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Bedside Assessment of Valvular Lesions
- 1. Bedside Assessment of the Severity of Valvular Lesion Samir Poudel MD(Internal Medicine), DM(Cardiology) Asst. Prof. of Cardiology NAMS, Bir Hospital
- 2. Outlines Introduction Severity of Individual Valvular Lesions Assessment of Dominance in combined valvular lesions Clinical Assessment of LV Function How to write the Diagnosis
- 3. Multivalvular Heart Disease Examiner Examinee
- 6. Prevalence of Valvular Lesions Patterns of anatomic/hemodynamic combinations of valve lesions C.N. Manjunath, P. Srinivas, K.S. Ravindranath, C. Dhanalakshmi,Incidence and patterns of valvular heart disease in a tertiary care high-volume cardiac center: A single center experience,Indian Heart Journal,Volume 66, Issue 3,2014,Pages 320-326,ISSN 0019-4832,
- 7. Systematic, etiology-specific analysis of various combinations of lesions 17 70 26 1835 1046 918 12 34 96 11 3 42 538 226 4 14 1 10 100 1000 10000 MS+MR MS+AR MR+AR AS+AR MR+AS MS+AS Congenital Rheumatic Degenerative Post-Surgical 26.5% 23.2% 46.6% 0.3% 0.8% 2.4% C.N. Manjunath, P. Srinivas, K.S. Ravindranath, C. Dhanalakshmi,Incidence and patterns of valvular heart disease in a tertiary care high-volume cardiac center: A single center experience,Indian Heart Journal,Volume 66, Issue 3,2014,Pages 320-326,ISSN 0019-4832,
- 8. Etiology Significant stenosis at multiple valves are usually Rheumatic Significant regurgitation at multiple valves are likely Non- Rheumatic Significant stenosis and regurgitation together are usually Rheumatic Quadrivalvular disease is most likely due to combination of causes – congenital , rheumatic, infective, degenerative disease A unitary cause for quadrivalvular disease is either rheumatic or myxomatous degeneration
- 9. Global Prevalence of RHD
- 10. Age-wise Involvement of Valve in RHD Distribution of valvular heart lesion classifications among cases of rheumatic heart disease (n=83). Data shown as raw frequencies with percentages (n (%)), both overall and age stratified Copyright © Asia Pacific Heart Association, British Cardiovascular Society & BMJ Publishing Group Ltd. All rights reserved.
- 11. Age and Sex- wise distribution of Rheumatic Mitral Stenosis cases C.N. Manjunath, P. Srinivas, K.S. Ravindranath, C. Dhanalakshmi; Incidence and patterns of valvular heart disease in a tertiary care high-volume cardiac center: A single center experience,Indian Heart Journal,Volume 66, Issue 3,2014,Pages 320-326,ISSN 0019-4832,
- 14. Prevalence of RHD in Nepal
- 15. Progression from pharyngitis to chronic rheumatic heart disease https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.114.009857
- 17. Distribution of cases with pulmonary hypertension C.N. Manjunath, P. Srinivas, K.S. Ravindranath, C. Dhanalakshmi,Incidence and patterns of valvular heart disease in a tertiary care high-volume cardiac center: A single center experience,Indian Heart Journal,Volume 66, Issue 3,2014,Pages 320-326,ISSN 0019-4832,
- 18. Symptoms Correlation Angina---------------------------à AS Syncope--------------------------à AS Hemoptysis----------------------à MS Palpitation-----------------------à AR Prominent Pulsations-----------------------à AR/TR Head nodding----àAnteroposterior: AR Lateral: TR
- 19. Mitral Stenosis ØExertional dyspnoea – 1st and most common symptom v5-10 yrs from ARF to symptoms (15-20 yrs in western population) vProgresses over 3-5 yrs from NYHA II to IV(5-10 yrs in western population) ØPND ØOrthopnea ØHemoptysis ØSystemic embolism ØRVF
- 20. Severe MS Diastolic Thrill A2-OS gap- shorter Prolonged diastolic murmur Pulmonary hypertension Congestive Heart failure Cardiomegaly-RV dilatation
- 21. Pulmonary HTN Prominent parasternal heave Palpable P2 Palpable pulmonary artery pulsation Pulmonary ejection click Graham Steel murmur Prominent a wave in JVP If patient has developed significant TR--à CV wave in JVP/ Obliteration of X-descent/Prominent Y-descent
- 22. Mitral Regurgitation • Long asymptomatic period – 10-20 yrs from ARF to symptom (A decade longer than MS) • History Once severe MR – Symptomatic within 6-10 yrs Symptoms herald LVSD or AF – Rapid decline in survival Chronic weakness/Fatigue/Exercise Intolerance Dyspnoea – less common and late
- 23. Severe MR Hyperdynamic LV type apex Functional flow mid diastolic murmur S3 Wide split S2 Pulmonary Hypertension Congestive Heart failure Cardiomegaly
- 24. Mitral Regurgitation with- • Acute severe MR • Associated significant aortic valve disease S4- • MVP with holosystolic murmur • Significant MS with pliable leaflets Loud S1-
- 26. Acute Severe MR Normal-sized LA Normal or reduced LA compliance LA pressure rises abruptly: • Pulmonary edema • Marked elevation of pulmonary vascular resistance • Right-sided heart failure
- 27. Acute Severe MR Murmur may be decrescendo rather than holosystolic, ending well before A2 Lower pitched and softer than the murmur of chronic MR A left-sided S4 frequently is found • Increased intensity of P2 • Murmurs of pulmonary regurgitation and tricuspid regurgitation • A right-sided S4 Pulmonary hypertension: V wave is markedly elevated A v wave (late systolic pressure rise) in the pulmonary artery pressure pulse may rarely cause premature closure of the pulmonary valve----> an early P2, and paradoxical splitting of S2
- 28. Mitral Valve Prolapse • Mid-systolic click- a high-pitched sound • Multiple clicks can be heard as different parts of the mitral leaflets prolapse at different times of systole • The clicks of MVP happen after the beginning of the upstroke à ØAortic ejection click occurs with the beginning of the carotid pulse upstroke
- 29. Mitral Valve Prolapse • The clicks are often but not always followed by a mid or late systolic murmur • The duration of the murmur usually corresponds with the severity of MR • When the murmur is restricted only to the later part of the systole, MR is not severe • • As the MR progresses, the systolic murmur becomes holosystolic
- 30. Mitral Valve Prolapse Physical findings in MVP vary significantly from patient to patient as well as in the same patient at different times Some patients can present with both mid-systolic click and murmur Others with either one of them The same patient can have only a click at one time and a murmur at another time, both on another occasion and no abnormality at another time Mid-systolic click can happen in tricuspid valve prolapse and also in atrial septal aneurysm
- 31. Murmur of MVP: Effect of Maneuvers Prolongs/ Increase in Intensity Systolic click and murmur will move towards the first sound and the murmur will become longer Cause the mitral valve leaflets to prolapse earlier in systole Anything that decreases the left ventricular volume Decreased venous return Tachycardia Increased myocardial contractility Reduced afterload Shortens/ Decrease in Intensity Will delay the onset of click and murmur Anything that increases the left ventricular volume Increased venous return Increased afterload Decreased myocardial contractility Bradycardia
- 32. The intensity and duration of HCM murmur increases after a premature ventricular beat compared to MVP murmur where the intensity decreases or remains unchanged
- 33. Murmur of MVP • Not infrequently, the murmur of mitral valve prolapse is holosystolic (either spontaneously or following interventions to decrease left ventricular volume) • Such a murmur: ØGenerally retains a medium pitch ØMay radiate to the axilla ØMay reach an intensity of grade 5 or 6 ØMay have a musical whooping or honking quality.
- 34. Aortic Stenosis History v Long asymptomatic period – 10-20 yrs from ARF symptoms (a decade longer than MS) v 10-15 yrs from Mild to Severe AS v Once severe AS – Symptomatic within 2 yrs Symptoms – Rapid decline in survival : 6mth Afib/2yr HF/3yr Syncope/5yr Angina ØExercise intolerance and dyspnoea – most common ØExertional Angina ØExertional Presyncope (> than Syncope)
- 35. Severe AS Pulsus parvus et tardus Apico-carotid delay Thrill Paradoxical split S2 Longer and late peaking of systolic murmur LV S4 in youngs < 40 years LV dysfunction (S3 / Short and soft AS murmur) Pulmonary hypertension Congestive Heart failure Cardiomegaly
- 36. In Severe AS SBP/Pulse pressure is low In elderly, SBP can be >160mmHg because of high PVR SBP>200mmHg almost exclusively rules out Severe AS If the murmur becomes soft and sort-> LV dysfunction
- 37. Aortic Regurgitation Longer asymptomatic period • – After ARF • – After development of AR Once symptomatic – Course is similar to AS Exercise intolerance and dyspnoea – Most common Palpitations – exertional and resting – even painful – may precede other symptoms by months-yrs Nocturnal (and exertional) angina
- 38. Severe AR High volume collapsing pulse Narrowly split S2 Longer duration of diastolic murmur Austin Flint murmur Displaced apex Hill’s Sign >60 mmHg LV S3 Pulmonary HTN
- 39. LV Dysfunction in Severe AR Soft S1 S3 Presystolic component of Austin Flint murmur disappears
- 40. Fate of Severe AR Severe AR LV Dysfunction @ 6%/yr Symptomatic @ 25%/yr Mortality @ 10%/yr
- 41. Tricuspid Regurgitation Functional TR is more frequent than organic TR and is due to severe Pulmonary hypertension Severe organic TR is almost always due to rheumatic origin 10.4% of RHD cases had TR(C.N. Manjunath et al) Severe organic TR coexists with Mitral or Aortic valve disease Common features of RHF- Edema, Ascites, tender hepatomegaly
- 42. Tricuspid Stenosis Never solitary but very rare: 0.3% involvement in RHD series (C.N. Manjunath et al) Almost exclusively (~90%) seen with rheumatic MS RVF – (Tender hepatomegaly, ascites, anasarca) – without disabling dyspnoea Fatigue/Exercise intolerance more prominent than dyspnoea – d/t low CO
- 43. Severe PS • Prominent a-wave in JVP • Left parasternal heave (if IVS is intact) • Systolic thrill in 2nd left intercostal area with radiation upwards and to the left • Long late-peaking ejection systolic murmur extending beyond A2 which is often inaudible
- 44. Severe PR Causes: • Usually 2ndary to pulmonary HTN (High pressure PR) • Congenital pulmonary valve regurgitation – Uncommon • Post-op TOF with transannular patch- Frequent Palpable pulmonary artery Parasternal pulsations
- 45. Diastolic Murmur of Low- pressure PR • Low-medium frequency • Crescendo-decrescendo • Starts slightly after P2 • Short in duration • Occasionally louder in inspiration • Parasternal heave is unusual
- 46. Diastolic Murmur of High Pressure PR • Higher pitched • Starts immediately after P2 • P2 is loud and often palpable • Constant vascular pulmonary ejection click is present • Left parasternal heave (in intact IVS) • Long and even pan-diastolic decrescendo murmur • Doesn’t show respiratory variation
- 47. Non valvular factors that modify/precipitate presentation Associated arrhythmias –atrial fibrillation etc. Infective endocarditis Rheumatic activity Volume overload states – Anemia, Worsening Renal failure, Dietary non- compliance Pressure overload states – Uncontrolled HTN Thyrotoxicosis, and other high output states Ischemia(CAD) Respiratory illness Altitude Pregnant status –regurgitant lesions generally tolerated better SIRS – Infection: most common Pneumonia
- 48. Presentation of Multivalvular Lesions • Severity and chronicity of individual lesions • Hemodynamic and pathophysiological influences of one lesion on the other • Proximal versus distal effect • Generally proximal lesions tend to influence distal lesions more , than vice versa • Cardiac output and ventricular function • Associated cardiac conditions –e.g. ASD + MS • Systemic factors
- 49. General Rules for Multivalvular Lesions Severe lesion dominate Proximal lesion dominate Lesions not always additive
- 50. Multivalvular Heart Disease- In Practice Scant data and guidelines Classical symptoms and clinical findings may be masked/modified Assessment of ‘dominance’ of a lesion has great therapeutic implications
- 51. JVP BP Pulse Apical Impulse Thrill Parasternal Heave Heart Sounds Murmurs Added Sounds Assessment of Severity of Lesions
- 52. Severity of PAH Severity of PVH
- 53. Combined MS + MR Parasternal heave - prominence Apical impulse - prominence Apical MDM Apical PSM
- 54. Combined MS+MR Dominant MS • Pulmonary symptoms • Parasternal lift – early systolic & brisker • Tapping apical impulse • S1 - loud • OS • MDM/LDM Dominant MR • Easy fatigability • Parasternal impulse- slower & late systolic • Hyperdynamic apical impulse • S1 - soft • S3 • Pansystolic murmur As in patients with mixed aortic VHD, the peak transmitral velocity, mean gradient, or mitral velocity-time integral may provide an assessment of the overall severity of the mixed mitral VHD
- 55. Combined MS+AS: This infrequent combination is usually poorly tolerated, and the reduction in cardiac output is usually greater than what is seen in isolated AS or MS Severe MS may lead to low LV outflow and, therefore, result in paradoxical low-flow, low-gradient AS Carotid pulse & Apex prominent Parasternal heave Loud S1 OS Ejection systolic murmur Grade < 3/6 Mid diastolic murmur
- 56. Combined MS+AS Dominant MS Dominant AS Angina Syncope Pulsus parvus et tardus Carotid thrill Apical impulse heave Ejection systolic murmur Dyspnea Pulmonic hypertension Atrial fibrillation Systemic thromboembolism MDM
- 57. Combined MS+AR Combined Features Wide pulse pressure Apical prominence Parasternal impulse Loud S1 OS S3 S4 Early diastolic murmur Mid diastolic murmur The continuity equation and pressure half-time methods are invalid to calculate mitral valve effective orifice area, transthoracic 3- dimensional echocardiography may be used to assess mitral valve anatomic orifice area and confirm MS severity
- 58. Combined MS+AR Dominant MS Dominant AR Dyspnea, Effort intolerance, Systemic emboli Parasternal heave Loud S1 Angina, Palpitation Parasternal apical impulse S3/S4
- 59. Combined MR+AS AS augments the severity of MR Systemic hypotension Pulmonic hypertension Hyperdynamic AI S3 / S4 Mitral – PSM Aortic – ESM
- 60. Combined MR+AS Dominant MR Dominant AS Easy fatigability Pulmonary symptoms S3 Murmur decreased/unchanaged after handgrip/squatting Syncope Angina S4 Murmur increased with squatting and decreased with handgrip
- 61. Combined MR+AR • When MR > AR , it attenuates AR • When AR > MR , it worsens MR • Pulmonary symptoms are earlier and severe with MR + AR combination than in isolation • MR is worsened by AR • Wide pulse pressure • Peripheral signs • Diffuse apical impulse • P2/ S3/ S4 • Mitral PSM/ Aortic EDM MR associated with AR may be primary or secondary to LV remodeling as a consequence of AR Mitral valve competency normally protects the left atrium and the pulmonary veins from the deleterious effects of the increased LV pressure related to AR
- 62. Combined MR+AR Dominant MR Dominant AR Pulmonary symptoms Atrial fibrillation Parasternal heave PSM Angina Wide pulse pressure Longer EDM S4
- 63. Combined AS+AR Apico carotid delay S2 paradoxical split A2 – soft or absent S3 S4 Prolonged Aortic ESM Prolonged Aortic EDM Austin Flint Murmur
- 64. Combined AS+AR Dominant AS Dominant AR Angina, syncope Anacrotic pulse Apex heave Systolic decapitation Systolic Ejection click S2 reverse split S4- early Systolic murmur – late peaking, loud and longer Palpitation Wide pulse pressure/ Pulsus bisferiens Diffuse apical impulse Early diastolic murmur S4- late (High LVEDP) Peripheral signs
- 65. Mitral Valve Disease+ TS Dyspnoea and orthopnoea predominate Easy fatigability PND/ hemoptysis/pulmonary edema conspicuously absent JVP- giant a wave and slow y descent Split S1 Parasternal heave usually absent MDM at left lower parasternal border
- 66. Mitral Valve Disease + TS • MS precedes TS • TS masks MS • TS is to be suspected when RHF persists after adequate mitral valvotomy.
- 67. Combined TS + TR TS > TR • Tricuspid OS • The Tricuspid diastolic murmur increases and whereas Tricuspid systolic murmur decreases with inspiration
- 68. Combined TS + TR TR > TS • Tricuspid S3 • The Tricuspid diastolic murmur decreases and whereas Tricuspid systolic murmur increases with inspiration.
- 69. LV Dysfunction Assessment In Severe AR- • Soft S1 • S3 • Disappearance of presystolic component of Austin Flint murmur • Sustained apex In Severe AS- • S3 • Dilated heart and diffuse apex In Severe MR- • Sustained apex Bisferience pulse- Intact LV function in Severe AR/HOCM S3 in severe MR tells about severity only not LV dysfunction
- 70. How to write the diagnosis ? Etiological diagnosis Anatomical diagnosis ? Heart failure NYHA class Rhythm PVH/PAH LV Function ? Evidence of Rheumatic fever? Features of Infective endocarditis ? Precipitating factors eg- Anemia ?