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IM - CONGENITAL HEART DISEASES

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tonystep1's version from 2017-08-29 22:08

CONGENITAL HEART DISEASES CLINICAL FEATURES AND DIAGNOSIS

 

Question Answer
Atrial Septal Defect lAS D)l. Mild systolic ejection murmur at pulmonary area secondary to increased pulmonary blood flow
2. Wide, fixed splitting of s2
3. Diastolic flow "rumble" murmur across tricuspid valve area secondary to increased blood flow
4.TEE is diagnostic (better than transthoracic echocardiogram)
Ventricular Septal Defect1. A large shunt with very high PVR (Eisenmenger's reaction) gives rise to SOB,
dyspnea on exertion, chest pain, and cyanosis.
a. Harsh, blowing holosystolic murmur with thrill
• At fourth left intercostal space
• Murmur decreases with Valsalva and handgrip
Echocardiogram is diagnostic
Coarctation of the Aortal. HTN in upper extremities with hypotension in lower extremities
2. Well-developed upper body with underdeveloped lower half
3. Midsystolic murmur heard best over the back
4. Symptoms include headache, cold extremities, claudication with exercise, and leg
fatigue.
CXR
a. Notching of the ribs
b. "Figure 3" appearance due to indentation of the aorta at site of coarctation,
with dilatation before and after the stenosis
Patent Ductus Arteriosus 􀂍PDA)l. May be asymptomatic
2. Signs of heart failure
3. Loud P 2 (sign of pulmonary HTN)
4. LVH: secondary to left-to-right shunt
5. Right ventricular hypertrophy: secondary to pulmonary HTN
6. Continuous "machinery murmur" at left second intercostal space (both systolic
and diastolic components)
7. Wide pulse pressure and bounding peripheral pulses
8. Lower extremity clubbing: toes more likely than fingers to be cyanotic (differential
cyanosis)
l. CXR
a. Increased pulmonary vascular markings
b. Dilated pulmonary artery
c. Enlarged cardiac silhouette
d. Sometimes calcifications of ductus
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CONGENITAL HEART DISEASES PATHOPHYSIOLOGY

Question Answer
Atrial Septal Defect lAS D)l. Oxygenated blood from the LA passes into the RA, increasing right heart output
and thus pulmonary blood flow.
2. Leads to increased work of the right side of heart As shunt size increases, RA and
RV dilatation occurs with pulmonary-to-systemic flow ratios greater than 1 .5: 1.0.
3 . Pulmonary HTN is a serious sequelae, but is rare in ASD.
Ventricular Septal Defecta. Blood flows from the LV (high pressure) into the RV (low pressure) through a
hole, resulting in increased pulmonary blood flow. As long as the pulmonary
vascular resistance (PVR) is lower than the systemic vascular resistance
(SVR), the shunt is left to right. If the PVR increases above the SVR, the
shunt reverses.
b. Large defects eventually lead to pulmonary HTN, whereas small defects do not
change pulmonary vascular hemodynamics
Coarctation of the AortaNarrowing/constriction of aorta, usually at origin of left subclavian artery near ligamentum
arteriosum, which leads to obstruction between the proximal and distal
aorta, and thus to increased left ventricular afterload
Patent Ductus Arteriosus 􀂍PDA)Pathophysiology
a. Large left-to-right shunting results in volume overload, pulmonary HTN, and
right-sided heart failure.
b. Cyanosis occurs late.
c. May eventually see reversal of blood flow
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CONGENITAL HEART DISEASES TREATMENT AND MANAGEMENT

Question Answer
Atrial Septal Defect lAS D)Surgical repair when pulmonary-to-systemic blood flow ratio is greater than 1.5:1 or 2.0:1 or if symptomatic
Ventricular Septal Defectl. Endocarditis prophylaxis is important.
2. Surgical repair is indicated if the pulmonary flow to systemic flow ratio is greater
than 1 .5: l or 2: l .
3 . For the asymptomatic patient with a small defect, surgery i s not indicated
Coarctation of the Aortal. Standard treatment involves surgical decompression.
2. Percutaneous balloon aortoplasty is also an option in selected cases
Patent Ductus Arteriosus 􀂍PDA)l. If pulmonary vascular disease is absent: surgical ligation
2. If severe pulmonary HTN or right-to-left shunt is present, do not correct PDA.
Surgery is contraindicated
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