Pathophysiology of Rheumatic Heart Disease
Predisposing Factors:
LEGEND:
SIGNS AND SYMPTOMS
Laboratory results
Nursing Diagnosis
Treatment
Reference: Reference:
Lemore,P. , Burke,K. (2007)
Principles of medical
Surgical Nursin: Critical Care
thinking in Client care.4th
edition.volume 2
Precipitating Factors:
 Family history of RHD Etiology
 Environmental factors
(paternal side) Group A Beta-
 Low Socioeconomic Status
 Age (36 years old) Hemolytic
 Geographical Location
 Female Streptococcus
Bacteria invades the upper respiratory tract (tonsils and pharynx)
Inflammation of affected tissues
RHEUMATIC HEART DISEASE
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
RESOLVED Sedimentation
A Temp:36.5 Rate (ESR)
 A

Immune system Immune system

cross-reacts with cross-reacts with
Synovial membrane myocardial tissue

Leakage of plasma
proteins and fluid

Swelling of the joint

Compression of
nerve endings Endocarditis Pericarditis Myocarditis

Acute pain (joints) Pain and tenderness Mechanical Increased Myocardium loses
related to ongoing of the joint injury caused by permeability of its contractility
disease process inflammation and
capillaries
tachycardia
Arthritis migrates Digoxin Decreased Cardiac
Epirosone 50 mg TID upward to different 0.25mg OD Shifting of plasma Output
Carvedilol
joints Erosion of mitral and fibrinogen to
6.25mg OD
valve leaflets pericardial sac
Decreased Perfusion Ineffective tissue
Migratory perfusion
Polyarthritis Aggregation of Swelling of
platelets and fibrin pericardium Sympathetic
along the valve Response: Increased -Delayed capillary
Heart Rate, Increased refill: 3 seconds
C Contractility, -Body Weakness
Vasoconstriction -Dizziness
Fomation of vegetations along -Pale skin, lips and
the edges of the leaflets MILD CADIOMYOPATHY nails
ECG: Enlargement of chambers of -clubbing nails
D
heart, arrhythmia -equal,weak
B peripheral pulse
Echocardiogram: damage heart
valves and infection
 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
leaflets of the valve Irregular heart
Compression
rhythm Increased Volume in LA
of nerves

Mitral Stenosis Mitral Regurgitation

Increased Volume in Pulmonary Vein
Sharp, stabbing
localized pain
Warfarin 5mg Increased Pressure in
OD HS
Pulmonary
Decreased Cardiac output Pulmonary capillary bed
edema, dyspnea
Acute chest pain related to
tissue ischemia
Pulmonary
Decrease blood in the bone marrow
Hypertension

Decrease RBC production

Blood cell production slows down Increased Pressures in the RV and RA
Ineffective
RBC:3.42
Decrease WBC production Hemoglobin: Decrease in tissue
perfusion r/t Dilatation/Hypertrophy of RV
102 hemoglobin and
low
iron rich protein
Decrease immune hemoglobin Risk for fall
defense reaction count Decreased CO despite Risk for self-care deficit
Decrease oxygenation compensatory mechanisms

Infection
Hypoxia Generalized
Shortness of breath and Tachycardia weakness,pale

Fatigue related to poor condition Activity Intolerance related to imbalance between oxygen and carbon dioxide demand