Abdominal Aortic Aneurysm Overview

Narrowing of the aorta, obstructing blood flow, increasing blood pressure risk, and leading to LVH (left ventricular hypertrophy).

Four heart defects: Pulmonic stenosis, VSD (ventricular septal defect), overriding aorta, and RVH (right ventricular hypertrophy).

Poor feeding, breathing difficulties, and failure to thrive.

High blood pressure, headaches, leg cramps, or exercise intolerance.

Diagnosis of TOF typically includes a chest X-ray that shows a 'boot-shaped heart', ECG (detecting right ventricular hypertrophy), and echo (to assess the obstruction).

ECHO, MRI, or CT angiography is used to assess aorta narrowing.

Referral to cardiologists/cardiosurgeons is crucial for diagnosis and management in cases of suspected congenital heart disease.

TOF patients may be comfortable at rest but experience cyanotic spells with agitation. This shows progressing worsening of heart function.

Abdominal aortic aneurysm; dilation of the abdominal aorta by 3cm or more.

Involves all three layers of the vessel wall; the most common type of aneurysm, including AAA.

A pseudoaneurysm; occurs when the inner and middle layers of the vessel wall are disrupted, often from trauma or infection.

Conditions such as atherosclerosis, cerebrovascular disease, family history, hypertension, high cholesterol, smoking, obesity, and old age increase the risk of Abdominal Aortic Aneurysms.

A sudden onset of severe hypotension, pulsatile abdominal pain, and abdominal or back pain are classic signs of a ruptured AAA and constitute a medical emergency.

Ultrasound is the standard for detecting AAAs, primarily for men aged 65-75 who are smokers or have a family history of AAAs.

Surgical intervention to repair the aneurysm; often endovascular, particularly if size exceeds a certain threshold.

Atherosclerotic narrowing of the internal carotid arteries, frequently 60-99%, causing potential for stroke.

A hole in the atrial septum (wall between the atria) causing blood to shunt from the left to right side of the heart.

Often asymptomatic, but may present as fatigue, thin build, or frequent respiratory infections.

ASD is the 2nd most common congenital heart defect in adults, often asymptomatic until adulthood, usually by age 40+.

Small defects during infancy may close spontaneously. Larger defects require intervention after one year of age.

Untreated ASD can lead to RV enlargement, fibrosis, pulmonary hypertension, and potentially, atrial arrhythmias.

Persistent opening of the fetal blood vessel (ductus arteriosus) between the aorta and pulmonary artery after birth. This causes blood to be shunted from the aorta to the lungs.

Symptoms in infants with PDA may include heart failure (difficulty feeding, breathing problems), and failure to thrive.

Diagnosis of PDA often involves EKG, chest X-ray, and an echocardiogram (ECHO) to visualize the heart and blood flow.

Prematurity is the primary risk factor for PDA, along with being born at high altitude.

Uncorrected large PDA in adults can manifest as a systolic murmur and signs of cyanotic heart disease, such as bluish skin or clubbed fingers.

Condition impacting blood flow in the carotid arteries, potentially leading to stroke.

Sound heard during auscultation suggesting turbulent blood flow, potentially linked to atherosclerosis.

Risk factors for diseases like CAD which can be changed with lifestyle changes.

Risk factors for disease that cannot be changed.

Surgical procedure to remove plaque buildup in the carotid arteries.

Sudden, temporary loss of vision in one eye.

Heart defects present at birth, due to problems during development.

Bluish discoloration of the skin due to low oxygen in the blood.

Hole in the wall separating the upper heart chambers.

A blood vessel that should close after birth remains open.

A hole in the wall between the two lower chambers of the heart.

Blood flows from the left to right ventricle in a VSD, overloading the left ventricle and potentially causing pulmonary hypertension.

A harsh, high-pitched murmur heard at the left lower sternal border, usually a sign of a small ventricular septal defect.

Symptoms like a low-pitched murmur, a thrill, and signs of Congestive Heart Failure (CHF) may appear in babies with large defects.

A significant percentage (78%) of small VSDs close on their own within the first two years.

Large VSDs can lead to increased blood pressure in the lungs if left uncorrected, potentially reversing the blood flow and causing cyanosis.

Echocardiogram (Echo) is a crucial diagnostic tool for confirming and assessing the size and type of the ventricular septal defect.

Adults with asymptomatic small VSDs may develop complications like aortic regurgitation, while those with larger defects often experience symptoms in childhood, such as shortness of breath and tiredness.