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Valvular Disorders & Infecive Endocarditis Normal Valve Function Prevent backward flow of blood Permit forward flow of blood Abnormal valve function Allows backward flow Valve is “leaky;” “regurgitant;” “incompetent” Backwards jet causes turbulence that is audible as murmur Prevents forward flow Valve does not open well Greek stenōsis, a narrowing Typically causes hypertrophy and dilatation of the cardiac chamber All valvular diseases have characteristic murmurs Damaged valve disrupts blood flow=turbulence & sound! Caused by Rheumatic Heart Disease Acute conditions (infective endocarditis) Acute MI Congenital Heart Defects Aging Auscultation Use the diaphragm for high pitched sounds and murmurs Use the bell for low pitched sounds and murmurs Sequence of auscultation { Z Pattern } Apex Lower left sternal border (LLSB) Upper left sternal border (ULSB) Upper right sternal border (URSB) Common Murmurs and Timing Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve prolapse Tricuspid insufficiency Diastolic Murmurs Aortic insufficiency Mitral stenosis S1 S2 S1 Grading the Intensity of Murmurs Grade 1 Grade 2 Murmur associated with a thrill Grade 5 Murmur hears with stethoscope on chest wall, louder than grade 2 but without a thrill Grade 4 Faint murmur heard with stethoscope on chest wall Grade 3 Murmur heard with stethoscope, but not at first Murmur heard with just the rim held against the chest Grade 6 Murmur heard with the stethoscope held away and in from the chest wall Cardiac Murmurs Most mid systolic murmurs of grade 2/6 intensity or less are benign Associated with physiologic increases in blood velocity: Pregnancy Elderly In contrast, the following murmurs are usually pathologic: Systolic murmurs grade 3/6 or greater in intensity Continuous murmurs Any diastolic murmur Innocent Murmurs Common in asymptomatic adults Characterized by Grade I – II @ LSB Systolic ejection pattern - no with Valsalva – – – – S1 S2 Normal precordium, apex, S1 Normal intensity & splitting of second sound (S2) No other abnormal sounds or murmurs No evidence of LVH Characteristic Pathological Murmur Diastolic murmur Loud murmur - grade IV or above Regurgitant murmur Murmurs associated with a click Murmurs associated with other signs or symptoms e.g. cyanosis Abnormal 2nd heart sound – fixed split, paradoxical split or single Valvular Aortic Stenosis Normal valve area 3-4 cm2 Failure of valve to open normally during systole, requiring LV to develop excess pressure to overcome increased resistance Mild AS >1.5 cm2 Moderate >1.0 cm2 Severe AS when area ¼ normal <1 cm2 for large person <0.75 cm2 for normal person Causes concentric hypertrophy Symptoms of exertional chest pain, syncope, dyspnea Mandate valve replacement to prevent sudden death A.S : Etiology Clinical Presentation of Aortic Stenosis Cardinal symptoms: Angina Syncope CHF Physical Findings S1 S2 Mild-Moderate S1 S2 Severe Management of Aortic Stenosis Prognosis in asymptomatic disease excellent Conservative approach with monitoring for symptoms recommended Once symptoms occur, AVR needed Only should be considered: If other cardiac surgery (such as CABG) planned Severe LVH or systolic dysfunction Women contemplating pregnancy Aortic Regurgitation Aortic Regurgitation: Etiology Any conditions resulting in incompetent aortic leaflets Congenital Acquired Bicuspid valve Aortopathy Cystic medial necrosis Collagen disorders (e.g. Marfan’s) Rheumatic heart disease Dilated aorta (e.g. hypertension..) Degenerative Connective tissue disorders E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis ) Syphilis (chronic aortitis) Acute AI: aortic dissection, infective endocarditis, trauma Aortic Regurgitation: Symptoms Dyspnea, Orthopnea, PND Chest pain. Nocturnal angina >> exertional angina Peripheral Signs of Severe Aortic Regurgitation Quincke’s sign: capillary pulsation Corrigan’s sign: water hammer pulse Bisferiens pulse (AS/AR > AR) De Musset’s sign: systolic head bobbing Mueller’s sign: systolic pulsation of uvula Durosier’s sign: femoral retrograde bruits Traube’s sign: pistol shot femorals Hill’s sign:BP Lower extremity >BP Upper extremity by > 20 mm Hg - mild AR > 40 mm Hg – mod AR > 60 mm Hg – severe AR Aortic Regurgitation: Physical Exam Widened pulse pressure Systolic – diastolic = pulse pressure High pitched, blowing, decrescendo diastolic murmur at LSB Best heard at end-expiration & leaning forward S1 S2 S1 Aortic Regurgitation: Natural History Asymptomatic Normal LV function (~good prognosis) Abnormal LV function Progression to cardiac symptoms (25 % ) Symptomatic (Poor prognosis) Mortality > 10 % TX: Medical Surgery BEFORE LV dysfunction Mitral Stenosis Almost always rheumatic in origin >40% of cases of RHD result in mitral stenosis Presentation 20-40 years after the initial episode of rheumatic fever Diastolic murmur Women affected more than men (2:1) classic presentation is during vaginal delivery. Tachycardia, straining, volume increase cause pulmonary edema Patients eventually have exertional dyspnea, atrial fibrillation (often with thromboembolism), chest pain Always look for MS in patient with new Atrial fibrillation Mitral Stenosis Pathophysiology Normal valve area: 4-6 cm2 Mild mitral stenosis: MVA 1.5-2.5 cm2 Minimal symptoms Mod mitral stenosis MVA 1.0-1.5 cm2 usually does not produce symptoms at rest Severe mitral stenosis MVA < 1.0 cm2 Mitral Stenosis Symptoms Fatigue Palpitations Cough SOB Orthopnea PND Palpitation A. Fibrillation Systemic embolism Pulmonary infection Hemoptysis Right sided failure Hepatic Congestion Edema Worsened by conditions that cardiac output. Exertion,fever, anemia, tachycardia, Afib, intercourse, pregnancy, thyrotoxicosis Mitral Stenosis Physical Exam S1 S2 OS S1 First heart sound (S1) is accentuated Opening snap (OS) Low pitch diastolic rumble at the apex Pre-systolic accentuation (esp. if in sinus rhythm) MS Mortality Minimal symptoms >80% 10 year survival Limiting symptoms <15% 10 year survival Untreated patients 60-70% progressive pulmonary edema 20-30% systemic embolism 1-5% endocarditis/infection Mitral Regurgitation Incompetent mitral valve allows loss of stroke volume back into Left Atrium Mitral valve prolapse most common cause Rheumatic disease and endocarditis Physical Examination Loud pan-SYSTOLIC murmur, loudest at apex and radiating into axilla Typically soft S1 Presence of S3 suggests severe MR Mitral Regurgitation: Etiology Valvular-leaflets Rheumatic Endocarditis Chordae Fused/inflammatory Torn/trauma Degenerative Endocarditis Annulus Papillary Muscles Calcification, IE (abcess) CAD (Ischemia, Infarction, Rupture) LV dilatation & functional regurgitation Trauma MR Symptoms Dyspnea, Orthopnea, PND Fatigue Pulmonary HTN, Right sided failure Hemoptysis Systemic embolization in A Fib Mitral Insufficiency: Physical Exam S1 Mitral regurgitation S2 S1 MR Treatment No medical therapy Most difficult clinically By the time symptoms occur, it may be too late Drop in Ejection Fraction or development of atrial fibrillation enough to justify surgery Mitral Valve Prolapse : Epidemiology Affects 5-10% of population Most common cause of isolated severe MR Females >> males; Ages of 14 - 30years Strong hereditary component (? Autosomal Dominant) 2º to failure of apposition/coaptation of the anterior and posterior mitral valve leaflets. Cause is unknown in a majority of pts Mitral Valve Prolapse: Symptoms Majority are asymptomatic for entire life Palpitations Chest pain (atypical). Often substernal, prolonged, poorly related to exertion, and rarely resembles typical angina Syncope Mitral Valve Prolapse: Physical Exam S1 C S2 Most important finding: mid late systolic click. Variable murmurs: high pitched late systolic crescendo-decrescendo murmur, Mitral Valve Prolapse: Complications Arrhythmias (Usually PVC, PSVT>>VT) Transient cerebral ischemic (embolic – rare) Infective endocarditis (if associated with MR) Sudden death (rare) Tricuspid Valve Disease Tricuspid stenosis is rare Associated with rheumatic heart disease More common than regurgitation Result in R. atrial enlargement > inc. systemic venous pressure > atrial fibrillation, peripheral edema, ascites TR usually occurs secondary to: Pulmonary hypertension RV chamber enlargement with annular dilatation Endocarditis (associated with IV drug use) Other secondary causes: carcinoid, radiation therapy Symptoms are manifestations of systemic venous congestion Ascites & Pedal edema Echo is diagnostic in most cases Severe tricuspid regurgitation is difficult to treat and carries a poor overall clinical outcome Other Valve disorders: Pulmonic stenosis Thrombus on valves – Hypercoag., DIC, Malignancy, etc. May cause strokes, sec. bacterial infection. Libman-Sacks: Uncommon valve disorders NBTE: Non bacterial thrombotic… Result in R. ventricular hypertension and hypertrophy Fatigue , loud midsystolic murmur Sterile Immune complex vegetations SLE. Carcinoid Heart Disease: Carcinoid tumour, 5HT, seratonins etc.. Endocardial fibrosis Valvular Disease Rheumatic fever Endocarditis causes regurgitation Regurgitation frequently present acutely Long term predominant effect is stenosis Patients with valve disease should take antibiotics prior to dental work to prevent endocarditis All patients with symptomatic valvular disease (i.e. dyspnea, chest pain, syncope) need to be evaluated for surgical correction Some asymptomatic subjects also need correction “before it’s too late” Valvular Disease General Principles Left sided valvular disease more prone to cause serious hemodynamic problems Regurgitation causes volume overload- eccentric hypertrophy (dilatation) Stenotic lesions cause pressure overload on proximal chamber- concentric hypertrophy (thickened walls) Stenotic lesions cause symptoms sooner than regurgitant lesions but respond to therapy better Common Murmurs and Timing Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve prolapse Tricuspid insufficiency Diastolic Murmurs Aortic insufficiency Mitral stenosis S1 S2 S1 General Appearance Marfan Syndrome Large stature, coarse facial features, “spade” hands Associated with: Cardiac hypertrophy Turner Syndrome Tall, long extremities Associated with: aortic root dilitation, MV prolapse Acromegaly Web neck, hypertelorism, short stature Associated with: Aortic coarctation, pulmonary stenosis Pickwickian Syndrome Severe obesity, somnolence Associated with: Pulmonary hypertension Fredreich ataxia Duchenne muscular dystrophy Pseudohypertrophy of the calves Cardiomyopathy Ankylosing spondylitis Lurching gait, hammertoe, pes cavus Associated with: hypertrophic cardiomyopathy Straight back syndrome, stiff (“poker”) spine Associated with: AI, CHB (rare) Lentigines (LEOPARD syndrome) Brown skin macules that do not increase with sunlight Associated with: HOCM, PS General Appearance- 2 Hereditary hemorrhagic telangiectasia (Osler-WeberRendu) Butterfly rash on face, Raynaud phenomenon- hands, Livedo reticularis Associated with: Verrucous endocarditis, Myocarditis, Pericarditis Sarcoidosis Lupus Small capillary hemangiomas on the face or mouth Associated with: Pulmonary arteriovenous fistula Tuberous Sclerosis Pale diaphoretic skin, neurofibromatosis- café-au-lait spots Associated with: Catecholamineinduced secondary dilated CM Angiofibromas (face; adenoma sebaceum) Associated with: Rhabdomyoma Myxedema Pheochromocytoma Cutaneous nodules, erythema nodosum Associated with: Secondary cardiomyopathy, heart block Coarse, dry skin, thinning of lateral eyebrows, hoarseness of voice Associated with: Pericardial effusion, LV dysfunction Prosthetic Valve Complications Common complications include: Endocarditis prophylaxis required for patients with all types of prosthetic valves Suspect valve dysfunction in: Structural valve deterioration Valve thrombosis Embolism Bleeding Endocarditis Acute CHF in the immediate postoperative period New cardiac symptoms Embolic phenomena Hemolytic anemia New murmurs TEE is the diagnostic procedure of choice Postoperative TTE should be done 2-3 months after surgery 2007: Who gets Prophylaxis? Only patients with the highest risk of adverse outcomes (heart failure, surgery, death) from endocarditis: 1. Prosthetic cardiac valve 2. Previous Infective Endocarditis 3. Cardiac transplant recipients who develop cardiac valvulopathy 4. Congenital Heart Disease Which categories of Congenital Heart Disease? Unrepaired cyanotic CHD Tetralogy of Fallot, Transposition of Great Arteries, including palliative shunts and conduits Completely repaired congenital heart defect with prosthetic material or device during 1st 6 months after surgery Repaired CHD with residual defects at or near a prosthetic patch/device (which inhibit endothelialization) Dental Procedures “If it bleeds, give prophylaxis” High-risk pts undergoing all dental procedures that involve manipulation of gingival tissues OR periapical region of teeth OR perforation of oral mucosa i.e. biopsies, suture removal, placing orthodontic bands NO PROPHYLAXIS: X ray, anesthetic injections, fluoride treatments Shedding of deciduous teeth Placement/adjustment of removable prosthodontic or orthodontic appliances Prophylaxis for Dental Procedures Goal: cover Strep Viridans Single dose, 30-60 min prior to procedure PO Amoxicillin 2g PO, PCNallergic Cephalexin 2g IV: Ampicillin 2gm IV/IM OR Clindamycine 600mg OR Azithromycine 500mg **Don’t use Cephalexin if anaphylaxis, angioedema, or urticaria w/PCNs or ampicillin OR Cefazolin 1g IV/IM OR Ceftriaxone 1g IV/IM IV, PCNallergic Cefazolin 1g IV/IM OR Ceftriaxone 1g IV/IM OR Clindamycine 600mg IV/IM Summary: IE prophylaxis Need high-risk pt PLUS high-risk procedure High-risk pts: 1. Prosthetic cardiac valve 2. Previous IE 3. Cardiac transplants w/ valvulopathy 4. Congenital Heart Disease High-risk procedures: 1. 2. Dental: “If it bleeds, give prophylaxis” Respiratory: Consider if pt will be cut or biopsied No Prophylaxis Endotracheal intubation Cardiac cath/stent Pacer/ICD implantation EGD, Colonoscopy Barium Enema TEE Incision/Bx of surgically scrubbed skin Circumcision Vaginal delivery Hysterectomy Endocarditis Etiology Damaged valve (RHD) exposed to bacteria in blood stream S. viridans, S. aureus Clinical acute, subacute, chronic fever, new murmur, ESR (+) blood cultures Treatment Antibiotic according to organism Future prophylaxis for procedures Endocarditis Classification Acute Subacute (SBE) Virulent! Staph aureus, Gram Negative Rods Normal valves Acute course with rapid valve destruction, Heart Failure Streptococci, Enterococcus, Staph epidermoides Underlying cardiac disease More indolent presentation: low-grade fever, murmur Native valve, addict, prosthetic valve, culture-neg Diagnosis of IE Fever, new murmur or heart failure, bacteremia Systemic findings of emboli Neurologic impairment ECG New AV block or BBB suggests perivalvular invasion CXR Septic pulmonary emboli Trans Thoracic Echocardiography: 98% Specificity for veg Sensitivity <60%; less in obesity, COPD Begin with TTE if pt is good candidate for imaging surface, has native valves, or has low probability of IE Trans Esophageal Echocardiography: Invasive, costly Sens 75-95%, Spec 85-98%. Neg TEE: NPV >92% Consider for pts w/prosthetic valves, high probability of endocarditis, and to evaluate myocardial abscess, perivalvular extension Septic Emboli Osler's Nodes: Painful, erythematous nodules associated with bacterial endocarditis. 4 P’s: Pink Painful Pea-sized Pulp of fingers/toes Splinter Hemorrhages: in the nail bed. Roth Spots Janeway Lesions Nontender, erythematous, hemorrhagic or pustular lesions on palms, soles Petechiae • Not specific for IE but common • Splinter Hemorrhages –Linear, under nailbeds • Conjunctival Petechiae –Hemorrhages on eversion of eyelid Prosthetic Valve Endocarditis Risk of IE EARLY: < 2 months post-op 1% at 12 mos, 2-3% at 60 mos post-op #1 cause: Staph aureus (used to be staph epi) Usually acquired in the hospital: direct intra-op contamination or post-op hematogenous spread Anchoring sutures and valve ring are not yet endothelialized, so more vulnerable LATE: > 2 months post-op Endothelialization occurs over months, making it more difficult for bugs to adhere. Community-acquired. IVDU Classic teaching: IVDU Right-sided IE But left-sided IE may actually be more common 50% Staph Aureus 15% Enterococcus 8% each: Strep, GNR (Pseudomonas or Serratia), Candida May be polymicrobial Major Duke’s Criteria Definite IE: 2 major, 1 major + 3 minor, or 5 minor (+) Blood cultures with appropriate organism Evidence of Coxiella burnetii infection New Valvular regurgitation + Echo findings Minor Duke’s Criteria High-risk for IE, or h/o IVDU Temperature > 38oC Vascular Phenomena Immunologic phenomena Arterial embolism, septic pulm infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions Osler’s nodes, Roth spots, GN, Rheumatoid factor Serologic studies Blood cultures or echo results not meeting the major criteria Therapy: General comments Prolonged IV administration of bactericidal agents(s) x 4-6 wks Culture-negative native-valve endocarditis should be individualized and generally includes penicillin, ampicillin, ceftriaxone, or vanc, +/aminoglycoside Indications for Surgery Refractory CHF, Severe valvular dysfunction Uncontrolled infection Valve perforation, dehiscence, fistula, abscess 1 embolic event with persistent large vegetation, or >1 episode of embolization Prosthetic valve infection Fungal IE New heart block… Conclusions Valvular heart disease associated with spectrum of presentations Recognition prior to the onset of symptoms may be life saving Careful physical exam almost always diagnostic “Pearls” Diastolic murmurs usually represent pathological conditions as do most continuous murmurs. Most important issue in patient with a cardiac murmur is the presence or absence of symptoms. Many asymptomatic children and young adults with grade 2/6 midsystolic murmurs and no other cardiac physical findings need no further cardiac evaluation Many asymptomatic elderly patients have midsystolic murmurs related to sclerotic aortic valve leaflets, flow into tortuous, noncompliant great vessels Such murmurs must be distinguished from murmurs caused by mild to severe valvular aortic stenosis (AS) which is prevalent in this age group.