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.

7. 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.

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

10. 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

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

12. 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

13. 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.

14. AORTIC INSUFFICIENCY/REGURGITATION
Causes:
• Congenital,
• RF,
• Endocarditis,
• Aortic root disease,
• Other (e.g., rheumatic arthritis, SLE)

15. 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

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

17. 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.

18. • 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.

19. • 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.

20. PATHOPHYSIOLOGY

21. 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)

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

23. • 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.

24. MITRAL INSUFFICIENCY
Aetiology
• LV dilatation,
• Calcification,
• RF,
• Infective endocarditis,
• Papillary muscle dysfunction,
• Chordal rupture,
• MVP

27. CLINICAL FEATURES
• Fatigue
• Irregular heart sound (heart murmur)
• Irregular heartbeat
• Shortness of breath

28. 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.

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

31. 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.

32. • 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.

33. 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.

34. 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

35. 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

36. 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.

37. SPECIFIC TREATMENT

38. 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

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

40. • 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