Mitral Valve Diseases PDF

VALVULAR HEART DISEASE By Dr.ibrahim A.elhamid MD lecturer of cardiology MUST Intended learning objectives : Discuss the common etiologies of valvular stenosis and regurgitation. Recognize the signs and symptoms of valvular mitral stenosis and regurgitation which progres...

VALVULAR HEART DISEASE By Dr.ibrahim A.elhamid MD lecturer of cardiology MUST Intended learning objectives : Discuss the common etiologies of valvular stenosis and regurgitation. Recognize the signs and symptoms of valvular mitral stenosis and regurgitation which progress and increase with increased mitral valve lesions Be able to quickly, diagnose and treat acute mitral regurgitation or mitral stenosis and identify complications Identify patients who should be referred for surgical replacement of their valves and how to follow up after MVR OVERVIEW Mitral Stenosis Mitral Regurgitation Acute and Chronic  Pathophysiol Physical Etiology ogy Exam Natural Testing Treatment History  Definition: Obstruction of LV inflow that MITRL prevents proper filling during diastole STENOSIS Normal MV Area: 4-6 cm2 OVERVIEW Transmitral gradients and symptoms begin at areas less than 2 cm2 Rheumatic carditis is the predominant cause Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.  ETIOLOGY OF MITR AL STENOSIS Organic Rheumatic heart disease: 77-99% of all cases Infective endocarditis: 3.3% Mitral annular calcification: 2.7%  ETIOLOGY OF MITRAL STENOSIS Functional During rheumatic activity (Carey coomb’s murmur) Severe AR (Austin flint murmur) the reurgitant blood interfere with the full opening of the mitral valve. VSD (over blood flow across the mitral valve)  MS PATHOPHYSIOLOGY Progressive Dyspnea (70%): LA dilation  pulmonary congestion (reduced emptying) worse with exercise, fever, tachycardia, and pregnancy Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. Right heart failure symptoms: due to Pulmonary venous HTN Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure  NATURAL HISTORY OF MS Disease of plateaus: Mild MS: 10 years after initial RHD insult Moderate: 10 years later Severe: 10 years later (1.5 cm2 or less) Is there tight MS? Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism. Clinical picture symptoms symptoms of pulmonary venous congestion: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, hemoptysis, recurrent chest infections Symptoms of low cardiac output: dizziness, easy fatigue, muscle weakness, oliguria, cold extremities Symptoms of systemic venous congestion: when??? lower limb swelling, dyspepsia, right hypochondrial pain  Chest pain ( with severe PH) hoarseness of voice : due to compression of the left recurrent laryngeal nerve by greatly dilated left atrium (Ortner syndrome)  Signs General - Malar flush -PVC: bilateral fine basal crepitations. - Low COP: Low SBP, weak pulse volume, pallor, peripheral cyanosis, cold extremities - SVC: congested neck veins (prominent a wave), tender hepatomegaly, lower limb edema - AF may occur  prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in PHYSICAL advanced disease EXAM FINDINGS Mitral facies: When MS is severe and OF MS the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks (malar flush)  Local inspection and palpation - Stage of PVC: diastolic thrill on apex (in left lateral position) palpable S1 - stage of PH: pulsating pul. Area palpable S2 (pulmonary hypertension) accentuated P2 & narrow splitting of S2 left parasternal heave ( dilated right ventricle)- - Graham steel murmur: early diastolic murmur of pulmonary regurgitation at left sternal border Stage of right sided failure: - S3 gallop on the tricuspid area - murmur of functional TR on the tricuspid area  Auscultation: - Accentuated S1: Caused by : rapidity with which left ventricular pressure rises at time of mitral valve closure wide closing excursion of the leaflets. Opening snap (OS): Due to opening of rigid mitral valve Most audible at the apex value: - Diagnosis of organic MS, - Pliable MV - It is absent in calcified MS, - A2-OS interval varies in severity of MS (short A2-OS interval indicates severe MS)  HEART SOUNDS IN MS Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex. Heard best with the patient lying on the left side in held expiration using the con Intensity of the diastolic murmur does not correlate with the severity of the stenosis  HEART SOUNDS IN MS Loud S1, Opening snap heard at the apex when leaflets are still mobile Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips. A shorter S2 to opening snap interval indicates more severe disease. - Murmur of mitral stenosis: low pitched rumbling mid diastolic murmur with presystolic accentuation best heard at the apex with the bell of the stethoscope and with the patient in the left lateral position  EVALUATION OF MS ECG: may show atrial fibrillation or LA enlargement CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area Transesophageal echocardiography ATRIAL FIBRILLATION Left atrial enlargement Right atrial enlargement  Serial echocardiography: Mild: 3-5 Moderate:1-2 Severe: yearly years years Managem ent of MS Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression b-blockers, CCBs, Digoxin which control heart rate and hence Duiretics for fluid prolong diastole for overload improved diastolic filling  MANAGEMENT OF MS Identify patient early who might benefit from percutaneous mitral balloon valvotomy. IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures. SIMPLIFIED INDICATIONS FOR MITRAL VALVE REPLACEMENT ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms Asymptomatic moderate or Severe MS with a valve not suitable for PMBV Feed back quiz 1 The intensity of the murmur is not correlated with the severity of MS First symptoms to show up are systemic venous congestion AF complications is not uncommon one with MS MITRAL REGURGITATI ON CHRONIC MITR AL R EGURGITATION OV ERVIEW Definition: Backflow of blood from the LV to the LA during systole Mild (physiological) MR is seen in 80% of normal individuals.  ACUTE MR Endocarditis Acute MI: Malfunction or disruption of prosthetic valve  Myocardial infarction: Cardiac cath or thrombolytics Management of Acute MR Most other cases of mitral regurgitation is afterload reduction: nitroprusside, even in the Diuretics and setting of a nitrates normal blood pressure. MANAGEMENT OF ACUTE MR Do not attempt to alleviate tachycardia with beta- blockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.  Balloon Pump T R E AT M E N T O F Nitroprusside even if ACUTE MR hypotensive Emergent Surgery  Myxomatous degeneration (MVP) ET I O L O G I E S O F C H RO N I C Ischemic MR MITRAL R E G U RG I TAT I O N Rheumatic heart disease Infective Endocarditis PATHOPHYSIOLOGY OF MR Pure Volume Overload Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension. Progressive left ventricular volume overload leads to dilation and progressive heart failure. PHYSICAL EXAM FINDINGS IN MR Auscultation: soft S1 and a holosystolic murmur at the apex radiating to the axilla S3 (CHF/LA overload) In chronic MR, the intensity of the murmur does correlate with the severity. Exertion Dyspnea: ( exercise intolerance) Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation THE NATURAL HISTORY OF MR Compensatory phase: 10-15 years Patients with asymptomatic severe MR have a 5%/year mortality rate Once the patient’s EF becomes