased LV diastolic wall stress -->eccentric hypertrophy and left ventricular enlargement-->worse MR
What is the change you expect to see in the left-ventricular pressure-volume relationship in acute mitral regurgigration? insufficient time for remodeling --> compliance remains same --> left ventrcile responds to shift in loading conditions by shifting along FIXED pressure volume curve; if shift large enough --> pulmonary edema
What is the change you expect to see in the left-ventricular pressure-volume relationship in subacute mitral regurgigration? Rises less dramatically --> ventricular remodeling through eccentric hypertrophy --> increase in LV volume and compliance --> shifts patient to new left ventricular pressure-volume relationship --> chornic compensated phase of mitral regurgitation
What is the change you expect to see in the left-ventricular pressure-volume relationship in chronic mitral regurgigration? Left ventricle becomes increaseing dysfunctional during systole --> LV pressure rises --> congestive heart failure and CHRONIC DECOMPENSATED PHASE of mitral regurg.
What changes would you see in the atrial pressure curves in patients with mitral regurgitation? Prominent V-waves (simultaneous filling of LA from lung and contracting LV); rapid y-descent due to augmented antegrade flow (due to increased atrial preload)
What auscultatory findings would you find in patients with significant mitral regurgitation? Best heard in 5th intercostal space in anteroaxillary line + radiation into axilla: Pan-or holosystolic murmur (S1-->slightly beyond A2), early dystolic rumble (with possible S3); murmur location can vary based on direction of jet
What is the cause of mitral valve prolapse? Myxomatous degeneration of mitral valve with redundant leflets that are inappropriately elongated relative to ventricular diameter
What happens during mitral valve prolapse? Ventricle contracts --> redundant mitral valve leaflets bow/prolapse into atria --> inappropriate coaptation of leaflet tips
What auscultatory finding would you find in mitral valve prolapse? mid-to-late systolic click as the leaflets tense during prolapse; if leaflets don't coapt well-->mid-to-late systolic regurgitatn murur following systolic click
How does the position of the mitral valve click change with systole? Increasing left ventricular volume --> mitral valve click and murmur later in systole
How is mitral regurgitation treated? Relieve pulmonary vascular congestion (DIURETICS); reduce peripheral vascular resistance to augment forward blood flow (VASODILATORS or if critically ill, SODIUM NITROPUSSIDE); intra-aortic balloon; surgical repair or replacement of mitral valve
How does an intra-aortic baloon pump work and why does it help patients in cardiogenic shock? Percutaneous catheter based therapy; during diastole, IABP inflates, displacing blood in descending thoracic aorta in retrograde and antegrade direction, improving coronary perfusion; deflates in systole to facilitate foward flow
What is the definitive treatment for patients with mitral regurgitation? Surgical repair or replacement of mitral valve
What is the mechanism of action of sodium nitroprusside? Potent arteriolar vasodilator: metabolized into NO --> guanylate cyclase activation in vascular smooth muscle cells --> stimulates cGMP production, which promotes calcium reuptake from cytoplasm into endoplasmic reticulum --> smooth muscle relaxation
What are the advatages and disadvantages of using nitroprusside? Pro: short half-life, easily titrated; Con: cyanide is metabolic byproduct, so monitor CN if used over long period of time
Medical management of chronic mitral regurgitation focuses on: 1) diuretics to manage volume overload and 2) vasodilator therapy in patients with systemic hypertension (no definitive data on benefit of chronic vasodilator therapy in normotensive patients)
What are the surgical treatment options for patients with mitral valve prolapse? Mitral valve replacement (mechanical or bioprostetic); Mitral valve repair (avoids need for long term anticoagulation and minimiszed amount of prosthetic material implanted)
How is post-operative survival affected by LV ejection fraction? Postoperative survival decreases as LV function decreases.
When should a patient be recommended for mitral valve surgery? Rule of thumb: mitral valve surgery for patients with severe regurgitation PRIOR to patient developing significant symptoms or left ventricular dysfunction
Created by: karkis77



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