Radiologic Diagnosis of Heart

Diseases

An Atlas of Cardiac X-rays

Part 2

Pulmonary vasculature

Dr. Khairy Abdel DayemProfessor of Cardiology

Ain Shams University

Radiologic Diagnosis of Heart

Diseases

An Atlas of Cardiac X-rays

Part 2

Pulmonary vasculature

Dr. Khairy Abdel DayemProfessor of Cardiology

Ain Shams University

Pulmonary vasculature The normal pulmonary vasculature

Pulmonary congestion

Pulmonary Plethora

Pulmonary Oligemia

Pulmonary embolism and Infarction

Pulmonary Hypertension

Pulmonary vasculature The normal pulmonary vasculature

Pulmonary congestion

Pulmonary Plethora

Pulmonary Oligemia

Pulmonary embolism and Infarction

Pulmonary Hypertension

Content

The Lung Fields The Normal Pulmonary Vasculature

The Lung Fields The Normal Pulmonary Vasculature

Characteristics of the Normal Pulmonary Vasculature

The normal pulmonary vessels include, (Fig. 11):

a) The pulmonary arterial tree starts at the hilum with the right

and left main pulmonary arteries. Each artery divides

repeatedly until very small terminal branches are seen in the

peripheral third of the lung fields.

b) The pulmonary veins drain the lung and end into four main

pulmonary veins that run alongside the arteries and open into

the left atrium.

Characteristics of the Normal Pulmonary Vasculature

The normal pulmonary vessels include, (Fig. 11):

a) The pulmonary arterial tree starts at the hilum with the right

and left main pulmonary arteries. Each artery divides

repeatedly until very small terminal branches are seen in the

peripheral third of the lung fields.

b) The pulmonary veins drain the lung and end into four main

pulmonary veins that run alongside the arteries and open into

the left atrium.

The pulmonary vessels to the lower lung fields are slightly larger

than those of the upper lung fields because gravity aids the flow of

blood the lower half of the lungs.

The pulmonary vessels to the lower lung fields are slightly larger

than those of the upper lung fields because gravity aids the flow of

blood the lower half of the lungs.

Fig. (11): Left: Normal distribution of pulmonary blood flow. Note that the vessels in the lower lung zone (3) are larger than those of the upper lung zone (1).Middle: Redistribution (inversion of flow) in case of pulmonary congestion.Right: Increased but balanced flow distribution (pulmonary plethora) resulting from left to right shunt

c-The major pulmonary arteries accompany the major

bronchi. When seen in cross section they are equal in size.

Abnormalities in the Pulmonary Vasculature

Four types of pathological changes in the pulmonary

vasculature must be recognized:

A. Pulmonary Congestion (Fig. 12):

When the venous return from the lungs is interfered with,

pulmonary congestion results. The pressure in the

pulmonary veins and capillaries rises and this pressure

elevation is passively transmitted to the pulmonary artery

raising its pressure. Its most common causes are:

Left ventricular failure

Mitral stenosis

Fig. (12): Left: vasoconstriction of the pulmonary arterioles supplying the lung bases in response to congestion (redistribution or cephalization of flow).Right: Radiological signs of pulmonary congestion: (1) hilar veiling, (2) small pleural effusions, (3) thickened transverse fissure, (4) Kerely’s B lines, (5) dilated upper lobe veins, (6) hemosiderosis.

Fig. (12): Left: vasoconstriction of the pulmonary arterioles supplying the lung bases in response to congestion (redistribution or cephalization of flow).Right: Radiological signs of pulmonary congestion: (1) hilar veiling, (2) small pleural effusions, (3) thickened transverse fissure, (4) Kerely’s B lines, (5) dilated upper lobe veins, (6) hemosiderosis.

The X-ray shows the following:

1. Pulmonary arteriolar vasoconstriction occurs early and starts

first in the lower lobes of the lungs because congestion is more

severe in the base. The vasoconstriction diverts blood from the

lower lobes to the upper lobes. The lower lungs zones become

more radiotranslucent in the X-ray relative to the upper zone. The

upper lobe veins dilate. This is called redistribution or

cephalisation of the pulmonary vasculature, (Fig. 12, 13 & 14).

2. Transudation of fluid in the interstitial septa between lung

lobules renders them thick. They become visible in the X-ray as

short transverse lines near the base (Kereley’s B lines).

3. Transudation of fluid around the bronchi causes a radio opaque

ring around the air filled bronchus. This is called bronchial

cuffing, (Fig. 15). Bronchi with thick congested walls may be

seen along their course as longitudinal lines running towards the

hilum (Kereley’s A lines).

The X-ray shows the following:

1. Pulmonary arteriolar vasoconstriction occurs early and starts

first in the lower lobes of the lungs because congestion is more

severe in the base. The vasoconstriction diverts blood from the

lower lobes to the upper lobes. The lower lungs zones become

more radiotranslucent in the X-ray relative to the upper zone. The

upper lobe veins dilate. This is called redistribution or

cephalisation of the pulmonary vasculature, (Fig. 12, 13 & 14).

2. Transudation of fluid in the interstitial septa between lung

lobules renders them thick. They become visible in the X-ray as

short transverse lines near the base (Kereley’s B lines).

3. Transudation of fluid around the bronchi causes a radio opaque

ring around the air filled bronchus. This is called bronchial

cuffing, (Fig. 15). Bronchi with thick congested walls may be

seen along their course as longitudinal lines running towards the

hilum (Kereley’s A lines).

Fig. (13): Pulmonary congestion: in a case mitral stenosis showing increased translucency of both lung bases with dilated upper pulmonary veins (A) Interstitial edema of the right hilum makes its components difficult to recognize individually. Kerley’s B lines are apparent in the right costophrenic angle.

Fig. (14): Pulmonary congestion in mitral valve disease showing: radiotransluscent bases and dilated pulmonary veins draining the upper lobe.

Fig. (15): Left: the wall of normal bronchus is invisible or very thin.Right: pulmonary congestion causing thickened bronchial wall (bronchial cuffing)

Fig. (15): Left: the wall of normal bronchus is invisible or very thin.Right: pulmonary congestion causing thickened bronchial wall (bronchial cuffing)

4. In extreme cases transudation of fluid occurs in the pulmonary

alveoli and round the main bronchi causing picture of acute

pulmonary edema which characteristically results in butterfly

opacities extending from the hila of both lung fields, (Fig. 16 & 17).

Fig (16): Pulmonary edema in an adult shown diagrammatically (left) and PA view of x-ray (right).

Fig. (17): Butterfly or bat-wing appearance of pulmonary edema in PA view in an infant.

5. Pleural effusion may be seen as obliteration of right or left costophrenic angles. Effusion may also fill the interlobar fissure (interlobar effusion). When it is absorbed it leaves a thickened transverse fissure (Fig. 18).

6. Multiple very small extravasations of red cells in the interstitial tissue of the lungs lead to collections of hemosiderin particles resulting in foreign body reaction. In the X-ray this is seen as miliary shadows in both lung fields (hemosiderosis) (Fig. 19).

5. Pleural effusion may be seen as obliteration of right or left costophrenic angles. Effusion may also fill the interlobar fissure (interlobar effusion). When it is absorbed it leaves a thickened transverse fissure (Fig. 18).

6. Multiple very small extravasations of red cells in the interstitial tissue of the lungs lead to collections of hemosiderin particles resulting in foreign body reaction. In the X-ray this is seen as miliary shadows in both lung fields (hemosiderosis) (Fig. 19).

Fig. (18): Case of mitral stenosis and pulmonary congestion showing small pleural

effusions in both costophrenic angles

Fig. (19): Mitral stenosis and pulmonary congestion showing miliary small

nodules of hemosiderosis

B. Pulmonary Oligemia:

The amount of blood flowing into the pulmonary vessels is

reduced in cases of:

Pulmonary stenosis

Pulmonary hypertension

Pulmonary embolism

Right ventricular failure

The X-ray signs consist of rapid or sudden narrowing (pruning)

of the peripheral branches of the pulmonary artery which become

very thin and invisible in the peripheral third of the lung fields.

The lungs become more radiotranslucent (Fig. 20). Pulmonary

oligemia may be accompanied by right ventricular enlargement

and right atrial dilatation, (Fig. 21).

Fig. (20): Valvular pulmonary stenosis showing pulmonary oligemia and poststenotic dilatation of the pulmonary artery

Fig. (21): Pulmonary Oligemia: No vascular markings can be recognized in the peripheral two thirds of the lung fields. The right

ventricle and the atrium are dilated

C. Pulmonary Plethora:

Increased arterial blood flowing in the lungs is called plethora.

The pulmonary vessels dilate to accommodate the excessive flow.

When the flow exceeds twice the normal the pulmonary blood

pressure starts to rise because of overfilling.

Pulmonary plethora always results from shunt of blood from the

arterial to the venous side of the circulation as in cases of:

Atrial septal defect

Ventricular septal defect

Patent ductus arteriosus

C. Pulmonary Plethora:

Increased arterial blood flowing in the lungs is called plethora.

The pulmonary vessels dilate to accommodate the excessive flow.

When the flow exceeds twice the normal the pulmonary blood

pressure starts to rise because of overfilling.

Pulmonary plethora always results from shunt of blood from the

arterial to the venous side of the circulation as in cases of:

Atrial septal defect

Ventricular septal defect

Patent ductus arteriosus

X-ray Picture:

1. The main pulmonary artery and its branches in the hilum are

enlarged.

2. The peripheral pulmonary arteries are larger than normal and

are well seen in the outer third of lung field. When seen in cross

section the pulmonary artery is larger than accompanying

bronchus, (Fig. 22 & 23).

Fig. (22): Pulmonary plethora in a case of ventricular septal defect. A catheter was introduced from an arm vein to the superior vena cava then to the right ventricle and through the defect to the left ventricle and aorta. The pulmonary arteries are over-filled.

Fig. (23): 3 degrees of severity of pulmonary plethora: mild (a), moderate (b) and severe (c).

D. Pulmonary Embolism:

Small pulmonary emboli produce no pathological effects apart

from obstruction of small arteries in the lungs. Moderately large

emboli may produce pulmonary infarction that occurs only in 10%

of cases because the lungs have double blood supply from both

the pulmonary artery and the bronchial arteries. Massive

pulmonary embolism may obstruct one or both of the main

pulmonary arteries (Fig. 24).

D. Pulmonary Embolism:

Small pulmonary emboli produce no pathological effects apart

from obstruction of small arteries in the lungs. Moderately large

emboli may produce pulmonary infarction that occurs only in 10%

of cases because the lungs have double blood supply from both

the pulmonary artery and the bronchial arteries. Massive

pulmonary embolism may obstruct one or both of the main

pulmonary arteries (Fig. 24).

Fig. (24): Effects of pulmonary emboli of different sizes: (1) single very small embolus, (2) bigger emboli cause pulmonary infarction, (3) massive embolus obstructing the main pulmonary artery and its branches, (4) repeated pulmonary emboli cause right ventricular hypertrophy

Fig. (24): Effects of pulmonary emboli of different sizes: (1) single very small embolus, (2) bigger emboli cause pulmonary infarction, (3) massive embolus obstructing the main pulmonary artery and its branches, (4) repeated pulmonary emboli cause right ventricular hypertrophy

The radiologic signs depend on the pathologic effects of the embolism, Fig. (24):

a. There may be no radiologic signs in cases of small emboli.

b. Large emboli may cause abrupt cut-off or sudden tapering of one pulmonary artery associated with radiotranslucency in the corresponding lung zone due to absent or decreased blood flow (Westermark’s Sign).

c. Signs of pulmonary infarction are:

i. The infarcted area is seen in the X-ray either as a triangular radio-opaque shadow with its base towards the chest wall and its apex at the site of the embolus or as “Hampton’s Hump”: a homogenous, wedge-shaped density in the peripheral field, convex to the hilum, Fig. (25).

ii. The copula of the diaphragm is high on the side of infarction.

iii. There may be a small pleural effusion.

iv. After healing, fibrosed and contracted infarction may show as a linear opacity.

d. Signs of pulmonary hypertension and right ventricular enlargement.

Fig. (25): Case of Pulmonary embolism causing pulmonary infarction. Hampton’s Hump is seen in the lower zone of the right lung. The right copula or

the diaphragm is elevated and the right atrium is dilated

Fig. (25): Case of Pulmonary embolism causing pulmonary infarction. Hampton’s Hump is seen in the lower zone of the right lung. The right copula or

the diaphragm is elevated and the right atrium is dilated

E. Pulmonary Hypertension: The basic mechanism of pulmonary hypertension is increased

pulmonary vascular resistance. This can be due to one of the two

main causes:

1. Pulmonary arteriolor vasoconstriction which occurs most

commonly as a response to longstanding pulmonary venous

congestion or to increased pulmonary arterial flow (pulmonary

plethora).

2. Organic obliteration or destruction of pulmonary arterioles

causing obstruction to blood flow. This may be:

a. Primary (primary pulmonary hypertension), or

b. Due to lung disease as extensive fibrosis or emphysema

(chronic obstructive pulmonary disease), or

c. Obliteration of pulmonary vessels by clots or emboli

(thromboembolic pulmonary hypertension) or bilharzia ova.

E. Pulmonary Hypertension: The basic mechanism of pulmonary hypertension is increased

pulmonary vascular resistance. This can be due to one of the two

main causes:

1. Pulmonary arteriolor vasoconstriction which occurs most

commonly as a response to longstanding pulmonary venous

congestion or to increased pulmonary arterial flow (pulmonary

plethora).

2. Organic obliteration or destruction of pulmonary arterioles

causing obstruction to blood flow. This may be:

a. Primary (primary pulmonary hypertension), or

b. Due to lung disease as extensive fibrosis or emphysema

(chronic obstructive pulmonary disease), or

c. Obliteration of pulmonary vessels by clots or emboli

(thromboembolic pulmonary hypertension) or bilharzia ova.

The X-ray may show the following, (Fig. 26):

1. Signs of pulmonary vasoconstriction and pulmonary

oligemia. These consist of narrowing of the peripheral

branches of the pulmonary artery which become very thin

or even invisible in the peripheral third of the lung fields.

The lungs become more radiotranslucent.

2. Dilatation of the main pulmonary artery and of its proximal

branches. The dilated main pulmonary artery is seen as a

prominence of the left border of the heart at the medial end

of the second left intercostal space anteriorly. Its main

branches are seen dilated in the hila.

3. Signs of right ventricular hypertrophy.

4. Right atrial dilatation causes outwards displacement of the

right border of the heart.

The X-ray may show the following, (Fig. 26):

1. Signs of pulmonary vasoconstriction and pulmonary

oligemia. These consist of narrowing of the peripheral

branches of the pulmonary artery which become very thin

or even invisible in the peripheral third of the lung fields.

The lungs become more radiotranslucent.

2. Dilatation of the main pulmonary artery and of its proximal

branches. The dilated main pulmonary artery is seen as a

prominence of the left border of the heart at the medial end

of the second left intercostal space anteriorly. Its main

branches are seen dilated in the hila.

3. Signs of right ventricular hypertrophy.

4. Right atrial dilatation causes outwards displacement of the

right border of the heart.

Fig. (26): Two cases of aneurysmal dilatation of the main pulmonary artery and its right branch and pulmonary oligemia in

bilharzial pulmonary hypertension