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Valvular Heart disease PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Valvular Heart disease" by Dr. Ashraf Abdelfatah Deyab.

This medical PowerPoint presentation talks about Valvular Heart disease.

Valvular heart disease refers to a group of conditions in which one or more of the heart valves (mitral, aortic, tricuspid, or pulmonary) do not function properly. The heart valves regulate the flow of blood through the heart, and when they are damaged or diseased, the heart has to work harder to pump blood. This can lead to symptoms such as fatigue, shortness of breath, chest pain, and fainting.

There are several types of valvular heart disease, including Aortic stenosis, Mitral regurgitation, Tricuspid regurgitation, Pulmonary stenosis, and Mitral stenosis.

Tags : Valvular Heart disease, heart valves, Aortic stenosis, Mitral regurgitation, Tricuspid regurgitation, Pulmonary stenosis, Mitral stenosis, cardiology, cardiology PowerPoint presentation

Published on : Mar 19, 2023 | Views : 3335 | Downloads : 1

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Slide 1-

Valvular Heart Disease Kenneth S. Korr M.D. Associate Professor of Medicine, Brown Medical School Director, Division of Cardiology The Miriam Hospital
Slide 2-

Normal Valve Function Maintain forward flow and prevent reversal of flow. Valves open and close in response to pressure differences (gradients) between cardiac chambers.
Slide 3-

Abnormal Valve Function Valve Stenosis Obstruction to valve flow during that phase of the cardiac cycle when the valve is normally open. Hemodynamic hallmark -“pressure gradient” ~ flow// VA Valve Regurgitation, Insufficiency, Incompetence Inadequate valve closure--- back leakage A single valve can be both stenotic and regurgitant; but both lesions cannot be severe!! Combinations of valve lesions can coexist Single disease process Different disease processes One valve lesion may cause another Certain combinations are particularly burdensome (AS & MR)
Slide 4-

Mitral Valve Competence: Integrated function of several anatomic elements Posterior LA wall Anterior & Posterior valve leaflets Chordae tendineae Papillary muscles Left ventricular wall where the papillary muscles attach
Slide 5-

Mitral Valve Disease: Etiology Mitral Stenosis Rheumatic - 99.9%!!! Congenital Prosthetic valve stenosis Mitral Annular Calcification Left Atrial Myxoma Acute Mitral Regurgitation Infective endocarditis Ischemic Heart disease Papillary ms rupture Mitral valve prolapse Chordal rupture Chest trauma Chronic Mitral Regurgitation Ischemic Heart disease Papillary ms dysfunction Inferior & posterior MI Mitral Valve prolapse Infective endocarditis Rheumatic Prosthetic Mitral annular calcification Cardiomyopathy LV dilatation IHSS
Slide 6-

Mitral Regurgitation-Pathophysiology MR: Leakage of blood into LA during systole 10 Abnormality -Loss of forward SV into LA Compensatory Mechanisms Increase in SV (& EF) Forward SV + regurgitant volume LV (LA) dilatation Left Ventricular Volume Overload (LVVO)
Slide 7-

Chronic Mitral Regurgitation - LVVO LVVO LV dilatation Eccentric hypertrophy Increased LA pressure Pulmonary HTN Dyspnea Atrial arrhythmias Low output state
Slide 8-

Pathophysiology –Acute vs Chronic Mitral Regurgitation Acute MR Normal (noncompliant) LA Increase LA pressure large “V” waves Acute Pulmonary Edema Chronic MR Dilated, compliant LA LA pressure normal or slightly increased Fatigue, low output state Atrial arrhythmias- a. fib. Most patients fall between these two extremes!!
Slide 9-

Mitral Regurgitation: Physical Findings Auscultatory Findings S1 – soft or normal P2 – increased Holosystolic blowing murmur @ apex MVP – mid-systolic click IHSS – murmur increases with Valsalva Acute MR – descrescendo systolic murmur S3 gallop & diastolic flow rumble Hyperdynamic Left Ventricle Brisk carotid upstrokes Hyperdynamic LV apical impulse LA lift; RV tap
Slide 10-

Mitral Stenosis -Pathophysiology Restriction of blood flow from LALV during diastole. Normal MVA 4-6cm2. Mild MS 2-4cm2. Severe MS < 1.0cm2. MV Pressure gradient – MV grad ~ MV flow//MVA. Flow = CO/DFP (diastolic filling period). As HR increases, diastole shortens disproportionately and MV gradient increases.
Slide 11-

Relationship between MV gradient and Flow for different Valve Areas Cross hatched area indicates range of normal resting flow. The vertical line represents the threshold for developing pulmonary edema. Pressure gradient increases as flow increases: to a small degree with normal valve area(4-6cm2). to greater degrees with smaller valve areas. in severe stenosis, a significant gradient is present at rest.
Slide 12-

Mitral Stenosis-Pathophysiology MV gradient Incr LA pr Pulmonary HTN Passive Reactive- 2nd stenosis RV Pressure Overload RVH RV failure Tricuspid regurgitation Systemic Congestion Paradoxes of MS Disease of Pulm Arts & RV LV unaffected (protected) As RV fails, pulmonary symptoms diminish
Slide 13-

Mitral Stenosis- Clinical Symptoms Symptoms related to severity of MVA reduction- Symptoms unrelated to severity of MS- Atrial fibrillation Systemic thromboembolism Symptoms due to Pulmonary HTN and RV failure- Fatigue, low output state Peripheral edema and hepato-splenomegaly Hoarseness –recurrent laryngeal nerve palsy
Slide 14-

Mitral Stenosis: Physical Findings Auscultatory findings S1 – variable intensity; increased early, progressively decreases OS –opening snap, variable intensity A2-OS interval – varies inversely with severity of MS; shortens as MVA diminishes Low-pitched diastolic rumble @ apex Duration of murmur correlates with severity of MS Pre-systolic accentuation Increased P2 Body habitus – thin, asthenic, female Low BP LA lift & RV tap
Slide 15-

Mitral Valve Disease – Echo findings Mitral Stenosis Thickened, deformed MV leaflets 2D MVA Doppler Gradient Associated LAE, RVH, PHTN, TR,MR, LV function Mitral Regurgitation Determine etiology – leaflets, chordae, MVP, MI Doppler severity of MR jet LV function
Slide 16-

Mitral Valve Disease : Treatment Mitral Stenosis Medical Rx for Class I & II HR control – Dig & BB Anticoagulation Afib, >40yrs, LAE, MR, prior embolic event Surgical Rx -Class III &IV Balloon Mitral Valvuloplasty Commissural fusion pliable, noncalcified leaflets No MR of LA thrombus Mitral Valve Surgery Open commissurotomy MV replacement Chronic Mitral Regurgitation Medical Rx for mild to mod MR with vasodilators, diuretics, anticoagulation Surgical Rx –ideally before LV systolic function declines. MV replacement MV ring & CABG MR repair – associated with improved long-term LV funvtion MVP, ruptured chords, infective endocadritis, pap ms rupture.
Slide 17-

Balloon Mitral Commissurotomy
Slide 18-

Aortic Valve Disease: Etiology Aortic Stenosis Degenerative calcific (senile) Congenital – Uni or bicuspid Rheumatic Prosthetic Acute Aortic Insufficiency Infective endocarditis Acute Aortic Dissection Marfan’s Syndrome Chest trauma Chronic Aortic Insufficiency Aortic leaflet disease Infective endocarditis Rheumatic Bicuspid Aortic valve Prolapse & congenital VSD Prosthetic Aortic root disease Aortic aneurysm/dissection Marfan’s syndrome Connective tissue disorders Syphilis HTN Annulo-aortic ectasia
Slide 19-

Aortic Stenosis - Pathophysiology Normal AVA 2.5-3.0cm2 Severe AS <1.0cm2 Critical AS <0.7cm2; <0.5cm2/m2 Hemodynamic Hallmark Systolic pressure gradient AV grad ~ AV flow//AVA AV flow = CO/SEP (systolic ejection period) 50-100mmHg gradients are common in severe AS
Slide 20-

Relationship between AV gradient and Flow for different Aortic valve areas. Like Mitral Stenosis – as flow increases so does the gradient. Unlike Mitral Stenosis – Resting flows are higher smaller AV area shorter SEP Larger gradients Significant (>50mmHg) gradient can be present at rest in asymptomatic individuals.
Slide 21-

Pathophysiology of Aortic Stenosis- LVPO Chronic LV Pressure Overload Concentric LVH “Stiff” noncompliant LV Increased LVEDP Increased LV mass Increased MVO2 Well tolerated for decades LV fails CHF Atrial fibrillation Poorly tolerated Loss of atrial “kick” Rapid HR Acute pulmonary edema and hypotension.
Slide 22-

Aortic Stenosis: Natural History & Clinical Symptoms Asymptomatic for many years Symptoms develop when valve is critically narrowed and LV function deteriorates Bicuspid AV 5th - 6th decade Senile AS 7th-8th decades Classic Symptom Triad Angina pectoris – 5 years CHF 1-2 years Syncope 2-3 years Sudden Death Natural History Studies- Pts grad 25mmHg –20% chance of intervention in 15 years Pts with asymptomatic severe AS require close f/u Gradient progression 6-10mmHg/yr Risk Factors Age > 70 CAD, hyperlipidemia Chronic renal failure
Slide 23-

Aortic Stenosis: Physical Findings
Slide 24-

Aortic Insufficiency- Pathophysiology 10 abnormality – LVVO Severity of LVVO Size of regurgitant orifice Diastolic pressure gradient between Ao & LV HR or duration of diastole Compensatory Mechanisms LV dilatation & eccentric LVH Increased LV diastolic compliance Peripheral vasodilation
Slide 25-

LV Volume vs Pressure Overload
Slide 26-

Acute vs Chronic AR Pathophysiology and Clinical Presentation Acute Aortic Regurgitation Sudden AoV incompetence Noncompliant LV Acute Pulmonary Edema Emergency AVR Chronic Aortic Regurgitation Long asymptomatic phase Progressive LV dilatation DOE, orthopnea, PND Frequent PVC’s
Slide 27-

Chronic Aortic Regurgitation: Physical Findings Widened Pulse Pressure > 70mmHg (170/60) Low diastolic pressure <60mmHg Hyperdynamic LV – DeMusset’s signs Corrigan’s pulse Quincke’s pulsations, Durozier’s murmur Auscultation: Diminished A2 Descrescendo diastolic blowing murmur @ LSB Austin-Flint murmur – diastolic flow rumble @ apex Due to interference with trans-mitral filling by impignement from aortic regurgitant jet. DDx - mitral stenosis(increases intensity with amyl nitrite)
Slide 28-

Aortic Valve Disease:Diagnostic Testing Aortic Stenosis EKG- NSR, LVH with strain, LAE,LAD CXRay – frequently normal 2D-ECHO Aortic cusps –thickened, calcified, decreased mobility Assessment of LVH & LV systolic function Concomitant MR, AR Doppler assesment of AoV gradient Planimetry of AV area Aortic regurgitaiton EKG- LVH without strain CXRay- Chronic AI – “cor bovinum” Acute AI – pulmonary edema with nl heart size 2D ECHO Assess Ao valve and root Assess LV function/dilatation LVES dimension>55mm Doppler severity of regurgitant jet
Slide 29-

Relationship between AV gradient and Flow for different Aortic valve areas. Like Mitral Stenosis – as flow increases so does the gradient. Unlike Mitral Stenosis – Resting flows are higher smaller AV area shorter SEP Larger gradients Significant (>50mmHg) gradient can be present at rest in asymptomatic individuals.
Slide 30-

Balloon Aortic Valvuloplasty Indications for BAV in critical Aortic Stenosis Younger patients with congenital AS and predominant commissural fusion Bridge to eventual AVR Moderate to severe heart failure/cardiogenic shock Extremely high risk for AVR Urgent/emergent need for noncardiac surgery Patient with limited lifespan – cardiac or noncardiac Patient refuses surgery
Slide 31-

Aortic Valve Surgery: Ross Procedure Autotransplant of pulmonic valve to the aortic position Reimplantation of the coronary arteries Homograft valve in the pulmonic position Indications Younger patients No anticoagulation Requires similar sized aortic and pulmonic roots
Slide 32-

Valvular Heart Disease The End