Infectious Heart Diseases

PREDISPOSING FACTORS
Non-Modifiable Factors: Age (5 15 years old) Genetic Predisposition Modifiable Environmental Conditions (overcrowding) Economic Factors (malnutrition and poor access to health care) Immunodeficiency

PRECIPITATING FACTORS
Exposure to GABS

Entry of the microorganisms

Upper airway organs are affected pharynx tonsils

Local inflammatory response

pharynx

tonsils

Local inflammatory response PAIN Inadequate intake (loss of weight) Increase WBC on to the site in order to retard GABS and prevent it from entering the systemic circulation Increase in WBC WBC vs M.O. Release of pyrogens Fever Breakage of the endothelial lining Entry of GABS in the bloodstream bacteremia The foreign body will stimulate the production of antibodies GABS travel in the entire body via the circulatory and lymphatics system Absorption of GABS via the lymphatic veins

bacteremia The foreign body will stimulate the production of antibodies

GABS travel in the entire body via the circulatory and lymphatic system

The body codes the The body codes the antigens antigens CHON STREPTOLYSIN-O located in their cell membrane Formation of ANTIFormation of STREPTOLYSIN-O M CHON (ASO) antibodies antibodies Increase in ASO titer ANTI ASO vs GABS Failure of the antiASO to retard GABS Increased hemolyisis of the RBCs Elevated ESR and decrease in hgb and hct Increase in MCHON titer

JOINTS

SKIN

CNS

HEART

B JOINTS Vascular changes occur in the blood vessel Permeability of the capillaries supplying the synovial membrane of the joints

Extravasation of plasma from the capillaries to the synovial fluid (prostaglandin and arachidonic acid)
Local inflammatory reaction in the synovial membrane

ARTHRITIS (POLYARTHRITIS)

C By way of the stratum germinativum, GABS reach the skin surface Local inflammation Formation of inflammatory lesions Erythema Marginatum Inflammation of the tendon sheaths Formation of inflammatory nodules

Subcutaneous Nodules

D Entry via the midcerebral artery Affects the upper motor neuron (caudate nucleus) Firing of impulses Afferent neuron to the anterior motor horn of the spinal cord Reception of the lower motor neuron Chorea (Sydenhams Chorea or St. Vitus Dance)

E
Venous return (carries GABS)

Comes in contact with the endocardium Inflammation of the endocardium ENDOCARDITIS

Follows the normal flow of blood

Infected blood enters the lungs Pulmonary Infections

Damage and shortening of the chordae tendinae

Infected deoxygenated blood exits the left ventricle Formation of tiny Infected blood enters the coronary arteries translucent vegetations around the valve Inflammation of the Inflammation of the leaflets MYOCARDIUM PERICARDIUM MYOCARDITIS
PERICARDITIS

Calcifications of the valves and partial opening (stenosed) VALVULAR DISORDERS (Mitral Valve Stenosis)

MURMURS

MYOCARDITIS

PERICARDITIS

ASCHOFFS BODIES

Restrictions to Contraction Decrease in stroke volume Decrease in cardiac output Baroreceptor reflex Increased SNS stimulation Tachycardia and vasoconstriction

Left ventricle has to increase preload in order to resist increase afterload (but with decrease volume) Restrictions to contraction progresses

Further decrease in cardiac output

HEART FAILURE (LEFT or RIGHT SIDE)

Microbial infection of the endothelial surface of the heart, especially the valves.

Infective Endocarditis

MODIFIABLE

NON-MODIFIABLE
age (47-64years old)

dental procedures
upper respiratory tract infection and urinary tract infection intravenous drug users (2-5%)

reproductive condition
pre-existing heart diseases

NON-MODIFIABLE FATORS
AGE: 47 64 year sold

MODIFIABLE FACTORS
Dental procedures, URTI, UTI, intravenous drug users, reproductive condition, preexisting heat condition

Entry of the microorganisms via the various routes Systemic affectation Incorporation in the bloodstream

WBC vs M.O. Release of the chemical pyrogen

FEVER Contaminated blood enters the heart via the venous return Colonization of the other endothelial structures Formation of bacterial colonies on the edges of the heart valves Irregularly shaped bacterial colonies would attract platelet aggregates Formation of vegetations

Damage on the endocardium

ENDOCARDITIS

ENDOCARDITIS

Formation of vegetations

Damage and shortening of the chordae tendinae

Formation of tiny translucent vegetations around the valve leaflets

Growth of the vegetations by further attraction of more platelet aggregates Further damage to the valves

Platelet aggregates are loosely attached on the valvular lining Dislodgement of clots/thrombi Embolism

Vegetations continue to release infectious substances SYSTEMIC INFECTION Travels to the skin via the stratum germinativum Inflammatory lesions (rashes)/ nodules on the fingertips (Oslers nodes)

Calcifications of the valves and partial opening (stenosed) VALVULAR DISORDERS (Mitral Valve Stenosis) Decreased preload Decrease stroke volume Decrease cardiac output Baroreceptor reflex Increase SNS activity

Tachycardia, vasoconstriction Marked increase in preload and increase in afterload

Marked decrease in stroke volume and cardiac output

Heart failure

Abdominal aorta
Abdominal pain

Renal Artery

MCA

Retinal artery Retinal damage Formation of round necrotic tissues around the retina Roths Spots

Coronary artery Angina Pectoris/Myocar dial infarction

Renal parenchymal damage

Proteinuria, hematuria, casts, acidosis, electrolyte imbalance

TIA, CVA, ataxia, aphasia

Flank pain

Loss of vision

Pulmonary artery Difficulty of breathing and pulmonary vasculature damage

Radial/ulnar artery koilonychia

MYOCARDITIS

Entry of the microorganisms via the respiratory system Local inflammatory process

Toxic effects of exogenous substance

FLU-LIKE SYMPTOMS

Release of endogenous toxins of the microorganisms

Damage of the myocytes (myocardium) Decrease contractile state of the myocardium Decrease in preload hypotension Baroreceptor reflex Increase in SNS stimulation Tachycardia, tachypnea, vasoconstriction

Tachycardia, tachypnea, vasoconstriction Decrease in ventricular filling Preload decreases Further decrease in stroke volume Further decrease in cardiac output Further stimulation of adrenergic system (SNS) Decrease in pressure in the ventricles Faint heart sounds Left atrial enlargement Atrial tachycardia/ atrial fibrillation leading to mural thrombi formation Pooling of blood in the atria Further damage in the myocardium (elevation of the cardiac enzymes) serum creatinine kinase troponin T troponin I ECG Changes: ST segment elevation, T wave inversion, transient Q waves Loss of ventricular compliance S3 gallop

Increase SA node activity

Pooling of blood in the atria PULMONARY HYPERTENSION

Further damage in the myocardium

Compensation of the other heart muscles

Portions that are damaged regenerate and are replaced by non pliable fibrous tissues

Hypertrophy of the myocardium

Conduction system defects (dysrhythmias) CHEST PAIN

Myofibril damage and stretching of the remaining functional fibers

HEART FAILURE

PERICARDITIS

Entry of the microorganisms via the respiratory system

Local inflammatory process FLU-LIKE SYMPTOMS BACTEREMIA

Damage on the endothelial surface

Reaches the alveolar capillary membranes

Incorporation of the microorganism in the systemic circulation Vascular changes take place in response to the microorganism/s Hydrostatic pressure increases

Edema on the dependent parts of the body

Increase in capillary permeability (particularly of the capillaries supplying the serous membrane of the heart)

Synovial membrane of the joints (ARTHRITIS)

extravasation of fluids, together with the microorganisms, fibrin deposits and the chemical mediators of inflammation

extravasation of fluids, together with the microorganisms, fibrin deposits and the chemical mediators of inflammation

Formation of fibrous exudates in the pericardial space

Inflammation of the visceral and parietal pericardium

ACUTE PERICARDITIS

Formation of fibrous exudates in the pericardial space Slow filling

Decrease amount of serous fluid in the pericardial space

Impaired contraction of the ventricles Decrease in stroke volume Decrease in cardiac output

PERICARDIAL with EFFUSION Muffled heart sounds

Rubbing of the inflamed layers PERICARDIAL FRICTION RUB

Hypotension Baroreceptor reflex Adrenergic receptor stimulation (increased SNS activity) Tachycardia, tachypnea, vasoconstriction

Pressure of the inflamed pericardium over the intercostal muscles Chest Pain

Tachycardia, tachypnea, vasoconstriction

Decrease in ventricular filling Preload decreases Further decrease in stroke volume Further decrease in cardiac output Increase in left ventricular diastolic volume and pressure Decrease ventricular filling

Further decrease in cardiac output Pooling of blood in the left atrium

Further stimulation of adrenergic system (SNS)

Decrease in pressure in the ventricles Pulmonary HPN Rise in pulmonary artery pressure Rise in right ventricular pressure Mitral valve damage

Faint heart sounds

Hypertrophy

Inflammation of the pericardium and thickening of the exudate causes fusion of the two layers
CHRONIC CONSTRICTIVE PERICARDITIS Entire pericardium restricts myocardial contraction Contraction of the heart increases but becomes inefficient Hypertrophy of the heart muscles Conduction system defects Right Sided Heart Failure Left Sided Heart Failure

EXUDATIVE PERICARDITIS Agents/ processes causing pericardial inflammation Formation of exudate: fibrin, WBC, endothelial cells

Acute Pericarditis

CO

Restricts heart filling & emptying

Cardiac tamponade Exudates accumulates in pleural sac Localization of fibrinous exudate

Exudate covers pericardium Further inflam. of serous pleura & tses.

DRY PERICARDITIS
Delicate adhesions from within the pericardial space along with serous fibrin deposits, hge & calcification Adhesion obliterate the pericardial sac Inflammation of the pericardium Penetration to the myocardium myopericarditis

 Chronic inflammatory condition in which the pericardium changes into a thick, fibrous band of tissue.
Repeated cases of acute pericarditis Formation of thick, fibrous band of tse Encircles, encases, and compresses the heart Prevents proper ventricular filling and emptying CO/ heart failure

Chronic Constrictive Pericarditis

Pericardial Effusion
Rapid Fluid Accumulation
Sudden Fluid Accumulation Stretching of pericardium Loss of elasticity of pericardium Fibrosis of pericardium

Compression of heart Ventricular filling CO