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What are congenital heart defects (CHD)?
Structural abnormalities of the heart that are present at birth.
What is the most common cause of heart disease in children?
Congenital heart defects.
Do all congenital heart defects require treatment?
No. Some heal over time, while others require medical or surgical treatment.
What is the cause of congenital heart defects in most cases?
Unknown in approximately 90% of cases.
What genetic conditions are associated with congenital heart defects?
Trisomies 13, 15, and 18, and Turner syndrome.
What maternal factors increase the risk of congenital heart defects?
Tobacco use, alcohol use during pregnancy, and maternal rubella infection.
What are the two main categories of congenital heart defects?
Left-to-right shunts (non-cyanotic) and right-to-left shunts (cyanotic).
What is cyanosis?
A bluish discoloration of the skin or mucous membranes caused by decreased oxygen in the blood.
Which type of shunt typically causes cyanosis?
Right-to-left shunts.
What congenital heart defects are classified as left-to-right shunts?
Atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA).
Are left-to-right shunts cyanotic at birth?
No, they are initially non-cyanotic.
What complication can cause left-to-right shunts to become cyanotic later in life?
Pulmonary hypertension with right ventricular hypertrophy.
What is the foramen ovale?
A normal fetal opening between the atria that allows blood to bypass the lungs before birth.
What normally happens to the foramen ovale after birth?
It closes or becomes very small within weeks to months.
What is an atrial septal defect?
A persistent opening between the atria that does not close after birth.
What is a patent foramen ovale (PFO)?
A small residual opening between the atria that remains in some healthy adults.
What happens when a large atrial septal defect is present?
Oxygenated blood flows from the left atrium to the right atrium and is sent back to the lungs.
Why does a large ASD increase workload on the heart and lungs?
Excess blood is repeatedly pumped into pulmonary circulation.
What cardiac changes result from a large ASD?
Right ventricular hypertrophy and pulmonary hypertension.
What causes pulmonary hypertension in ASD?
Increased blood volume damages pulmonary vessels.
How are small ASDs managed in infants?
They often close or narrow spontaneously.
How are large ASDs treated?
They may require surgical closure.
What is the most common congenital heart defect?
Ventricular septal defect.
What happens in a large ventricular septal defect?
Oxygenated blood flows from the left ventricle into the right ventricle and back to the lungs.
What effect does a VSD have on the heart?
Increased workload causes cardiac enlargement.
What structural changes result from a VSD?
Right ventricular hypertrophy and pulmonary hypertension.
What long-term complication can develop from pulmonary hypertension in VSD?
Permanent damage to pulmonary blood vessels.
How does a VSD eventually lead to cyanosis?
Right-to-left shunting sends deoxygenated blood into the aorta.
What is tardive cyanosis?
Cyanosis that develops later in life after heart failure.
What is the ductus arteriosus?
A fetal channel between the pulmonary artery and the aorta.
What is the function of the ductus arteriosus before birth?
Allows blood to bypass the lungs.
When does the ductus arteriosus normally close?
Within 1–2 days after birth.
What happens in patent ductus arteriosus?
Blood flows from the aorta into the pulmonary artery.
What complications can result from PDA?
Pulmonary hypertension and eventual cyanosis.
Which congenital heart defects are right-to-left shunts?
Tetralogy of Fallot and transposition of the great vessels.
What are the four components of Tetralogy of Fallot?
Ventricular septal defect, overriding aorta, pulmonary stenosis, and right ventricular hypertrophy.
Why does Tetralogy of Fallot increase the risk of infective endocarditis?
Abnormal blood flow damages endocardial surfaces.
What is a “Tet spell”?
A sudden drop in oxygen causing cyanosis, tachypnea, and irritability in babies/children.
What is transposition of the great vessels?
The aorta arises from the right ventricle and the pulmonary artery from the left ventricle.
Why is transposition of the great vessels fatal if untreated?
Deoxygenated blood is continuously pumped back into circulation. Needs to be treated with surgery for survival.
What conditions allow survival in transposition of the great vessels?
Presence of a VSD, ASD, or PDA.
What is congestive heart failure?
Inability of the heart to pump sufficient oxygenated blood to meet tissue needs.
How common is heart failure?
Approximately 10 out of 100 people are affected.
How many deaths annually are attributed to heart failure?
Approximately 300,000.
How does age affect heart failure prevalence?
It increases with advancing age.
Why is CHF important in optometry?
It damages delicate ocular blood vessels and increases risk for glaucoma and macular degeneration.
What is the most common cause of heart failure?
Coronary artery disease.
What other causes of heart failure exist?
Dilated cardiomyopathy, hypertension, and heart valve disease.
What is cardiac hypertrophy?
Increase in ventricular size with reduced filling capacity and stiffened muscle.
What is compensated heart failure?
Hypertrophy plus physiologic mechanisms temporarily maintain circulation.
What compensatory mechanisms occur in compensated heart failure?
Tachycardia, increased contractility, fluid retention, and sympathetic stimulation.
What is cardiomegaly?
Enlargement of the heart due to hypertrophy or dilation.
What is decompensated heart failure?
Failure of compensatory mechanisms leading to inadequate circulation.
What happens during ventricular dilation?
Chambers enlarge but stroke volume does not increase (Frank-Starling law fails).
What occurs in left-sided heart failure?
The left ventricle fails to pump blood into the aorta.
What causes left ventricular failure?
Excessive thickness, stiffness, or weakness of the ventricle.
Where does blood back up in left-sided heart failure?
Left atrium and lungs.
What pulmonary complications occur in left-sided heart failure?
Pulmonary hypertension and pulmonary edema.
What respiratory symptoms are seen in left-sided heart failure?
Dyspnea, tachypnea, orthopnea, paroxysmal nocturnal dyspnea, cough.
What are heart failure cells?
Hemosiderin-filled macrophages in lung alveoli (appear brown).
What usually causes right-sided heart failure?
Left-sided heart failure.
What is cor pulmonale?
Right heart failure due to primary lung disease.
Where does blood back up in right-sided heart failure?
Systemic and portal venous circulation.
What systemic signs occur in right-sided heart failure?
Dependent edema, jugular venous distension, passive hepatic congestion.
What is nutmeg liver?
Chronic passive congestion of the liver causing mottled appearance.
What is pitting edema?
Edema that retains an indentation after pressure is released. Often occurs with right-sided heart failure.
How should optometrists monitor patients with CHF?
Regular comprehensive exams assessing retinal vessels and hemorrhage.
Why is blood pressure monitoring important in CHF patients?
Persistent hypertension worsens vascular damage.
Why is interdisciplinary communication important in CHF?
Ocular findings should be shared with cardiologists and primary care providers.
What is ischemic heart disease?
An imbalance between myocardial oxygen supply and demand.
What does ischemia mean?
Reduced blood flow and oxygen delivery to tissue.
What happens when ischemia is severe?
Myocardial infarction (cell death).
What is the most common cause of ischemic heart disease?
Atherosclerosis of coronary arteries.
What is atherosclerosis?
Accumulation of atheromas in arterial walls that narrow the lumen.
What is an atheroma composed of?
Lipids, foam cells, smooth muscle cells, fibrous cap, damaged endothelium.
What is a fatty streak?
Early accumulation of foam cells beneath endothelium. Usually first sign of developing atherosclerosis.
Can fatty streaks be present in children?
Yes, even in normal arteries.
How does atherosclerosis progress?
Fatty streaks enlarge into plaques that narrow arteries.
What causes plaque rupture?
Enzymes released by macrophages.
What happens after plaque rupture?
Thrombus formation causing ischemia and infarction.
What is calcification of atheromas?
Transformation of endothelial cells into osteoblast-like cells.
Why is atherosclerosis called “hardening of the arteries”?
Due to calcification of plaques.
What causes myocardial infarction?
Thrombus in coronary arteries at a ruptured atheroma; causing lack of oxygen and tissue death.
What is coronary thrombosis?
Disease caused by a thrombus in coronary arteries.
What are major modifiable risk factors for atherosclerosis?
Hypertension, diabetes, smoking, hyperlipidemia.
What additional risk factors contribute to atherosclerosis?
Abdominal obesity and insulin resistance.
What unmodifiable risk factors increase atherosclerosis risk?
Male and older age.