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Pulmonary vascular diseases

Dr Mohammed Bader .
Pulmonary oedema
Pulmonary edema is the term used to indicate an abnormal accumulation of fluid in the extravascular pulmonary tissues. There is a constant flow of fluid and proteins from the microvascular spaces (arterioles, capillaries, and venules) in the lung into the interstitial space. The interstitial space includes the alveolar wall interstitium and the interlobular, perivascular, peribronchial, and subpleural connective tissue spaces.
The pulmonary lymphatic vessels begin in loose connective tissue spaces proximal to but not in the alveoli.
(1) Pleural—common over the lower lobes
(2) Interlobular—arise at the periphery of the acinus (not in the alveolar walls) and extend in the septa to join with the veins
(3) the perivenous group, which extend to the hilum.
(4) Peribronchial—arise at the junctions of the alveolar septa and accompany the pulmonary arteries
(5) Anastomotic—run in the deep interlobular septa.
The pulmonary lymphatics carry the excess microvascular filtrate into the systemic venous system. When the capacity of the lymphatics is exceeded, edema results

The major causes of pulmonary edema

I.Hemodynamic pulmonary edema (elevated capillary hydrostatic pressure)
Left heart failure, mitral diseases , and LT atrial tumours
2. Pulmonary venous obstruction.
II.Permeability pulmonary edema
1. Narcotic overdose ?,smoke and chemical fume inhalation
3. rapid re expansion lung, and high attitude
III.Combined hemodynamic and permeability edema
1. Shock lung, including septic shock
2. Adult respiratory distress syndrome (ARDS)—a variety of causes
IV. Lymphatic obstruction edem
V. Renal failure oedema
VI. Edema of unknown origin
Radiological features of interstitia oedema
1.Perivascular blurring or cuffing
2.Peribronchial blurring or cuffing with loss of clear definition of the outer bronchial wall
3. “Hilar haze”—a loss of definition of large central pulmonary vessels with a slight general increase in opacity


4. Appearance of septal lines
a. Kerley B lines are dense, horizontal lines that measure about 1.5 to 2.0 cm in length. They represent secondary interlobular septa thickened by fluid
b .Kerley A lines are longer and range in length from 5 to 10 cm. They tend to be straight extend from the hila or parahilar area toward the periphery. They are seen in the upper lobes and tend to appear in acute interstitial edema. They represent fluid in the secondary interlobular septa, chiefly in the upper lobes
5. A diffuse, reticular pattern may be observed
Subpleural edema may be observed best adjacent to the minor fissure on the right
ALVEOLAR EDEMA
-bilateral opacities that extend outward in a fan-shaped manner from the hilum on both sides .
-The peripheral lungs are relatively clear. This includes the bases as well as the apices except in congestive failure, in which basal congestive changes and edema produce changes there.
-air bronchogram :the fluid-filled alveoli surrounding the bronchi produce contrast with the air-containing bronchi
-Usually bilateral but some reported cases unilateral oedema is seen
-upper-lobe blood diversion
In 50% of patients with cardiogenic oedema there was upper-lobe blood diversion; in the remaining 50%, however, a ‘normal’ (lower zones > upper zones) or ‘balanced’ (lower zone = upper zone) pattern were noted. In patients with increased permeability oedema due to the acute respiratory distress syndrome (ARDS), only 10% showed an inverted pattern; normal or balanced flow were more commonly seen. A peripheral distribution of oedema was strikingly absent in patients with cardiogenic oedema but, in contrast, it was the commonest pattern seen in ARDS. Based on these findings and some ancillary features, the authors claimed an overall accuracy for chest radiography of 86–89%[44] .
. Clearly, analysis of the radiographic pattern may sometimes allow a distinction to be made but the inconsistency of the radiographic signs suggests that differentiation between the various forms of pulmonary oedema, on radiographic features alone, is unreliable.
PULMONARY INFARCTION
the roentgen signs are (1) elevation of the hemidiaphragm on the involved side, indicating decrease in lung volume; (2) unilateral pleural effusion, usually small; (3) pulmonary parenchymal consolidation; (4) atelectasis; and (5) linear shadows. An infarct must be differentiated from pneumonia, edema, and atelectasis as well as other local conditions, including infected cysts and abscesses.
The lower lobes are most frequently involved, but the lesion can occur in any lobe.
EMBOLISM WITHOUT INFARCTION
Pulmonary embolism with out infarction can be massive and life-threatening and is more common than embolism with infarction.
findings are often absent
The central pulmonary arteries may be increased in size. The descending branch of the right pulmonary artery, measured at total lung capacity from the level of the bronchus intermedius to its outer border, is a maximum of 16 mm in adult men and 15 mm in adult women. Any measurement greater than these suggests the possibility of embolism. This finding is particularly useful when there is a change??
Occasionally a small pleural effusion may be present
PULMONARY HYPERTENSION
Pulmonary hypertension may be predominantly arterial (precapillary) or venous (postcapillary), or it may represent a combination of the two.
I.Precapillary (arterial) hypertension )
A.Increased resistance
1. Obstructive—pulmonary embolism, idiopathic or primary pulmonary hypertension, pulmonary schistosomiasis, reverse shunts (ventricular septal defect, atrial septal defect, or patent ductus arteriosus)
2. Obliterative—pulmonary emphysema, diffuse interstitial diseases (granulomatous, neoplastic, or infectious)
3. Constrictive—anoxia
B. Increased flow
1. Large left-to-right shunts—patent ductus arteriosus, ventricular septal defec
II. Postcapillary (venous) hypertension
A. Acute—Left ventricular failure regardless of cause
B. Chronic—Mitral valvular disease, left atrial myxoma, anomalous pulmonary venous return, mediastinal fibrosis, idiopathic or primary veno-obstructive disease
III.Combined precapillary and postcapillary hypertensi


Arterial (Precapillary) Hypertension
dilatation of the pulmonary artery and its central branches on either side and narrowing of the peripheral pulmonary arteries
The lungs are relatively clear unless the underlying pulmonary disease has produced considerable change.
The heart may show alteration consistent with the initial defect. However, eventually the right ventricle may enlarge to become the predominant chamber (cor pulmonale).

Venous (Postcapillary) Hypertension

often accompanied by changes that cause a considerable increase in pulmonary density (e.g., edema)
constriction of the pulmonary arteries and veins in the lower zones and dilatation of the arteries and veins in the upper zones caused by redistribution of blood flow to the upper lobes are the most reliable early signsAs the venous pressure increases, additional findings of early interstitial edema can be observed; they include the appearance of Kerley B lines and Kerley A lines. A slight perihilar haze may be evident
vasculitis
The vasculitides are a group of clinically diverse conditions charac. by
involvement of blood vessels in an inflammatory, occlusive and often destructive process.
Wegener's granulomatosis is characterized by necrotizing vasculitis and granulomatous inflammation which affects primarily the upper and lower respiratory tracts and kidneys
Radiological finding of vasculitis
widely distributed multiple irregular masses / nodules of varying sizes (up to 9 cm), especially in lower lung fields
thick-walled cavities with irregular shaggy inner lining (25-50%)
pleural effusion in 25%
lymphadenopathy exceedingly rare
C Carcinoma
A Auto-Immune (Wegener’s,
Rheumatoid nodules)
V Vascular (Pulmonary emboli and
septic emboli)
I Infection (especially tuberculosis,
f ungal, staphlococcal)
T Trauma (pneumatocele)
Y Young = congenital
Differential diagnosis of nodular lung disease
-Neoplasm Metastases
-Malignant lymphoma
-Inflammatory Granulomas
-Fungal infection
-Rheumatoid nodules
-Vasculitis
-Langerhan’s cell histiocytosis
-Congenital Arterio-venous malformation
-Miscellaneous Haematoma
-Pulmonary infarcts
-Occupa



رفعت المحاضرة من قبل: عادل احمد هلال الجميلي
المشاهدات: لقد قام 16 عضواً و 132 زائراً بقراءة هذه المحاضرة








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