n S2=Aortic valve closure, pulmonic n S3=Very healthy or very sick LV n Children and young athletes, CHF n S4=Stiff LV, incr LVEDP, HTN, hypertrophy

Transcription

1 Cardiac Physical Exam Valvular Heart Disease Susan Schima MD September 29, 2015 S1=mitral valve closure (can t really hear tricuspid component) S2=Aortic valve closure, pulmonic S3=Very healthy or very sick LV Children and young athletes, CHF Healthy=suckers Sick=pushers S4=Stiff LV, incr LVEDP, HTN, hypertrophy Cannot hear in afib. Occurs during atrial contraction Physiologic Splitting S1 S2 Expiration M1,T1 A2,P2 Persistent Splitting RBBB, Pulm HTN S1 S2 Expiration M1,T1 A2 P2 Inspiration M1,T1 A2 P2 Inspiration M1,T1 A2 P2 Delayed activation of the RV, so delayed closure of P2 Fixed Splitting ASD S1 S2 Expiration M1,T1 A2 P2 Inspiration M1, T1 A2 P2 Increased venous return balanced by reciprocal decr flow through shunt Paradoxical Splitting LBBB Expiration S1 P2 A2 Inspiration S1 P2A2 Delayed LV activation, ejection and AV closure 1

2 Paradoxical Splitting Summary- Splitting of S2 Delayed LV activation LBBB RV pacing Delayed LV outflow LV systolic failure AS, HOCM Physiologic Splitting=respiratory flow variation Paradoxical=LBBB, AS Persistent=RBBB, pulm HTN, MS Fixed=ASD Murmurs Stages of Progression of VHD Innocent/functional murmur Short, soft <grade 2 Right sternal border No increase with valsava Normal S2 No other abnormal sounds No LV enlargement on exam or ecg Stage Definition Description A At risk Risk factors for development of VHD B Progressive Mild to moderate, asymptomatic C Asymptomatic Severe C1: LV or RV remains compensated C2: LV or RV decompensated D Symptomatic Severe Symptoms due to VHD Frequency of Echo in Asymptomatic pts with VHD and Normal EF Stage AS AR MS MR Progressive (stage B) Severe (Stage C) 3-5 yr if mild, 1-2 y if mod 3-5 yr if mild 1-2 y if mod 6-12 m 6-12 m Dilating LVmore frequently 3-5 yr (MVA >1.5 cm2) 1-2 y (MVA 1-1.5cm2) Every yr (MVA < 1 cm2) 3-5 yr if mild 1-2 y if mod 6-12 m Dilating LVmore frequently Medical Therapy Most valve disease is ultimately surgical, however benefit to ACE inhibitor or ARB and beta blockers if LV dysfunction Care taken not to abruptly lower BP in pts with stenotic lesions Rheumatic fever and IE prophylaxis Maintenance of optimal oral health Influenza and pneumococcal vaccines to appropriate pts 2

3 Medical Therapy Exercise Testing All patients should be optimized with goal directed medical therapy Safety and efficacy of exercise programs in VHD not established Pts benefit from regular aerobic exercise program to ensure CV fitness Heavy isometric repetitive training may increase AL, but resistive training with small free weights or repetitive isolated muscle training may be used Class IIa Reasonable in selected patients with asymptomatic severe VHD to Confirm absence of symptoms Assess hemodynamic response to exercise Determine prognosis Rheumatic Fever Secondary Prevention of Rheumatic Fever Important cause of VHD, slight increase in cases since 1987 Group A strep-prompt recognition and rx for primary prevention Pts with prior episodes of RF or those with evidence of RHD, long-term antistreptococcal prophylaxis is indicated for secondary prevention Agent PCN G benzathine PCN V potassium Sulfadiazine Macrolide or azalide abx (PCN/sulfa allergic) Dosage 1.2 million units IM q 4 wks 200 mg po BID 1g po daily Varies Duration of Secondary Prophylaxis for RF IE Prophylaxis Type RF with carditis and persistent VHD RF with carditis but no residual VHD RF without carditis Duration after Last Attack 10y or until pt is 40 yo (whichever longer) 10 yr or until pt is 21 yo (whichever longer) 5 y or until pt 21 yo (whichever longer) IIa : Reasonable for the following pts at highest risk for adverse outcomes from IE before dental procedures that involve manipulation of gingival tissue, manipulation of the periapical region of teeth, or perforation of the oral mucosa 3

4 IE Prophylaxis Prosthetic cardiac valves Previous IE Cardiac transplant recipients with valve regurgitation due to structurally abnormal valve Congenital heart disease with: Unrepaired cyanotic CHD, incl palliative shunts Repaired CHD with prosthetic material or device during first 6 m after procedure Repaired CHD with residual defects at site or adjacent to site of prosthetic patch or prosthetic device IE Prophylaxis No Benefit Class III Not recommended in patients with VHD who are at risk of IE for nondental procedures (eg TEE, EGD, colonoscopy or cystoscopy) in the absence of active infection Aortic Stenosis Etiology Senile degenerative (calcific) > 70 Most common Rheumatic Calcified bicuspid Congenital <30 Unicuspid, bicuspid Associated with other abnormalities (aortic disease) 1-2% of all live births Familial-AD with low penetrance DNA transcription error, defective myofibrils Screen relatives of patients with bicuspid valve Bicuspid Clinical Presentation: Physical Exam -Loud, late peaking systolic murmur that radiates to carotids, crescendodecrescendo -Single or paradoxically split S2 -Delayed and diminished carotid upstroke (parvus et tardus) -Only reliable sign to exclude severe AS is normally split S2 4

5 Symptoms Syncope Clinical Presentation CHF (worst prognosis) Angina Medical Therapy AS Control of blood pressure in those at risk for AS and those with asymptomatic AS (stages A,B,C). Start at low dose and titrate up Avoid diuretics if small LV chamber size because may result in fall in CO. Statins have no role in AS (although many have CAD) Evaluation of Severity When to operate AVA AREA MEAN GRADIENT JET VELOCITY MILD >1.5 cm2 <25mmHg <3 m/s MODERATE cm mmH g 3-4 m/s Class I Symptomatic with Severe AS Severe AS and undergoing CABG, aorta or other valve surgery Severe AS and LV systolic dysfunction (EF < 50%) SEVERE <1 cm2 >40mmHg >4 m/s Surgical Treatment of AS Surgical AVR for patients with low or intermediate surgical risk TAVR if prohibitive surgical risk and predicted post-tavr survival greater than 12 months (Class I) TAVR is reasonable alternative to surgical AVR in those with high surgical risk (Class IIa) Evaluation of Surgical and Interventional Risk Individualized Operative mortality estimated from different risk scoring systems (STS risk estimate or Euroscore) Fraility should be considered 5

6 Pre-op Coronary Angiogram Low Risk (all) Intermed. Risk (any 1) High Risk (any 1) Prohibitive Risk (Any 1) STS PROM <4% AND 4-8% OR >8% OR Risk of death or major morbidity > 50% at 1 yr Fraility None AND 1 Index (mild) OR Major Organ System Compromise not to be improved postop None AND 1 Or > Or = 2 Indices (mod to severe) OR No more than 2 Ø Or= 3 OR Males > 35 yo Premenopausal women > 35 with risk factors Postmenopausal women Aortic Regurgitation Etiology Congenital, calcific, rheumatic, IE, HTN, Marfans, RA, syphilis, anorectic drugs, inflammatory (psoriatic arthritis, ankylosing spondylitis) Trauma, MI Acute and Chronic Acute Severe AI Presentation Sudden large regurgitant volume on unprepared LV. Abrupt increase in LVEDP and LAP, LV can t compensate quickly and get decrease in forward SV. Tachycardia is compensatory but insufficient Pulmonary congestion S3 and S4 AR murmur may be absent Pulse pressure may not be increased because systolic pressure is reduced and aortic diastolic pressure equilibrates with elevated LV diastolic pressure 6

7 Treatment Urgent surgery IABP contraindicated Beta-blockers contraindicated (unless dissection) because increase diastolic filling time and worsen the AI, blunt compensatory tachycardia Nitroprusside is an option (augment forward flow and reduce LVEDP) Chronic AI Compensatory increase in ED volume, increase in chamber compliance to accommodate increased volume without increase in filling pressures- concentric and eccentric hypertrophy Greater diastolic volume allows LV to eject large total SV to maintain forward CO Pressure and Volume overload Chronic AI Preload reserve can be exhausted and hypertrophic response may be inadequate, so that further increase in afterload results in reduced EF. May have prolonged asymptomatic interval Dyspnea and exertional angina Physical Exam Most consistent finding is wide pulse pressure (if don t have, not severe) Head nodding (de Mussets) Capillary pulsations (Quinke s) Rapid carotid upstroke, rapid collapse (Corrigan s pulse) Pistol shot femoral pulse (Duroziez s) Physical Exam Diastolic decrescendo murmur May also have short SEM with ejection click (if bicuspid) Displaced LV impulse Austin-Flint murmur specific for severe AI Severe AR jet/lvot diameter > 60% Flow reversal in proximal desc thoracic aorta Regurgitant volume > 60ml Regurgitant fraction > 55% Evaluation 7

8 Surgical Treatment of AR Medical Treatment of AR Symptomatic pts with severe AR regardless of LV systolic function Asymptomatic EF < 50% Nl EF but LVESD > 50 mm, stage C2 Nl EF but LVEDD > 65 mm if surgical risk is low Treat hypertension, ideally with CCB or ACEI/ARB. Reduced HR with BB may cause higher stroke volume, which contribute to elevated SBP in pts with chronic severe AR If LV dysfunction/symptoms and surgery not option, treat with vasodilators (CCB, ACEI/ARB,BBL). Not needed if LV function normal and asymptomatic Mitral Stenosis Etiology Almost always Rheumatic! W:M 2:1 Pathophysiology Clinical Presentation Diastolic transmitral gradient is the fundamental expression of MS Results in increased LA pressure, which is reflected back to pulmonary circulation atrial arrhythmias Right sided heart failure First symptoms usually precipitated by exercise, emotional stress, infection, pregnancy or afib with RVR (increase in transmitral flow or decr in diastolic filling period rise in LAP) Dyspnea, PND, orthopnea Hemoptysis Palpitations Emboli 8

9 Physical Exam Evaluation Accentuated S1, opening snap, low pitched mid diastolic rumble, and presystolic murmur Shorter A2-os interval and longer diastolic rumble indicate more severe MS S2-OS interval <70msec severe, >110 mild AS MS worsens, pressure increases, leading to earlier opening of MV and shortening of A2-Os interval Echo for severity Mean Gradient MVA PASP Mild <5mmHg >1.5 cm2 <30m mhg Moderate 5-10mmHg mmhg Severe >10 mmhg <1 >50 mmhg Treatment Anticoagulation if AF Intervention if symptoms Percutaneous Mitral Balloon Valvotomy Success rate depends on morphology of MV (pliable) Absent 0s, soft S1- probably calcified and won t do well Crisp OS and loud S1- should do well Contraindications- MR > 2+, LA thrombus Mitral Balloon Valvotomy Severe MS and non-pliable Valve Class I or II: Observe Class III or IV: MVR 9

10 Severe MS, pliable Valve, Mitral Regurtiation Class II, III, IV : Consider PMBV Asymptomatic PAP > 60mmHg New onset Afib Acute MR Acute MR Etiology Chordal rupture IE Ischemic heart disease Consider if hyperdynamic LV function and shock Pulmonary congestion/edema S3 and S4 MR murmur may be absent or soft Acute MR Management Sudden volume overload on unprepared LA and LV. Increased preload and increased SV. Without time to develop LVH, forward SV and CO are reduced Papillary mm rupture- poor prognosis without surgery IE- depends on response to abx (if CHF- OR) Chordal rupture-depends on tolerance of severe MR 10

11 Treatment Chronic MR Unstable: IV nitroprusside, IABP, Surgery Stable: IV vasodilators, diuretics, abx. IE- OR if progressive CHF, no response to abx, abscess or recurrent emboli Etiology Most is degenerative (MVP) Ischemic IE Rheumatic Pathophysiology Presentation Compensatory increase in LVEDV to increase SV and restore forward CO. Eventually, prolonged burden of volume overload results in LV dysfunction, reduced forward output and pulm congestion. By the time symptoms develop, LV dysfunction may have already occurred Once there is LV dysfunction, prognosis poor Physical Exam Displaced of LV apical impulse S3 Holosystolic murmur May also have diastolic rumble without MS due to early diastolic filling (sign of severity) Assessment of Severity Management Regurgitant volume > 60 ml Regurgitant fraction > 50% ERO >.4 cm2 LV gram If normal sized LA and LV- can t be severe Surgery for- Symptoms (Class II-IV) LV dysfunction (EF < 60%, ESD > 40mm) Prophylactic? Reasonable in asymptomatic pt if low operative mortality (<1%) and high chance of successful repair 11