1. CHEST X-RAY FINDINGS: Left-to-Right Shunt

2. Uncomplicated ASD: Left-to-Right shunt
enlargement of central and all segments of pulmonary arteries
increased pulmonary vascularity, prominent hilar markings
“shunt vascularity”

3. Uncomplicated ASD: Left-to-Right shunt
No enlargement of left heart in simple ASD
RA enlargement
RV enlargement: filling in of retrosternal space; posterior displacement of the LV toward the spine

4. Uncomplicated ASD: Left-to-Right shunt
RV enlargement: increased opacification posterior to the sternum

5. Uncomplicated ASD: Left-to-Right shunt
enlargement of the cardiac silhouette
enlarged central and peripheral pulmonary arteries
normal- to small-sized aorta
absent SVC shadow- bec. of rotation of the heart from right-sided cardiac enlargement

6. Long Standing Shunt CXR findings:
lead to pulmonary arterial hypertension
Eisenmeger Physiology
when pulmonary arterial pressure exceeds systemic arterial pressure, reversal of shunting of blood from left-to-right to right-to-left occurs
CXR findings:
marked central pulmonary artery dilatation
narrowing of peripheral pulmonary artery branches
central pulmonary arteries become aneurysmal and rarely, be calcified

7. Long Standing Shunt (Eisenmeger Physiology)
enlargement of the right heart
absence of the SVC shadow
aneurysmal enlargement and calcification central pulmonary arteries

8. Pulmonary ARTERIAL Congestion vs. Pulmonary VENOUS Congestion

9. Pulmonary Arterial Congestion Pulmonary Venous Congestion
active congestion
-arteriolar dilation leads to increased blood flow
passive congestion
- dilation of veins and capillaries due to impaired venous outflow
Affected tissues turn red (erythema) because of the engorgement of vessels with oxygenated blood
tissues take on a dusky reddish-blue color (cyanosis) due to red cell stasis and the accumulation of deoxygenated hemoglobin

10. Pulmonary Arterial Hypertension
medial hypertrophy, eccentric and concentric intimal fibrosis, recanalized thrombi appearing as fibrous webs, and plexiform lesions
Abnormalities in molecular pathways regulating the pulmonary vascular endothelial and smooth-muscle cells
loss of apoptosis of the smooth-muscle cells allowing their proliferation
emergence of apoptosis-resistant endothelial cells which can obliterate the vascular lumen

11. Pulmonary Arterial Hypertension
three types of changes in the pulmonary arteries:
Muscular walls of the arteries may tighten up  narrower lumen
Walls may thicken as the amount of muscle increases in some arteries. Scar tissue may form in the walls of arteries. As the walls thicken and scar, the arteries become increasingly narrow.
Tiny blood clots may form within the smaller arteries, causing blockages

12. Pulmonary Venous Hypertension
occurs in the setting of elevated left sided filling pressure
often associated with diastolic dysfunction of the left ventricle; diseases affecting the pericardium or mitral or aortic valves; or rare entities such as cor triatriatum, left atrial myxoma, extrinsic compression of the central pulmonary veins from fibrosing mediastinitis, and pulmonary venoocclusive disease.
the degree of elevation in pulmonary artery pressure is concordant with the degree of elevation in left atrial pressure.

13. Pulmonary Venous Congestion
arterialization of the external elastic lamina, medial hypertrophy, and focal eccentric intimal fibrosis
Microcirculatory lesions: capillary congestion, focal alveolar edema, and dilatation of the interstitial lymphatics