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Cardiology Review: Heart Failure and Valve Disease March 30, 2009

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

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Cardiology Review: Heart Failure and Valve Disease March 30, 2009

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  1. Cardiology Review:Heart Failure and Valve DiseaseMarch 30, 2009 Dr. Lisa Mielniczuk Assistant Professor Medicine University of Ottawa Heart Institute

  2. Outline • Heart Failure • Causes • Symptoms • Treatments • Approach to valve disease • Aortic stenosis and regurgitation • Mitral stenosis and regurgitation

  3. HF Prevalence in Canada Chow C-M et al. Can J Cardiol 2005;21(14):1265-71.

  4. Majority of HF Patients Treated by GPs/FPs Tu K et al. Can J Cardiol 2004;20:282-91.

  5. 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!

  6. 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

  7. Cardiomyopathy • Characterized by ventricular • Dilatation • Hypertrophy • Frank Starling: CO = SV x HR • Laplace: Tension = Press x rad/ 2 x thick

  8. Gross Pathologic Findings • Enlargement of all 4 chambers • Normal valves with regurgitation • Enlargement and distortion of the subvalvular apparatus • Intracavitary thrombi

  9. Heart Failure Increased contractility Normal Stroke volume (cardiac output) A Heart Failure B C Hypotension Pulmonary congestion Left ventricular end diastolic pressure (volume)

  10. Classification of Cardiomyopathy • Multiple ways to consider classification: • Etiologic • Systolic vs. Diastolic • Right vs. Left • Pathologic

  11. General Causes of HF • Coronary artery disease • Myocardial infarction • Valve disease • Idiopathic cardiomyopathy • Hypertension • Myocarditis / pericarditis • Arrhythmias • Thyroid disease • Pregnancy • Toxins (alchohol, chemotherapy)

  12. CAD is the most common cause of systolic dysfunction What are the other non-ischemic causes of a dilated cardiomyopathy? Idiopathic (50%) Familial Substance abuse Myocarditis Infiltrative disease Peripartum HIV Chemotherapy Electrolyte imbalance Nutritional: thiamine,scurvy Dilated Cardiomyopathy

  13. 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 Impaired ventricular relaxation • LVH • Hypertrophic cardiomyopathy • Restrictive cardiomyopathy • Transient ischemia Obstruction of LV filling • MS • Pericardial constriction or tamponade

  14. Mechanisms and Causes of HF • Cardiac Causes • Left sided HF • Pulmonary stenosis • Right ventricular infarction Right Sided HF • Parenchymal pulmonary disease • COPD • Interstitial lung disease • Chronic infections • Adult respiratory distress syndrome • Pulmonary Vascular Disease • Pulmonary emobolism • Pulmonary HTN • Right ventricular infarction

  15. The Heart Failure Continuum

  16. 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) • CLASS IV • Severe limitation, may experience symptoms at rest INCREASING SEVERITY OF HEART FAILURE

  17. Stages of Heart Failure STAGE A High risk but no structural heart disease STAGE B Structural heart disease but no symptoms STAGE C Current or prior symptoms HF STAGE D Refractory HF • Marked symptoms despite maximal meds • hospitalized • Previous MI • LVH, low EF • Valvular disease • Structural disease plus symptoms • HTN, ASCD • DM, obesity • FH • cardiotoxins • Routine: ACE, BB and diuretics • Selected: aldo agents, ARBs, dig, nitrates • Devices:CRT/ICD • End of life • MCS • transplant • ACE or ARB • BB • Treat HTN, lipids • Smoking cessation • ACE or ARB if appropriate

  18. Diagnosis of HF • Constellation of symptoms and signs • CXR • Alternative Methods • Invasive hemodynamic studies • Echocardiogram • Serum BNP testing

  19. Symptoms and Signs of HF Increased filling pressures Poor Cardiac Output Congestion Poor Perfusion

  20. Evaluating the JVP • Consensus: <2 cm above the sternal angle considred normal and >4cm ASA is abnormal • http://cal.fmc.flinders.edu.au/gemp/ClinicalSkills/clinskil/year1/cardio/cardio04.htm

  21. 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 Congestion

  22. Symptoms Fatigue Confusion Dyspnea sweating Signs Hypotension Tachycardia Cool extremities Altered mental status Rising creatinine Liver enzyme abnormalities Assessing Perfusion

  23. 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)

  24. 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) Cardiogenic vs. Noncardiogenic pulmonary edema

  25. cardiogenic pulmonary edema Kerley B lines (septal lines) 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 Non-cardiogenic pulmonary edema 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 CXR Findings of Pulmonary Edema

  26. cuffing Alveolar edema Kerley B

  27. Goals of Therapy • Identify and Treat the Underlying Cause • Eliminate the acute precipitant • Manage HF symptoms • Modulate the neurohormonal response • Improve long-term survival

  28. 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

  29. Pharmacotherapy ↓cardiac function + inotropes  wall stress ↓renal/tissue perfusion Peripheral/pulmonary edema vasodilators BB Neurohormonal changes  vascular resistance  ANF diuretics ACE I  norepinephrine  aldosterone sprionolactone Na/fluid accumulation  angiotensin II

  30. Management Strategy Severe symptoms: refer to specialist, ER or HF clinic If EF>40%: treat cause (HTN) If EF<40% • Education • Risk factor reduction • Fluid/salt regimen intolerant Prescribe ARB ACE I +Beta blocker Consider nitrates Titrate to target doses If QRS>120, consider CRT Continue therapy Clinically stable If EF<30% consider ICD • Add ARB • Digoxin or nitrates NYHA III • Combo diuretics • spironolactone Class IIIb-IV Can J Cardiol 2007; 23

  31. Beta Blockers MERIT HF Study The MERIT-HF Study Group, Lancet 1999; 353:2001

  32. Beta Blockers and Functional Class US CARVEDILOL TRIAL SOLVD-P Exner, DV, Dries, DL, Waclawiw, MA, et al. J Am Coll Cardiol 1999; 33:916.

  33. ACE Inhibitors and Survival CONSENSUS Trial Study Group, N Engl J Med 1987; 316:1429

  34. ACE Inhibitors and Heart Failure meta-analysis of five trials involving 12,763 patients Flather, MD, Yusuf, S, Kober, L, et al. Lancet 2000; 355:1575

  35. Valvular Disease

  36. Restriction and narrowing of mitral valve Impairment of left ventricular filling Mitral Stenosis

  37. 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

  38. MS - Pathophysiology • LA pressure increases • Increased pulmonary pressures • LA dilatation • Atrial fibrillation • Stagnation of blood in LA • thromboembolism

  39. 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

  40. 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

  41. MS - Diagnosis • ECG • LAE, RVH • Atrial fibrillation • CXR • LAE, pulmonary vascular redistribution • Prominent pulmonary arteries • Echo • Thickened MV • LAE

  42. Percutaneous balloon valvuloplasty Surgical repair Antibiotics at time of risk Diuretics for vascular congestion Decrease HR if AF anticoagulation MS - Treatment

  43. Mitral Regurgitation • Structural abnormality of mitral valve apparatus resulting in leaking of blood back to LA during systole

  44. MR - Causes • Mitral Annulus • Annular calcification • Leaflets • Rheumatic disease • Endocarditis • Myxomatous disease • prolapse MOST COMMON: Myxomatous degeneration Papillary muscle dysfunction or cavity dilatation • Chordae Tendinae • Rupture • endocarditis • Papillary muscle • Dysfunction (MI or ischemia) • Left ventricle • Cavity dilatation

  45. 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

  46. MR – Clinical Presentation • Chronic • Fatigue • If LV contractile dysfunction – heart failure • Acute • Pulmonary edema • hypotension

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