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

Uncomplicated ASD: Left-to-Right shunt

• enlargement of central and all segments of pulmonary arteries

• increased pulmonary vascularity, prominent hilar markings

“shunt vascularity”

• RA enlargement• RV enlargement: filling in of retrosternal space;

posterior displacement of the LV toward the spine

Uncomplicated ASD: Left-to-Right shunt

• RV enlargement: increased

opacification posterior to the

sternum

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

Uncomplicated ASD: Left-to-Right shunt

Long Standing Shunt• 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

Long Standing Shunt (Eisenmeger Physiology)

• enlargement of the right heart• absence of the SVC shadow�• aneurysmal enlargement and calcification central

pulmonary arteries

Pulmonary ARTERIAL Congestionvs.

Pulmonary VENOUS Congestion

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

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

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

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.

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