This document discusses valvular heart disorders, focusing on mitral valve stenosis and regurgitation. It defines stenosis as a narrowing of the valve orifice, while regurgitation is the incomplete closure of the mitral valve, allowing blood to flow back into the left atrium. The most common cause of both is rheumatic heart disease. Symptoms of mitral stenosis include dyspnea and fatigue, while regurgitation causes fatigue, dyspnea, and palpitations. Diagnosis is via echocardiogram. Treatment depends on severity but may include medications, balloon valvuloplasty, or valve replacement surgery.

1. 1
Valvular Heart Disorders
Hizbullah Khan
BScN, MScN
Asst. Professor (CNM)

2. Objectives
Review the valves of the heart
Discuss the disorders of mitral valve
List the etiology of mitral valve disorders
Explain the pathophysiology of mitral stenosis and
regurgitation
Describe the signs and symptoms of mitral stenosis and
regurgitation
Discuss briefly the management mitral valve disorders.
2

3. 3

4. 4

5. 5

6. Mitral Valve Stenosis
Stenosis: It refers to narrowing
Valve orifice is smaller, impending the forward flow
of blood.
The valve leaflets or cusps may become fused or
thickened that the valve cannot open freely; obstructs
the normal flow of blood
Mitral valve stenosis represents the incomplete
opening of the mitral valve during diastole, with left
atrial distention and impaired filling of the LV.
Most common valvular disorder
6

7. Causes
Rheumatic heart disease
Infections – bacterial endocarditis, thrombus
formation, calcification
Heart attack/MI – damage to the heart muscle,
papillary muscles
Congenital heart disease
7

8. Pathogenesis
Mitral valve stenosis is characterized by fibrous
replacement of valvular tissue, along with stiffness
and fusion of the valve apparatus.
The mitral cusps fuse at the edges and involvement of
the chordae tendineae causes shortening, which pulls
the valvular structures more deeply into the
ventricles.
As the resistance to flow through the valve increases,
the left atrium becomes dilated and left atrial
pressure rises.
The increased left atrial pressure eventually is
transmitted to the pulmonary venous system, causing
pulmonary congestion.
8

9. Pathogenesis
Symptoms develop as the gradient across the valve
becomes worse so that the left atrial pressure is
greater than the left ventricular pressure.
As the condition progresses, symptoms of decreased
cardiac output occur during extreme exertion.
In the late stages of the disease, pulmonary vascular
resistance increases with the development of
pulmonary hypertension; this increases the pressure
against which the right heart must pump and
eventually leads to right-sided heart failure.
The normal mitral valve orifice area is 4 to 6 cm2
.
Symptoms usually develop when mitral valve area is
less than 1.5 cm2
.
9

10. Pathophysiology
10

11. Clinical Manifestations
Exertional dyspnea, weakness and fatigue (most
common)
Orthopnea, cough, hemoptysis
Cyanosis
Right-sided heart failure – distended neck veins,
peripheral edema, hepatomegaly, abdominal
discomfort
Cardiac murmurs
Atrial fibrillations and premature atrial beats due to
fibrosis of the internodal (SA & AV) and interatrial
tracts, along with damage to the sinoatrial node.
11

12. Clinical Manifestations
Palpitations, chest pain
The risk of arterial embolization, particularly stroke,
is significantly increased in people with atrial
fibrillation.
12

13. Mitral Valve Regurgitation
Mitral valve regurgitation is characterized by
incomplete closure of the mitral valve, with the left
ventricular stroke volume being divided between the
forward stroke volume that moves into the aorta and
the regurgitant stroke volume that moves back into
the left atrium during systole.
13

14. Causes
Rheumatic heart disease (RHD) is associated with a
rigid and thickened valve that does not open or close
completely.
Mitral regurgitation can result from rupture of the
chordae tendineae or papillary muscles, papillary
muscle dysfunction, or stretching of the valve
structures due to dilation of the LV or valve orifice.
Myocardial infarction
Infective endocarditis
14

15. Pathophysiology
15

16. Clinical Manifestations
Fatigue & weakness – due to decreased CO
(predominant complaint)
Exertional dyspnea & cough – pulmonary congestion
Palpitations – due to atrial fibrillation (occur in 75%
of patients)
Right-sided heart failure – distended neck veins,
edema, ascites, hepatomegaly
Cardiac Murmurs
May or may not have chest pain
16

17. Diagnosis
Echo
Echocardiography is used to assess the anatomy of
the mitral valve, including the degree of leaflet
thickening, calcification, changes in mobility, and
extent of involvement of the sub-valvular structures.
Echocardiography also allows evaluation of cardiac
chamber dimensions, pulmonary hypertension, left and
right ventricular function, and other valvular disease,
and examination of the left atrial appendage for the
presence or absence of thrombus
17

18. MANAGEMENT
Minor symptoms – medical treatment
Diuretics - pulmonary congestion↓
Digoxin, β-blockers , CCB, antiarrhythmic drugs -
control ventricular rate in AF
Anticoagulants - risk of embolism↓
Antibiotic prophylaxis - infective endocarditis & RF
Definitive treatment – Surgical
Balloon valvuloplasty, mitral valvotomy (for MS),
Mitral valve replacement for both MS & MR
18

19. 19

20. 20

21. 1. Emanuel Rubin & John L. Farber, Essential Pathology,
Philadelphia, 1990.
2. Kumar, Vinay; Abbas, Abul K; Aster, Jon. (2009).
Robbins & Cotran pathologic basis of diseases (8th ed.).
St. Louis, Mo: Elsevier Saunders. ISBN 1-4160-3121-9.
3. Porth CM. Pathophysiology: Concepts of altered Health
States. 7th
edition; 2005. Lippincott Williams & Wilkins.
Reference
s