Etiology: -Unknown

Togavirus infects mother via airborne droplets

Modifiable Risk Factors: -Maternal Illness (Rubella during the 8th week of pregnancy) -Poor nutrition during pregnancy -Maternal alcoholism - smoking

Invades nasopharynx

Travels to the lymph glands

Enters the bloodstream

Maternal viremia occurs

Enters placenta

Retards cell mitosis of the fetus

Structural malformations in the mesoderm

Ventricular Septal Defect

Aorta Dextroposition

Pulmonary Artery Stenosis

Right Ventricular hypertrophy

Mixing of deoxygenated and oxygenated blood

Increase blood volume going through VSD

Heart works harder to push out blood to the pulmonary artery

Heart Murmur Increased contractility

Tet Spell

Reduced blood flow to lungs

Cardiomegly

Decreased oxygenated blood circulating in body

Decreased oxygenation

Decreased oxygen saturation

Decreased energy

Hypoxemia and Hypoxia

Stimulates respiratory center hyperapnea Stimulates erythropoiesis

Tires easily

Feeding problems

Cyanosis

Clubbing of fingers and toes

Growth retardation

Decreased nutrients needed to strengthen immune system

Failure to thrive Increased RBC Decreased immune system

Frequent infections

Right Blalock Taussig Shunt with 5mm anastamosis

Excessive blood flow through shunt

Pooling of blood into lungs

Oxygenated blood goes back to heart via pulmonary artery

Crackles

Pulmonary congestion

Goes to the left ventricle via the bicuspid valve

Pulmonary edema

Blood flows back to the right ventricle due to the VSD

Lung tissue is destroyed Blood overfills due to hypertrophied right ventricle and pulmonary artery stenosis

Pulmonary capillary bed is reduced

Increase pressure in ventricles both left and right Dyspnea Cough Ventricles pumping ability decreased

Stretched cardiac muscle

Ventricles continuously filled with blood

Blood backs up into systemic circulation

Lesser blood is pumped out of the heart

Distended neck veins

Peripheral edema Decreased Stroke volume Decreased cardiac output Decreased blood pressure

Bodys initial response is to compensate: reverse the impending insult

Sympathetic response activated

Increase cathecolamines: epi and norepi

Hypoperfusion to other organs to supply vital organs with enough nutrients and oxygen

Gluconeogensis

Inflammatory response activated

Glycogenolysis

Autoregulation

GIT

Musculoskeletal system

Skin

Liver

Insulin resistance

Localized effect on vasculature

Kidney

Hypermetabolism

RAAS

Increase blood volume

Cant remove excess fluid in blood Hypoactive bowel sounds Increase fluid in bloodstream Cold, clammy skin Cyanosis Increase workload of failing heart Vicious cycle will occur Increase blood pressure Increase cardiac output

Tires easily

Decreased exercise tolerance

SYSTEMIC AFFECTATION

RESPIRATORY SYSTEM

INTEGUMENTARY SYSTEM

LIVER

KIDNEY

BRAIN

HEART

MUSCU-SKELETAL SYSTEM

Lung will be already hypoperfused

Cells and tissues are not receiving enough oxygen

The liver will continuously receive unoxygenated blood

Kidney will be furtherly hypoperfused

Brain hypoxia

Heart will try to pump and contract to compensate

Muscle will receive less

Decrease level of consciousness tachycardia

Oxygen transport from alveolar sac to the blood stream is altered

PALLOR

Anaerobic respiration will occur

Less blood is received by the blood

Infiltration of glycogen in the liver

RAAS will continuously be triggered

Filtration will be altered

Heart will be exhausted

Respiratory acidosis will occur

Further cyanosis will occur

Glycogen interfere with the portal circulation

Chronic increase in Blood Pressure

Excretion of body waste product is decreased

**Note: Signs and Symptoms Four Primary Defects

Liver edema

Increase in serum creatine and serum BUN level

Treatment

HEPATOMEGALY