* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Heart Failiure and Valve disease
Survey
Document related concepts
Cardiovascular disease wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Rheumatic fever wikipedia , lookup
Heart failure wikipedia , lookup
Aortic stenosis wikipedia , lookup
Coronary artery disease wikipedia , lookup
Antihypertensive drug wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Jatene procedure wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Transcript
Cardiology Review: Heart Failure and Valve Disease March 30, 2009 Dr. Lisa Mielniczuk Assistant Professor Medicine University of Ottawa Heart Institute Outline • Heart Failure – Causes – Symptoms – Treatments • Approach to valve disease – Aortic stenosis and regurgitation – Mitral stenosis and regurgitation HF Prevalence in Canada 4 Chow C-M et al. Can J Cardiol 2005;21(14):1265-71. Leadership. Knowledge. Community. Majority of HF Patients Treated by GPs/FPs 5 Tu K et al. Can J Cardiol 2004;20:282-91. Leadership. Knowledge. Community. Why Heart Failure? Projected number of incident hospitalizations for CHF patients, using high, medium and low population growth projections in Canada 1996-2050 HF Cases are on the rise! Definition • Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body • Clinically – Ventricular dysfunction – Reduced exercise capacity – Impaired quality of life – Shortened life expectancy Cardiomyopathy • Characterized by ventricular – Dilatation – Hypertrophy • Frank Starling: CO = SV x HR • Laplace: Tension = Press x rad/ 2 x thick Gross Pathologic Findings • Enlargement of all 4 chambers • Normal valves with regurgitation – Enlargement and distortion of the subvalvular apparatus • Intracavitary thrombi Increased contractility Normal A Heart Failure Hypotension Stroke volume (cardiac output) Heart Failure B C Pulmonary congestion Left ventricular end diastolic pressure (volume) Classification of Cardiomyopathy • Multiple ways to consider classification: – Etiologic – Systolic vs. Diastolic – Right vs. Left – Pathologic General Causes of HF • • • • • • • • • • Coronary artery disease Myocardial infarction Valve disease Idiopathic cardiomyopathy Hypertension Myocarditis / pericarditis Arrhythmias Thyroid disease Pregnancy Toxins (alchohol, chemotherapy) Dilated Cardiomyopathy • CAD is the most common cause of systolic dysfunction • Idiopathic (50%) • Familial • Substance abuse • What are the other nonischemic causes of a dilated cardiomyopathy? • • • • • • • Myocarditis Infiltrative disease Peripartum HIV Chemotherapy Electrolyte imbalance Nutritional: thiamine,scurvy Mechanisms and Causes of HF Impaired Contractility Myocardial infarction Transient ischemia Chronic volume overload MR/AR Dilated cardiomyopathy Increased Afterload AS Uncontrolled HTN Systolic Dysfunction Left Sided HF Diastolic Dysfunction Obstruction of LV filling MS Pericardial constriction or tamponade Impaired ventricular relaxation LVH Hypertrophic cardiomyopathy Restrictive cardiomyopathy Transient ischemia Mechanisms and Causes of HF Cardiac Causes Left sided HF Pulmonary stenosis Right ventricular infarction Right Sided HF Pulmonary Vascular Disease Pulmonary emobolism Pulmonary HTN Right ventricular infarction Parenchymal pulmonary disease COPD Interstitial lung disease Chronic infections Adult respiratory distress syndrome The Heart Failure Continuum Functional Classification ACC/AHA STAGES OF HEART FAILURE STAGE A •High risk for developing HF (diabetes, CKD, HTN) •No structural disorder of the heart STAGE B •Structural disorder of the heart (e.g.. Previous MI) •Not yet developed symptoms of HF STAGE C •Past or current symptoms of HF •Symptoms associated with underlying structural heart disease STAGE D •End stage disease •Requires specialized treatment strategies NYHA FUNCTIONAL CLASS CLASS I •No symptoms and no limitations in physical activity •No shortness of breath when walking, climbing stairs etc. CLASS II •Mild symptoms and slight limitation during ordinary physical activity CLASS III •Marked limitation in activity due to symptoms (fatigue, shortness of breath) with less than ordinary activity (e.g.. Short distances or ADL’s) INCREASING SEVERITY OF HEART FAILURE CLASS IV •Severe limitation, may experience symptoms at rest Stages of Heart Failure STAGE A High risk but no structural heart disease •HTN, ASCD •DM, obesity •FH •cardiotoxins Treat HTN, lipids Smoking cessation ACE or ARB if appropriate STAGE B STAGE C STAGE D Structural heart disease but no symptoms Current or prior symptoms HF Refractory HF •Previous MI •LVH, low EF •Valvular disease •Structural disease plus symptoms •Marked symptoms despite maximal meds •hospitalized ACE or ARB BB Routine: ACE, BB and diuretics Selected: aldo agents, ARBs, dig, nitrates Devices:CRT/ICD End of life MCS transplant Diagnosis of HF • Constellation of symptoms and signs • CXR • Alternative Methods – Invasive hemodynamic studies – Echocardiogram – Serum BNP testing Symptoms and Signs of HF Increased filling pressures Congestion Poor Cardiac Output Poor Perfusion Evaluating the JVP • Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal • http://cal.fmc.flinders.ed u.au/gemp/ClinicalSkills /clinskil/year1/cardio/car dio04.htm Congestion • Left-Sided – Symptoms • Dyspnea • Orthopnea • Paroxysmal nocturnal dyspnea • Fatigue – Signs • • • • • S3 gallop Displaced apex MR Pulmonary rales Loud P2 • Right-Sided – Symptoms • • • • Peripheral edema Abdominal bloating Nausea Anorexia – Signs • • • • Elevated JVP Hepatomegaly Ascites Edema Assessing Perfusion • Symptoms – – – – Fatigue Confusion Dyspnea sweating • Signs – – – – – – Hypotension Tachycardia Cool extremities Altered mental status Rising creatinine Liver enzyme abnormalities Pulmonary Edema • General Considerations – Increase in the fluid in the lung – Generally, divided into cardiogenic and non-cardiogenic categories. • Pathophysiology – Fluid first accumulates in and around the capillaries in the interlobular septa (typically at a wedge pressure of about 15 mm Hg) – Further accumulation occurs in the interstitial tissues of the lungs – Finally, with increasing fluid, the alveoli fill with edema fluid (typically wedge pressure is 25 mm Hg or more) Cardiogenic vs. Noncardiogenic pulmonary edema • Cardiogenic pulmonary edema – Heart failure – Coronary artery disease with left ventricular failure. – Cardiac arrhythmias – Fluid overload -- for example, kidney failure. – Cardiomyopathy – Obstructing valvular lesions -for example – Myocarditis and infectious endocarditis • Non-cardiogenic pulmonary edema -- due to changes in capillary permeability – – – – – – – Smoke inhalation. Head trauma Overwhelming sepsis. Hypovolemia shock Acute lung re-expansion High altitude pulmonary edema Disseminated intravascular coagulopathy (DIC) – Near-drowning – Overwhelming aspiration – Acute Respiratory Distress Syndrome (ARDS) CXR Findings of Pulmonary Edema • cardiogenic pulmonary edema • Non-cardiogenic pulmonary • Kerley B lines (septal lines) edema • • • – Seen at the lung bases, usually no more than 1 mm thick and 1 cm long, perpendicular to the pleural surface Pleural effusions – Usually bilateral, frequently the right side being larger than the left – If unilateral, more often on the right Fluid in the fissures – Thickening of the major or minor fissure Peribronchial cuffing – Visualization of small doughnut-shaped rings representing fluid in thickened bronchial walls – Bilateral, peripheral air space disease with air bronchograms or central bat-wing pattern – Kerley B lines and pleural effusions are uncommon – Typically occurs 48 hours or more after the initial insult – Stabilizes at around five days and may take weeks to completely clear – On CT • Gravity-dependent consolidation or ground glass opacification • Air bronchograms are common cuffing Alveolar edema Kerley B Goals of Therapy • • • • • Identify and Treat the Underlying Cause Eliminate the acute precipitant Manage HF symptoms Modulate the neurohormonal response Improve long-term survival Precipitants of HF • Increased metabolic demands – Fever, anemia, infection, tachycardia, hyperthyroidism, pregnancy • Increased circulating volume – Excessive salt or fluid in diet – Renal failure • Increased afterload – Hypertension – PE • Impaired contractility – Negative inotropes – Ischemia • Failure to take medications Progression of underlying disease Pharmacotherapy ↓cardiac function + inotropes wall stress ↓renal/tissue perfusion vasodilators Peripheral/pulmonary edema BB Neurohormonal changes ANF vascular resistance norepinephrine ACE I diuretics aldosterone sprionolactone Na/fluid accumulation angiotensin II Management Strategy Education Severe symptoms: refer to specialist, ER or HF clinic Risk factor reduction Fluid/salt regimen If EF>40%: treat cause (HTN) If EF<40% ACE I +Beta blocker intolerant Prescribe ARB Consider nitrates Titrate to target doses If QRS>120, consider CRT If EF<30% consider ICD Clinically stable •Add ARB NYHA III •Digoxin or nitrates •Combo diuretics •spironolactone Continue therapy Class IIIb-IV Can J Cardiol 2007; 23 MERIT HF Study The MERIT-HF Study Group, Lancet 1999; 353:2001 US CARVEDILOL TRIAL SOLVD-P Exner, DV, Dries, DL,Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916. CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429 meta-analysis of five trials involving 12,763 patients Flather, MD,Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575 Valvular Disease Mitral Stenosis • Restriction and narrowing of mitral valve • Impairment of left ventricular filling Mitral Stenosis - Causes • Rheumatic Fever (>90% cases) – 50% patients will have known history – Average 20 years prior to clinical symptoms • Congenital stenosis of MV • Extensive calcification • endocarditis MS - Pathophysiology • LA pressure increases – Increased pulmonary pressures • LA dilatation – Atrial fibrillation • Stagnation of blood in LA – thromboembolism MS - Clinical Presentation • Natural history variable • 10 year survival (symptoms) – 50-60% • Early onset – Dyspnea and reduced exercise capacity • Advanced – – – – SOB at rest Pulmonary congestion (orthopnea, PND etc) Pulmonary HTN (RHF) Hoarseness from laryngeal nerve compression MS - Examination • Loud S1 – From high pressure gradient from LA and LV • Opening snap – Sudden tensing of chordae and stenotic leaflets on valve opening • Diastolic murmur – Low frequency – Severity relates to duration MS - Diagnosis • ECG – LAE, RVH – Atrial fibrillation • CXR – LAE, pulmonary vascular redistribution – Prominent pulmonary arteries • Echo – Thickened MV – LAE MS - Treatment • Percutaneous balloon valvuloplasty • Surgical repair • Antibiotics at time of risk • Diuretics for vascular congestion • Decrease HR if AF • anticoagulation Mitral Regurgitation • Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole MR - Causes Mitral Annulus •Annular calcification Leaflets •Rheumatic disease •Endocarditis •Myxomatous disease •prolapse Chordae Tendinae •Rupture •endocarditis Papillary muscle •Dysfunction (MI or ischemia) Left ventricle •Cavity dilatation MR - Pathophysiology • Portion of the LV stroke volume ejected into LA – Forward CO is les than total LV CO • • • • Elevation of LA volume Reduction of forward CO Volume related stress on LV Severity depends on: – – – – Size of orifice during regurge SVR opposing LV blood flow LA compliance Duration of regurgitation MR – Clinical Presentation • Chronic – Fatigue – If LV contractile dysfunction – heart failure • Acute – Pulmonary edema – hypotension MR - Examination • Murmur – Pansystolic murmur heard at apex • S3 – Reflects increased volume returning to LV in early diastole • LV displacement – If LV enlargement present MR - Diagnosis • CXR – Pulmonary edema if acute – Left atrial and ventricular dilatation – Calcification of MV • Echo – Identifies structural cause of MR – LV /LA size and function MR - Treatment • Acute MR – Vasodilators and diuretics – Reduce the resistance to forward flow – Relieve pulmonary edema • Chronic – Operative repair once symptoms develop or LV starts to dilate Aortic Stenosis • Thickened and restricted opening of aortic valve • Obstruction to LV outflow AS - Causes • Age related calcification of valve • Rheumatic heart disease • Congenital bicuspid AV AS - Pathophysiology • Blood flow across the AV is impeded • Once AVA reduced by 50%: – Significant LV pressure needed to drive blood into aorta – Results in LV hypertrophy – Reduced LV compliance • Increased end diastolic pressure AS – Clinical Presentation • Angina – Imbalance b/w myocardial oxygen supply and demand • Syncope – Peripheral vasodilation with inability to augment CO with exercise • HF – Increased LAP from high LVEDP – Contractile dysfunction if longstanding pressure overload Symptom Median survival Angina 5 yrs Syncope 3 years HF 2 years AF 6 months AS -Exam • Murmur – Late peaking systolic ejection murmur • Carotid pulse – Weakend (parvus) and delayed (tardus) due to LV obstruction • S4 – Atrial contraction into stiff LV AS - Treatment • Only effective treatment for severe symptomatic disease is surgical correction • What if asymptomatic? – 20% of patients will progress over 20 years if mild disease only – Endocarditis prophylaxis Aortic Regurgitation AR - Causes • Abnormalities of valve leaflets – Congenital (bicuspid valves) – Endocarditis – Rheumatic • Dilatation of aortic root – Aortic aneursym – Aortic dissection – syphilis AR - Pathophysiology • Severity of AR – Size of regurgitant orifice – Pressure gradient across valve in diastole – Duration of diastole • Acute – LV noncompliant – LVEDP rises quickly – pulmonary edema • Chronic – Chronic volume/pressure overload – Dilates – well compensated AR – Clinical Manifestations • SOB on exertion • Fatigue • Decreased exercise tolerance AR - Examination • Murmur – Blowing diastolic along LSB • Widened pulse pressure Name Description Bisferins Double impulse Corrigans Marked distention and collapse deMusset Head bobbing Duroziez To and fro murmur Hill Greater popliteal SBP Muller Uvula pulsations Quincke Nail bed pulsation Traube Pistol shot femoral art AR - Treatment • Asymptomatic disease progresses very slowly • Surgery if: – Symptoms – Impaired LV function • Death occurs within 4 years after angina or 2 years after HF Summary Slide • Heart Failure – Understand causes of systolic and diastolic HF – Awareness of the presentation of left vs. right HF – Know treatment priniciples • Valve Disease – Identify the most common causes of 4 common valve lesions – Remember clinical presentations – Surgery treatment of choice any time symptoms present