Pathophysiology of Rheumatic Heart Disease

Predisposing Factors:
Family history of RHD
Age (5-15 years old)
Past history of Rheumatic
Fever

Precipitating Factors:
Environmental factors
Low Socioeconomic Status
Geographical Location

Etiology
Group A Beta-
Hemolytic
Streptococcus

Bacteria invades the upper
respiratory tract (tonsils and
pharynx)
Macrophages attack bacteria, and then
present its antigen to the immune system
Production of antibodies (IgG & IgM)
Inflammation of affected tissues
Activation of complement system, opsonic
phagocytosis, production of NK cells to
combat pathogens
Immune system cross-reacts and causes
tissue injury to normal body cells due to
Molecular Mimicry
Multi-systemic effects
Production of Cytokines, TNF,
Endogenous Pyrogens (IL 1 and IL 6)

A
Release of Prostaglandin
E2

Increased thermostat point
in the hypothalamus

Increased thermostat point
in the hypothalamus

Increased body
temperature

Hyperthermia

Stimulation of liver to produce
acute phase proteins

Increased C
Reactive
Protein

Increased
Fibrinogen

RBCs stick
together
(rouleaux)

Increased
Erythrocyte
Sedimentation
Rate (ESR)


A
Immune system cross-
reacts with Basal Ganglia
Disruption in
motor signals
Involuntary muscle
contractions
(Sydenhams Chorea)
Immune system
cross-reacts with
Synovial membrane
Leakage of plasma
proteins and fluid
Swelling of the joint
Compression of
nerve endings
Pain and tenderness
of the joint
Arthritis migrates
upward to different
joints
Migratory
Polyarthritis
Immune system
cross-reacts with Skin
Presence of ring-like
lesions (Erythema
Marginatum)
Immune system
cross-reacts with
subcutaneous tissue
Immune system
cross-reacts with
myocardial tissue
Presence of
subcutaneous
nodules
Pericarditis
Increased
permeability of
capillaries
Shifting of plasma
and fibrinogen to
pericardial sac
Swelling of
pericardium
C
Endocarditis Myocarditis
Myocardium loses
its contractility
Mechanical injury
caused by
inflammation and
tachycardia
Erosion of mitral
valve leaflets
Aggregation of
platelets and fibrin
along the valve
Fomation of vegetations along
the edges of the leaflets
B
Decreased Cardiac
Output
Decreased Perfusion
Sympathetic
Response: Increased
Heart Rate, Increased
Contractility,
Vasoconstriction
D
E


B C D
Vegetations heal
with fibrosis and
calcifications
Permanent
distortions of the
leaflets of the valve
Mitral Stenosis Mitral Regurgitation
E
Pericardial
layers rub
each other
Increased
pressure on
parietal
pericardium
Compression
of nerves
Sharp, stabbing
localized pain
Pericardial
friction rub on
auscultation
Increased Residual Volume of LV
Increased Pressure in LV
Dilatation/Hypertrophy of LV
Increased Volume in LA
Increased Volume in Pulmonary Vein
Increased Pressure in
Pulmonary capillary bed
Pulmonary
edema, dyspnea
Pulmonary
Hypertension
Cor Pulmonale
Dilatation/Hypertrophy of RV
Increased Pressures in the RV and RA
F
F
Decreased CO despite
compensatory mechanisms
Cardiogenic shock
Multi-organ failure
DEATH
Decreased Heart Rate
Hypoperfusion
Hypoxia