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Valvular heart lesions
This document provides a summary of various valvular heart lesions including: 1. Mitral stenosis causes narrowing of the mitral valve and leads to left atrial and pulmonary hypertension. Symptoms include dyspnea and right heart failure. 2. Mitral regurgitation results in blood flowing back to the left atrium, causing left atrial and ventricular enlargement. Symptoms develop later and include fatigue and cardiac cachexia. 3. Aortic stenosis narrows the aortic valve and increases left ventricular pressures, causing hypertrophy and later heart failure. Symptoms include exertional dyspnea and angina.
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Valvular heart lesions
- 1. A S YN O P S I S VALVULAR HEART LESIONS
- 2. MITRAL STENOSIS (MS) •Normal 4-6 cm2 • Stenosis <4 cm2 • Symptoms <2 cm2 • Severe stenosis <1 cm2 • Causes:- • Rheumatic heart disease • Calcification • Congenital • Lutembacher’s syndrome (acquired MS+ASD) • Carcinoid tumour metastases
- 3. MS • Pathophysiology:- • LAoutlet obstruction • LA pressure ↑, LA dilatation • LV filling ↓, dependent on LA contraction • Symptoms:- • ↑ing DoE, haemoptysis, cough, chest pain(Pulm cong, PAH) • Fatigue, pedal edema, ascites (Rt sided HF) • Palpitation (AF) • Systemic embolism:- CVA, Renal, Mesenteric, Peripheral ischaemia
- 4. MS EXAMINATION • Signs:- •Malar flush (AV anastamoses, venous stasis) • JVP ↑ (RVH, TR, PAH) • Pulse – SR, low volume, AF • Apex – localized tapping • RV – heaving, sustained (PAH, RVH) • Loud palpable S1, opening snap, loud P2 (PAH) • Mid-diastolic, rough, rumbling apical murmur + presystolic accentuation • Graham Steele – EDM (func PR)
- 5. MS INVESTIGATIONS • CXR:- •Enlarged LA • PVH, PAH, pulm edema • Calcified mitral valve • ECG:- • Bifid P (P mitrale) • RVH – RAD, tall R V1 • ECHO:- • Mitral valve – area, severity, calcific, mobility • PR, TR • Atria – size, LA thrombus • Ventricles – size, function • CAG – prior to MVR
- 6. MS TREATMENT • Diuretics(HF) • Digoxin, β-blocker, CCB, anticoag (AF) • Rheumatic fever prophylaxis • IE prophylaxis • Surgery – medical fails/not feasible • Trans-septal balloon valvotomy • Closed valvotomy • Open valvotomy • MVR
- 7. MITRAL REGURGITATION (MR) •Abnormality of:- • Valve leaflets • Valve annulus • Chordae tendinae • Papillary muscles • Left ventricle • Pathophysiology:- • Part of stroke vol back to LA • LA overload • CO ↓
- 8. MR • Acute:- • Largevol back to LA, acute LA press ↑ • PVH, pulm edema • Next LV enlarges, maintain stroke vol & CO • Chronic:- • LA dilates, LA press N/slight ↑ • Less PVH & pulm edema
- 9. MR CAUSES • Myxomatousvalvular degeneration • Ischaemic HD • Rheumatic HD • Infective endocarditis • DCM, HCM • Autoimmune – SLE • Collagen vascular – Marfan’s, Ehler Danlos • Congenital – 1o ASD • Drugs – Fenfluramine, cabergoline
- 10. MR SYMPTOMATOLOGY • Slowprogress – No symp for years • Sense forceful heartbeat - ↑ stroke volume • Fatigue, lethargy, cardiac cachexia - ↓ CO • Dyspnoea, orthopnoea –PVH, a/c pulm edema • Later – dyspnoea, ascites, pedal edema, ↑ JVP, palpitation (RVH, PAH, AF) • Sub a/c IE – PUO
- 11. MR EXAMINATION • Pulse:- •AF • SR, N/low volume • Apex:- • Forceful • Systolic thrill • Auscultation:- • S1 soft, S3+ • Apical PSM. Radiating to axilla • JVP ↑ if RV failure
- 12. MR INVESTIGATION • CXR:- •Cardiomegaly, LA & LV enlarged, valve calcific • ECG:- • AF, SR, bifid P mitrale, LVH • ECHO:- • LA & LV dilated • Valve leaflet motion • Papillary muscle anatomy & function • Regurg jet direction, severity
- 13. MR TREATMENT • MildMR – asymp – conservative • Vasodilators - ↓ pre & afterload • Diuretics – HF • Anticoag, antiarrhythmics – AF • β blockers – atrial arrhythmia • ICD – vent arrhythmia • Endocarditis prophylaxis • Symptomatic = Sx (prevent LVD) • MV repair – Sx, clip • MV replacement
- 14. BARLOW’S SYNDROME (MVP) •Pathophysiology:- • Large leaflet/ annulus • Long chordae • Papillary muscle dysfunction • Seen max in young females • Associations:- • Marfan’s • Thyrotoxicosis • RHD, IHD, ASD, HCM • Findings – early systolic click, PSM +/-
- 15. AORTIC STENOSIS (AS) •LV outflow obstruction • Causes:- • Calcific degeneration – elderly, male, DM, HTN, DLP • Congenital bicuspid vlave • Rheumatic HD • Misc – • CKD • Paget’s of bone • Radiation • Familial hypercholesterolemia
- 16. AS PATHOPHYSIOLOGY • LVemptying obstructed • LV pressures ↑ • LV hypertrophy (press overload) • LV ischaemia – angina, arrhythmia, HF • Exertion – • CO rises very little • Worsens angina and fatigue • Syncope/presyncope • Later LA press ↑, PVH = dyspnoea
- 17. AS SYMPTOMS • WhenAV area <⅓ normal • Exertional symptoms • Angina = 4 years • Syncope = 3 years • Dyspnoea = 2 years • Heart failure = 1.5 years • Cachexia, fatigue = end-stage
- 18. AS EXAMINATION • Pulse– SR, low vol, slow rising (parvus et tardus) • Apex – undisplaced, heaving • Aortic area – systolic thrill • Auscultation:- • Ejection click • Soft A2, reversed split +/- • S4 • Systolic, low pitched, ejection (crescendo-decrescendo) murmur – aortic area, radiating to carotids
- 19. AS INVESTIGATION • CXR:- •Cardiac size N, HF = cardiomegaly • AV calcification • Dilated ascending aorta • ECG:- • SR, Vent arrhythmia • LVH + strain = ST ↓, T ↓, Left leads • ECHO:- • AV area, calcific, jet velocity, severity • LVH, dysfunction • Aorta dilatation • MRI/CT:- • Aortic aneurysm, dilatation, coarcation
- 20. AS TREATMENT • Asymptomatic:- •Regular follow-up ECHO • IE prophylaxis • Valvotomy:- • Buys time, improves LV temporarily • Childhood, adolescents mainly • Surgery:- • Symptomatic • Aorta gross/rapidly progressing dilatation • AV replacement – open, percutaneous
- 21. AORTIC REGURGITATION (AR) •Pathophysology:- • Blood ejected into aorta in systole • Leaks back into LV in diastole • DBP ↓ • LV volume overload • ↑ Stroke vol to maintain effective CO • LV dilatation, later dysfunction
- 22. AR CAUSES • Acute:- •Rheumatic fever • Infective endocarditis • Aortic dissection • Rupture sinus of valslva • Prosthetic valve failure • Chronic:- • Rheumatic heart disease, syphilis, HTN • Bicuspid valve, valve calcification, subvalvular VSD • Arthritides – reactive, ankylosing spondylitis, rheumatoid • Marfan’s, osteogenesis imperfecta
- 23. AR SYMPTOMS • Latein disease, when LV fails • Pounding of heart • ↑ Stroke volume & force of contraction • Angina • DoE • Arrhythmias +/-
- 24. AR EXAMINATION • Pulse:- •SR, large vol, collapsing • Water hammer/Corrigan’s pulse • BP:- • SBP ↑, DBP ↓ • Wide pulse pressure • Apex:- Displaced down & out (LV dilatation) • Sounds:- • High pitched EDM at Lt sternal border • ESM at aortic area, radiating to carotids • MDM at apex (Austin-Flint)
- 25. AR PERIPHERAL SIGNS •Light-house – Flushing & blanching forehead • Landolfi’s – Pupillary size alternation • Becker’s – Retinal artery pulsation • De Musset’s – Head nodding • Muller’s – Uvula pulsation • Corrigan’s – Dancing carotids • Quincke’s – Capillary pulsation in nails • Locomotor brachii • Rosenbach’s – Liver pulsations • Gerhardt’s – Spleen pulsations • Traube’s – Pistol shot sounds over femorals • Duroziez’s – Systolic & diastolic murmurs over femorals • Hill’s – SBP popliteal>brachial
- 26. AR INVESTIGATIONS • CXR:- •LVH • Ascending aorta dilatation & calcification • AV calcific • ECG:- LVH • Tall R & deep T ↓ in left side leads • Deep S right side leads • ECHO:- • Dilated aortic arch • LV – dilatation, dysfunction • Severity of AR • TEE – Aortic valve & aortic root • MRI & CT – Assess thoracic aorta & root
- 27. AR TREATMENT • Rxfor specific cause • A/c AR – vasodilators, inotropes • LV dysfunction – ACEi • Surgery:- • Before LVD sets in – not completely reversible • Before significant symptoms develop • A/c severe AR • Symptomatic c/c severe AR • LVD present • LV dilatation present • Along with other cardiac Sx
- 28. TRICUSPID STENOSIS (TS) •Uncommon • Women > men • Associated mitral & aortic valve disease • Causes:- • RHD • Carcinoid • Pathophysiology:- • RA emptying impaired, CO ↓ • RA press ↑ • Venous congestion (↑JVP, hepatomeg, ascites, pedal edema)
- 29. TS • Symptoms:- • Abdpain + swelling • Pedal edema • Left sided failure symptoms • Signs:- • ↑ JVP, pedal edema • Pulsatile liver, hepatomegaly • Rumbling MDM @ lower LSE, louder on inspiration • Tricuspid OS
- 30. TS INVESTIGATIONS • CXR:- •Prominent right atrial bulge • ECG:- • Peaked, tall P waves (>3 mm) in lead II (RAE) • ECHO:- • Thickened & immobile tricuspid valve
- 31. TS TREATMENT • Medical:- •Diuretic therapy • Salt restriction • Surgical:- • Tricuspid valvotomy • Tricuspid valve replacement is often necessary • Other valves usually also need replacement
- 32. TRICUSPID REGURGITATION (TR) •RA pressure overload • Causes:- • Functional- • RV dilatation • Cor pulmonale, MI, pulmonary HTN • Organic- • RHD • IE • Carcinoid syndrome • Congenital - Ebstein’s anomaly
- 33. TR • Symptoms:- • Rightheart failure • Signs:- • Large jugular venous c & v waves • Hepatomegaly + pulsates in systole • Lt parasternal heave (RVH) • Blowing PSM @ LSE, best heard on inspiration • AF common • ECHO:- • Dilated RV • Thickened tricuspid valve
- 34. TR TREATMENT • Functional– Medical Rx • Severe organic:- • TV repair – plasty, plication • TV replacement
- 35. PULMONARY STENOSIS (PS) •Causes:- • Congenital – most common (isolated, ToF) • RHD • Carcinoid • Pathophysiology:- • RV press overload • RVH, then RAH • Rt heart failure
- 36. PS • Symptoms:- • Mild– asymptomatic • Moderate – fatigue, syncope, dyspnoea +/- • Severe – incompatible • Signs:- • JVP – prominent a wave • Lt parasternal heave • Delayed, soft P2 + pulmonary ejection click • Harsh midsystolic ejection murmur @ 2nd Lt ICS, best heard on inspiration, thrill + • RV S4
- 37. PS • Investigations:- • CXR:- •Prominent pulmonary artery • ECG:- • RAH – Tall P right leads • RVH – Tall R right leads • ECHO:- • Doppler – stenotic flow • RVH • RA hypertrophy/enlargement • Treatment:- • Pulmonary valvotomy (balloon,direct surgery)
- 38. PULMONARY REGURGITATION (PR) •Most common acquired pulm valve defect • Pulm HTN most common cause (annular dilatation) • Decrescendo diastolic murmur • No symptoms • Treatment rarely needed