Valvular Heart Disease.pptx

Physiotherapy in Valvular Heart Disease

1. Valvular Heart Disease Dr. Shilpasree saha (PT) ASSISTANT PROFESSOR, NIHS

2. contents INTRODUCTION STENOSIS REGURGITATION AORTIC STENOSIS AORTIC INSUFFICIENCY MITRAL STENOSIS MITRAL INSUFFICIENCY

3. Introduction Malfunction of the heart valves, which can be caused by infection, congenital abnormalities, aging, or disease, is much more common on the left side of the heart than on the right and often involves more than one valve. Valvular abnormalities are often asymptomatic for years to decades, but eventually cardiac function may become impaired, resulting in diastolic dysfunction, systolic dysfunction, or both, with consequent pulmonary or systemic vascular congestion, as well as decreased cardiac output.

4. When valve disease is severe, heart failure and sudden death may occur. Abnormal valvular structures create turbulent blood flow,,which increases the hemodynamic stress on these structures and leads to progressive damage and dysfunction. Compensatory mechanisms, including ventricular hypertrophy, chamber dilatation, and peripheral adaptations, can help to maintain the overall performance of the heart for may years, often decades, even when there is malfunction of more than one valve. Eventually, however, these compensatory mechanisms may become exhausted so that heart failure develops.

5. Valvular Stenosis Restriction of blood flow due to narrowing of valvular opening, creates an obstruction to forward flow through the valve and thus a pressure and volume load on the chamber preceding it and generates a pressure gradient across the valve that is proportional to the severity of stenosis. Concentric hypertrophy develops in response to the pressure load and attempts to normalize the SV that is pumped through the narrow valve.

6. Valvular Regurgitation/ Insufficiency Incompetent valve closure results in backward flow (regurgitation) of blood from the receiving chamber or vessel to the antecedent chamber or vessel. This creates a volume load (normal filling volume plus regurgitant volume) on the chambers or vessels on both sides of the affected valve, leading to dilatation and often hypertrophy.

7. Aortic Stenosis Causes: Congenital; Senile calcification; Valvulitis; Rheumatic fever; Severe atherosclerosis

8. Pathophysiology Restricted opening of the AoV Increase pressure load on LV Increase LV systolic pressure, prolongation of ejection Left ventricular hypertrophy Decrease Compliance Increase LV filling pressures dependence of adequate LV filling on atrial contraction Increase Risk of subendocardial ischemia Increase pressures in pulmonary vessels and RV

9. Most commonly, the left ventricular wall thickening occurs in response to pressure overload, and chamber dilatation occurs in response to the volume overload.

10. Clinical Manifestations May be asymptomatic, even with significant AS, for many years. Once symptoms develop, prognosis is poor. Dyspnea, especially on exertion Angina pectoris Lightheadedness, Syncope on exertion: Syncope is caused by the decrease in cerebral perfusion occurring during exertion when the arterial pressure declines due to systemic vasodilation and an inadequate increase in cardiac output related to stenosis. Sudden death Possible systemic emboli Harsh systolic ejection murmur at second ICS radiating to the neck

11. Evaluation Echocardiography remains the standard approach method to evaluate and follow-up patients with aortic stenosis and stratify them for the surgery. It allows imaging of the valve anatomy and the severity of valve calcification and can also allow direct imaging of the orifice area. Exercise testing helps in unmasking symptoms in asymptomatic patients, but it should be avoided in symptomatic patients. Cardiac computed tomography (CT) use is expanding in patients with calcific aortic valve disease. It is used when all the non-invasive tests are inconclusive. Cardiac magnetic resonance imaging (MRI) can assess LV mass, function, and volume when it cannot be obtained readily in echocardiography.

12. Aortic Insufficiency/Regurgitation Causes: Congenital, RF, Endocarditis, Aortic root disease, Other (e.g., rheumatic arthritis, SLE)

13. Incomplete closure of the AoV Backflow of blood to left ventricle Left ventricular hypertrophy & dialation Increase left atrial pressure Left sided heart failure (late stage) Left atrium hypertrophy Increase pulmonary pressure Right sided HF Increase right ventricular Pressure

14. Clinical Manifestations If chronic AI, gradual LV dilatation allows asymptomatic status for decades, then similar to AS, except for less angina and syncope.

15. Mitral Stenosis Mitral stenosis is almost always rheumatic in origin. In older people it can be caused by heavy calcification of the mitral valve apparatus. There is also a rare form of congenital mitral stenosis.

16. In rheumatic mitral stenosis, the mitral valve orifice is slowly diminished by progressive fibrosis, calcification of the valve leaflets, and fusion of the cusps and subvalvular apparatus. The flow of blood from LA to LV is restricted and left atrial pressure rises, leading to pulmonary venous congestion and breathlessness. There is dilatation and hypertrophy of the LA and left ventricular filling becomes more dependent on left atrial contraction.

17. The mitral valve orifice is normally about 5 cm2 in diastole and may be reduced to 1 cm2 in severe mitral stenosis. Patients usually remain asymptomatic until the stenosis is less than 2 cm2. Reduced lung compliance, due to chronic pulmonary venous congestion, contributes to breathlessness, and a low cardiac output may cause fatigue.

18. Pathophysiology

19. symptoms Breathlessness (pulmonary congestion) Fatigue (low cardiac output) Oedema, ascites (right heart failure) Palpitation (atrial fibrillation) Haemoptysis (pulmonary congestion, pulmonary embolism) Cough (pulmonary congestion) Chest pain (pulmonary hypertension) Thromboembolic complications (e.g. stroke, ischaemic limb)

20. Signs Atrial fibrillation Mitral facies Auscultation: Loud first heart sound, opening snap Mid-diastolic murmur Crepitations, pulmonary oedema, effusions (raised pulmonary capillary pressure)

21. The forces that open and close the mitral valve increase as left atrial pressure rises. The first heart sound (S1) is therefore loud and can be palpable (tapping apex beat). An opening snap may be audible and moves closer to the second sound (S2) as the stenosis becomes more severe and left atrial pressure rises. However, the first heart sound and opening snap may be inaudible if the valve is heavily calcified.

22. Mitral insufficiency Aetiology LV dilatation, Calcification, RF, Infective endocarditis, Papillary muscle dysfunction, Chordal rupture, MVP

23. Clinical features Fatigue Irregular heart sound (heart murmur) Irregular heartbeat Shortness of breath

24. Mitral Valve Prolapse Mitral valve prolapse is a type of myxomatous valve disease. The tissue of the mitral valve leaflets and chordae are abnormally stretchy, so that as the heart beats, the mitral valve bows or flops back into the left atrium.

25. Etiology MVP usually occurs as an isolated condition in connective tissue disorders such as Marfan syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum syndrome.

26. PATHOPHYSIOLOGY MVP is the primary myxomatous degeneration of one or both leaflets of the mitral valve. Myxomatous degeneration may involve valve leaflet abnormalities, chordae tendinaeae weakening, and elongation, mitral annular dilatation or thickened leaflet tissue, elongated chordae, mitral annular enlargement leading to segmental mitral leaflet prolapse. Other pathophysiological changes include fibroelastic deficiency characterized by thin, translucent and smooth leaflets or deficiency in elastin, proteoglycan, and collagen with connective tissue deficiency.

27. Endothelium disruption leads to complications such as infectious endocarditis and thromboembolism. Most MVP individuals have minimal mitral valve structure derangement which is not clinically significant. There is usually a gross redundancy of the mitral valve leaflets which fails coaptation of the leaflets during systole, leading to mitral insufficiency.

28. PHYSICAL SYMPTOMS Frequently asymptomatic. MVP can be asymptomatic and can also present with symptoms of atypical chest pain, palpitations, dyspnea on exertion, and exercise intolerance.

29. Over the years, it has been noted that patients with MVP do develop a range of autonomic symptoms that include: Panic attacks Anxiety Exercise intolerance Palpitations Fatigue Atypical chest discomfort Orthostasis Mood changes Syncope

30. DIAGNOSIS The most useful method of making a diagnosis of MVP is by echocardiogram. Mitral Valve Prolapse is defined as mitral valve displacement more than 2 mm above mitral annulus in long-axis view

31. MEDICAL AND SURGICAL TREATMENT MVP patients with no symptoms often require no treatment. MVP patients with symptoms of dysautonomia (chest pain, palpitations), should be treated with beta-blockers such as propranolol. MVP with severe mitral regurgitation may benefit from mitral valve repair or mitral valve replacement. Asymptomatic patients with mitral valve prolapse are managed conservatively with observation and monitoring. If the patient is symptomatic with palpitations, anxiety, chest pain, other etiologies should be ruled out. Symptomatic patients with severe mitral regurgitation, systolic heart failure, and symptom progression require surgical intervention.

32. Specific Treatment

33. Other Regular monitoring of cardiac function to determine necessity of surgical interventions before irreversible deterioration develops or risk of sudden death becomes significant Lifestyle modifications (e.g., salt restriction; avoidance of caffeine, alcohol, and nicotine) Prophylactic antibiotics to prevent endocarditis

34. Treatment for CHF Treatment for pulmonary edema and shock if acute Antiarrhythmic agents, as indicated

35. Surgical interventions once symptomatic: Balloon valvuloplasty or valvulotomy/commissurotomy for valvular stenosis Valvuloplasty or annuloplasty for valvular incompetence Valve replacement Heart transplantation for extremely high-risk individuals