Pathophysiology of Rheumatic Heart Disease

Predisposing Factors: Precipitating Factors:

Etiology
 Family history of RHD  Environmental factors
Group A Beta-
 Age (5-15 years old)  Low Socioeconomic Status
Hemolytic
 Past history of Rheumatic  Geographical Location
Streptococcus
Fever

Bacteria invades the upper

respiratory tract (tonsils and
pharynx)

Inflammation of affected tissues

Macrophages attack bacteria, and then Production of Cytokines, TNF,

present its antigen to the immune system Endogenous Pyrogens (IL 1 and IL 6)

Production of antibodies (IgG & IgM) Release of Prostaglandin Stimulation of liver to produce
E2 acute phase proteins

Activation of complement system, opsonic

Increased thermostat point
phagocytosis, production of NK cells to Increased C Increased
in the hypothalamus
combat pathogens Reactive Fibrinogen
Protein
Increased thermostat point
Immune system cross-reacts and causes in the hypothalamus RBCs stick
tissue injury to normal body cells due to together
Molecular Mimicry (rouleaux)
Increased body
temperature

Multi-systemic effects Increased

Hyperthermia Erythrocyte
Sedimentation
A Rate (ESR)
 A

Immune system cross- Immune system Immune system Immune system Immune system
reacts with Basal Ganglia cross-reacts with cross-reacts with Skin cross-reacts with cross-reacts with
Synovial membrane subcutaneous tissue myocardial tissue

Disruption in Presence of ring-like

motor signals Leakage of plasma lesions (Erythema Presence of
proteins and fluid Marginatum) subcutaneous
nodules
Involuntary muscle
contractions Swelling of the joint
(Sydenham’s Chorea)

Compression of
nerve endings Endocarditis Pericarditis Myocarditis

Pain and tenderness Mechanical injury Increased Myocardium loses

of the joint caused by permeability of its contractility
inflammation and capillaries
tachycardia
Arthritis migrates Decreased Cardiac E
upward to different Shifting of plasma Output
joints Erosion of mitral and fibrinogen to
valve leaflets pericardial sac
Decreased Perfusion
Migratory
Polyarthritis Aggregation of Swelling of
platelets and fibrin pericardium Sympathetic
along the valve Response: Increased
Heart Rate, Increased
C Contractility,
Vasoconstriction
Fomation of vegetations along
the edges of the leaflets
D
B
 B C D

Vegetations heal Increased Residual Volume of LV

with fibrosis and Pericardial Increased
calcifications layers rub pressure on
Increased Pressure in LV
each other parietal
Permanent pericardium
Dilatation/Hypertrophy of LV
distortions of the
Pericardial
leaflets of the valve
friction rub on Compression
auscultation Increased Volume in LA
of nerves

Mitral Stenosis Mitral Regurgitation

Increased Volume in Pulmonary Vein
Sharp, stabbing
F
localized pain
Increased Pressure in
Pulmonary
E Pulmonary capillary bed
Decreased CO despite edema, dyspnea
compensatory mechanisms
Pulmonary
Hypertension
Decreased Heart Rate

Cardiogenic shock Increased Pressures in the RV and RA

Hypoperfusion Dilatation/Hypertrophy of RV

Hypoxia Cor Pulmonale

Multi-organ failure
F

DEATH