Heart valvular disease - Basic concept.pptx

CVS

1. VALVULAR HEART DISEASE Dr.Haritha MEM

2. murmur A murmur is caused by turbulent blood flow. There are 3 main factors: Forward flow through a narrowed outlet Backwards or regurgitant flow through a leaking/ incompetent valve High blood flow in high output states such as anaemia, pregnancy, thyrotoxicosis, sepsis and fever

3. Benign or physiologic murmurs are common and do not cause symptoms or findings compatible with cardiovascular disease. They are generally soft systolic ejection murmurs that begin after S1, end before S2, and are not associated with other abnormal heart sounds. Anaemia Sepsis Volume overload, or other conditions causing an increased cardiac output. Any diastolic murmur or new systolic murmur with symptoms at rest is pathologic and warrants emergent echocardiography

4. types Mitral stenosis Mitral regurgitation Mitral valve prolapse Aortic stenosis Aortic regurgitation Right sided valvular heart disease Prosthetic valve disease The major valvular emergencies are: Infective endocarditis Papillary muscle rupture or flail mitral (posterior) leaflet due to ruptured chordae tendineae Prosthetic valve thrombosis / dehiscence

5. MITRAL STENOSIS Mitral stenosis prevents normal diastolic filling of the left ventricle. Symptoms may not occur until the valve area is reduced to 1-1.5 cm2 (normal 4-6 cm2)  Mitral annular calcification is a slowly progressive nonrheumatic cause of mitral stenosis. It is more common among women, the elderly, and those with hypertension or with chronic renal failure.

6. Pathophysiology of mitral stenosis

7. Clinical features Exertional dyspnea , Orthopnoea - Breathlessness on exertion is often the first symptom noticed. Acute pulmonary oedema – Hyperdynamic states with an associated tachycardia such as pregnancy, infection, uncontrolled AF and anaemia may result in a worsening of symptoms Atrial fibrillation - Risk of left atrial thrombus and systemic embolism Haemoptysis – used to be 2 nd most common presentation but rare. Fatigue (due to reduced cardiac output)

8. Opening snap after aortic valve closure Pre systolic attenuation

9. treatment Medical management focuses primarily on symptom control and anticoagulation. Patients in atrial fibrillation or with dyspnea on exertion may benefit from heart rate control with a β-blocker or calcium channel blocker Anticoagulants - left atrial diameter is >55 mm or the patient has atrial fibrillation, a left atrial thrombus, or history of systemic emboli. Haemoptysis from pulmonary HTN – may require bronchoscopy The primary treatment for symptomatic disease is percutaneous mitral commissurotomy, optimally performed before onset of severe pulmonary hypertension.

10. Mitral regurgitation Mitral regurgitation occurs when a dysfunctional valve allows retrograde blood flow from the left ventricle into the left atrium during systole. This causes volume overloading of the left atrium and an increased workload for the ventricle to maintain the ejection fraction. Mitral valve prolapse is another cause and is typically found in younger patients.

11. A high-pitched holosystolic murmur is best heard in the fifth intercostal space and mid-left thorax and radiates to the axilla. The first heart sound is soft and often obscured by the murmur. An S3 is usually heard and is followed by a short diastolic rumble, indicating increased flow into the left ventricle

12. treatment Think of acute mitral regurgitation in any patient with new-onset and marked pulmonary edema Acute mitral regurgitation due to papillary muscle rupture, emergency surgery is the treatment of choice. In the ED, start therapy with oxygen and positive-pressure ventilation for respiratory failure (pulmonary edema ) Nitrates - afterload reduction, which results in increased forward flow into the aorta Inotropes For severe mitral regurgitation from acute myocardial infarction includes emergent revascularization For chronic mitral regurgitation, emergency treatment is based on acute symptoms. Control atrial fibrillation with rapid ventricular response with β- blockers or calcium channel blockers, and start anticoagulation to avoid embolization

13. Mitral valve prolapse Mitral valve prolapse is a systolic billowing of one or both leaflets into the left atrium occurring with or without mitral regurgitation More commonly in women. Most cases are idiopathic or acquired secondary to IHD, Rheumatic heart disease and hypertrophic cardiomyopathy. It is characterized by myxomatous degeneration of the valve caused by heritable defects in connective tissue proteins.

14. pathophysiology One or both of the mitral valve leaflets show fibromyxomatous changes. At the end of diastole the valve closes normally but as the pressure in the LV rises the leaflet proplases back into the LA. Strain on the papillary muscles can lead to mitral regurgitation.

15. Most patients are asymptomatic, but symptoms may include chest pain, palpitations, fatigue, anxiety, and dyspnea unrelated to exertion.

16. The classic auscultatory finding is a mid-systolic click Manoeuvres that decrease preload, such as Valsalva or standing, will cause the click to occur earlier in diastole. Increasing preload by squatting or afterload by hand grips causes the systolic click to move later in systole. A late systolic murmur that crescendos into S2 may be present.

17. treatment Echocardiography will confirm the diagnosis Patients with palpitations attributed to mitral valve prolapse may respond to oral β-blockers, but that is typically left to the cardiologist or primary care physician Antithrombotic therapy is not routinely recommended unless complicated by transient ischemic attacks, stroke, or atrial fibrillation. Patients with concomitant mitral regurgitation require endocarditis prophylaxis

18. Aortic stenosis Aortic stenosis prevents left ventricular outflow. LV outflow obstruction can also be produced by a congenital abnormality above the valve (supra-valvular aortic stenosis) or by sub-valvular obstruction due to muscular hypertrophy as seen in hypertrophic cardiomyopathy. AS is severe once the valve area has decreased to 1cm 2  or less (normal 3-4 cm 2 ) Hypertension, smoking and raised cholesterol are all risk factors for aortic valve calcification

19. Clinical features Breathlessness is usually the first symptom, followed by paroxysmal nocturnal dyspnoea, exertional syncope, angina and acute myocardial infarction. The sudden onset of atrial fibrillation (AF) may cause an acute progression of symptoms. GI bleeding from angiodysplasia may occur.

20. Classic physical examination findings are a late peaking systolic murmur at the right second intercostal space radiating to the carotids, a single or paradoxically split S2, an S4 gallop, and a diminished carotid pulse with a delayed upstroke. Brachioradial delay may also be a useful early finding, as is a narrowed pulse pressure.

21. treatment Low-dose dobutamine stress echocardiography aids identification prior to the development of classic symptoms Pulmonary edema - oxygen and positive-pressure ventilation. Negative inotropic drugs like β-blockers or calcium channel blockers, are often poorly tolerated. Use nitrates, vasodilators, and diuretics with close monitoring because reducing preload may cause significant hypotension. New-onset atrial fibrillation may require cardioversion to maintain cardiac output. Surgical management, either open or by transcatheter approach, is a mainstay of treatment. Endocarditis in isolated aortic stenosis is uncommon, and antibiotic prophylaxis is not routinely recommended

22. Aortic regurgitation Aortic regurgitation occurs when valve leaflets fail to close fully, causing blood to flow from the aorta into the left ventricle during diastole

23. pathophysiology

24. Clinical features Acute aortic regurgitation generally presents rapidly, with dyspnea and pulmonary edema . To maintain cardiac output, tachycardia develops but is often inadequate, resulting in cardiogenic shock or cardiac arrest. Sudden-onset ripping or tearing interscapular pain suggests aortic dissection. Fever or history of IV drug abuse suggests endocarditis Chronic aortic regurgitation typically present with exertional dyspnea or fatigue. Chest pain may occur from myocardial ischemia due to low diastolic pressures that decrease coronary blood flow. Symptoms of left ventricular failure may occur late in the disease, but greater than one quarter of patients with chronic aortic regurgitation die or develop left heart dysfunction before symptoms occur

25. The classic finding is a high-pitched blowing diastolic murmur heard immediately after S2, in the second or third intercostal space at the left sternal border. In acute disease, the murmur may be inaudible due to tachycardia, tachypnea , and rales. A systolic ejection murmur due to increased stroke volume and an S3 due to ventricular dilatation may exist. In the left lateral decubitus position, listen for a mid-diastolic rumble (Austin Flint murmur) using the bell of the stethoscope at the cardiac apex

26. Diagnosis & treatment The most common abnormality is left ventricular hypertrophy. Ischemic changes or ST elevation may be seen from aortic dissection involving the coronary arteries. In chronic aortic regurgitation, the chest radiograph reveals cardiomegaly, aortic dilatation, and, possibly evidence of congestive heart failure. Echocardiography confirms the diagnosis and determines the cause and severity of regurgitation. Unstable patients require emergency echocardiography edema without cardiac enlargement. If due to aortic dissection, the chest radiograph may show a widened mediastinum. If suspecting aortic dissection, perform CT angiogram

27. treatment Acute aortic regurgitation requires immediate surgical intervention. Treat pulmonary edema with oxygen and intubation for respiratory failure. Vasodilators such as nitroprusside, combined with inotropic agents such as dobutamine or dopamine, may augment forward flow and reduce left ventricular end-diastolic pressure. Diuretics and nitrates are usually ineffective. Although β-blockers are commonly used in aortic dissection, avoid these in acute aortic regurgitation because they block the compensatory tachycardia that is critical in maintaining cardiac output. Chronic aortic regurgitation is treated with vasodilators such as angiotensin-converting enzyme inhibitors or dihydropyridine calcium channel blockers. If acute symptoms such as pulmonary edema or chest pain occur, admit the patient for stabilization and further management. Patients who become symptomatic, have a low ejection fraction, or have significant left ventricular dilatation are candidates for aortic valve replacement , either open or by transcatheter approach.

28. Right sided valvular heart disease The incidence of true right-sided valvular heart disease is unknown because normal subjects frequently have a small amount of tricuspid and pulmonary valve regurgitation at baseline. Pathologic tricuspid regurgitation is usually due to elevated right heart pressure or volume overload, such as from pulmonary hypertension, chronic lung disease, pulmonary embolism, or atrial septal defects. Tricuspid stenosis is rare and is generally accompanied by regurgitation. The pulmonic valve is the least likely valve to be affected by acquired disease. Most pulmonic valvular disease is congenital, although pulmonary hypertension, rheumatic heart disease, and carcinoid syndrome can rarely cause some degree of pulmonic valve disease. Acute onset of symptomatic tricuspid disease is most often due to endocarditis. Tricuspid valve endocarditis typically involves aggressive organisms, such as Staphylococcus aureus, which can cause rapid valve destruction.

29. Clinical features Clinically significant right-sided valvular disease causes signs and symptoms of right heart failure such as Jugular venous distention Peripheral edema Hepatomegaly Splenomegaly Ascites. Exertional dyspnea is often the first symptom in patients with right-sided valvular disease associated with pulmonary hypertension.

30. TRICUSPID REGURGITATION Patients with tricuspid valve regurgitation from endocarditis may have signs of sepsis. The murmur of tricuspid valve regurgitation is soft, blowing, and holosystolic. It is best heard along the lower left sternal border and increases with inspiration. A systolic waveform in the jugular vein, hepatic pulsations, and systolic eyeball propulsion may be seen in severe tricuspid incompetence

31. TREATMENT

32. TREATMENT Treatment of right-sided valvular heart disease is aimed at the underlying cause. Treat endocarditis with antibiotics. For patients with functional tricuspid or pulmonic regurgitation, treat the cause of pulmonary hypertension or right-sided failure. Diuretics treat the effects of elevated venous pressure, such as lower extremity edema , ascites, and hepatic congestion. Patients with symptomatic pulmonic or tricuspid stenosis may be candidates for balloon valvotomy, and those with severe tricuspid regurgitation due to a structural valve abnormality may require valve replacement

33. Prosthetic valve disease Mechanical valves are more durable with lower failure rates, but have a higher risk for thromboembolic complications. Lifelong anticoagulation is necessary to reduce the thromboembolic risk. Embolic risk is highest during the first 3 postoperative months. Emboli are more common from mitral rather than from aortic valves. Bioprosthetic valves , from porcine, bovine, or human sources, are less thrombogenic but are more likely to fail and require repeat surgery. Antiplatelet therapy is recommended for all patients with prosthetic valves

34. Clinical features Acute onset of respiratory distress, pulmonary edema , and cardiogenic shock may be associated with mechanical valve failure, tearing of a bioprosthesis , or a large clot obstructing the valve or preventing closure. Failures often result in sudden death. A paravalvular leak also presents with congestive heart failure. The severity of symptoms is dependent on leak size and how rapidly the leak develops

35. Diagnosis & treatment Patients with bioprostheses usually have a normal S1 and S2, with no abnormal opening sounds. Mechanical valves normally have a loud, clicking, metallic sound associated with valve closure. Systolic murmurs of prosthetic aortic valves are common, but loud diastolic murmurs should be considered pathologic; a “quiet” mechanical valve is concerning. A loud holosystolic murmur indicates prosthetic mitral valve dysfunction. Aortic bioprostheses usually cause a short mid-systolic murmur, and mitral bioprostheses may cause a short diastolic rumble. Emergency cardiothoracic counsultation is recommended.

36. REVERSAL OF ANTICOAGULATION WITH PROSTHETIC VALVES Prosthetic valves patients seen in the ED are frequently on prophylactic anticoagulation. Emergency physicians must know how to treat supratherapeutic anticoagulation with or without bleeding. An INR >5 confers a high risk of excess bleeding, but rapid changes in anticoagulation pose an equally ominous risk of valve thrombosis and thromboembolism. Patients with an INR of 5 to 10 without bleeding have warfarin withheld; another possible added step is low-dose oral vitamin K reversal, 1.0 to 2.5 milligrams. Patients with severe bleeding complications are best treated with fresh frozen plasma or prothrombin complex concentrate.3 Avoid parenteral, high-dose vitamin K due to risk of overcorrection.

37. Infective endocarditis Infective endocarditis (IE) is a infection of the heart's lining or valves. It's a serious condition that can be life-threatening if not treated promptly.  Bacteria >>> Viral Endocarditis patients often have nonspecific signs and symptoms, but endocarditis has the potential for multiorgan involvement.

38. Causative organism Staphylococcus is the single most common cause, followed by streptococci (including viridans group streptococci) and enterococci. Other rarer causes of infectious endocarditis include Rickettsia, Chlamydophila, Bartonella, Coxiella burnetii , Legionella, Candida, and Aspergillus. Early prosthetic valve endocarditis is most commonly caused by perioperative colonization from Staphylococcus epidermidis, Aspergillus, or Candida albicans. Blood cultures are the best method for detection, but are negative in about 5% of patients; 33% to 50% of culture-negative endocarditis is attributed to prior antibiotic administration. For culturenegative cases without prior antibiotic administration, infection is most often due to fastidious organisms (usually from the HACEK group— Haemophilus, Aggregatibacter , Cardiobacterium , Eikenella , and Kingella — and also Bartonella and Coxiella burnetii ).25

39. RISK FACTORS High risk Prosthetic valves. Previous bacterial endocarditis. Aortic valve disease. MR or mixed mitral disease. Cyanotic congenital heart disease. PDA. Uncorrected left-to-right shunt. Intracardiac and systemic–pulmonary shunts. Moderate risk Mitral valve prolapse (MVP) with regurgitation or valve thickening. Isolated mitral stenosis. Tricuspid valve disease. Pulmonary stenosis. Hypertrophic cardiomyopathy. Bicuspid aortic valve disease. Degenerative valve disease in the elderly. Mural thrombus (e.g. post-infarction).

40. RISK FACTORS Low risk MVP without regurgitation. Tricuspid regurgitation without structural valve abnormality. Isolated ASD. Surgically corrected left-to-right shunt, with no residual shunt. Calcification of MV annulus. IHD and/or previous CABG. Permanent pacemaker. Atrial myxoma. Other predisposing factors Arterial prostheses or AV fistulae. Recurrent bacteraemia (e.g. IV drug users, severe periodontal disease, colon carcinoma). Conditions predisposing to infections (e.g. diabetes, renal failure, alcoholism, immunosuppression). Recent central line.

41. Clinical features Infection malaise, anorexia, weight loss, fever, rigors, and night sweats. Long-standing infection anaemia, clubbing, and splenomegaly. Cardiac manifestations congestive cardiac failure (CCF), palpitations, tachycardia new murmur, pericarditis, or AV block. Signs due to immune complex deposition: Skin: petechiae (most common), Splinter haemorrhages Osler’s nodes [small tender nodules (pulp infarcts) on hands and feet, which persist for hours to days] Janeway lesions (non-tender, erythematous, and/or haemorrhagic areas on the palms and soles).

42. Eye Roth spots (oval retinal haemorrhages with a pale centre, located near the optic disc) conjunctival splinter haemorrhages retinal flame haemorrhages. Renal microscopic haematuria Glomerulonephritis Renal impairment. Cerebral: toxic encephalopathy. Musculoskeletal: arthralgia or arthritis.

43. Dukes criteria for ie Major criteria Positive blood culture Typical microorganism for IE from two separate blood cultures. Persistently positive blood culture Evidence of endocardial involvement : Positive echocardiogram Oscillating intracardiac mass (vegetation). Abscess. New partial dehiscence of prosthetic valve. New valve regurgitation. Minor criteria Predisposing condition or drug use. Fever >38°C. Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial and conjunctival haemorrhage, Janeway lesions. Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor. Microbiological evidence: positive blood cultures, but not meeting major criteria, or serological evidence of organism consistent with IE. Echo: positive for IE, but not meeting major criteria

44. Dukes criteria for ie Definite endocarditis:  2 major criteria or 1 major and 3 minor criteria or 5 minor criteria. Possible endocarditis:  findings which fall short of definite endocarditis but are not rejected. Rejected diagnosis : firm alternative diagnosis, or sustained resolution of clinical features with <4 days of antibiotic therapy.

45. diagnosis Chest radiographs may demonstrate pulmonic emboli (often in multiple areas) in patients with right-sided valvular involvement or may show acute heart failure in those with left-sided valvular involvement. Echocardiography – inflammative changes There are no definitive laboratory tests that diagnose endocarditis - Common findings are anemia (70% to 90%), hematuria , and elevation of erythrocyte sedimentation rate (>90%), C-reactive protein, or procalcitonin. In patients with confirmed endocarditis, repeat blood cultures every 48 to 72 hours to assess treatment progress.

46. treatment DEFINITIVE TREATMENT OF ENDOCARDITIS Base definitive antibiotic treatment on culture and sensitivity results. Most patients will require 4 to 6 weeks of antibiotic therapy.

47. references Valvular Heart Disease – RCEMLearning Washington manual of medical therapeutics Tintinally manual of emergency medicine Rosens emergency medicine concepts and clinical practice Oxford text book of acute medicine