1. Murmurs and valvular heart disease Dr. John Edmond MD FRCP

2. Objectives By the end of this session, you will be able to; –Describe the symptoms and clinical findings of the most common valvular abnormalities –Discuss the clinical importance of identifying cardiac murmurs –Understand the limitations of auscultation

3. What is a murmur? Abnormal heart sounds that are produced as a result of turbulent blood flow which is sufficient to produce audible noise.

4. Are murmurs important? Of course! But only if taken into account as part of the clinical examination of the patient

5. Clinical vs. noise Ventricular septal defect; Small hole; High pressure maintained between LV and RV throughout systole. High velocity flow, all through systole. Big noise, all through systole

6. Clinical vs. noise Ventricular septal defect; Big hole; Pressure quickly equalises between LV and RV. High volume flow, but no great velocity and only at beginning of systole. Little noise, early systole only

7. How the system works The heart is a pump. –Passive flow Gravity Pressure from muscle pumps –Active flow Atrial and ventricular contractions –Both require valves to ensure flow is in correct direction.

8. The system works in series; –Venous return –Right atrium –Right ventricle –Pulmonary artery –Pulmonary veins –Left atrium –Left ventricle –Aorta Tricuspid valve Pulmonary valve Mitral valve Aortic valve

9. Basic valvular anatomy

10. Small groups, 15 minutes Aortic stenosis Aortic regurgitation Mitral stenosis Mitral regurgitation Describe; –Haemodynamics –Symptoms –Clinical signs

11. Aortic stenosis

13. Haemodynamics –Left ventricle hypertrophies –Massively increased LV pressures –High LV filling pressure increases LA pressure –Low systemic blood pressure

14. Aortic Stenosis NB: Pullback gradient is different to PIG obtained by echo

15. Aortic Stenosis

16. Aortic stenosis Haemodynamics –Massively increased LV pressures –Low systemic pressure Symptoms –Breathlessness –Angina –(Pre) syncope –Sudden cardiac death

17. Aortic stenosis Signs –Low pulse pressure –Slow rising pulse –Heaving apex –Murmur, radiating to neck –Quiet A2

18. Aortic stenosis TimingSystolic ShapeCrescendo-decres’ LocationUpper right sternal border RadiationTo carotids IntensityVariable PitchHigh QualityHarsh

19. Aortic regurgitation

21. Haemodynamics –Left ventricle dilates –Increased diastolic pressure leads to increased atrial pressures. Clinical –Breathlessness –Angina

22. Aortic regurgitation Haemodynamics –Left ventricle dilates –Increased diastolic pressure leads to increased atrial pressures. Clinical –Breathlessness –Angina

23. Aortic regurgitation Signs –Quinkes sign –Corrigans sign –De Musset’s sign –Duroziez’s sign –Large volume, collapsing pulse –Apex displaced, thrusting –Murmur(s)

24. Aortic regurgitation TimingEarly….diastole ShapeDecrescendo LocationAortic RadiationLower L sternal edge IntensityVaried PitchHigh QualityBlowing

25. Mitral stenosis

27. Haemodynamics –Increased left atrial pressure –Increased back pressure into lungs, R heart Clinical –Atrial arrhythmias, potentially emboli –Fatigue –Breathlessness –Central cyanosis with “Mitral facies”

28. Mitral stenosis

29. Mitral Stenosis

30. Mitral stenosis Haemodynamics –Increased left atrial pressure –Increased back pressure into lungs, R heart Clinical –Atrial arrhythmias, potentially emboli –Fatigue –Breathlessness –Central cyanosis with “Mitral facies”

31. Mitral stenosis Signs –Mitral facies –Low volume pulse, often irregular (AF) –Apex not displaced (possibly tapping) –Left parasternal heave –Murmur

32. Mitral stenosis TimingEarly-mid diastole (OS) ShapeDecrescendo LocationApex RadiationAxilla IntensityVaried PitchLow QualityRumbling

33. Mitral regurgitation

35. Haemodynamics –Left ventricle dilates –Left atrium dilates –Increased pressure in lungs and R heart

36. Mitral regurgitation Haemodynamics –Left ventricle dilates –Left atrium dilates –Increased pressure in lungs and R heart Clinical –Atrial arrhythmias –Breathlessness –May be asymptomatic for many years

37. Mitral regurgitation Signs –Normal pulse (?irregular) –Thrusting displaced apex –Left parasternal heave –Murmur

38. Mitral regurgitation TimingHolosystolic ShapePansystolic LocationApex RadiationTo axilla IntensityVariable PitchHigh pitched QualityBlowing

39. Ventricular septal defect TimingThroughout systole ShapePansystolic LocationLower L sternal edge RadiationOften widely IntensityVaried PitchVaried QualityHarsh

40. WHAT IS THE MOST IMPORTANT QUESTION IN MEDICINE???

41. WHY?

42. Always ask “WHY?” Rheumatic fever Infection (endocarditis) Ischaemic heart disease (acute/chronic) LV dilatation (but again, why?) Aortic dissection Aging (degenerative) Congenital

43. Rheumatic fever Streptococcal infection, usually as child Generalised febrile illness, sore throat Joint disease Heart disease “Rheumatic fever licks the joints but bites the heart”

44. Rheumatic fever Generally a disease of poverty Extremely rare in the UK Endemic in 3 rd World Important part of any introductory history.

45. What happens if something goes wrong Nothing! –Compensation over many years –Haemodynamics slowly worsen –Patient feels “old” Breathless Tired all the time Chest pain –Final decompensation…..

47. Acute mitral regurgitation Acute ventricular septal defect Infective endocarditis leading to valve destruction Acute valvular changes are much less well tolerated than chronic disease, leading to acute heart failure, often fatal. Things can develop acutely

48. What can be done? Early assessment of patient –Clinical history –Clinical examination –ECG –Chest xray –Echocardiography –Cardiac catheterisation Regular assessment of patient

49. Echocardiography Ultrasound examination of the heart and great vessels Can be transthoracic (TTE) or transoesphageal (TOE)

51. Echocardiography pitfalls Ultrasound waves used; –Limited discrimination –Have to pass through fat, past lungs etc –Takes time to get good images. Transoesphageal echo can help.

52. What can be done? Medical therapy –Diuretics –Vasodilators –Anti-arrhythmics –Aspirin or anticoagulation Surgery –Percutaneous –Open surgery

53. Valve surgery Alter the native valve –Valvotomy –Open repair Replace the valve –Homograft –Xenograft –Metalic valve

54. Xenograft Do not require anticoagulation Can degenerate

55. Metallic valve Do require anticoagulation; –INR often >3.0 Apparently last for ever! Audible valve clicks

56. Infective endocarditis Infection on a heart structure –Usually an already abnormal valve –Can be any other structure or abnormality –Usually bacterial –Can be fungal Overall mortality 20%

57. Infective endocarditis Presents as generalised sepsis –Fevers, night sweats, weight loss –New murmur –Raised inflammatory markers –Positive blood cultures “Duke Criteria” for diagnosis. A)+ve blood cultures, endocardial involvement B)Predisposition, fever, vascular phenom’, serological tests, etc.

58. Infective endocarditis Commonly; –Prosthetic valve –Prior endocarditis –Aortic valve disease –Mitral valve disease –Coarctation –Congenital heart disease –Tricuspid valve in drug addicts Uncommon; –HCM –Pacing wires –ASD –Coronary stents –Surgically repaired VSD or ASD with no residual defect

59. Duke criteria MAJOR CRITERIA –+ve blood culture for typical organism –Evidence of endocardial involvement MINOR CRITERIA –Predisposition –Fever –Vascular phenomena –Immunological phenomena –Microbiological evidence –Echocardiographic evidence Diagnosis; 2 major 1 major + 3 minor 5 minor

60. Questions??

61. Valvular heart disease; summary Valvular heart disease is a common cause of cardio-respiratory symptoms Ausculatation alone dose not help diagnose or classify the disease As always in medicine; –Put THE WHOLE picture together –Ask yourself why this is happening to your patient